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Textbook of Surgery
Textbook of
Surgery
EDITED BY
Julian A. Smith
MBBS, MS, MSurgEd, FRACS, FACS, FFSTRCSEd, FCSANZ, FAICD
Head, Department of Surgery (School of Clinical Sciences at Monash Health), Monash University
Head, Department of Cardiothoracic Surgery, Monash Health
Editor‐in‐Chief, ANZ Journal of Surgery
Andrew H. Kaye AM
MBBS, MD, FRACS
Head, Department of Surgery, The University of Melbourne
Christopher Christophi AM
MBBS (Hons), MD, FRACS, FRCS, FACS
Head of Surgery (Austin Health), The University of Melbourne
Wendy A. Brown
MBBS (Hons), PhD, FRACS, FACS
Head, Department of Surgery (Central Clinical School, Alfred Health), Monash University
Director, Centre for Obesity Research and Education (CORE), Monash University
FOURTH EDITION
This edition first published 2020 © 2020 by John Wiley & Sons Ltd
Edition History
1e (1997); 2e (2001); 3e (2006) Blackwell Publishing Ltd.
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Library of Congress Cataloging‐in‐Publication Data
Names: Smith, Julian A., editor. | Kaye, Andrew H., 1950– editor.
Title: Textbook of surgery / edited by Julian A. Smith, MBBS, MS, MSurgEd, FRACS, FACS, FFSTRCSEd, FCSANZ,
FAICD Head, Department of Surgery (School of Clinical Sciences at Monash Health), Monash University, Head,
Department of Cardiothoracic Surgery, Monash Health, Editor-in-Chief, ANZ Journal of Surgery, Andrew H. Kaye,
AM, MBBS, MD, FRACS, Head, Department of Surgery, The University of Melbourne, Christopher Christophi, AM,
MBBS (Hons), MD, FRACS, FRCS, FACS, Head of Surgery (Austin Health), The University of Melbourne, Wendy A.
Brown, MBBS (Hons), PhD, FRACS, FACS, Head, Department of Surgery (Central Clinical School, Alfred Health),
Monash University Director, Centre for Obesity Research and Education (CORE), Monash University.
Other titles: Surgery
Description: Fourth edition. | Hoboken, NJ : Wiley-Blackwell, 2020. | Includes bibliographical references and index.
Identifiers: LCCN 2019030070 (print) | LCCN 2019030071 (ebook) | ISBN 9781119468080 (paperback) |
ISBN 9781119468172 (adobe pdf) | ISBN 9781119468165 (epub)
Subjects: LCSH: Surgery.
Classification: LCC RD31 .T472 2020 (print) | LCC RD31 (ebook) | DDC 617–dc23
LC record available at https://lccn.loc.gov/2019030070
LC ebook record available at https://lccn.loc.gov/2019030071
Cover image: © gchutka/Getty Images
Cover design by Wiley
Set in 9/11.5pt Sabon by SPi Global, Pondicherry, India
10 9 8 7 6 5 4 3 2 1
Contents
Contributors, viii 16 Peptic ulcer disease, 133

Preface, xiii Paul A. Cashin and S.C. Sydney Chung
Acknowledgements, xiv 17 Gastric neoplasms, 143
John Spillane
Section 1 Principles of Surgery 18 Obesity and bariatric surgery, 151
1 Preoperative management, 3 Yazmin Johari and Wendy A. Brown
Julian A. Smith
2 Assessment of surgical risk, 13 Section 3 Hepatopancreaticobiliary Surgery
Benjamin N.J. Thomson 19 Gallstones, 163
Arthur J. Richardson
3 Anaesthesia and pain medicine, 19
David Story 20 Malignant diseases of the hepatobiliary
system, 173
4 Postoperative management, 25
Thomas J. Hugh and Nigel B. Jamieson
Peter Devitt
21 Liver infections, 191
5 Surgical techniques, 35
Vijayaragavan Muralidharan, Marcos V. Perini
Benjamin N.J. Thomson and David M.A. Francis
and Christopher Christophi
6 Management of surgical wounds, 45
22 Pancreatitis, 199
Rodney T. Judson
Peter S. Russell and John A. Windsor
7 Nutrition and the surgical patient, 49
23 Pancreatic tumours, 209
William R.G. Perry and Andrew G. Hill
David Burnett and Mehrdad Nikfarjam
8 Care of the critically ill patient, 57
24 Portal hypertension and surgery on the patient
Jeffrey J. Presneill, Christopher MacIsaac
with cirrhosis, 219
and John F. Cade
Michael A. Fink
9 Surgical infection, 65
Marcos V. Perini and Vijayaragavan Section 4 Lower Gastrointestinal Surgery
Muralidharan 25 Principles of colorectal and small bowel
10 Transplantation surgery, 75 surgery, 229
Michael A. Fink Ian Hayes
11 Principles of surgical oncology, 87 26 Physiology of small and large bowel: alterations
G. Bruce Mann and Robert J.S. Thomas due to surgery and disease, 237
12 Introduction to the operating theatre, 93 Jacob McCormick and Ian Hayes
Andrew Danks, Alan C. Saunder 27 Small bowel obstruction and ischaemia, 243
and Julian A. Smith Ian Hayes and the late Joe J. Tjandra
13 Emergency general surgery, 109 28 The appendix and Meckel’s diverticulum, 249
Benjamin N.J. Thomson and Rose Shakerian Rose Shakerian and the late Joe J. Tjandra
29 Inflammatory bowel disease, 255
Section 2 Upper Gastrointestinal Surgery Susan Shedda, Brit Christensen and
14 Gastro‐oesophageal reflux disease and hiatus the late Joe J. Tjandra
hernias, 115 30 Diverticular disease of the colon, 267
Paul Burton and Geraldine J. Ooi Ian Hastie and the late Joe J. Tjandra
15 Tumours of the oesophagus, 123 31 Colorectal cancer, 273
Ahmad Aly and Jonathan Foo Ian T. Jones and the late Joe J. Tjandra
v
vi Contents
32 Large bowel obstruction, 285 Section 11 Orthopaedic Surgery

Raaj Chandra 50 Fractures and dislocations, 457
33 Perianal disorders I: excluding sepsis, 293 Peter F. Choong
Ian Hayes and Susan Shedda 51 Diseases of bone and joints, 465
34 Perianal disorders II: sepsis, 301 Peter F. Choong
Ian Hayes and the late Joe J. Tjandra
Section 12 Neurosurgery
Section 5 Breast Surgery 52 Head injuries, 483
35 Breast assessment and benign breast Andrew H. Kaye
disease, 309 53 Intracranial tumours, infection and
Rajiv V. Dave and G. Bruce Mann aneurysms, 493
36 Malignant breast disease and surgery, 317 Andrew H. Kaye
Rajiv V. Dave and G. Bruce Mann 54 Nerve injuries, peripheral nerve entrapments
and spinal cord compression, 511
Section 6 Endocrine Surgery Andrew H. Kaye
37 Thyroid, 331
Jonathan Serpell Section 13 Vascular Surgery
38 Parathyroid, 339 55 Disorders of the arterial system, 527
Jonathan Serpell Raffi Qasabian and Gurfateh
39 Tumours of the adrenal gland, 345 Singh Sandhu
Jonathan Serpell 56 Extracranial vascular disease, 537
Raffi Qasabian and Gurfateh Singh Sandhu
Section 7 Head and Neck Surgery 57 Venous and lymphatic diseases
40 Eye injuries and infections, 353 of the limbs, 545
Helen V. Danesh‐Meyer Hani Saeed and Michael J. Grigg
41 Otorhinolaryngology, 359 58 Endovascular therapies, 553
Stephen O’Leary and Neil Vallance Timothy Buckenham
42 Tumours of the head and neck, 369
Rodney T. Judson Section 14 Urology
59 Benign urological conditions, 565
Section 8 Hernias Anthony J. Costello, Daniel M. Costello and
43 Hernias, 381 Fairleigh Reeves
Roger Berry and David M.A. Francis 60 Genitourinary oncology, 577

Homayoun Zargar and Anthony J. Costello

Section 9 Skin and Soft Tissues
44 Tumours and cysts of the skin, 397 Section 15 Cardiothoracic Surgery
Rodney T. Judson 61 Principles and practice of cardiac surgery, 587
45 Soft tissue tumours, 403 James Tatoulis and Julian A. Smith
Peter F. Choong 62 Common topics in thoracic surgery, 603
46 Infection of the extremities, 415 Julian A. Smith
Mark W. Ashton and David M.A. Francis
47 Principles of plastic surgery, 423 Section 16 Problem Solving
Mark W. Ashton 63 Chronic constipation, 617
Kurvi Patwala and Peter De Cruz
Section 10 Trauma 64 Faecal incontinence, 625
48 Principles of trauma management, 431 Andrew Bui
Scott K. D’Amours, Stephen A. Deane and 65 Rectal bleeding, 633
Valerie B. Malka Adele Burgess
49 Burns, 443

66 Haematemesis and melaena, 637
Ioana Tichil and Heather Cleland Wendy A. Brown
Contents vii
67 Obstructive jaundice, 643 76 Massive haemoptysis, 707

Frederick Huynh and Val Usatoff Julian A. Smith
68 The acute abdomen, peritonitis and

77 Epistaxis, 711
intra‐abdominal abscesses, 649 Robert J.S. Briggs
Paul Cashin, Michael Levitt and 78 Low back and leg pain, 715
the late Joe J. Tjandra Jin W. Tee and Jeffrey V. Rosenfeld
69 Ascites, 659 79 Acute scrotal pain, 727

David A.K. Watters, Sonal Nagra and Anthony Dat and Shomik Sengupta
David M.A. Francis 80 Post‐traumatic confusion, 735
70 Neck swellings, 667

John Laidlaw
Rodney T. Judson 81 Sudden‐onset severe headache, 745
71 Acute airway problems, 675 Alexios A. Adamides
Stephen O’Leary 82 The red eye, 749
72 Dysphagia, 679 Christine Chen
Wendy A. Brown 83 Double vision, 757
73 Leg swelling and ulcers, 685 Christine Chen
Alan C. Saunder, Steven T.F. Chan and
David M.A. Francis Answers to MCQs, 763
74 Haematuria, 693 Index, 767
Kenny Rao and Shomik Sengupta
75 Postoperative complications, 699

Peter Devitt
Contributors
Alexios A. Adamides Andrew Bui

BMedSci, BMBS, MRCS (Edin), MD, FRACS MBBS, MSc, FRACS
Clinical Senior Lecturer, University of Melbourne Lecturer in Surgery, University of Melbourne
Neurosurgeon, Royal Melbourne Hospital Colorectal Surgeon, Austin Health
Melbourne, Victoria, Australia Melbourne, Victoria, Australia
Ahmad Aly Adele Burgess

MBBS, MS, FRACS BMedSci (Hons), MBBS, FRACS
Clinical Associate Professor of Surgery, University of Senior Lecturer in Surgery, University of Melbourne
Melbourne Head, Colorectal Surgery, Austin Health
Head, Upper Gastrointestinal Surgery, Austin Health Melbourne, Victoria, Australia
Melbourne, Victoria, Australia
David Burnett
Mark W. Ashton BSc, MBBS, FRACS
MBBS, MD, FRACS Hepatopancreaticobiliary Surgeon
Clinical Professor of Surgery, University of Melbourne John Hunter Hospital
Plastic Surgeon, Royal Melbourne Hospital Newcastle, New South Wales, Australia
Paul Burton
MBBS(Hons), PhD, FRACS
Roger Berry
Senior Lecturer in Surgery, Monash University
MBBS, FRACS
Upper Gastrointestinal Surgeon, Alfred Health
Upper Gastrointestinal and Hepatobiliary Surgeon,
Monash Health
Melbourne, Victoria, Australia John F. Cade AM
MD, PhD, FRACP, FANZCA, FCICM
Professorial Fellow, Department of Medicine, University
Robert J.S. Briggs of Melbourne
MBBS, FRACS, FACS Emeritus Consultant in Intensive Care, Royal Melbourne
Clinical Professor of Surgery, University of Melbourne Hospital
Clinical Executive Director of Otolaryngology; Head, Melbourne, Victoria, Australia
Otology and Medical Director, Cochlear Implant Clinic,
Royal Victorian Eye and Ear Hospital Paul A. Cashin
Melbourne, Victoria, Australia MBBS, FRACS
Clinical Associate Professor of Surgery, Monash
Wendy A. Brown University
MBBS (Hons), PhD, FRACS, FACS Director of General Surgery, Monash Health
Head, Department of Surgery (Central Clinical School, Melbourne, Victoria, Australia
Alfred Health), Monash University
Director, Centre for Obesity Research and Education Steven T.F. Chan
(CORE), Monash University MBBS, PhD, FRACS
Melbourne, Victoria, Australia Professor of Surgery, University of Melbourne
Upper Gastrointestinal Surgeon, Western Health
Timothy Buckenham Melbourne, Victoria, Australia
MBChB, FRANZCR, FRCR, FCIRSE, EBIR
Professor of Vascular Imaging and Intervention, Monash Raaj Chandra
University MBBS, BMed Sci, MEd, FRACS
Head, Vascular Services, Department of Imaging, Adjunct Senior Lecturer in Surgery, Monash University
Monash Health Colorectal Surgeon, Royal Melbourne Hospital
viii
Contributors ix
Christine Chen Andrew Danks

MBBS, PhD, FRANZCO MBBS, MD, FRACS
Clinical Associate Professor of Surgery, Monash University Associate Professor of Surgery, Monash University
Head, Department of Ophthalmology, Monash Health Head, Department of Neurosurgery, Monash Health
Peter F. Choong Anthony Dat

MBBS, MD, FRACS, FAOrthA, FAAHMS MBBS, MS
Professor of Surgery, University of Melbourne Urology Registrar, Eastern Health
Director of Orthopaedics, St. Vincent’s Hospital Melbourne, Victoria, Australia
Chair, Bone and Soft Tissue Sarcoma Service
Peter MacCallum Cancer Centre Rajiv V. Dave
Melbourne, Victoria, Australia MBChB, FRCSEd, MD, BSc(Hons)
Fellow in Oncoplastic Breast and Endocrine Surgery,
Britt Christensen Royal Melbourne Hospital
BSc, MBBS(Hons), MPH, FRACP Melbourne, Victoria, Australia
Head, Inflammatory Bowel Disease Unit, Department of The Nightingale Centre, Manchester University NHS
Gastroenterology, Royal Melbourne Hospital Foundation Trust
Melbourne, Victoria, Australia Manchester, UK
Christopher Christophi AM Stephen A. Deane AM

MBBS, FRACS, FACS, FRCSC, FRCSEd (ad hom),
MBBS (Hons), MD, FRACS, FRCS, FACS
FRCSThailand (Hon)
Head of Surgery (Austin Health), University of
Associate Dean, Clinical Partnerships, Macquarie
Melbourne
University, Sydney
Conjoint Professor of Surgery, University of Newcastle
Honorary Consultant Surgeon, Hunter and New
S.C. Sydney Chung
England Local Health District
MD, FRCS (Edin), FRCP (Edin)
New South Wales, Australia
Formerly Dean, Faculty of Medicine, Chinese University
of Hong Kong Peter De Cruz
Senior Consultant in Surgery, Union Hospital MBBS, PhD, FRACP
Hong Kong Senior Lecturer in Medicine, University of Melbourne
Gastroenterologist and Director, Inflammatory Bowel
Heather Cleland Disease Service, Austin Health
MBBS, FRACS Melbourne, Victoria, Australia
Director, Victorian Adult Burns Service and Plastic
Surgeon, Alfred Health Peter Devitt
Melbourne, Victoria, Australia MBBS, MS, FRCS, FRACS
Associate Professor of Surgery, University of Adelaide
Anthony J. Costello AM General and Upper Gastrointestinal Surgeon, Royal
MBBS, MD, FRACS, FRCSI (Hon) Adelaide Hospital
Professorial Fellow, University of Melbourne Adelaide, South Australia, Australia
Head, Department of Urology, Royal Melbourne Hospital
Melbourne, Victoria, Australia Michael A. Fink
MBBS, MD, FRACS
Daniel M. Costello Senior Lecturer in Surgery, University of Melbourne
MBBS, DipSurgAnat Hepatopancreatobiliary and Liver Transplant Surgeon,
Surgical Resident, St. Vincent’s Hospital Austin Health
Scott K. D’Amours Jonathan Foo

BSc, MDCM, FRCSC, FRACS, FRCS(Glasg), FACS MBChB, DipGrad(Arts), PhD, FRACS
Conjoint Senior Lecturer in Surgery, University of New Upper Gastrointestinal Surgery Fellow, Austin Health
South Wales Melbourne, Victoria, Australia
Director, Department of Trauma Services, Liverpool
Hospital David M.A. Francis
Sydney, New South Wales, Australia BSc (Med Sci), MS, MD, PhD (Arts), FRCS (Eng), FRCS
(Edin), FRACS
Helen V. Danesh‐Meyer Renal Transplant Surgeon, Department of Urology, Royal
MBChB, MD, PhD, FRANZCO Children’s Hospital, Melbourne, Victoria, Australia
Professor of Ophthalmology, School of Medicine, Visiting Professor of Surgery and Renal Transplant
University of Auckland Surgeon, Department of Surgery, Tribhuvan University
Auckland, New Zealand Teaching Hospital, Kathmandu, Nepal
x Contributors
Michael J. Grigg Andrew H. Kaye AM

AM, MBBS, FRACS MBBS, MD, FRACS
Professor of Surgery, Monash University Head, Department of Surgery, University of Melbourne
Director of Surgery, Eastern Health Neurosurgeon, Royal Melbourne Hospital
Ian Hastie John Laidlaw

MBBS, FRACS MBBS, FRACS
Senior Lecturer in Surgery, University of Melbourne Clinical Associate Professor of Surgery, University of
Colorectal Surgeon, Royal Melbourne Hospital Melbourne
Melbourne, Victoria, Australia Neurosurgeon, Royal Melbourne Hospital
Ian Hayes
MBBS, MS, MEpi, FRCS(Gen Surg), FRACS Michael Levitt
Clinical Associate Professor of Surgery, University of MBBS, FRACS
Melbourne Colorectal Surgeon, St. John of God Healthcare, Subiaco
Head, Colorectal Surgery Unit, Royal Melbourne Perth, Western Australia, Australia
Hospital
Melbourne, Victoria, Australia Jacob McCormick
BMedSci, MBBS, FRACS
Andrew G. Hill Colorectal Surgeon, Royal Melbourne Hospital and Peter
MBChB, MD, EdD, FRACS, FACS MacCallum Cancer Centre
Professor of Surgery, University of Auckland Melbourne, Victoria, Australia
Colorectal Surgeon, Middlemore Hospital
Auckland, New Zealand Christopher MacIsaac
MBBS (Hons), PhD, FRACP, FCICM
Thomas J. Hugh Associate Professor in Medicine
MD, FRACS Director, Intensive Care Unit, Royal Melbourne Hospital
Professor of Surgery, University of Sydney Melbourne, Victoria, Australia
Head, Upper Gastrointestinal Surgery Unit, Royal North
Shore Hospital Valerie B. Malka
Sydney, New South Wales, Australia MBBS, FRACS, MIPH, MA
Senior Lecturer in Surgery, University of New South Wales
Frederick Huynh General and Trauma Surgeon, Deputy Director of
BSc(Hons), MBBS(Hons), FRACS Trauma, Liverpool Hospital
ANZHPBA Fellow, Alfred Health Sydney, New South Wales, Australia
G. Bruce Mann
Nigel B. Jamieson MBBS, PhD, FRACS
MBChB, BSc(Hons), FRCS, PhD Professor of Surgery, University of Melbourne
Lecturer in Surgery and Cancer Research UK Clinician Director of Breast Tumour Stream, Victorian
Scientist, University of Glasgow Comprehensive Cancer Centre
Honorary Consultant in HPB Surgery, Glasgow Royal Melbourne, Victoria, Australia
Infirmary
Glasgow, UK Vijayaragavan Muralidharan
BMedSci, MBBS (Hons), MSurgEd, PhD, FRACS
Yazmin Johari Associate Professor of Surgery, University of Melbourne
MBBS(Hons) Hepatopancreatobiliary Surgeon, Austin Health
General Surgery Registrar, Alfred Health Melbourne, Victoria, Australia
Sonal Nagra
Ian T. Jones MBBS, MMed(Surg), FRACS
MBBS, FRCS, FRACS, FASCRS Senior Lecturer in Rural General Surgery
Clinical Professor of Surgery, University of Melbourne Deakin University
Colorectal Surgeon, Royal Melbourne Hospital Consultant Surgeon, University Hospital Geelong
Melbourne, Victoria, Australia Geelong, Victoria, Australia
Rodney T. Judson Mehrdad Nikfarjam

MBBS, FRACS, FRCS MD, PhD, FRACS
Associate Professor of Surgery, University of Melbourne Associate Professor of Surgery, University of Melbourne
Head of Trauma Service, Royal Melbourne Hospital Hepatopancreatobiliary Surgeon, Austin Health
Contributors xi
Stephen O’Leary Jeffrey V. Rosenfeld AC, OBE

MBBS, BMedSci, PhD, FRACS MBBS, MS, MD, FRACS, FRCS(Ed), FACS, IFAANS,
Professor of Otolaryngology, University of Melbourne FRCS (Glasg, Hon), FCNST(Hon), FRCST(Hon),
Ear, Nose and Throat Surgeon, Royal Victorian Eye and FACTM, MRACMA
Ear Hospital Director, Monash Institute of Medical Engineering
Melbourne, Victoria, Australia Senior Neurosurgeon, Alfred Health
Geraldine J. Ooi
MBBS, BMedSci (Hons) Peter S. Russell
Senior Registrar, Centre for Obesity Research and BSc, PGDipSci, MBChB
Education (CORE), Monash University Research Fellow, Department of Surgery, University of
Senior Registrar in General Surgery, Alfred Health Auckland
Melbourne, Victoria, Australia Auckland, New Zealand
Kurvi Patwala Hani Saeed

MBBS(Hons) MD, BPharm
General Medical Registrar, Austin Health Vascular Surgery Registrar, Eastern Health
Marcos V. Perini Gurfateh Singh Sandhu

MD, PhD, FRACS BSc (Advanced), MBBS
Senior Lecturer in Surgery, University of Melbourne Vascular Surgery Registrar, Royal Prince Alfred Hospital
Hepatopancreaticobiliary and Liver Transplant Surgeon, Sydney, New South Wales, Australia
Austin Health
Melbourne, Victoria, Australia Alan C. Saunder
MBBS, FRACS
William R.G. Perry Senior Lecturer in Surgery, Monash University
BSc, MBChB, MPH, FRACS Vascular and Transplant Surgeon and Medical
Senior Clinical Fellow, Department of Colorectal Surgery, Director, Surgery and Interventional Services Program,
Oxford University Hospitals NHS Foundation Trust Monash Health
Oxford, UK Melbourne, Victoria, Australia
Jeffrey J. Presneill Shomik Sengupta

MBBS(Hons), PhD, MBiostat, PGDipEcho, FRACP, FCICM
MBBS, MS, MD, FRACS
Associate Professor in Medicine
Professor of Surgery, Monash University
University of Melbourne
Urologist, Eastern Health
Deputy Director, Intensive Care Unit
Royal Melbourne Hospital
Jonathan Serpell
MBBS, MD, MEd, FRACS, FACS, FRCSEd (ad hom)
Raffi Qasabian
Professor of Surgery, Monash University
BSc(Hons), MBBS(Hons), FRACS
Director of General Surgery and Head, Breast, Endocrine
Vascular and Endovascular Surgeon, Royal Prince Alfred
and General Surgery Unit, Alfred Health
Hospital
Sydney, New South Wales, Australia
Kenny Rao Rose Shakerian

MBBS, MS MBBS, DMedSci, FRACS
Urology Registrar, Eastern Health General Surgeon, Royal Melbourne Hospital
Fairleigh Reeves Susan Shedda

MBBS (Hons), DipSurgAnat MBBS, MPH, FRACS
Urology Registrar, Royal Melbourne Hospital Colorectal Surgeon, Royal Melbourne Hospital and
Melbourne, Victoria, Australia Royal Women’s Hospital
MBBS, DClinSurg, FRACS, FACS Julian A. Smith
Associate Professor of Surgery, University of Sydney MBBS, MS, MSurgEd, FRACS, FACS, FFSTRCSEd,
Head, Hepatopancreatobiliary Surgery, Westmead FCSANZ, FAICD
Hospital Head, Department of Surgery (School of Clinical
Sydney, New South Wales, Australia Sciences at Monash Health), Monash University
xii Contributors
Head, Department of Cardiothoracic Surgery, Ioana Tichil

Monash Health MD
Melbourne, Victoria, Australia Burns Fellow, Victorian Adult Burns Service, Alfred Health
John Spillane
MBBS, FRACS Joe J. Tjandra (deceased)
Lecturer in Surgery, University of Melbourne MBBS, MD, FRACS, FRCS(Eng), FRCPS, FASCRS
Surgical Oncologist, Division of Cancer Surgery, Peter Formerly Associate Professor of Surgery, University of
MacCallum Cancer Centre Melbourne
Melbourne, Victoria, Australia Colorectal Surgeon and Surgical Oncologist, Royal
Melbourne Hospital
David Story Melbourne, Victoria, Australia
MBBS (Hons), MD, BMedSci (Hons), FANZCA
Chair of Anaesthesia, Centre for Integrated Critical Care, Val Usatoff
University of Melbourne MBBS(Hons), MHSM, FRACS, FCHSM
Melbourne, Victoria, Australia Associate Professor of Surgery, University of Melbourne
Head, Upper Gastrointestinal and
Hepatopancreatobiliary Surgery, Western Health
James Tatoulis AM
MBBS, MS, MD, FRACS, FCSANZ
Professor of Cardiothoracic Surgery, University of
Melbourne
Neil Vallance
MBBS, FRACS
Director of Cardiothoracic Surgery, Royal Melbourne
Hospital
Emeritus Head, Department of Otolaryngology, Head
and Neck Surgery, Monash Health
Jin W. Tee
BMSc, MBBS, MD, FRACS David A.K. Watters AM, OBE
Associate Professor of Surgery, Monash University BSc (Hons), ChM, FRCSEd, FRACS
Complex Spine and Neurosurgeon, Spine Oncology Professor of Surgery, Deakin University
Surgery, Alfred Health Alfred Deakin Professor of Surgery
Head, Spine and Neurotrauma, National Trauma Deakin University and Barwon Health
Research Institute General and Endocrine Surgeon
Melbourne, Victoria, Australia University Hospital Geelong
Geelong, Victoria, Australia
Robert J.S. Thomas OAM
MBBS, MS, FRACS, FRCS(Eng) John A. Windsor
Professorial Fellow and Special Advisor on Health, BSc, MBChB, MD, FRACS, FACS
University of Melbourne Professor of Surgery, University of Auckland
Melbourne, Victoria, Australia General, Pancreatobiliary, Gastro‐oesophageal and
Laparoscopic Surgeon, Auckland City Hospital
Benjamin N.J. Thomson Auckland, New Zealand
MBBS, DMedSci, FRACS, FACS
Clinical Associate Professor in Surgery, University of Homayoun Zargar
Melbourne MBChB, FRACS
Head, Department of General Surgical Specialties Senior Lecturer in Surgery, University of Melbourne
Royal Melbourne Hospital Urologist, Royal Melbourne Hospital
Preface
Medical students and trainees must possess an grounding for students in surgical diseases, problems
understanding of basic surgical principles, a knowl- and management. Apart from forming the core cur-
edge of specific surgical conditions, be able to per- riculum for medical students, surgical trainees will
form a few basic procedures and be part of a also find the Textbook of Surgery beneficial in their
multidisciplinary team that manages the patient in studies and their practice.
totality. All students of surgery must also be aware The fourth edition of the Textbook of Surgery
of the rapid developments in basic sciences and includes new or extensively revised chapters on the
technology and understand where these develop- assessment of surgical risk, the management of sur-
ments impinge on surgical practice. gical wounds, introduction to the operating theatre,
The Textbook of Surgery is intended to supply emergency general surgery, obesity and bariatric
this information, which is especially relevant given surgery, lower gastrointestinal surgery, endovascu-
the current content of the surgical curriculum for lar therapies, benign urological conditions, genitou-
undergraduates. Each topic is written by an expert rinary oncology, sudden‐onset severe headache and
in the field from his or her own wisdom and experi- the red eye.
ence. All contributors have been carefully chosen With ever‐expanding medical knowledge, a core
from the Australasian region for their authoritative amount of instructive and up‐to‐date information
expertise and personal involvement in undergradu- is presented in a concise fashion. Important leading
ate teaching and postgraduate training. references of classic publications or up‐to‐date
In this textbook we have approached surgery literature have been provided for further reading. It
from a practical viewpoint while emphasising the is our aim that this textbook will stimulate students
relevance of basic surgical principles. We have to refer to appropriate reviews and publications for
attempted to cover most aspects of general surgery additional details on specific subjects.
including its subspecialties and selected topics of We have presented the textbook in an attractive
other surgical specialties, including cardiothoracic and easily readable format by extensive use of
surgery, neurosurgery, plastic surgery, ophthalmol- tables, boxes and illustrations. We hope that this
ogy, orthopaedic surgery, otolaryngology/head and fourth edition will continue to be valuable to
neck surgery, urology and vascular surgery. undergraduate, graduate and postgraduate stu-
Principles that underlie the assessment, care and dents of surgery, and for general practitioners and
treatment of surgical patients are outlined, followed physicians as a useful summary of contemporary
by sections on various surgical disorders. The final surgery.
section presents a practical problem‐solving approach
to the diagnosis and management of common surgi- Julian A. Smith
cal conditions. In clinical practice, patients present Andrew H. Kaye
with symptoms and signs to the surgeon who then Christopher Christophi
has to formulate care plans, using such a problem‐ Wendy A. Brown
solving approach. This textbook provides a good Melbourne, Australia
xiii
Acknowledgements
This book owes its existence to the contributions of we owe a debt of gratitude to our loving families,
our talented surgeons and physicians from through- specifically our spouses and partners – Sally Smith,
out Australia, New Zealand and Asia. We are Judy Kaye, Helena Fisher and Andrew Cook – as it
indebted to the staff of Wiley in Australia (Simon was precious time spent away from them which
Goudie) and in Oxford (Claire Bonnett, Jennifer allowed completion of this textbook.
Seward, Deirdre Barry and Nick Morgan) for their The editors wish to dedicate this edition to two
support and diligence. We thank Associate Professor highly esteemed previous editors, the late Joe
David Francis, Mr Alan Cuthbertson and Professor J. Tjandra and the late Gordon J.A. Clunie. Both
Robert Thomas for their assistance with previous were inspirational surgical educators who left an
editions, which laid the foundation for this fourth enduring legacy amongst the many students, train-
edition. ees and colleagues with whom they interacted over
Our patients, students, trainees and surgical men- many years.
tors have all been an inspiration to us, but above all
xiv
Section 1
Principles of Surgery
1 Preoperative management
Julian A. Smith
Department of Surgery (School of Clinical Sciences at Monash Health), Monash University
and Department of Cardiothoracic Surgery, Monash Health, Clayton, Victoria, Australia
act of placing a signature on a form. That signature

Introduction in itself is only meaningful if the patient has been
through a reasonable process that has left them in a
This chapter covers care of the patient from the
position to make an informed decision.
time the patient is considered for surgery through
There has been much written around issues of
to immediately prior to operation and deals with
informed consent, and the medico‐legal climate has
important generic issues relating to the care of all
changed substantially in the past decade. It is
surgical patients. Whilst individual procedures each
important for any doctor to have an understanding
have unique aspects to them, a sound working
of what is currently understood by informed con-
understanding of the common issues involved in
sent. Although the legal systems in individual juris-
preoperative care is critical to good patient out-
dictions may differ with respect to medical
comes. The important elements of preoperative
negligence, the standards around what constitutes
management are as follows.
informed consent are very similar.
• History taking: the present surgical condition
Until relatively recently, the standard applied to
and a general medical review.
deciding whether the patient was given adequate and
• Physical examination: the present surgical condi-
appropriate information with which to make a deci-
tion and a general examination.
sion was the so‐called Bolam test – practitioners are
• Reviewing available diagnostic investigations.
not negligent if they act in accordance with practice
• Ordering further diagnostic and screening
accepted by a reasonable body of medical opinion.
investigations.
Recent case law from both Australia and overseas
• Investigating and managing known or discovered
has seen a move away from that position. Although
medical conditions.
this area is complex, the general opinion is that a doc-
• Obtaining informed consent.
tor has a duty to disclose to a patient any material
• Scheduling the operation and any special prepa-
risks. A risk is said to be material if ‘in the circum-
rations (e.g. equipment required).
stances of that particular case, a reasonable person in
• Requesting an anaesthetic review.
the patient’s position, if warned of the risk would be
• Marking the operative site/side.
likely to attach significance to it or the medical prac-
• Prescribing any ongoing medications and proph-
titioner is, or should reasonably be aware that the
ylaxis against surgical site infection and deep
particular patient, if warned of the risk would attach
venous thrombosis.
significance to it’. It is important that this standard
• Planning postoperative recovery and possibly
relates to what a person in the patient’s position
rehabilitation.
would do and not just any reasonable person.
Important factors when considering the kinds
of information to disclose to patients include the
Informed consent following.
• The nature of the potential risks: more common
Although often thought of in a purely medico‐legal and more serious risks require disclosure.
way, the process of ensuring that a patient is • The nature of the proposed procedure: complex
informed about the procedure they are about to interventions require more information as do
undergo is a fundamental part of good‐quality procedures when the patient has no symptoms or
patient care. Informed consent is far more than the illness.
Textbook of Surgery, Fourth Edition. Edited by Julian A. Smith, Andrew H. Kaye, Christopher Christophi and Wendy A. Brown.
© 2020 John Wiley & Sons Ltd. Published 2020 by John Wiley & Sons Ltd.
3
4 Principles of Surgery
• The patient’s desire for information: patients ◦◦ ensure care is provided in an appropriate
who ask questions make known their desire for environment.
information and they should be told. • To identify important social issues which may
• The temperament and health of the patient: anx- have a bearing on the planned procedure and the
ious patients and patients with health problems or recovery period.
other relevant circumstances that make a risk more • To familiarise the patient with the planned proce-
important for them may need more information. dure and the hospital processes.
• The general surrounding circumstances: the Clearly the preoperative evaluation should include
information required for elective procedures a careful history and physical examination, together
might be different from that required in those with structured questions related to the planned
conducted emergently. procedure. Simple questions related to exercise
Verbal discussions concerning the therapeutic tolerance (such as ‘Can you climb a flight of stairs
options, potential benefits and risks along with without being short of breath?’) will often yield as
common complications are often supplemented much useful information as complex tests of cardi-
with procedure‐specific patient explanatory bro- orespiratory reserve. The clinical evaluation will
chures. These provide a straightforward illustrated be coupled with a number of blood and radio-
account for the patient and their relatives to con- logical tests. There is considerable debate as to the
sider and may be a source of clarification and/or value of many of the routine tests performed, and
further questions about the proposed operation. each hospital will have its own protocol for such
What does this mean for a medical practitioner? evaluations.
Firstly, you must have an understanding of the legal Common patient observations, investigations
framework and standards. Secondly, you must docu- and screening tests prior to surgery include:
ment how appropriate information was given to • vital signs (blood pressure, pulse rate, respiratory
patients – always write it down. If discussion points rate, temperature) and pulse oximetry
are not documented, it may be argued that they • body weight
never occurred. On this point, whilst explanatory • urinalysis
brochures can be a very useful addition to the p rocess • full blood examination and platelet count
of informed consent they do not remove the need to • urea and electrolytes, blood sugar, tests of liver
undertake open conversations with the patient. function
Doctors often see the process of obtaining • blood grouping and screen for irregular antibod-
informed consent as difficult and complex, and this ies (‘group and hold’)
view is leant support by changing standards. • tests of coagulation, i.e. international normalised
However, the principles are relatively clear and not ratio (INR) and activated partial thromboplastin
only benefit patients but their doctors as well. A fully time (APTT)
informed patient is much more likely to adapt to the • chest X‐ray
demands of a surgical intervention, and should a • electrocardiogram (ECG).
complication occur, they and their relatives almost On the basis of the outcomes of this preoperative
invariably accept such misfortune far more readily. evaluation a number of risk stratification systems
have been proposed. One in widespread daily use is
the relatively simple ASA (American Society of
Preoperative assessment Anesthesiologists) system (see Chapter 3, Table 3.3).
The preoperative assessment and work‐up will
The appropriate assessment of patients prior to sur- be guided by a combination of the nature of the
gery to identify coexisting medical problems and to operation proposed and the overall ‘fitness’ of the
plan perioperative care is of increasing importance. patient. Whilst there are a number of ways of look-
Modern trends towards the increasing use of day‐ ing at the type of surgery proposed, a simple three‐
of‐surgery admission even for major procedures way classification has much to commend it.
have increased the need for careful and systematic • Low risk: poses minimal physiological stress and
preoperative assessment, much of which occurs in a risk to the patient, and rarely requires blood
pre‐admission clinic (PAC). transfusion, invasive monitoring or intensive
The goals of preoperative assessment are: care. Examples of such procedures would be
• To identify important medical issues in order to groin hernia repair, cataract surgery and
◦◦ optimise their treatment arthroscopy.
◦◦ inform the patient of additional risks associ- • Medium risk: moderate physiological stress
ated with surgery (fluid shifts, cardiorespiratory effects) and risk.
1: Preoperative management 5
Usually associated with minimal blood loss. Evaluation of the elderly

Potential for significant problems must be appre- asymptomatic patient
ciated. Examples would be laparoscopic chole-
Ageing increases the likelihood of asymptomatic
cystectomy, hysterectomy and hip replacement.
conditions and screening investigations are therefore
• High risk: significant perioperative physiological
more stringently applied to older, apparently healthy
stress. Often requires blood transfusion or infu-
patients. Elderly patients (aged over 70 years) have
sion of large fluid volumes. Requires invasive
increased mortality and complication rates for surgi-
monitoring and will often need intensive care.
cal procedures compared with young patients.
Examples would be aortic surgery, major gastro-
Problems are related to reduced functional reserve,
intestinal resections and thoracic surgery.
coexisting cardiac and pulmonary disease, renal
A low‐risk patient (ASA I or II) will clearly require
impairment, poor tolerance of blood loss and greater
a far less intensive work‐up than a high‐risk patient
sensitivity to analgesics, sedatives and anaesthetic
(ASA III or IV) undergoing a high‐risk operation.
agents.
Areas of specific relevance to perioperative care
Complications of atelectasis, myocardial infarc-
are cardiac disease and respiratory disease. It is
tion, arrhythmias and heart failure, pulmonary
important that pre‐existing cardiorespiratory dis-
emboli, infection and nutritional and metabolic
ease is optimised prior to surgery to minimise the
disorders are all more frequent. Separation of the
risk of complications. Patients with cardiac disease
effects of ageing, frailty and of associated diseases
can be stratified using a number of systems (New
is difficult. Most of the increased mortality and
York Heart Association Functional Class for angina
morbidity is due to associated disease.
or heart failure; Goldman or Detsky indices) and
Special attention needs to be paid to the assess-
this stratification can be used to guide work‐up and
ment of cardiac, respiratory, renal and hepatic func-
interventions and provide a guide to prognosis.
tion along with patient frailty before operation in
One of the most important respiratory factors is
elderly patients.
whether the patient is a smoker. There is now clear
evidence that stopping smoking for at least 4 weeks
prior to surgery significantly reduces the risk of res-
piratory specific or generic complications. Patient safety (see also Chapter 12)
Once in hospital, and particularly once under

Evaluation of the healthy patient
anaesthetic, patients rely upon the systems and
Patients with no clinically detectable systemic illnesses policies of individuals and healthcare institutions
except their surgical problem are classified into to minimise the risk of inadvertent harm. Whilst
ASA class I. Mortality for low‐risk surgical proce- every hospital will have slightly different policies
dures in this group is very low and complications the fundamental goals of these include the
are likely to be due to technical errors. The mortality following.
for major high‐risk surgical procedures in such • The correct patient gets the correct operation on
patients is also low, of the order of a few per cent. the correct side or part of their body. An appro-
All such patients require detailed systems review priate method of patient identification and
by history and physical examination prior to the patient marking must be in place. It must be clear
operation. Preoperative special tests may be added in to all involved in the procedure, particularly for
order to detect any subclinical disease that may operations on paired limbs or organs when the
adversely affect surgery and to provide baseline val- incorrect side could be operated upon.
ues for comparison in the event of postoperative • The patient is protected from harm whilst under
complications. These tests should be sufficiently sen- anaesthetic. When under a general anaesthetic
sitive to detect an abnormality, yet specific enough to the patient is vulnerable to a number of risks.
avoid the chances of over‐diagnosis. The prevalence Important amongst these are pressure effects on
of the disease or condition being looked for is likely nerves, for example those on the common pero-
to be low in a healthy asymptomatic patient popula- neal nerve as it winds around the head of the
tion. Thus, most tests are likely to be within the nor- fibula.
mal range. Inappropriate and excessive tests increase • Previous medical problems and allergies are iden-
the likelihood of a false‐positive result due to chance. tified and acted upon.
With extensive multiphasic screening profiles of • Protocols for the prevention of perioperative
healthy individuals, about 5% of healthy normal infection and venous thromboembolism are
people will show one abnormal result. followed.
can, when used appropriately, significantly reduce

Prophylaxis infectious complications, inappropriate or pro-
longed use can leave the patient susceptible to
Infection infection with antibiotic‐resistant organisms such
Infections remain a major issue for all surgical as MRSA or VRE.
procedures and the team caring for the patient
Factors related to both the patient and the
needs to be aware of relevant risks and act to planned procedure govern the appropriate use of
minimise such risks. antibiotics in the prophylactic setting.
Before discussing the use of prophylactic antibiot-
ics for the prevention of perioperative infection, it is Patient‐related factors
very important that issues of basic hygiene are dis-
Patients with immunosuppression and pre‐existing
cussed (see also Chapters 9 and 12). Simple measures
implants and patients at risk for developing infec-
adopted by all those involved in patient care can
tive endocarditis must receive appropriate prophy-
make a real difference to reducing the risk of hospi-
laxis even when the procedure itself would not
tal‐acquired infection. The very widespread and sig-
indicate their use.
nificant problems with antibiotic‐resistant organisms
such as meticillin‐resistant Staphylococcus aureus
Procedure‐related factors
(MRSA) and vancomycin‐resistant Enterococcus
faecalis (VRE) have reinforced the need for such Table 1.1 indicates the risk of postoperative surgi-
basic measures. cal site infections with and without the use of pro-
• Wash your hands in between seeing each and phylactic antibiotics. In addition to considering
every patient. the absolute risk of infection, the potential conse-
• Wear gloves for removing/changing dressings. quences of infection must also be considered; for
• Ensure that the hospital environment is as clean example, a patient undergoing a vascular graft (a
as possible. clean procedure) must receive appropriate antibi-
These measures, especially hand hygiene, should be otic cover because of the catastrophic consequences
embedded into the psyche of all those involved in of graft infection.
patient care.
In addition to the very important matters of
Venous thromboembolism
hygiene and appropriate sterile practice, antibiotics
should be used in certain circumstances to reduce Deep vein thrombosis (DVT) is a not uncommon
the risk of perioperative surgical site infection. Each and potentially catastrophic complication of sur-
hospital will have individual policies on which par- gery. The risk for developing DVT ranges from a
ticular antibiotics to use in the prophylactic setting fraction of 1% to 30% or greater depending on
(see also Chapters 9 and 12). The antibiotics are both patient‐ and procedure‐related factors. Both
usually administered at or shortly before the induc- patient‐ and procedure‐related factors can be
tion of anaesthesia and continued for no more than classified as low, medium or high risk (Table 1.2).
24 hours postoperatively. It is also important to High‐risk patients undergoing high‐risk operations
state that whilst the use of prophylactic antibiotics will have a risk for DVT of up to 80% and a
Table 1.1 Risks of postoperative surgical site infection.
Wound infection rate (%)
Without prophylactic With prophylactic

Type of procedure Definition antibiotics antibiotics
Clean No contamination; gastrointestinal, 1–5 0–1

genitourinary or respiratory tracts not
breached
Clean‐contaminated Gastrointestinal or respiratory tract 10 1–2
opened but without spillage
Contaminated Acute inflammation, infected urine, bile, 20–30 10
gross spillage from gastrointestinal tract
Dirty Established infection 40–50 10
Table 1.2 Prevention of deep vein thrombosis.
Operative risk factors
Low (e.g. hernia Medium (e.g. general High (e.g. pelvic cancer,
repair) abdominal surgery) orthopaedic surgery)
Patient risk Low (age <40, no No prophylaxis Heparin Heparin and mechanical
factors risk factors) devices
Medium (age >40, Heparin Heparin Heparin and mechanical
one risk factor) devices
High (age >40, Heparin and Heparin and Higher‐dose heparin,
multiple risk factors) mechanical devices mechanical devices mechanical devices
pulmonary embolism risk of 1–5% when prophy- in‐depth preoperative preparation. Whilst the prin-
laxis is not used. These risks can be reduced by at ciples already outlined are still valid, a number of
least one order of magnitude with appropriate additional issues are raised.
interventions.
Whilst a wide variety of agents have been trialled Informed consent
for the prevention of DVT, there are currently only
Whilst there is still a clear need to ensure that patients
three widely used methods.
are appropriately informed, there are fewer opportu-
• Graduated compression stockings: these stock-
nities to discuss the options and potential complica-
ings, which must be properly fitted, reduce
tions with the patient and their family. In addition,
venous pooling in the lower limbs and prevent
the disease process may have resulted in the patient
venous stagnation.
being confused. The team caring for the patient needs
• Mechanical calf compression devices: these work
to judge carefully the level of information required in
by intermittent pneumatic calf compression and
this situation. Although it is very important that fam-
thereby encourage venous return and reduce
ily members are kept informed, it has to be remem-
venous pooling.
bered that the team’s primary duty is towards the
• Heparin: this drug can be used in its conventional
patient. This sometimes puts the team in a difficult
unfractionated form or as one of the fractionated
position when the views of the patient’s family differ
low‐molecular‐weight derivatives. The fraction-
from those which the team caring for the patient
ated low‐molecular‐weight heparins offer the
hold. If such an occasion arises then careful discus-
convenience of once‐ or twice‐daily dosing for
sion and documentation of the decision‐making pro-
the majority of patients. It must however be
cess is vital. Increasingly, patients of very advanced
remembered that the anticoagulant effect of the
years are admitted acutely with a surgical problem in
low‐molecular‐weight heparins may not easily
the setting of significant additional medical prob-
be reversed, and where such reversal may be
lems. It is with this group of patients that specific
important, standard unfractionated heparin
ethical issues around consent and appropriateness of
should be used.
surgery occur. It is important that as full as possible a
The three methods are complementary and are
picture of the patient’s overall health and quality of
often used in combination, depending on the patient
life is obtained and that a full and frank discussion of
and operative risk factors (Table 1.2).
the options, risks and benefits takes place.
The systematic use of such measures is very
important if optimal benefit is to be gained by the
Preoperative resuscitation
potential reduction in DVT.
It is important that wherever possible significant
fluid deficits and electrolyte abnormalities are cor-
Preoperative care of the acute surgical rected prior to surgery. There is often a balance to
patient be made between timely operative intervention and
the degree of fluid resuscitation required. An early
A significant number of patients will present with discussion between surgeon, anaesthetist and, when
acute conditions requiring urgent or emergency required, intensivist can help plan the timing of sur-
surgical operations. There may be little time for an gical intervention.
Pre‐existing medical comorbidities Diabetes mellitus

There is clearly less time to address these issues and Diabetes mellitus is one of the most frequently seen
it may not be possible to address significant ongo- medical comorbidities that complicate periopera-
ing medical problems. Clearly such comorbidities tive care. It is clearly important that patients with
should be identified, and all involved with planning diabetes mellitus are appropriately worked up for
the operation should be informed. The issues are surgery.
most acute for significant cardiac, respiratory, In the weeks leading up to elective surgery the
hepatic or renal disease. management of the diabetes should be reviewed
and blood glucose control optimised. Particular
attention should be paid to HbA1c levels as an
Preoperative nutrition
index of diabetic control as well as cardiovascular
and renal comorbidities during the preoperative
An awareness of the nutritional status of patients is
assessment.
important and such awareness should guide the
Generally, patients with diabetes should be
decisions about nutritional support (see Chapter 7).
scheduled for surgery first case in the morning.
The well‐nourished adult patient should be fasted
Diet‐controlled patients require no special preop-
for at least 6 hours prior to anaesthesia to minimise
erative preparation. For patients taking oral hypo-
the risk of aspiration. Where possible regular medi-
glycaemic drugs, the drugs should be stopped the
cations, especially those for cardiovascular and res-
night before surgery and the blood glucose moni-
piratory conditions, should be continued.
tored. Patients with insulin‐dependent diabetes
Before an operation the malnourished patient
should receive a reduced dose of insulin and/or a
should, whenever possible, be given appropriate
shorter‐acting insulin or be commenced on an
nutritional support. There is no doubt that signifi-
intravenous insulin infusion. There are two
cant preoperative malnutrition increases the risk of
approaches to this.
postoperative complications (>10–15% weight
• Variable‐rate insulin infusion: the patient’s blood
loss). If possible, such nutrition should be given
glucose levels are monitored regularly and the
enterally, reserving parenteral nutrition for the
rate of insulin infusion adjusted. An infusion of
minority of patients in whom the gastrointestinal
dextrose is continued throughout the period of
tract is not an option. Parenteral nutrition is associ-
insulin infusion.
ated with increased costs and complications and is
• Single infusion of glucose, insulin and potassium
of proven benefit only in the seriously malnour-
(GIK): whilst this method has the advantage of
ished patient, when it should be given for at least
simplicity, it is not possible to adjust the rates of
10 days prior to surgery for any benefits to be seen.
glucose and insulin infusion separately and the
There is increasing evidence that enteral feeds spe-
technique can lead to the administration of exces-
cifically formulated to boost certain immune
sive amounts of free water.
parameters offer clinical benefits for patients about
The variable‐rate infusion is the most widespread
to undergo major surgery.
approach and although more involved in terms of
After operation any patient who is unable to take
monitoring offers better glycaemic control. This in
in normal diet for 7 days or more should receive
itself is associated with better patient outcomes.
nutritional support, which as before operation
should use the enteral route whenever possible.
Cardiac disease
Surgical risk is increased in the presence of cardiac
Specific preoperative issues
disease. Consideration must be given to balancing
the risk to the patient if the procedure is abandoned
Allergies
or delayed with the additional risk caused by the
A history of adverse or allergic reactions to medica- presence of cardiac disease. Emergency operations
tions or other substances must be documented and for life‐threatening conditions should proceed
repeat administration and/or exposure avoided as a regardless but elective surgery should be deferred in
life‐threatening anaphylaxis may result. Examples the presence of recent‐onset angina, unstable
of allergens within surgical practice include antibi- angina, recent myocardial infarction, severe aortic
otics, skin preparations (e.g. iodine), wound dress- valve stenosis, high‐degree atrioventricular block,
ing adhesives and latex. A complete latex‐free severe hypertension and untreated congestive car-
environment is required for those patients with a diac failure. Time should be spent investigating the
known latex allergy. condition and optimising therapy, frequently with
cardiological assistance. The introduction of beta‐ deferred in the presence of an active respiratory
blocker therapy to slow heart rate and occasionally infection or an acute exacerbation of asthma or
myocardial revascularisation (by percutaneous COPD.
coronary intervention or coronary artery bypass
Additional respiratory preparation may include
grafting) may be required in advance of surgery on chest physiotherapy, postural drainage, antibiotics
another system. for an acute infection with a positive sputum cul-
ture and inhaled bronchodilators or corticosteroid
Anticoagulant or antiplatelet therapy therapy. A formal preoperative pulmonary rehabili-
tation program may be indicated. Regional anaes-
Patients on warfarin should be transferred to hepa-
thesia is frequently preferred in patients with severe
rin or enoxaparin well in advance of surgery to
respiratory dysfunction.
ensure that the warfarin effect has worn off.
Heparin can be ceased for a short time in the perio-
perative period: withhold an infusion 4 hours Long‐term corticosteroid therapy
before surgery and recommence once the risk of Long‐term corticosteroid therapy results in adrenal
postoperative bleeding is low. Subcutaneously suppression and an impaired response to surgical
administered heparin or enoxaparin is withheld the stress. High‐dose intravenous hydrocortisone
day or evening before surgery and recommenced administration (100 or 250 mg every 6 hours) will
later that day or the day after. Warfarin recom- be required during the perioperative period and
mences once the patient can take oral medication. when the patient is unable to take their regular
Rapid reversal of warfarin prior to an emergency medication or in the presence of postoperative com-
operation may be achieved with vitamin K, pooled plications especially infection.
fresh frozen plasma or clotting factors.
The new oral anticoagulants (dabigatran, apixa- Cerebrovascular disease
ban or rivaroxaban) are difficult to reverse acutely
and need to be ceased 2–5 days preoperatively. A Stroke may complicate major surgery especially in
specific dabigatran reversal agent has recently elderly patients with severe intracranial or extrac-
become available. A bridging regimen such as that ranial atherosclerotic disease faced with fluctua-
described above is also required. tions in blood pressure or cerebral blood flow. An
The antiplatelet agents (aspirin, clopidogrel or asymptomatic carotid bruit related to an internal
ticagrelor) taken alone or in combination should be carotid artery stenosis confirmed with Doppler
ceased at least 5 days prior to an operation. Bleeding ultrasonography may be the first indicator of such
will be highly problematic at the time of surgery disease. Patients with symptomatic carotid disease
especially if multiple antiplatelet agents are contin- (e.g. transient ischaemic attacks) should undergo
ued. Combined usage often follows coronary artery carotid endarterectomy prior to the planned sur-
stenting and so their withdrawal in the context of gery. However, there is no evidence that a prophy-
surgery should be discussed with the treating inter- lactic carotid endarterectomy is of benefit in the
ventional cardiologist. Elective surgery may need to asymptomatic patient.
be postponed if dual antiplatelet therapy cannot be
safely ceased. Chronic liver disease and obstructive
jaundice
Active smoking and respiratory disease
Chronic liver disease of any cause may predispose
All active smokers should be encouraged to cease the patient to surgical complications such as poor
for at least 4 weeks in advance of elective surgery in wound healing, sepsis, excessive bleeding, renal
order to lessen the risk of respiratory problems impairment and acute delirium. Each of the previ-
(atelectasis, acute pneumonia and respiratory fail- ously discussed screening investigations will be
ure) in the postoperative period. Patients unwilling required in addition to specific liver and biliary tree
or incapable of stopping smoking should be referred imaging and possibly liver biopsy. The decision to
to a dedicated support service to assist with such. operate on a patient with severe liver insufficiency
Patients with chronic obstructive pulmonary dis- must be carefully considered. Elective surgery
ease (COPD), asthma and obstructive sleep apnoea should be deferred whilst liver function is opti-
require a detailed respiratory assessment (including mised. Emergency surgery can often result in
peak flow, spirometry and arterial blood gas esti- acute liver decompensation especially in the
mation) especially if the patient reports significant presence of sepsis, haemorrhage, electrolyte distur-
exercise limitation. Elective surgery should be bances, hypoxia and hypoglycaemia.
Patients with obstructive jaundice (see through such physiological mechanisms as

Chapter 67) frequently have an abnormal coagula- increased cardiac output. The signs and symptoms
tion profile and require vitamin K, coagulation fac- of anaemia vary with its severity and are more
tors or pooled fresh frozen plasma to correct the marked if the anaemia has developed over a short
defect. Close attention needs to be paid to the period. Symptoms of weakness and tiredness,
patient’s fluid and electrolyte status in order to pre- breathlessness, palpitations and angina can occur
vent acute renal failure. The hepatic clearance of with moderate or severe anaemia. Pallor is the out-
some commonly administered medications may be standing physical sign. Pallor of the conjunctiva
impaired. and the palmar creases becomes apparent when the
haemoglobin level falls below 10 g/dL. Tachycardia
Chronic kidney disease and cardiac failure may accompany severe anae-
mia. Patients with significant or symptomatic anae-
All patients aged over 40 years should have their
mia should be evaluated by a specialist physician or
kidney function evaluated (urinalysis, serum creati-
haematologist, frequently in a dedicated anaemia
nine, estimated glomerular filtration rate and
clinic.
serum albumin) when major surgery is planned.
In the surgical patient, it is often possible to insti-
Documented chronic kidney disease does not man-
tute iron therapy prior to admission to hospital.
date deferral of elective surgery. Patients with
Anaemia is thus always best diagnosed and its
chronic kidney disease may experience an acute
cause determined during the first office consulta-
deterioration in kidney function if they become
tion in patients needing elective surgery. For iron
water or saline depleted. Acute kidney failure is the
deficiency anaemia caused by blood loss, oral iron
most significant complication of chronic kidney
therapy begins immediately so that anaemia can be
disease: prevention demands strict attention to
safely corrected prior to surgery. Patients with mod-
fluid and electrolyte balance (especially avoiding
erate iron deficiency or haemolytic anaemias do not
dehydration and maintaining a stable level of serum
pose an excessive risk provided the haemoglobin
potassium), maintaining kidney perfusion and
level and the blood volume are adequate (>10 g/dL)
accurate replacement of blood loss during surgery.
and cardiorespiratory function is normal.
Apart from acute kidney failure, the main compli-
In patients with megaloblastic anaemia surgery
cations of surgery in patients with chronic kidney
should be deferred, if possible, until specific therapy
disease are sepsis (including urinary tract infection),
such as vitamin B12 or folic acid has repaired the
poor wound healing and cardiovascular complica-
generalised tissue defect. In these cases, transfusion
tions (myocardial infarction and stroke).
alone may not render surgery safe, as protein metab-
olism of all cells is affected by the vitamin deficiency
Anaemia
that causes the macrocytic anaemia. Adequate tissue
As a general rule mild anaemia does not increase levels can be achieved with 1–2 weeks of oral treat-
the risk of surgery. However, if time permits the ment with vitamin B12 or folic acid or both.
cause of the anaemia should be identified before If it is not possible to correct the anaemia in a
elective surgery. Iron deficiency anaemia is best timely manner, the patient may be given concen-
detected early and treated by oral or intravenous trated red cells prior to surgery. A period of 3 days
iron. Patients with the anaemia of renal injury are should be allowed to elapse before operation as the
an exception to the general rule and can cope with transfused blood will not reach its maximum oxy-
quite low haemoglobin levels, due to an increase in gen‐carrying capacity until at least 2 days following
red cell 2,3‐diphosphoglycerate (2,3‐DPG) that transfusion. This period allows the transfused red
promotes better transfer of oxygen at the tissue cells to accumulate normal levels of 2,3‐DPG, nec-
level. However, in all patients the combination of essary for efficient delivery of oxygen to the tissues,
any degree of anaemia with decompensated cardio- and allows plasma dispersal restoring normovolae-
vascular disease (e.g. angina or obstructive airways mia. Elective surgery should seldom be undertaken
disease) warns that intensive perioperative care will when the haemoglobin concentration is less than
be necessary. 9–10 g/dL. Patients with long‐standing anaemia are
Preoperative haemoglobin measurement should able to tolerate a reduced level of haemoglobin bet-
be performed as a routine examination in all ter than those who have become acutely anaemic.
patients. Patients may have significant anaemia but This tolerance in chronic anaemia is a result of
no symptoms if the anaemia has developed slowly altered 2,3‐DPG concentration in the red cells, with
over a period of months and the body has compen- a favourable shift in the oxyhaemoglobin dissocia-
sated for the decreased oxygen‐carrying capacity tion curve to the right.
Woodhead K, Fudge L (eds) Manual of Perioperative Care:

Psychological preparation and mental an Eessential Guide. Oxford: Wiley Blackwell, 2012.
illness
All surgical patients must be in a relaxed state of MCQs

mind irrespective of the nature of the procedure
they are about to undergo. Anxiety and a fear Select the single correct answer to each question. The
of the unknown or of the potential complications correct answers can be found in the Answers section
of surgery are common, especially in the con- at the end of the book.
text of life‐threatening illnesses or procedures.
1 Without the use of prophylaxis the risk of deep calf
Reassurance can be achieved by empathetic sur-
vein thrombosis in a patient undergoing an anterior
geon communication with the patient and their
resection for rectal cancer is likely to be at least:
relatives and, in certain instances, by the provi-
a 10%
sion of specialised input from other healthcare
b 20%
professionals such as support nurses or
c 30%
psychologists.
d 50%
Patients with pre‐existing mental illness such as
anxiety, depression, psychoses, substance abuse or
2 Which of the following measures is most likely to
dementia who are preparing for an operation
reduce the risk of postoperative wound infection
require guidance from their treating healthcare pro-
with MRSA?
fessionals such that their condition is optimally
a 5 days of broad‐spectrum prophylactic antibiotics
managed in the perioperative period. The stress of
b ensuring the patient showers with chlorhexidine
surgery may worsen or unmask any pre‐existing
wash prior to surgery
mental condition. Care must be taken in the pre-
c a policy of staff hand washing between patients
scription of analgesics, anxiolytics, sedatives, anti-
d screening patients for MRSA carriage prior to
depressant and antipsychotic medications in these
surgery
patients.
3 Which of the following constitutes the legal standard

for the information that should be passed to a patient
Further reading to meet the requirements of ‘informed consent’?
a what a patient in that position would regard as
Smith JA, Yii MK. Pre-operative medical problems in sur-
reasonable
gical patients. In: Smith JA, Fox JG, Saunder AC, Yii
b what a reasoned body of medical opinion holds
MK (eds) Hunt and Marshall’s Clinical Problems in
Surgery, 3rd edn. Chatswood, NSW: Elsevier, as reasonable
2016:348–70. c a list of all possible complications contained
Wilson H. Pre-operative management. In: Falaschi P, within a patient explanatory brochure
Marsh DR (eds) Orthogeriatrics. Springer International d all serious complications that occur in more than
Publishing, 2017:63–79. 1% of patients
2 Assessment of surgical risk
Benjamin N.J. Thomson
University of Melbourne, Royal Melbourne Hospital Department of Surgery and Department of
General Surgery Specialties, Royal Melbourne Hospital, Melbourne, Victoria, Australia
For most surgical procedures the benefits of per-

Introduction forming surgery far outweigh the risks and the deci-
sion is easier, but for complex surgical procedures
This chapter reviews the assessment of risk for
the risks may outweigh any benefit. As outlined by
patients being considered for surgery or other inva-
the General Medical Council document the risks of
sive interventions.
not performing surgery also need to be considered.
Another important aspect is the likely outcome
from surgery. For example, most patients with ade-
Surgical risk
nocarcinoma of the head of the pancreas are not
suitable for surgical management due to the pres-
The definition of surgical risk is complex and dif-
ence of metastatic disease or involvement of the
fers depending on the point of view of the assessor.
major adjacent blood vessels. After appropriate
The risks of a particular surgical procedure may
preoperative staging only 5–10% of patients are
have a different value when considered by the sur-
suitable for surgery. Resection of the pancreatic
geon, anaesthetist, intensivist, patient or family
head (pancreaticoduodenectomy or Whipple’s pro-
member.
cedure) had a mortality of 50% in the 1950s,
What a surgeon may consider to be a small com-
whereas in 2018 the reported mortality in specialist
plication may be devastating to a patient depending
centres was 0.0–6.0%. Furthermore, operative
on their personal circumstances. For example, a
morbidity is close to 50%. Despite the high mor-
very rare risk of a unilateral recurrent laryngeal
bidity and mortality, the median survival for those
nerve injury leading to vocal cord palsy is well tol-
patients undergoing successful resection is only
erated by the majority of patients but is a disaster
14–24 months even in high‐volume centres. Clearly
for a professional singer. From a patient’s perspec-
any patient being considered for surgery needs also
tive surgical risk encompasses the mortality and
to understand the likelihood of successful treat-
morbidity relevant to their circumstances as well as
ment and to be able to balance this against their
the chance of successfully achieving the desired
own personal circumstances as well as the likeli-
outcome.
hood of morbidity and mortality.
The General Medical Council (GMC) of the UK
Another reason to assess surgical risk is identifica-
defines the risk of a proposed investigation or treat-
tion of high‐risk patients who may benefit from risk
ment using three criteria as well as the potential
reduction measures such as preoperative and intra-
outcome of taking no action (Box 2.1). This is an
operative optimisation as well as postoperative man-
integral component of the consent process required
agement in intensive care or high‐dependency units.
for each intervention or surgical procedure and
allows the patient and clinician to make a consen-
sual decision after considering the benefits of a pro-
cedure balanced against the associated risks. Assessment of surgical risk
However, there may be a number of treatment
options for each surgical pathology so the assess- There are three components to assessment of surgi-
ment of surgical risk also facilitates surgical cal risk. The first is the associated mortality and
decision‐making. morbidity of all surgical procedures. This can be
13
complications and other risks of surgery or inter-

Box 2.1 GMC‐UK definition of risk
ventions. It details the need for clear, accurate infor-
of investigation/treatment
mation about the risks of a proposed procedure
1 Side effects being presented in a way that the patient under-
2 Complications stands to enable them to make an informed
3 Failure of an intervention to achieve the desired decision. It is important to understand the patient’s
outcome views and preferences as well as the adverse out-
4 The potential outcome of taking no action comes that they are most concerned about. It is
Source: https://www.gmc‐uk.org/ethical‐guidance/ impossible to cover every possible side effect or
ethical‐guidance‐for‐doctors/consent/part‐2‐making‐ adverse outcome for each procedure but discussion
decisions‐about‐investigations‐and‐treatment#paragraph‐28 of the common adverse outcomes whether severe or
less serious is required as well as any possible
serious adverse outcomes.
obtained from multiple data sources that include There are a number of resources available to aid
personal audit, hospital audit, regional health data in the discussion, such as procedure‐specific infor-
or specialty group audits. Furthermore, there is mation pamphlets produced at a hospital level,
extensive published data available detailing the mor- surgical regulatory authorities or government

tality and morbidity of surgical procedures or inter- agencies.
ventions, although this is often reflective of leading
high‐volume centres. Therefore, publications that
report pooled data from all possible sources may Risk scoring systems
offer a clearer representation of surgical risks. A
brief overview of surgical risk is outlined in Table 2.1. Many tools have been developed to estimate both
The next two components of surgical risk assess- mortality and morbidity rates for individual
ment involve both subjective and objective parame- patients prior to a surgical procedure or interven-
ters. Subjective assessment includes information taken tion. Most are scoring systems that estimate risk for
from the history and examination of a patient as well all patients whilst others are specific for high‐risk
as recognition of patterns, clinical experience and patients or particular surgical procedures or disci-
intuition of the assessor. Often the experience of the plines. Like all tools they only provide an estimated
assessor in surgical practice may be pivotal in identify- risk and none are perfect. Most incorporate both
ing those patients at greater risk. Objective risk assess- physiological and comorbid data selected from
ment includes biochemical and haematological testing large databases of patients. These have then been
as well as assessment of physiological function, par- analysed with regression techniques to identify the
ticularly cardiac and respiratory function. Assessment key variables. Often a weighting is added to each of
of comorbidities also plays a role. There are also many the variables. Ideally these scoring systems should
risk prediction models and scoring systems available be validated in multiple other centres to analyse
that can be general or surgery specific. their usefulness for particular patient groups.
ASA
Discussing the risks of surgery
One of the first scoring systems developed was by
The General Medical Council of the UK has pub- the American Society of Anesthesiologists (ASA) in
lished guidance on the consent process and in par- 1963. It was a five‐point classification system for
ticular on the discussion of the side effects, assessment of a patient prior to surgery. It was
Table 2.1 Overview of the morbidity and mortality of common surgical procedures.
Surgical procedure Morbidity (%) Mortality (%)
Inguinal hernia repair 8–32 0–0.5

Appendicectomy 3.0–28.7 0.9–2.8
Laparoscopic cholecystectomy 14.7–21.4 0.3
Pancreaticoduodenectomy 20–54 0–6.0
Oesophagectomy 25–45 0.7–10.0
Coronary artery bypass grafting 30 1.5–2.5
2: Assessment of surgical risk 15
Table 2.2 American Society of Anesthesiologists expansion and improvement in the prognostic esti-
classification of mortality rates. mates led to the development of APACHE III.
APACHE was never designed to predict mortal-
ASA rating Number Deaths (%) ity in individual patients. Furthermore, the ability
1 92 227 0.001 to predict an individual’s probability of survival
2 367 161 0.002 depends upon response to therapy over time. The
3 195 829 0.028 APACHE system is predominantly a guide for
4 45 118 0.304 intensive care patients and therefore assessment of
5 353 6.232 critically ill patients rather than a guide for elective
1E 3 018 0.000 surgery.
2E 12 188 0.033
3E 7 109 0.155
4E 5 000 3.280 POSSUM
5E 899 19.911
The Physiological and Operative Severity Score for
the enumeration of Mortality and morbidity
Source: Hopkins TJ, Raghunathan K, Barbeito A et al.
Associations between ASA physical status and
(POSSUM) was first described in 1991. Rather than
postoperative mortality at 48 h: a contemporary a system for intensive care patients it was designed
dataset analysis compared to a historical cohort. as a scoring system to estimate morbidity and mor-
Perioper Med 2016;5:29. tality following surgery. It provides a risk‐adjusted
prediction of outcome. It is the most widely used
surgical risk scoring system in the UK. Various
subsequently revised with a sixth category coding modifications have been described and validated
for emergency patients. It is a combination of sub- for colorectal, oesophagogastric and vascular
jective anaesthetic opinion with an objective assess- patient groups. The Portsmouth P‐POSSUM was
ment of the patient’s fitness for surgery. The developed in 1998 and is now the most commonly
majority of hospitals and anaesthetists in Australia used in the UK.
use it routinely.
The ASA classification is as follows.
• ASA I: a normal healthy patient.
Pre‐admission clinics
• ASA II: a patient with mild systemic disease.
• ASA III: a patient with severe systemic disease.
Pre‐admission clinics have been established for
• ASA IV: a patient with severe systemic disease
more than 20 years. They have many different roles
that is a constant threat to life.
that include administration, surgical clerking, con-
• ASA V: a moribund patient who is not expected
sent, preoperative education as well as anaesthetic
to survive without the operation.
review. They provide an excellent environment for
• ASA VI: a declared brain‐dead patient whose
assessing surgical risk as well as for optimising
organs are being removed for donor purposes.
patients’ medical conditions prior to surgery. There
The coding for emergency patients is marked
are very few studies assessing the efficacy of pre‐
with the addition of an E.
admission clinics in determining a patient’s fitness
The ASA system correlates with mortality, as out-
but there are studies demonstrating increased
lined in Table 2.2 that details the outcome of
patient satisfaction as well as a decrease in hospital
732,704 patients.
length of stay.
Risk scoring systems lack sensitivity and specific-
APACHE
ity when applied to individuals. Assessment by an
First introduced in 1979, the Acute Physiology And anaesthetist in a pre‐admission clinic allows any
Chronic Health Evaluation (APACHE) system was scoring system to be used as an adjunct to informa-
developed to measure the severity of illness in intention obtained through clinical assessment of each
sive care patients. It consisted of both acute physi- individual patient. The three objectives of an anaes-
ological abnormalities as well as a chronic health thetic preoperative assessment are firstly to identify
evaluation measure. This was updated in 1985 with the risk of the patient developing an adverse out-
APACHE II with a reduction in the physiological come. The second is to assess any comorbidities
values from 34 to 12 as well as adding a points that may be optimised prior to surgery. The third
score for diminished physiological reserve due to objective is to individualise perioperative manage-
immune deficiency and ageing as well as chronic ment to attempt to minimise any remaining adverse
cardiac, pulmonary, renal or liver disease. Further outcomes.
There are a number of common comorbidities Neurological risk assessment

that should be assessed to minimise surgical risk.
There are a number of risk factors for cerebrovas-
cular complications in the postoperative period
Cardiac disease
that include age, cerebrovascular disease, hyperten-
Ischaemic heart disease is the commonest cause of sion, atrial fibrillation and the type of surgery.
serious cardiac adverse outcomes at the time of sur-
gery. There is a greater risk amongst patients with a Haematological risk assessment
past history of myocardial infarction, particularly
A past history of deep venous thrombosis, pulmo-
within 3–6 months. The presence of angina is less
nary embolism or haematological disorders (i.e.
clear as a marker of increased risk but congestive
protein C and S deficiency) increases the risk of
cardiac failure has consistently been found to be an
thromboembolism in the postoperative period.
indicator of worse outcomes.
There are a number of investigations that can be
Operative risk in the elderly
used to assess cardiac risk, the commonest being an
electrocardiogram. Non‐invasive assessments of Operative risk is greater in the elderly, with a two to
reversible cardiac ischaemia that may allow optimi- five times greater risk of death in comparison with
sation prior to surgery include exercise electrocar- younger patients. In general, elderly patients have a
diogram, radionuclide stress cardiac imaging and lower reserve when challenged by a surgical procedure
stress echocardiography. or complication. In the original National Confidential
Enquiry into Patient Outcome and Death (NCEPOD)
Respiratory disease released in 1987, 79% of perioperative deaths
occurred in the over‐65 age group, although that only
Patients with pulmonary disease are at risk of peri-
represented 22% of the surgical population.
operative complications such as hyperreactive air-
ways, prolonged ventilation, atelectasis, pneumonia
and respiratory failure. The site of the surgical inci- Summary
sion is important in determining risk due to impair-
ment of pulmonary function. Median sternotomy, Assessment of surgical risk is a key component to
upper abdominal incisions and thoracotomy are both preoperative surgical and anaesthetic care.
associated with the greatest risk. The assessment of surgical risk is critical in provid-
Pulmonary function tests are the main investiga- ing consent as well as for identifying those at risk
tion for assessment of pulmonary disease and treat- who can be optimised prior to surgery or managed
ment of reversible airway disease may be required in an appropriate environment to allow for the best
prior to surgery. possible outcome.
Renal risk assessment

Acute renal failure after surgical procedures is Further reading
associated with a higher mortality rate. Many ter-
tiary referral hospitals also have large nephrology Burnand KG, Young AE, Lucas J, Rowlands BJ, Scholefield J
services and surgical procedures on patients with (eds) The New Aird’s Companion in Surgical Studies,
3rd edn. Edinburgh: Elsevier Churchill Livingstone, 2005.
end‐stage renal failure are common. Again optimi-
Paterson‐Brown S (ed.) A Companion to Specialist
sation of the biochemical consequences of renal
Surgical Practice: Core Topics in General and
failure with preoperative renal dialysis is often Emergency Surgery, 6th edn. Edinburgh: Elsevier, 2018.
required for those patients with end‐stage renal
failure.
MCQs
Hepatic risk assessment
Select the single most appropriate answer to each
There are a number of risk assessments for chronic
question. The correct answers can be found in the
liver disease, including the Child–Pugh classifica-
Answers section at the end of the book.
tion and the Model for End‐stage Liver Disease
(MELD). Patients with liver failure are at a high 1 Discussion of the risks of a surgical procedure
risk of death even following basic surgical proce- should include:
dures so management in a specialist centre is a the side effects
required to reduce the risk of an adverse outcome. b likely complications
2: Assessment of surgical risk 17
c failure of the proposed surgery to achieve the b can be adequately assessed by electrocardiogra-
desired outcome phy alone
d the potential outcome if no action is taken c is not required if the patient continues to smoke
e all of the above d is only required for high‐risk cardiac surgical
patients
2 The American Society of Anesthesiologists (ASA) e may involve assessment of reversible cardiac
risk scoring system: ischaemia with radionuclide stress cardiac
a consists of 12 acute physiological abnormalities imaging or stress echocardiography
as well as a chronic health evaluation measure
b was designed for assessment of critically ill 4 Operative risk in patients over 65 years of age is:
intensive care patients a no greater than for younger patients
c can be adjusted according to various different b dependent on regular aspirin intake
surgical procedures c greater than younger patients
d is a 6‐point classification system for assessment d only a greater risk if surgery is required for
of patients prior to surgery trauma
e is assessed by the surgical team prior to surgery e greater for procedures performed under local
anaesthesia rather than general anaesthesia
3 Optimisation of cardiac ischaemia prior to surgery:
a is not necessary as ischaemic heart disease does
not increase operative risk
3 Anaesthesia and pain medicine
David Story
Centre for Integrated Critical Care, University of Melbourne, Melbourne, Victoria, Australia
anaesthetists but also general practitioners, general

Introduction physicians, specialty physicians, pain medicine spe-
cialists, and nursing and allied health practitioners
Anaesthetists aim to minimise the risks of surgery
such as physiotherapists and cancer support nurses.
and anaesthesia for individual patients and provide
The anaesthetist’s assessment will include review-
optimal operating conditions leading to the best
ing assessments from others including the surgical
possible surgical outcomes. This requires direct
team and physicians. Anaesthetists want to know
patient care before, during and after surgery. The
about coexisting conditions (comorbidity), includ-
foundations of anaesthesia practice are general
ing (i) the nature and extent of the patient’s condi-
anaesthesia, regional anaesthesia, airway manage-
tion, (ii) the preferred treatment for this condition,
ment, perioperative medicine, pain medicine, resus-
and (iii) whether the patient is maximally opti-
citation crisis management, and safety and quality.
mised. Anaesthetists are experts in translating this
In contemporary anaesthesia these all centre on evi-
information into a perioperative plan. As with all
dence‐based cost‐effective practice.
good clinical assessment, anaesthetists consider
history, examination and tests.
The history often starts with a health question-
Before surgery
naire and then follow‐up questions during a face‐
to‐face meeting. Current medications and any
The aim of preoperative assessment is to identify
adverse reactions to medications, particularly aller-
and reduce risks and develop an individualised plan
gic reactions, are important. Another important
for the patient for the perioperative period (before,
area is prior experience of surgery and anaesthesia.
during and after surgery) to achieve the goals of
The initial focus of anaesthesia assessment is ABC
care, including being (ideally) cured of the surgical
(airway, breathing and circulation) or, more specifi-
condition (particularly cancer) and returning to the
cally, potential airway problems and respiratory or
best possible quality of life. About 20% of adult
cardiovascular dysfunction. Examination will focus
patients undergoing surgery and anaesthesia are at
on these areas. Tests will depend on the patient’s
high risk of postoperative complications, disability
comorbidity, age and planned surgery.
or death after surgery. Preoperative factors increas-
ing the risk of poor outcome range from severe
Airway
heart disease to severe anxiety to long‐term com-
plex pain syndromes. However, for patients with The aim is to detect potential airway problems
robust health, failure to achieve an expected return that may adversely affect the intraoperative and/
to competitive sport or full employment would be a or postoperative period. An increasing number of
poor outcome. patients have anatomy and disease states that may
make intraoperative airway management both
difficult and risky. Several factors (Box 3.1) are
Preoperative assessment associated with difficult endotracheal intubation,
All patients should receive timely appropriate pre- and which are also associated with difficult mask
operative assessment. Increasingly, this includes a ventilation and airway obstruction during
team approach including not only surgeons and sedation.
19
Box 3.1 Factors associated with Box 3.2 Preoperative fasting

difficulty of airway management recommendations
including during sedation
• For adults having an elective procedure, limited
• Previous difficult endotracheal intubation solid food may be taken up to 6 hours prior to
• Poor mouth opening anaesthesia and clear fluids may be taken up to 2
• Poor jaw advancement hours prior to anaesthesia. Clear fluids are regarded
• Prominent teeth as water, pulp‐free fruit juice, clear cordial, black
• Large tongue tea and coffee. This excludes particulate or milk‐
• Limited neck movement based drinks.
• Short, large neck (bull neck) • Prescribed medications may be taken with a sip of
• Extreme obesity water less than 2 hours prior to anaesthesia unless
• Obstructive sleep apnoea otherwise directed (e.g. oral hypoglycaemics and
• Large breasts anticoagulants).
Breathing (lung disease)

The greatest aspiration risk is for patients undergo-
The most common lung conditions are asthma,
ing emergency surgery particularly abdominal sur-
chronic obstructive pulmonary disease (COPD)
gery and in patients with known gastrointestinal
and recent cigarette smoking. Patients with severe
obstruction, pain requiring opioids, and active
asthma can deteriorate progressively or suddenly
vomiting. A relatively new aspiration risk is previ-
during the perioperative period; however, endotra-
ous gastric banding for obesity (see Chapter 18).
cheal intubation that directly stimulates the trachea
When possible, patients are fasted before surgery,
can be a strong trigger for asthma. Patients with
including all elective surgery, to reduce the risk of
COPD may have a reactive asthma‐like component
aspiration, particularly from large amounts of solid
as well as underlying structural lung disease.
material. Over the last 10 years fasting guidelines
Oxygen saturation on finger pulse oximetry of less
have been relaxed and fasting is not a barrier
than 92% on room air is associated with severe
for patients receiving their regular medications
lung disease and is a strong predictor of postopera-
(Box 3.2). However, patients with vomiting or gut
tive pulmonary complications including pneumo-
obstruction often need parenteral drug substitution
nia. The anaesthesia plan will depend on the
for important medications and pharmacist advice
severity of the asthma or COPD and the nature of
should be sought.
the surgery, with a preference for regional anaesthe-
sia where possible for patients with severe lung dis-
Cardiovascular
ease. Care of patients with severe disease will often
require coordination with optimisation plans, Symptomatic heart disease caries significant periop-
including preoperative oral steroids. While cigarette erative risk of complications and death, usually in
smoking is associated with perioperative respira- the first few days after surgery. Cardiac complica-
tory complications, smoking is also associated with tions are more common in patients with sympto-
surgical site infection and patients should be sup- matic ischaemic heart disease, heart failure or severe
ported with smoking cessation plans. Patients with heart valve disease. The aim of cardiac assessment is
very severe lung disease who may require prolonged to identify and minimise the risks of cardiac compli-
mechanical ventilation in the intensive care unit cations, such as myocardial injury after non‐cardiac
(ICU) need very careful consideration of whether to surgery including myocardial infarction, worsening
proceed with surgery. cardiac failure and significant arrhythmia notably
Another factor in respiratory assessment is aspi- atrial fibrillation. Previous stroke is a risk factor for
ration risk. Aspiration occurs when stomach con- both further stroke and cardiac complications.
tents are vomited or passively regurgitated and Several drugs for cardiovascular disease may be
contaminate the trachea and lower airways. withheld prior to surgery depending on individual
Aspiration can be acidic gastric fluid and/or bile circumstances, including opinion from the patient’s
and/or food. Aspiration may be associated with cardiologist, to reduce perioperative risks, for exam-
chemical pneumonitis, bacterial pneumonia or air- ple anticoagulants (including aspirin) to reduce
way obstruction and is a medical emergency. bleeding risk and some antihypertensives (ACE
Aspiration continues to be an important cause of inhibitors and angiotensin receptor blockers) to
complications and death before and after surgery. reduce the risk of persisting hypotension. Patients
3: Anaesthesia and pain medicine 21
with significant cardiovascular disease often require deficiency is with iron infusion. However, some
more intensive monitoring and intervention during patients will have functional anaemia, also known as
surgery, such as continuous monitoring of intra‐arte- anaemia of chronic disease, which is harder to treat.
rial pressure and use of vasopressors and then ongo-
ing care in high dependency or ICU after surgery. Postoperative nausea and vomiting
Other frequent and important comorbidities
include diabetes, anaemia and kidney disease. Postoperative nausea and vomiting (PONV) is called
the ‘big little problem’. PONV is common but usually
preventable and treatable. However, patients find
Diabetes
PONV distressing and may have delayed mobilisa-
Type 2 diabetes now affects up to 30% of surgical tion and prolonged admission and occasionally seri-
patients, with many previously undiagnosed. Poorly ous complications such as pneumonia. The Apfel risk
controlled diabetes in surgical patients is associated score for PONV includes four factors: (i) female sex;
with increased complications including infection. (ii) history of motion sickness or PONV; (iii) non‐
Patients with type 2 diabetes frequently have, or smoker; and (iv) planned postoperative opioid treat-
need to be screened for, chronic kidney disease and ment. The incidence of PONV ranges from 10% with
cardiovascular disease. Preoperative assessment no Apfel factors to 80% with four factors. Patients at
includes measurement of haemoglobin (Hb)A1c to high risk will often receive multimodal intraoperative
screen for diabetes in patients aged over 50 years anti‐emetic prophylaxis. Further, the anaesthesia and
and for diabetes control in those with known diabe- analgesia plan will have greater emphasis on non‐
tes. The key to managing diabetes in the periopera- opioid modalities, particularly regional analgesia.
tive period is to frequently measure the blood sugar Patients at high risk of PONV will also have regular
and respond to both hyperglycaemia and hypogly- rather than just rescue postoperative anti‐emetics.
caemia. To avoid hypoglycaemia, most oral diabe-
tes drugs will be withheld before surgery and insulin Pain
dosing will be modified. Many patients undergoing
major surgery will need temporary change to insu- Preoperative pain syndromes, particularly those
lin while in hospital in collaboration with the treated with opioids and often requiring orthopae-
diabetes team. dic or spinal surgery, require close attention and
specific planning. Multimodal pain management
plans with regional analgesia blocks should be
Chronic kidney disease
discussed with patients before surgery to outline
Even mild chronic kidney disease, defined as an risks and benefits. Chronic post‐surgical pain is
estimated glomerular filtration rate (eGFR) of less an under‐recognised complication of surgery.
than 60 mL/min per m2, carries a significant increase Approximately 10% of patients have chronic pain
in the risk of death after surgery. Patients should be (months to years) after major surgery, with about
on optimal treatment for the severity of their kid- one‐third of these patients having severe pain. This
ney disease. Maintaining adequate hydration is the incidence is higher in specific types of surgery,
most important strategy in reducing the risks of notably thoracic and breast surgery. Pain manage-
chronic kidney disease. ment plans individualised to the patient and the
surgery are important for reducing these risks.
Anaemia Some drugs, such as gabapentin, will need to be
started preoperatively. The pain plan must include
Identifying preoperative anaemia, and the underlying rescue for both poor postoperative pain control
cause, by measuring the haemoglobin and often and complications of pain control such as excessive
undertaking iron studies is important for risk mini- sedation.
misation. Some surgical conditions, particularly colo-
rectal cancer, have a high incidence of anaemia (see
Quantifying risk of complications
Chapter 1). Preoperative anaemia carries an increased
and mortality
risk of complications and mortality after surgery, in
addition to an increased risk of red cell transfusion While we often focus on the risks of complication,
which also carries risks of complications. The risks of death and disability, patient‐focused outcomes also
anaemia and transfusion may be reduced by identify- include pain, nausea and safe return to activities of
ing and managing preoperative iron deficiency and daily living, as well as anaesthesia‐specific risks
minimising intraoperative blood loss: patient blood including regional anaesthesia and adverse drug
management. The most effective way to treat iron reaction. Following comprehensive anaesthesia

Table 3.1 American Society of Anesthesiologists Physical Score (ASA‐PS).
ASA‐PS class Definition Examples
ASA I Healthy Healthy, non‐smoking, minimal alcohol use

ASA II Mild systemic disease Current smoker, well‐controlled hypertension, or mild
asthma
ASA III Severe systemic disease Poorly controlled diabetes, active hepatitis, or moderate
reduction of left ventricular ejection fraction
ASA IV Severe systemic disease that is a constant Ongoing cardiac ischaemia, sepsis, end‐stage cirrhosis
threat to life
ASA V A moribund patient who is not expected Examples include ruptured abdominal aneurysm, or gut
to survive without the operation ischaemia with septic shock
Source: https://www.asahq.org/
http://www.google.co.uk/url?sa=t&rct=j&q=&esrc=s&source=web&cd=1&cad=rja&uact=8&ved=2ahUKEwjX__
LSmLPeAhWlTt8KHRBzDX0QFjAAegQICBAC&url=http%3A%2F%2Fwww.asahq.org%2F~%2Fmedia%2Fsites
%2Fasahq%2Ffiles%2Fpublic%2Fresources%2Fstandards‐guidelines%2Fasa‐physical‐status‐classification‐system.
pdf&usg=AOvVaw2VpwTL1ioJ7‐XXfFM7Smwq Reproduced with permission of American Society of
Anesthesiologists.
assessment, patients should be allocated a score using

Box 3.3 Example of calculating risks
the American Society of Anesthesiologists Physical
for patients and related decisions
Score (ASA‐PS) (Table 3.1). This single‐variable score
is a remarkably strong predictor of postoperative Risk calculation for a 74‐year‐old woman for elective
complications and mortality. However, increased partial colectomy with colostomy using the American
accuracy can be achieved by including other risk College of Surgeons Risk Calculator
factors for complications and mortality such as • If assessed as ASA 2 (e.g. has hypertension), risk of
increasing age, frailty and emergency surgery. Risk death within 30 days of surgery is at least 0.5%
calculators, such as the American College of Surgeons and risk of complications is 20%. This patient is
online risk calculator (Box 3.3), allow quantitative suitable for ward care.
risk assessment of complications and mortality, usu- • If assessed as ASA 4 (e.g. has diabetes, cardiac
ally the risk of dying within 30 days of surgery (30‐ failure and chronic renal impairment), risk of death
day mortality). Patients with a 5% or greater risk of is at least 5% and risk of complication 35%.
30‐day mortality require higher levels of specialised Clinicians should strongly consider critical care
care including admission to ICU after surgery. Patients admission after surgery.
with a 5% risk of mortality are likely to have a risk of • If assessed as ASA 4, frail and having emergency
major complications exceeding 20% and risk of poor surgery (a growing number of patients), risk of
death is 13% and risk of complications 42%. The
functional recovery. Increasingly, in assessing the
goals of care should be discussed with the patient
goals of care these high‐risk patients undergo more
(and family) and some may decide for supportive
limited surgery or non‐surgical treatment.
care only or limitations on medical treatment if she
deteriorates after surgery.
Intraoperative care
block) and general anaesthesia, all of which have
The intraoperative care plan will depend on the
many additional options.
nature and extent of the surgery and the patient.
The broad aspects of anaesthesia are one or more
of pain relief, sleep or sedation, no memory (amne-
Intravenous access
sia), muscle relaxation and stable physiology, par- For many procedures intravenous access is predomi-
ticularly haemodynamic stability. The fundamental nantly used to administer drugs to provide appropri-
keys to safe anaesthesia are appropriate intrave- ate and safe anaesthesia, with fluid therapy being a
nous access and control of the airway. minor component. The small cannulas (blue, 22G,
The broad options for anaesthesia involve one or 0.41 mm diameter) have a maximum flow rate of
more of the following: local anaesthesia, sedation, about 30 mL/min but because flow is related to the
regional anaesthesia (spinal, epidural or nerve fourth power of the radius, a large cannula (orange,
3: Anaesthesia and pain medicine 23
14G, 1.6 mm diameter) has 10 times the flow (300 some supplemental oxygen due to respiratory
mL/min). Flow is enhanced in cannulas sited in larger depression or in order to wash out carbon dioxide
veins. For adult trauma patients, the standard of care and to reduce claustrophobia under drapes.
is two 16‐gauge cannulas in large cubital fossa veins Contemporary supplemental oxygen is often accom-
with a total flow of up to 400 mL/min (2 × 200 mL/ panied by continuous monitoring of expired carbon
min). This would be similar to intravenous access for dioxide. This safety measure detects hypoventilation
major surgery. Long catheters placed in central veins and airway obstruction due to apnoea.
(central lines), particularly the internal jugular vein,
are used for reliable and robust intravenous access
for drugs that could cause harm if they passed into Postoperative pain medicine
interstitial tissue through damaged peripheral veins
or if the drugs were suddenly stopped. Such drugs All anaesthetists, and many surgeons, are trained in
include potent vasoconstrictors whose sudden cessa- acute pain medicine. Advanced pain medicine is
tion can lead to severe shock and where extravasa- now a medical speciality with many practitioners
tion can lead to tissue necrosis. Central lines also also being anaesthetists. Good pain control after
allow easy venous blood sampling for analysis and surgery is a central part of postoperative care. The
for measurement of central venous pressure. most important cause of chronic post‐surgical pain
is severe acute postoperative pain.
Intraoperative monitoring Pharmacological therapy will be combined with
strategies such as physiotherapy and proactive
The most important intraoperative monitor is the
nursing care to effectively and efficiently return the
pulse oximeter, which allows continuous non‐
patient to the best possible function and recovery
invasive measurement of blood oxygen saturation
from their surgical condition. Other aims include
and heart rate. Falling oxygen saturation is most fre-
minimising the risks of pain therapies for the indi-
quently due to inadequate ventilation or inadequate
vidual and the spread of drugs of addiction (par-
inspired oxygen in patients who are anaesthetised
ticularly opioids) into the broader community.
but spontaneously breathing. Other fundamental
Collaboration with an anaesthetist‐led acute pain
monitoring includes ECG to detect changes or
service greatly facilitates these aims. Further, acute
abnormalities in heart rate and rhythm, and blood
pain medicine is more complex at extremes of age
pressure monitoring with either intermittent non‐
and in those with complex comorbidity, those suf-
invasive cuff measurements (usually the brachial
fering from opioid tolerance or dependence, obese
artery) or continuous invasive arterial monitoring
patients and those with complex pain syndromes.
(usually the radial artery).
While anaesthetists will usually plan and estab-
Contemporary anaesthesia machines can per-
lish a postoperative pain management plan, ward
form extensive electronic monitoring of multiple
clinicians need to measure a patient’s pain, often
patient and machine variables. In addition to the
with a 0–10 visual analogue scale and alter the plan
fundamental monitoring previously outlined,
if patients have poor pain control or side effects,
anaesthesia machines monitor inspired and expired
particularly excess sedation. Postoperative care also
gases (oxygen, carbon dioxide and anaesthetic
involves weaning from analgesia as appropriate
gases). Further, anaesthesia machines have complex
and moving the patient to oral pain relief appropri-
alarm systems that enhance safety monitoring indi-
ate for community discharge and subsequent cessa-
vidualised to the patient and procedure. Modern
tion. Chronic post‐surgical pain is an important
machine ventilators allow both full mechanical
complication after surgery. While some operations,
ventilation and assisted spontaneous ventilation.
particularly surgery via thoracotomy, carry a major
Depth of anaesthesia can be routinely monitored
risk of chronic post‐surgical pain, one in ten patients
with specialised EEG, and depth of muscle relaxa-
will have chronic pain after abdominal surgery.
tion with neuromuscular monitoring
Multimodal analgesia aims to combine the bene-
fits of different mechanisms to treat pain to provide
Oxygen therapy and airway interventions
high‐quality pain relief and minimise side effects.
Intraoperative airway interventions range from sup- The following list gives an indication of the postop-
plemental oxygen via nasal prongs through to erative analgesic options that can be individualised
endotracheal intubation. Even patients undergoing to patients and operations.
procedures under local anaesthesia and sedation, • Paracetamol: regular paracetamol is an effective
such as minor plastic surgery, or those undergoing foundation for multimodal analgesia. With appro-
major surgery under spinal anaesthesia may require priate dosing paracetamol has minimal side effects.
• Non‐steroidal anti‐inflammatory drugs arrhythmias and cardiac arrest but are dose
(NSAIDs): these drugs form the next tier of anal- related and rare with contemporary practice.
gesics. While being very effective analgesics,
NSAIDs can increase the risk of bleeding and Further reading
acute kidney injury. For most patients the bene-
fits greatly outweigh these relatively rare risks. American College of Surgeons. Surgical Risk Calculator.
• Opioids: morphine has been a mainstay of pain Available at https://riskcalculator.facs.org/RiskCalculator/
relief for centuries. In contemporary practice National Institute for Health and Care Excellence.
morphine is administered in many ways: oral, Routine Preoperative Tests for Elective Surgery. Nice
subcutaneous, intramuscular, intravenous, epi- Guideline NG45. London: NICE, 2016. Available at
dural and spinal. Many patients receive mor- https://www.nice.org.uk/guidance/ng45
Schlug SA, Palmer GM, Scott DA, Halliwell R, Trinca J.
phine via patient‐controlled analgesia (PCA) that
Acute pain management: scientific evidence, fourth edi-
aims to empower the patient and reduce risks. All
tion, 2015. Med J Aust 2016;204:315–17.
routes of morphine administration carry the risk Thilen SR, Wijeysundera DN, Treggiari MM. Preoperative
of life‐threatening respiratory depression and consultations. Anesthesiol Clin 2016;34:17–33.
death. Hospital protocols aim to minimise these
risks. However, far more frequent complications
include nausea, constipation and itch. Other fre- MCQs
quently used alternative opioids are fentanyl and
Select the single most appropriate answer to each
oxycodone. Tramadol is an atypical opioid with
less respiratory depression, constipation and
potential for abuse. However, tramadol can have
important drug interactions that can limit its use,
1 A fit and healthy patient having their anterior
including a serotonin syndrome with some anti-
cruciate ligament repaired:
depressants. There is a strong trend towards min-
a has no cardiopulmonary perioperative risks
imising use of opioids around the time of surgery
b is American Society of Anesthesiologists Society
to reduce the frequency of in‐hospital opioid
Physical Status 1
complications (nausea and vomiting, constipa-
c will require minimal analgesia
tion and itch), reduce long‐term opioid use and
d will require a postoperative critical care bed and
reduce community opioid abuse.
prolonged hospital stay
• Ketamine: this drug acts on different receptors
e is likely to have obstructive sleep apnoea
from the opioids and provides complementary but
different analgesia and is opioid sparing. Ketamine 2 Anaesthesia assessment:
infusion is often introduced for inadequately a is usually just before induction of anaesthesia
treated pain after major surgery and for patients b requires blood tests
at significant risk with opioid analgesia. The major c excludes patients with complex pain syndromes
complication with ketamine is hallucinations. d requires history, examination and further tests
• Anticonvulsants: gabapentin and pregabalin are e is independent of surgical assessment
two anticonvulsants used to treat chronic as well
as acute pain from nerve injury, which can occur 3 Which of the following risk factors for postopera-
in many types of surgery. These drugs are also tive nausea and vomiting (PONV) is incorrect?
opioid sparing and reduce opioid side effects. a old age
• Local anaesthetics: increasingly, patients on b gender
wards have infusions of local anaesthetic through c previous nausea and vomiting
specialised catheters placed by anaesthetists that d non‐smoking
provide direct analgesia to major nerves and e use of opioids
nerve plexuses, or wound catheters placed by sur-
geons. Epidural infusions are still used in some 4 Opioids:
major thoracic and abdominal surgery, usually on a are the foundation of all pain management plans
an individualised basis. These infusions may pro- b have excitation as a major side effect
vide better postoperative analgesia, less opioid c cause diarrhoea
use and less PONV, itch and sedation than only d can be administered by several routes
using systemic analgesia. The most important side e are contraindicated for patients taking
effects of local anaesthetics are fitting, cardiac paracetamol
4 Postoperative management
Peter Devitt
Department of Surgery, University of Adelaide and Royal Adelaide Hospital, Adelaide,
South Australia, Australia
anaesthetist by the end of the procedure. In check-

Introduction ing the charts of the patient after the procedure,
care will be taken that these and any other medica-
Good postoperative management will have started
tions required are prescribed and administered.
before the procedure with appropriate counselling
These may include antibiotics (prophylactic or ther-
and preparation (see Chapter 1). This preparation
apeutic), sedatives, anti‐emetics and anticoagulants.
will have included an assessment of fitness for the
procedure and identification and management of
Monitoring
any risk factors. The patient will have been provided
with a clear explanation of the procedure (emer- Depending on the nature of the procedure and the
gency or elective), the risks and benefits, and the underlying state of health of the patient, the vital
likely outcome. This will have included a description signs (blood pressure, pulse and oxygen saturation)
of what the patient should expect in terms of short‐ will be measured and recorded regularly. If an arte-
and long‐term recovery from the procedure, possi- rial catheter has been inserted, blood pressure and
ble complications and the necessity for any drains, pulse readings can be observed on a monitor con-
stomas, catheters or other bits of tubing, the details stantly. The intensity and frequency of monitoring
of which would be alien to most of the population. will be maximal in the recovery room and this level
The anticipated length of time in hospital will have of scrutiny maintained if the patient is in an inten-
been discussed, as well as details of how long it will sive care or high‐dependency area.
take to make a full recovery from the procedure and Measurement of the central venous pressure may
how long the patient will be away from or unable to be required for patients with poor cardiorespira-
participate in their usual activities. The patient will tory reserve or where there have been large volumes
have been reassured about pain control measures of fluid administered or major fluid shifts are
and, perhaps most difficult of all, the doctor will expected.
have tried to ensure that the patient’s expectations The patient chart will also record all fluid that
match those of the health professional. has been given during and since the operation,
This chapter will focus on the care of the patient in together with fluid lost. Ideally, these figures will
the immediate postoperative period, up until the time have been balanced by the end of the procedure, so
of discharge from hospital. The immediate and short‐ that the duty of the attending doctor will be to
term needs of the patient and care to be provided will monitor ongoing losses (digestive and urinary
depend on the magnitude and type of surgery. tracts, drains, stomas) and replace these. The nor-
mal daily fluid and electrolyte requirements will
also be provided. If there has been major fluid shifts
or if renal function is precarious, a urinary catheter
Immediate management of the patient will be inserted and regular (hourly) checks made
of fluid losses. Serum electrolytes and haematologi-
Pain management
cal values will be checked frequently, again the fre-
Pain relief is of paramount importance (see quency depending on any abnormalities present
Chapter 3) and an appropriate drug regimen will and the magnitude of any fluid and electrolyte
have been prescribed by the surgeon and/or replacement.
25
Mobilisation Prophylaxis against venous

thromboembolism
Early mobilisation is encouraged. Unless there are
specified orders to the contrary, all patients are This is a key part of the management of any hospi-
encouraged to get up and move around as much talised individual, particularly the surgical patient.
as their underlying condition will allow. Obvious A risk analysis will have been performed preopera-
exceptions to this policy include patients with epi- tively (see Chapter 1) and depending on the nature
dural catheters and those with severe multiple of the procedure and the individual’s risk, some
injuries. The aim of early mobilisation is to form of chemoprophylaxis may be started in the
encourage good pulmonary ventilation and to postoperative period. This will require day‐to‐day
reduce venous stasis. For those who cannot mobi- monitoring and for major procedures, such as hip
lise, physiotherapy should be provided to help joint replacement or many cancer operations, the
with breathing and measures taken to either prophylaxis may be continued after discharge from
increase venous flow (pneumatic calf compression hospital. For patients being managed in intensive
devices) or reduce risks of deep vein thrombosis care settings and who, for various reasons, will
(heparin). The timing of any planned heparin have limited or no mobility, intermittent mechani-
administration will depend on the nature of the cal calf compression will be used in addition to
procedure and the risks of haemorrhage from that chemoprophylaxis.
procedure.
Enhanced recovery after surgery (ERAS)
Communication programs
When problems arise, they are frequently com- These structured programs are starting to replace
pounded by a failure of communication. Whilst traditional surgical practices, with implementation
the doctor’s duty of care is to the patients them- of protocols for early postoperative feeding, early
selves, the needs of the relatives must be taken mobilisation and more effective pain control meas-
into account. Simple things – which are often for- ures. Evidence now exists showing that these ERAS
gotten – include a reassuring telephone call to the systems can significantly reduce length of hospital
nearest relative after a procedure, informing them stay and complications rates, with overall reduction
(usually in general terms) of how the procedure in healthcare costs.
went. Whilst this is most obvious in the paediatric
setting, the same principles should be followed Respiratory care
with adult healthcare. The patients themselves
In the otherwise fit and healthy patient, maintenance
will seek some form of reassurance in the immedi-
of respiratory function is usually not a problem, par-
ate postoperative period. They will want to know
ticularly if there is optimal management of pain.
how the procedure went and how they are pro-
Even with upper abdominal or thoracic procedures,
gressing. They will also want reassurance that all
most patients will require little respiratory support
the tubes, lines and equipment to which they are
provided they are able to mobilise themselves and
attached are quite normal and not an indication
breathe unimpeded by pain. When assistance is
of impending disaster. Ideally, this will have been
required simple breathing exercises, with or without
discussed with them prior to the procedure. Any
the help of a physiotherapist, is usually sufficient.
unexpected findings or complications encoun-
Mechanical ventilation may be required in the early
tered during the procedure should be discussed
phase of recovery from a particular procedure. This
with the patient. The timing and detail of this dis-
can vary from prolonged endotracheal intubation, to
cussion is a matter of fine judgement and may be
intermittent positive pressure ventilation, to supple-
best done in the presence of the patient’s relatives
mental oxygenation by face mask or nasal prongs. In
and by the individual who performed the
these instances the patient may require prolonged
procedure.
monitoring in an intensive care or high‐dependency
unit with regular assessment of oxygen saturation
(pulse oximetry and arterial blood gas analysis).
Further care in the postoperative period For less fit patients, and particularly those with
chronic obstructive pulmonary disease (COPD), the
This covers the time from recovery from anaesthe- risks of respiratory failure will be considerable and
sia and initial monitoring to discharge from measures such as epidural local anaesthesia will be
hospital. Wound care is discussed in Chapter 6. employed. Control of pain, attention to regular
4: Postoperative management 27
hyperinflation (inhalation spirometry and physio-

Table 4.1 Electrolyte concentrations.
therapy) and early mobilisation are the keys to pre-
venting respiratory complications. Electrolyte Extracellular fluid Intracellular fluid
(mmol/L) (mmol/L)
Fluid balance Sodium 135 10

Potassium 4 150
The three principles of management of fluid bal-
Calcium 2.5 2.5
ance are:
Magnesium 1.5 10
• correct any abnormalities Chloride 100 10
• provide the daily requirements Bicarbonate 27 10
• replace any abnormal and ongoing losses. Phosphate 1.5 45
Ideally, any abnormalities will have been identi-
fied and corrected before or during the surgical
procedure. In the calculation of a patient’s fluid relatively simple regimen is 1 L of 0.9% saline and
requirements, there is a distinction to be made 1–2 L of 5% dextrose solution.
between the volume required to maintain the Both these solutions are isotonic with respect to
body’s normal functions and that required to plasma. The electrolyte solution contains the basic
replace any abnormal losses. The normal mainte- electrolyte requirements (154 mmol/L of sodium
nance fluid requirements will vary depending on and 154 mmol/L of chloride) and the total volume
the patient’s age, gender, weight and body surface can be adjusted with various amounts of dextrose
area. solution. Potassium can be added as required.
Other solutions (e.g. Ringer’s lactate) may contain
Basic requirements a more balanced make‐up of electrolytes, but are
rarely needed for a patient who is otherwise well
The total body water of a 70‐kg adult comprises
and only requires intravenous fluids for a few days.
45–60% of body weight. Lean patients have a
In the immediate postoperative period there is an
greater percentage of their body weight as body
increased secretion of antidiuretic hormone (ADH),
water and older patients a lesser proportion. Of the
with subsequent retention of water. In an adult of
total body water, two‐thirds is in the intracellular
average build, maintenance fluids can be restricted
compartment and one‐third is divided between
to 2 L per day with no potassium supplements until
plasma water (25% of extracellular fluid) and
a diuresis has occurred. This is not an absolute rule,
interstitial fluid (75% of extracellular fluid).
and potassium supplements can be given early, pro-
Therefore, a lean individual weighing 70 kg would
vided the patient has normal renal function.
have a plasma water of 3 L, an interstitial volume
Fluid and electrolyte replacement is that required
of 11 L and an intracellular volume of 28 L, making
to correct abnormalities. Volume depletion and
a total volume of 42 L.
electrolyte abnormalities are relatively common in
The normal daily fluid requirement to maintain a
surgical patients, particularly those admitted with
healthy 70‐kg adult is between 2 and 3 L. The indi-
acute illnesses. Volume depletion usually occurs in
vidual will lose about 1500 mL in the urine and
association with an electrolyte deficit, but can occur
about 500 mL from the skin, lungs and stool. Loss
in isolation. Reduced fluid intake, tachypnoea,
from the skin will vary with the ambient
fever or an increase in the ambient temperature
temperature.
may all lead to a unilateral volume loss. This will
The electrolyte composition of intracellular fluid
cause thirst and dehydration, which may progress
(ICF) and extracellular fluid (ECF) varies
to a tachycardia, hypotension and prostration. In
(Table 4.1). Sodium is the predominant cation in
severe cases there may be hypernatraemia and
ECF while potassium predominates in the ICF. The
coma. Intravenous administration of 5% dextrose
normal daily requirements of sodium and potas-
is used to correct the problem.
sium are 100–150 mmol and 60–90 mmol, respec-
More often volume depletion is accompanied
tively. This will balance the daily loss of these two
by an electrolyte deficit. Excessive fluid and elec-
cations in the urine.
trolyte may be lost from the skin (e.g. sweating,
burns), the renal tract (e.g. diabetic ketoacidosis)
Replacement
and the gastrointestinal tract (e.g. vomiting, ileus,
If an otherwise healthy adult is deprived of the nor- fistula, diarrhoea). There is considerable scope for
mal daily intake of fluid and electrolytes, suitable abnormal fluid losses in a surgical patient, par-
intravenous maintenance must be provided. One ticularly after a major abdominal procedure.
Table 4.2 Approximate electrolyte concentrations.
Sodium Potassium Chloride Bicarbonate Hydrogen

Secretions (mmol/L) (mmol/L) (mmol/L) (mmol/L) (mmol/L)
Salivary 50 20 40 50 —
Gastric 50 15 120 20 70
Duodenal 140 5 80 — —
Biliary 140 10 100 40 —
Pancreatic 140 10 80 80 —
Jejuno‐ileal 130 20 105 30 —
Faeces 80 10 100 25 —
Diarrhoea 100 30 50 60 —
There may be pooling of fluid at the operation nasogastric intubation to decompress the stomach
site itself, an ileus might develop, fluid could be after surgery for intestinal obstruction. Sump
lost through a nasogastric tube or drains, and drains are used to irrigate sites of contamination or
there might be increased cutaneous loss if there is infection.
a high fever. Drains can act as a point of access for infection,
The source of fluid loss will determine the type of and whilst this may be of little consequence if the
electrolyte lost. There is considerable variation in tube has been placed to drain an abscess cavity, all
the electrolyte content of different gastrointestinal efforts are made to reduce contamination of any
secretions (Table 4.2). Loss from the upper diges- wound. There is increased use of closed drainage
tive tract tends to be rich in acid, while loss from systems and dressings around drains are changed
the lower tract is high in sodium and bicarbonate. regularly. Any changes to tubes or bags on drains
Thus, patients with severe and prolonged vomiting must be carried out using aseptic techniques. Once
from gastric outlet obstruction may develop a met- a drain has served its purpose, it should be removed.
abolic alkalosis. The longer a drain stays in situ, the greater the risk
While the management of maintenance fluid of infection.
requirements can often be done on a daily basis, the The contents and volumes discharged through a
fluid and electrolyte replacement needs of an drain must be recorded. Large volumes, such as
acutely ill surgical patient is likely to be more those from the gastrointestinal tract, may need the
involved and necessitate close monitoring and equivalent amount replaced intravenously.
adjustment. Clinical assessment and appreciation
of the types of fluid loss will give an approximate
guide to the scale of the problem, but regular bio- Gut function
chemical electrolyte estimations will be required to
Some degree of gut atony is common after abdomi-
determine the precise composition of what needs to
nal surgery, particularly emergency surgery. The
be replaced. In most instances, measurement of
condition is usually self‐limiting and of little clini-
plasma electrolyte concentrations will provide suf-
cal consequence. There are three conditions that
ficient information, but occasionally it may be nec-
can produce massive gut dilatation and pose seri-
essary to estimate the electrolyte contents of the
ous problems for the patient:
various fluids being lost.
• gastric dilatation
• paralytic (small intestine) ileus
Drains and catheters • pseudo‐obstruction (large intestine).
Drains serve a number of purposes. They may be
Gastric dilatation
inserted into an operative site or into a wound as it
is being closed to drain collections or potential Gastric dilatation is rare and when it occurs tends
collections. Drains may also be put into the chest to be associated with surgery of the upper digestive
cavity to help the lungs re‐expand. They may be tract. It may occur suddenly 2–3 days after the
put into ducts and hollow organs to divert secre- operation and is associated with massive fluid
tions or to decompress that structure. Examples of secretion into the stomach, with the consequent
decompression include insertion of a tube into the risk of regurgitation and inhalation. Treatment is
common bile duct after duct exploration or by insertion of a nasogastric tube and
decompression of the stomach. Unfortunately, frequency in the patient undergoing an emergency

when gastric dilatation does occur, often the first procedure. The preoperative assessment will have
indication of the problem is a massive vomit and judged the individual’s risk and measures that
inhalation after the dilatation has occurred. By then might need to be taken to minimise respiratory
the damage is done and the value of a nasogastric problems (see Chapter 1). Apart from any comor-
tube at this stage is questionable. Traditionally, bidities, such as COPD, the likely cause of a patient’s
nasogastric tubes were used routinely for patients hypoxaemia will vary with the time of onset
following laparotomy, particularly in the emer- (Box 4.1).
gency setting. However, the nasogastric tube is Measures must be taken to minimise the risks of
often the patient’s major source of irritation and postoperative pulmonary complications, including
discomfort in the postoperative period and its rou- judicious use of pain medications, where local
tine use is gradually being abandoned. wound infiltration or nerve blocks may be more
appropriate than systemic measures. Early mobili-
Paralytic ileus sation and encouragement to cough and breathe
deeply must be actively promoted.
Paralytic ileus is less sinister and more common. In
Depending on the initial state of respiratory
the acutely ill patient who has undergone surgical
function and the degree of deterioration, the patient
intervention for peritonitis, paralytic ileus may be
may require anything from supplemental oxygen
present from the first postoperative day. Otherwise,
supplied by face mask to endotracheal intubation.
it tends to make its presence felt about 5 days after
A Pco2 above 45 mmHg, a Po2 below 60 mmHg
operation, and the patient may have been making
and a low tidal volume all indicate that mechanical
an apparently uneventful recovery. Abdominal dis-
ventilation will be required. Once appropriate ven-
tension occurs and the patient may vomit. Oral
tilatory support has been achieved, the cause of the
fluid restriction should be instituted and intrave-
respiratory failure can be addressed.
nous replacement may be required. Most cases
resolve spontaneously. Occasionally a prokinetic
Wound failure
agent may be considered.
Provided the surgical procedure has a minimal risk
Pseudo‐obstruction of infection (see Chapter 9) and has been performed
in an uneventful manner in a low‐risk patient, then
Classically, pseudo‐obstruction occurs in the
the chances of problems with the wound are mini-
elderly patient who has recently undergone sur-
mal and most such wounds can be left undisturbed
gery for a fractured neck of femur. The condition
is also often seen where there has been extensive
pelvic or retroperitoneal injury and sometimes the
condition appears to be more related to the use of Box 4.1 Factors contributing to
opiate analgesia rather than the type of surgery postoperative hypoxaemia
itself. The atony, with abdominal distension and
absence of bowel function, tends to occur 2–3 Immediate
days after surgery (or from the time the injury was Respiratory depression (anaesthetic agents, opioids)
sustained). Pseudo‐obstruction is often mistaken Within first 24 hours
for mechanical obstruction and the dilatation of Established respiratory disease (e.g. COPD)
the colon and caecum can be massive. If the condi- Obesity
tion does not resolve spontaneously, colonoscopic Excessive sedation
decompression is usually successful. Occasionally, Opiates
surgical intervention is required to prevent caecal Aspiration
perforation. Pneumothorax
Between days 2 and 5

Infection
Diaphragmatic splinting (secondary to abdominal
Important postoperative complications
distension)
Pleural effusion
Respiratory complications
Acute respiratory distress syndrome
Deterioration or impairment of respiratory func-
After day 5
tion is the commonest and more important postop- Pulmonary embolus
erative complication, occurring with greatest
until the patient leaves hospital. If there are identifi- dissection in subcutaneous tissues (e.g. mastec-
able risks the wounds may need to be attended to tomy) or where lymphatics may be damaged (e.g.
regularly. The problems that are likely to occur groin dissections). The seroma may not appear a
with wounds relate to: week after the procedure. Seromas will lift the skin
• discharge of fluid off the underlying tissues and impede wound heal-
• collection of fluid ing. They also make fertile ground for infection.
• disruption of the wound. Seromas should be aspirated under sterile condi-
Risk factors that may contribute to these prob- tions and the patient warned that several aspira-
lems include those that: tions may be required as the seroma may
• increase the risk of infection (see Chapter 9) re‐collect.
• increase the risk of wound breakdown.
There are general and local factors that increase
Confusion
the risk of breakdown of a wound. General factors
include those that interfere with wound healing, Confusion in surgical patients is common and has
such as diabetes mellitus, immunosuppression, many causes. Often the confusion is minor and
malignancy and malnutrition. Local factors include transient and does not need treatment. The patient
the adequacy of wound closure, infection and any- is typically elderly, has become acutely ill and in
thing that might put mechanical stress on the pain, is removed from the security and familiarity
wound. For example, abdominal wound failure is a of their home surroundings, is subject to emergency
potential problem in the obese, and in those with surgery and more pain, is put in a noisy environ-
chest infections, ascites or ileus. ment with strangers bustling around and is sleep‐
In the early stages of wound healing any abnor- deprived. These factors alone would make many
mal fluid at the wound site is likely to discharge otherwise healthy individuals confused. Add to that
rather than collect. The fluid may be blood, serous recipe the deprivation of the patient’s regular medi-
fluid, serosanguinous fluid or infected fluid of vary- cations (particularly alcohol), the upset to their
ing degrees up to frank pus. As discussed elsewhere body biochemistry, the presence of hypoxia and a
in this chapter, the discharge of blood from a wound variety of postoperative medications such as opi-
may have all sorts of consequences for the patient, oids, and it becomes understandable that some
which will vary from prompt opening of the neck degree of confusion is very common in the postop-
wound of a patient with a primary haemorrhage erative period. Confusion combined with restless-
after a thyroidectomy to evacuation of a haema- ness, agitation and disorientation is referred to as
toma after a mastectomy. delirium.
Serous fluid may be of little significance and be Important causes of confusion include:
the result of a liquefying haematoma from within • Sepsis (operative site, chest, urinary tract)
the depths of the wound. However, a serosan- • Hypoxia (chest infection, pulmonary embolus,
guinous discharge from an abdominal or chest pre‐existing pulmonary disease)
wound may herald a more sinister event, particu- • Metabolic abnormalities (hyponatraemia, hyper-
larly if it occurs between 5 and 8 days after the glycaemia/hypoglycaemia, acidosis, alkalosis)
operation. The discharge may have been preceded • Cardiac
by coughing or retching. Such a wound is in immi- • Hypotension (haemorrhage, dehydration)
nent danger of deep dehiscence with evisceration. • Cerebrovascular event
Should such an event occur, the wound must be • Drug withdrawal (alcohol, opiates, benzo-
covered in sterile moist packs and arrangements diazepines)
made to take the patient to the operating room for • Drug interaction (opiate sedation)
formal repair of the wound. • Exacerbation of pre‐existing medical conditions
Collections in and under a wound may be blood, (dementia, hypothyroidism).
pus or seroma. As mentioned, the rapidity with When a patient does become confused in the
which a haematoma appears and any pressure postoperative period, it is important to ensure that
effects such a haematoma may cause will determine no easily correctable cause has been overlooked.
its treatment. Collections of pus must be drained. Confusion is often secondary to hypoxia, where
Depending on its proximity or distance from the chest infection, over‐sedation, cardiac problems
skin surface, an abscess may be drained by opening and pulmonary embolism need to be considered.
the wound or inserting (under radiological control) Other important causes to consider include sepsis,
a drain into a deeper‐lying cavity. Seromas tend to drug withdrawal, metabolic and electrolyte distur-
occur where there has been a large area of bances and medications.
The management of the confused patient will operation is common and may reflect little more
include a close study of the charts, seeking informa- than the body’s metabolic response to injury.
tion on any coexisting disease (particularly cardi- A fever that is evident between 5 and 7 days after
orespiratory), drug record, alcohol consumption an operation is usually due to infection. While pul-
and the progress of the patient since the operation. monary infections tend to occur in the first few
Current medications should be noted, together with days after surgery, fever at this later stage is more
the nursing record of the vital signs. likely to reflect infection of the wound, operative
If possible, try to take a history and examine the site or urinary tract. Cannula problems and deep
patient. Ensure that the patient is in a well‐lit room vein thrombosis (DVT) should also be considered.
and give oxygen by face mask. Attention should be A fever occurring more than 7 days after a surgi-
focused on the cardiorespiratory system, as this cal procedure may be due to abscess formation.
may well be the site of the underlying problem. Apart from infection as a cause of fever, it is impor-
Some investigations may be required to help deter- tant to remember that drugs, transfusion and brain-
mine the cause of the confusion. These might stem problems can also produce an increase in body
include arterial blood gas analysis, haematological temperature.
and biochemical screens, blood and urine cultures, A careful history, review of the charts and physi-
a chest X‐ray and an electrocardiogram (ECG). cal examination will usually determine the cause of
Most patients with postoperative confusion do not the fever. The next stage in management will depend
require treatment other than that for the underlying on the state of health of the patient. The fever of a
cause. However, the noisy violent patient may need septic process, which has led to circulatory collapse,
individual nursing care, physical restraint or seda- will require resuscitation of the patient before any
tion. Sedation should be reserved for patients with investigation. Otherwise, appropriate investiga-
alcohol withdrawal problems, and either haloperidol tions may include blood and urine cultures, swabs
or diazepam should be considered in such circum- from wounds and drains, and imaging to define the
stances. Most hospitals have clearly defined proto- site of infection.
cols for the management of patients going through Treatment will depend on the severity and type of
alcohol withdrawal. These correlate the anxiety, vis- infection. The moribund patient will require resus-
ual disturbances and agitation of the patient with the citation and empirical use of antibiotics, the choice
degree of monitoring and sedation required. varying with the likely source of infection. Surgical
or radiological intervention (e.g. to drain an
abscess) may be required before the patient
Pyrexia
improves. However, the well patient may have anti-
The normal body temperature ranges between 36.5 microbial therapy deferred until an organism has
and 37.5°C. The core temperature tends to be been identified (e.g. Gram stain or culture).
0.5°C warmer than the peripheral temperature.
Thus an isolated reading of 37.5°C has little mean-
ing by itself and needs to be viewed in context with
Deep vein thrombosis and pulmonary
the other vital signs. Changes in temperature and
embolism
the pattern of change are more important. A tem- These complications can still occur despite prophy-
perature that rises and falls several degrees between laxis (see Chapter 1). Presentation of DVT may be
readings suggests a collection of pus and intermit- silent (60%) or as a clinical syndrome (40%). If
tent pyaemia, while a persistent high‐grade fever is suspected on clinical grounds (painful, tender and
more in keeping with a generalised infection. swollen calf), duplex ultrasonography is the investi-
Fever can be due to infection or inflammation. In gation of choice, with a sensitivity and specificity
determining the cause of the fever the following greater than 90%. In cases of suspected pulmonary
should be considered: embolism, a CT pulmonary angiogram is the appro-
• the type of fever priate investigation.
• the type of procedure which the patient has The treatment of DVT has now moved from
undergone unfractionated heparin infusion to subcutaneous
• the temporal relationship between the procedure low‐molecular‐weight heparin. This is maintained
and the fever. until the patient is fully anticoagulated on warfarin
Perhaps the most useful factor in trying to estab- and the latter is continued for 3–6 months to mini-
lish the cause of a patient’s fever is the relationship mise the risk of further thrombosis and the devel-
between the time of onset of the fever and the pro- opment of complications (see Chapters 73 and 75).
cedure. Fever within the first 24 hours of an A caval filter might have to be considered,
particularly for clot extending into the iliofemoral considered due to hypovolaemia until proven
segments. otherwise.
The treatment of a pulmonary embolus will
depend on the severity of the event. A relatively Hyponatraemia
minor episode, with no cardiovascular compro-
mise, can be managed with heparinisation, whereas Any reduction in the sodium concentration in the
a more serious embolus may need surgical interven- ECF may be absolute or secondary to water reten-
tion (embolectomy) or use of a fibrinolytic agent. tion. Loss of the major cation from the ECF leads to
a shift of water into the ICF. Any clinical manifesta-
Oliguria tion will reflect the expansion of the ICF (e.g. con-
Oliguria is a common problem in the postoperative fusion, cramps, and coma secondary to cerebral
period and is usually due to a failure by the attend- oedema) or the contraction of the ECF in absolute
ing medical staff to appreciate the volume of fluid hyponatraemia (e.g. postural hypotension, loss of
lost by the patient during the surgical procedure and skin turgor).
in the immediate postoperative period. For example, Hyponatraemia due to a total body deficiency of
the development of an ileus will lead to a large vol- sodium ions is an unusual scenario in the postop-
ume of fluid being sequestered in the gut and this erative surgical patient. Any hyponatraemia that
‘loss’ not being immediately evident. Before the occurs tends to be due to dilution and is caused by
apparent oliguria is put down to diminished output the administration of an excessive amount of water.
of urine, it is important to ensure that the patient is While this is a fairly frequent biochemical finding,
not in urinary retention. Such an assessment can be it rarely leads to any clinically significant problem.
difficult in a patient who has just undergone an Any hyponatraemia secondary to dilution may
abdominal procedure. If there is any doubt, a uri- also occur with inappropriate ADH secretion. The
nary catheter must be inserted. Alternately, most trauma of major surgery will produce an increase in
wards are now equipped with ultrasonographic ADH secretion and intravenous fluid must be
devices capable of providing an accurate estimation administered judiciously in the immediate postop-
of the bladder content. erative period. A safe rule of thumb is to restrict the
Diminished output of urine may be due to: patient to 2 L per day of maintenance fluid until a
• poor renal perfusion (pre‐renal failure due to diuresis has been established. Hyponatraemia can
hypovolaemia and/or pump failure) usually be corrected by the administration of the
• renal failure (acute tubular necrosis) appropriate requirements of isotonic saline. If the
• renal tract obstruction (post‐renal failure). patient has a severe hyponatraemia and associated
In the assessment of a patient with poor urine mental changes, an infusion of hypertonic sodium
output (<30 mL/h), these three possible causes must solution may be required.
be considered. Major surgery with large intraopera-
tive fluid loss and periods of hypotension during Hypernatraemia
the procedure might suggest renal tissue damage
Hypernatraemia in the postoperative patient is a
(acute tubular necrosis), while severe peritonitis
less common problem than hyponatraemia. Any
with large fluid shifts and no hypotension would be
hypernatraemia is usually relative rather than abso-
more in keeping with inadequate fluid
lute and occurs secondary to diminished water
replacement.
intake. Patients with severe burns or high fever may
The treatment of oliguria depends on the cause.
also develop hypernatraemia. An increase in the
Pre‐renal hypovolaemia is treated by fluid replace-
plasma sodium concentration will lead to a loss of
ment, while poor output secondary to pump failure
ECF volume and relative intracellular desiccation.
requires diuretic therapy and perhaps medications
The first clinical manifestation is thirst and if the
(e.g. inotropes, antiarrhythmics) to improve cardiac
hypernatraemia is allowed to persist, neurological
function. To give a hypovolaemic patient a diuretic
problems (e.g. confusion, convulsions, coma) may
in an attempt to improve urine output may be
ensue. Treatment is by administration of water by
counterproductive and detrimental.
mouth or intravenous 5% dextrose.
In acute renal failure the oliguria will not respond
to a fluid challenge. Management demands accu-
Hyperkalaemia
rate matching of input to output, monitoring of
electrolytes and even dialysis. With normal renal function, severe and life‐
In summary, most cases of postoperative oliguria threatening hyperkalaemia is rare. High concentra-
are secondary to hypovolaemia, and should be tions of potassium in the ECF can be associated
with cardiac rhythm disturbances and asystole. mechanical problem or local sepsis. Generalised
Hyperkalaemia may occur in severe trauma, sepsis bleeding may reflect a coagulation disorder and
and acidosis. Emergency treatment of arrhythmia‐ may be manifest by the oozing of fresh and unclot-
inducing hyperkalaemia consists of rapid infusion ted blood from wound edges and with bleeding
of a 1 L solution of 10% glucose with 25 units of from sites of cannula insertion.
soluble insulin. The insulin will help drive potas- Most cases of reactionary (and primary) haemor-
sium into the cells and the glucose will help coun- rhage are from a poorly ligated vessel or one that has
teract the hypoglycaemic effect of the insulin. At the been missed, and are not secondary to any coagula-
same time 20 mmol of calcium gluconate can be tion disorder. The bleeding point may go unnoticed
given to help stabilise cardiac membranes. If an during the operation if there is any hypotension, and
arrhythmia has already developed, the calcium glu- makes itself known only when the patient’s circulat-
conate should be given before the dextrose and ing volume and blood pressure have been restored to
insulin. Sodium bicarbonate (20–50 mmol) can be normal. The bleeding in secondary haemorrhage is
given if the patient is acidotic. If the level of potas- due to erosion of a vessel from spreading infection.
sium is not too high, an ion‐exchange resin (reso- Secondary haemorrhage is most often seen when a
nium) can be given. These resins can be administered heavily contaminated wound is closed primarily, and
by enema and they exchange potassium for calcium can usually be prevented by adopting the principle of
or sodium. Alternatively, the patient may be dia- delayed wound closure.
lysed (peritoneal or haemodialysis). In the manage- Postoperative haemorrhage can also be classified
ment of hyperkalaemia it is obviously as important according to its clinical presentation. The most com-
to treat the cause as it is to treat the effect. mon forms are wound bleeding, concealed intra-
peritoneal bleeding, gastrointestinal haemorrhage
Hypokalaemia and the diffused ooze of disordered haemostasis.
The approach to management will depend on the
Low levels of potassium in postoperative patients are overall condition of the patient and the assessment
common but hypokalaemia is rarely so severe as to of the type of bleed. A stable patient with a localised
produce muscle weakness, ileus or arrhythmias. blood‐soaked dressing will be managed differently
Patients with large and continuous fluid loss from the from a hypotensive patient with 2 L of fresh blood
gastrointestinal tract are prone to develop hypoka- in a chest drain, who in turn will be managed differ-
laemia. If potassium supplements are required they ently from a patient with a platelet count of 15 ×
may be given either orally or intravenously. If by the 109/L and fresh blood oozing from all raw areas.
latter route, the rate of infusion should not exceed In the first case the tendency might be to apply
10 mmol/h. Faster rates may precipitate arrhythmias another dressing in an attempt to achieve control by
and should only be undertaken on a unit where the pressure. A more positive approach is to remove the
patient can be monitored for any ECG changes. dressing and inspect the wound. In most instances, a
single bleeding point can be identified and con-
Haemorrhage trolled. In the next case, the patient has a major
bleed and this is probably from a bleeding vessel
The management of haemorrhage in the postopera-
within the operative site. Return to the operating
tive period may be approached in several ways. In
room and formal re‐exploration must be seriously
broad terms, bleeding may be classified as either
considered. In the third case, the prime problem is an
localised or generalised. If the former, it may be
anticoagulation defect requiring urgent correction.
classified as follows:
The diagnosis of postoperative haemorrhage is a
• primary (bleeding which occurs during the
clinical one, based on knowledge of the surgical pro-
operation)
cedure, the postoperative progress and an assess-
• reactionary (bleeding within the first 24 hours of
ment of the patient’s vital signs. The blood loss may
the operation)
not always be visible and could be concealed at the
• secondary (bleeding occurring at 7–10 days after
operative site or within the digestive tract. The treat-
the operation).
ment of postoperative haemorrhage depends on the
If localised, the bleeding is usually related to the
severity of the bleed and the underlying cause.
operative site and/or the wound. Occasionally, the
Hypovolaemia and circulatory failure will demand
bleeding may be at a point removed from both
urgent fluid replacement and consideration of the
these areas, for example gastrointestinal haemor-
likely cause and site of bleeding. Careful considera-
rhage from a stress‐related gastric erosion. Bleeding
tion must be given to control of localised haemor-
from the wound site is usually indicative of a
rhage and whether re‐operation is warranted.
Vomiting the dissection is difficult and the appendix is

found to be perforated and 100 mL of purulent
The causes of vomiting after surgery are many, and
fluid aspirated from the abdominal cavity, after
can be best determined by establishing the relation-
which a saline lavage is performed. The patient
ship between onset of vomiting and the time of the
cannot void postoperatively and requires a
operation. The two most common causes of post-
urinary catheter for 24 hours. He is kept on
operative vomiting are drug‐induced and gut atony.
intravenous antibiotics for 3 days and then
Vomiting that occurs in the immediate postoper-
discharged home on a 5‐day course of oral
ative period is usually drug related. If it is due to the
antibiotics. Three days after discharge he goes to
effects of anaesthesia, vomiting will usually settle
see his family doctor complaining of persistent
within 24 hours. Current anaesthetic techniques
diarrhoea. Which one of the following is the most
and modern anti‐emetics have rendered nausea and
likely diagnosis?
vomiting a relatively minor postoperative problem
a resolving paralytic ileus
for most patients.
b prostatitis
Vomiting that occurs several days after operation
c Clostridium difficile enteritis
may still be drug related, but in this instance is usu-
d leakage from the appendix stump
ally due to an opiate rather than an anaesthetic
e urinary tract infection
agent. Vomiting may be secondary to gut stasis, and
this atony is usually self‐limiting. If prolonged, a
3 A 56‐year‐old man undergoes a laparoscopic
prokinetic agent can be effective.
cholecystectomy 2 days after being admitted
If vomiting starts 7 days or so after abdominal
with acute cholecystitis. At operation some acute
surgery, a mechanical cause for the problem should
inflammatory changes are found around the
be considered.
gallbladder, which makes the procedure more
difficult than expected. A drain is placed in the
Further reading gallbladder bed at the end of the operation. The
following day the patient does not look well and is
Abeles A, Kwasnicki RM, Darzi A. Enhanced recovery complaining of right upper quadrant pain. He has
after surgery: current research insights and future direc- required regular morphine overnight to control his
tions. World J Gastrointest Surg 2017;9:37–45. pain. His blood pressure is 120/70 mmHg, heart
Marcantonio ER. Delirium in hospitalized older adults. rate 110 beats/min and temperature is 38.2°C. He
N Engl J Med 2017;377:1456–66.
has passed 100 mL of urine since the operation. On
pulmonary auscultation there are bibasal crackles
MCQs and there is guarding in the right upper quadrant.
Nothing has come out of the drain. Which one of
Select the single correct answer to each question. the following would be the most likely explanation
The correct answers can be found in the Answers for his current problem?
section at the end of the book. a aspiration pneumonia
b acute retention of urine
1 A previously well 56‐year‐old businessman is c bile leak
admitted with a perforated peptic ulcer and d duodenal perforation
undergoes surgery and repair of the perforation. He e pulmonary embolism
is making a satisfactory recovery but 3 days after
the operation becomes aggressive, shouting and 4 A 68‐year‐old man undergoes a semi‐elective
demands to be let home. He is still requiring laparoscopic cholecystectomy for acute cholecysti-
intravenous fluids for slow return of gut function. tis. The procedure is uncomplicated. Twelve hours
Which one of the following is the most likely later his blood pressure is 114/72 mmHg and his
explanation for his behaviour? urine output since operation has been 90 mL. He
a anxiety over work commitments has intravenous isotonic saline running at 80 mL/h.
b opiate toxicity Which one of the following is the most appropriate
c pneumonia next step in management?
d alcohol withdrawal a continue current management
e intravenous fluid overload b intravenous frusemide
c infusion of dopamine
2 A 21‐year‐old man undergoes a laparoscopic d infusion of noradrenaline
appendicectomy for appendicitis. At operation, e 1 L isotonic saline over 4 hours
5 Surgical techniques
Benjamin N.J. Thomson1 and David M.A. Francis2
1
University of Melbourne, Royal Melbourne Hospital Department of Surgery and Department of
General Surgery Specialties, Royal Melbourne Hospital, Melbourne, Victoria, Australia
2
Department of Urology, Royal Children’s Hospital, Melbourne, Australia and Department of Surgery,
Tribhuvan University Teaching Hospital, Kathmandu, Nepal
A face mask, which covers the nose and mouth,

Introduction prevents droplet spread of secretions and bacteria, is
worn for any invasive procedure and is changed after
This chapter reviews techniques used in surgical
each case. Eye protection in the form of plain plastic
practice and invasive procedures.
glasses or a visor attached to the face mask must be
worn to protect against droplet spray of infected
body fluids. Gloves are worn if there is a possibility of
The operating room (see also Chapter 12) coming into contact with patients’ body fluids. Clean
theatre attire, dedicated theatre shoes and a disposa-
The operating room is a dedicated area for surgical ble hair cover are worn while in the operating suite.
procedures and must be conducive to performing sur-
gery to the highest standards of safety for patients
and staff. The principal purpose of such a dedicated Aseptic techniques
area is to reduce the risk of infection of patients. The
operating room must be large enough for complex Joseph Lister, in 1865, first demonstrated the reduc-
procedures to be undertaken, for storage of appropri- tion in surgical site infections with disinfection
ate equipment, movement of staff, as well as the techniques. Aseptic techniques are clinical practices
maintenance of a sterile area around the operative that aim to prevent infection occurring in the
field. By changing the operating room air 20–25 times patient as a result of the surgical procedure by:
each hour at positive pressure relative to outside the • preparation and cleaning the patient’s skin with
room, low concentrations of airborne bacteria and antiseptic fluid before it is incised or punctured
particulate matter can be maintained. The number of • use of sterilised instruments, equipment or surgi-
people in the room and their movement should be cal materials which might come into contact with
minimised. Ambience within the operating theatre the operative field and surgical wound.
should be calm and professional, and procedures Personnel involved directly in the operative proce-
should be performed in a manner that is respectful to dure (surgeon, surgical assistant and ‘scrub’ nurse)
the patient and to all the staff involved. The air tem- wash their hands and forearms with antiseptic soap
perature should be such that inadvertent patient for 5 minutes before the first operation of the day
hypothermia does not occur. The operative field must and for 3 minutes before each subsequent case to
be well illuminated; surgeons sometimes wear a head reduce skin flora. More recently, alcohol‐based
light for procedures in body cavities that cannot be hand rubs have been developed that require appli-
illuminated easily by standard operating room lights. cation for 1 minute. Hands are dried with sterile
The surgeon’s assistant has the important role of towels, and a moisture‐impermeable sterile gown is
assisting and supporting the surgeon in the smooth worn. One or two pairs of sterile gloves prevent
conduct of operations. It is important to concen- transfer of bacteria from the surgeon’s hands to the
trate on the task at hand, to carry out the surgeon’s patient and also protect the surgeon from infected
instructions with speed and accuracy, to have a blood and body fluids from the patient.
sense of anticipation, and to notify the surgeon of After induction of anaesthesia, hair is removed
any potential problem during the operation. from the operative site by shaving with a razor
35
or electric clippers. The skin is cleansed with an anti-

Box 5.1 Methods of sterilisation
septic solution starting at the site where the incision
will be made and working away from the area, so Autoclave
that approximately 10–20 cm of skin around the Uses superheated steam at high pressure to reach a
incision site is prepared. The patient is covered with temperature of 121°C. Sterilisation is achieved when
sterile linen or impermeable drapes, leaving exposed droplets of superheated water evaporate immediately
only the cleansed area around the incision site, which upon reduction of pressure, thereby destroying
may be covered by a sterile adhesive plastic drape. microorganisms and leaving instruments dry. Most
surgical instruments and linen drapes are sterilised by
Surgical antiseptics autoclaving.
The commonest source of bacterial contamination Dry heat
in the operating room is from the patient. Therefore, Items which tolerate heat but not moisture can be
topical antiseptic agents are used to reduce the sterilised by dry heat, but it is less efficient and takes
number of skin organisms prior to any skin incision longer than autoclaving.
or puncture, and include the following.
Ethylene oxide gas
• Aqueous chlorhexidine (0.5%) is used to disin-
Takes several hours and is used for heat‐sensitive
fect mucous membranes and parts of the body
items such as endoscopes, electrical and optical
adjacent to structures which would be adversely
equipment and some plastics.
affected by more stringent antiseptics (e.g. the
skin around the eyes). Aqueous chlorhexidine is Glutaraldehyde
bactericidal and has low tissue toxicity. A 2% solution is used to sterilise equipment that can
• Cetrimide (2%) is bactericidal. tolerate moisture but not heat, such as urological
• Iodine‐based antiseptics, such as povidone iodine catheters, plastics and rubber.
10% (Betadine) and alcoholic iodine solution, Ionising radiation
destroy a wide range of bacteria, especially staph- Uses gamma rays and is particularly useful for
ylococci, by iodisation of microbial proteins. sterilising single‐use disposables such as plastics,
• Alcohol‐based (70%) antiseptics kill bacteria by dressings, scalpel blades and synthetic conduits.
evaporation.
• Chlorhexidine 2% can also be used in combina-
tion with 70% alcohol.
Hazards, other than those intrinsic to the anaes-
Sterility thetic and surgical operation, are organisational or
related to operating room equipment or the transfer
Anything that comes into contact with the surgical and positioning of the patient on the operating table.
wound must be sterile. The method of sterilisation
depends on the item being sterilised (Box 5.1). Organisational hazards
Universal precautions Organisational hazards should be entirely preventa-
The risk of transmission of infectious agents from ble. A full history and examination of the patient
patients to staff (and vice versa) is reduced by prac- must be made before surgery, including the past
tising universal precautions. Thus, it is assumed that medical history, drug history and allergies, so that
all patients harbour potentially dangerous patho- elementary errors are not made (e.g. unwittingly
gens (e.g. hepatitis C, HIV) no matter how innocu- operating on a patient with a pacemaker or who is
ous they appear, because carrier status cannot anticoagulated, or prescribing a drug to which the
definitely be excluded without repeated, expensive patient is allergic). Before surgery commences, the
and time‐consuming investigations. The principle of reason for and nature of the operation, together with
universal precautions is to establish a physical bar- its potential common and serious complications, and
rier between the patient and the carer to prevent the reasonable expectations from the procedure, are
direct contact with any potentially infected body discussed with the patient and family who are free to
fluid or tissue in either direction (Box 5.2). ask any questions. A consent or request for treat-
ment form, which states the nature of the operation
and the side on which the operation is to be per-
Hazards formed if the operation is a unilateral procedure, is
signed by the patient and the surgeon or deputy.
In addition to infection, there are many potential Once in the operating suite, a check is made to
sources of hazard in the operating environment. confirm that all the necessary safeguards have been
5: Surgical techniques 37
small point of contact (active electrode) through the

Box 5.2 Universal precautions
patient to a large contact site (indifferent electrode
Barrier protection or ‘diathermy plate’) to produce localised heat
Appropriate protective barriers are used during which coagulates protein. Diathermy produces
invasive procedures and handling contaminated (i) coagulation (haemostasis with a small amount
materials: gloves, face mask, eye shield, impermeable of adjacent tissue damage), (ii) cutting (tissue cut-
gown, shoe covers, hair cover. ting with minimal tissue damage), or (iii) fulgura-
tion (haemostasis with considerable tissue necrosis).
Minimising potential exposure
Potential dangers include electrocution, inadvertent
Decrease the risk of spreading potentially infected
burn to the patient at a remote site and to the sur-
body fluids by avoiding spillages, careful disposal of
geon, fire associated with pooled alcohol‐based
materials and equipment contaminated by body
fluids, having only essential personnel present during
antiseptics, explosion of flammable anaesthetic
invasive procedures, excluding personnel with open gases, and interference with the function of cardiac
wounds or abrasions, using impermeable dressings to pacemakers.
cover wounds, and using closed rather than open A variety of lasers with different wavelengths
drains. and effects on cells and tissues are used in surgical
practice for highly accurate tissue destruction (e.g.
Elimination of needlestick injuries
mucosal surgery, CNS tumours, dermatological
Do not handle uncapped needles, never re‐sheath
lesions, aerodigestive tumours), coagulating blood
used needles, and never remove a used needle from a
vessels (e.g. gastrointestinal tract, retinal photoco-
syringe. Use needles as little as possible. Immediately
agulation), and for photoactivation of intra‐tumour
dispose of used needles in a designated ‘sharps’
haematoporphyrin for malignant tumour destruc-
disposal container which has a one‐way opening.
tion (photodynamic therapy). Hazards include eye
Elimination of other penetrating injuries damage, explosion of anaesthetic gases, and shat-
Sharp objects (e.g. scalpels, needles) are transferred tering and destruction of other equipment.
between operating personnel in a ‘sharps dish’, not Limb tourniquets are used to provide a blood-
from hand to hand. Hand‐held needles are not used. less field in which to operate. The limb is ele-
Blunt suture needles are used where possible. Sharp vated and exsanguinated by a rubber bandage or
instruments are not placed on the operative field or
compressive sleeve, and the proximal tourniquet
anywhere on the patient. Alert personnel to the
inflated to 50 mmHg (upper limb) or 100 mmHg
presence of any sharp object in the operative field.
(lower limb) above systolic blood pressure. A tour-
niquet should not be kept inflated for more than
60–90 minutes. A record should be kept during the
performed for the patient. The World Health
operation of how long the tourniquet has been
Organization surgical safety checklist or variations
inflated. Tourniquet complications include arterial
are now mandatory in most Australian hospitals.
thrombosis, distal ischaemia, nerve compression
The checklist can be used at three stages: before the
and skin traction.
induction of anaesthesia (‘sign in’), before the inci-
sion of the skin (‘time out’) and before the patient
leaves the theatre (‘sign out’). The varied processes Positioning of the patient
in each hospital include checklists that ensure the
The patient is positioned on the operating table in
correct patient is having the correct procedure, the
such a way that the procedure is facilitated and the
correct site or side of the operation has been
airway can be protected. Pressure points are pad-
marked, that relevant equipment is available and
ded, and limbs are positioned so that peripheral
that the relevant imaging and clinical notes are
nerves, major blood vessels, joints and ligaments
available. At the start of each theatre list the ‘time
are not stretched or compressed. The anaesthetised
out’ for the first patients also includes an introduc-
patient must be in a stable position on the operat-
tion of all present in the theatre. Discussion of all
ing table and may need to be strapped in position
anticipated surgical and anaesthetic concerns are
with broad adhesive tape. There must be no contact
also discussed along with plans for prevention of
between the skin and any metallic surface because
deep venous thrombosis during and after theatre.
of the risk of diathermy burn and pressure necrosis.
Sections of the operating table can be angled so that
Equipment
the patient is optimally positioned for the particu-
Diathermy is used universally in surgical practice. lar procedure (e.g. flexed while lying supine or on
High‐frequency alternating current passes from a one side, head‐down, head‐up).
Endoscopy Endoscopic surgery
Endoscopy is performed by inserting a fibre‐optic There are two forms of endoscopic surgery that
telescope containing a light source and instrument both involve the insertion of a microchip video
channels into the gastrointestinal, respiratory and camera with a light source into the lumen or
urinary tracts. The operator undertakes the proce- through the wall of the aerodigestive tract into a
dure by manipulating the endoscope while viewing body cavity. The latter is performed through an
a video screen but occasionally the eyepiece of the incision in the wall of the gastrointestinal tract
instrument may be used. with placement of specially crafted surgical instru-
ments into a body cavity. For both techniques the
surgeon undertakes the procedure by manipulat-
Gastrointestinal endoscopy ing the instruments while viewing a video screen.
Endoscopy of the gastrointestinal tract allows the Some forms of endoscopic surgery utilise endo-
endoscopist to view the lumen of the oesophagus, scopic ultrasound for guidance of incisions or
stomach and proximal half of the duodenum placement of internal drains. Examples of endo-
(oesophagogastroduodenoscopy or upper gastro- scopic surgical procedures include resections of
intestinal endoscopy or gastroscopy), colon larger gastrointestinal tumours (endoscopic
(colonoscopy), rectum and distal sigmoid colon
mucosal resection), drainage of infected pancre-
(sigmoidoscopy), and distal rectum and anal canal atic collections into the stomach (endoscopic cyst‐
(proctoscopy). It is usually performed under seda- gastrostomy), oesophageal myotomy (per oral
tion. Intestinal endoscopy can also be performed at endoscopic myotomy or POEM), endoscopic sinus
laparotomy (enteroscopy) by making a small inci- surgery and natural orifice transluminal endo-
sion in the intestine and passing the endoscope scopic surgery (NOTES).
along the intestinal lumen. Procedures such as dila- The advantages of endoscopic or ‘closed’ surgery
tation of strictures, biospy and diathermy ablation are reduced postoperative pain and analgesic
of polyps, injection of adrenaline around bleeding requirements, earlier discharge from hospital and
gastric and duodenal ulcers, cholangiopancreatog- earlier return to normal function. However, many
raphy, removal of common bile duct calculi, biliary surgical procedures either cannot be undertaken
dilatation or stenting, injection of haemorrhoids endoscopically because of their very nature, or can-
and tumour phototherapy can be performed using not be completed endoscopically because of diffi-
fibre‐optic endoscopes. culty or patient safety, in which case the operation
is converted to an ‘open’ procedure. Some proce-
dures use endoscopic techniques to assist with the
Bronchoscopy procedure and an incision is made to either com-
The upper airway, trachea and proximal bronchi plete the operation or deliver the resected specimen.
can be inspected by bronchoscopy, which may be The range of endoscopically performed operations
performed under local or general anaesthesia. in many surgical specialties has increased enor-
Bronchoscopy is used for diagnosis (e.g. inspec- mously over the last 20 years.
tion and biopsy of lung tumours) or therapy (e.g.
removal of foreign bodies, aspiration of secre-
tions). Anaesthetists occasionally use the fibre‐optic Open surgery
bronchoscope to facilitate difficult endotracheal
intubation. Open surgery is the traditional or conventional
method of operating. In general terms, open surgery
involves making a surgical wound, dissecting tis-
Urological endoscopy
sues to gain access to and mobilise the structure or
The urethra (urethroscopy), bladder (cystoscopy) organ of interest, completing the therapeutic proce-
and ureters (ureteroscopy) can be inspected for dure, ensuring haemostasis is complete, and then
diagnostic purposes. Extensive therapeutic proce- closing the wound with sutures. Open surgery is
dures (e.g. resection of the prostate, diathermy and performed more with the hands and direct touch
excision of bladder tumours, extraction of calculi) than endoscopic procedures, and fingers may be
can be performed safely with far less morbidity used for ‘blunt’ dissection. The surgical wound
than the equivalent open procedures. accounts for much of the morbidity of open
surgery, particularly the cutting of muscle. The Orthopaedic surgery

range of open operations is extremely wide, as evi-
Large joints (e.g. knee, hip, ankle, shoulder, wrist)
denced by the procedures described throughout
can be inspected by arthroscopy. Therapeutic proce-
this book.
dures include removal of bone chips, cartilage exci-
sion and removal, and ligament repair. Arthroscopic
Minimally invasive surgery surgery has been enormously beneficial for ortho-
paedic patients and has allowed far more rapid
Minimally invasive surgery avoids the larger inci- return to function.
sions of open surgery to minimise morbidity.
Different types of microchip video cameras can be Robotic surgery
used to visualise the required cavity or space within Robotic surgery is a form of minimally invasive
the body. The cameras vary in size and their com- surgery where the surgeon is positioned remote to
plement of different angled lenses, which are either the patient but usually within the operating theatre.
fixed or manoeuvrable. Magnification of the image A robotic system operated by the surgeon is used to
often provides a superior view to that obtained at control the camera as well as the instruments that
open surgery. are placed through multiple ports. A surgical assis-
tant still makes the port site incisions and a theatre
Abdominal surgery nurse is scrubbed to change to robotic instruments
Laparoscopy refers to the technique of insufflat- when required. The robot is particularly useful for
ing the peritoneal cavity with gas, inserting a cam- work in cramped narrow spaces where robotic
era through most commonly a 10–15 mm suturing is far superior to laparoscopic suturing
subumbilical incision and inspecting the abdomi- techniques in such instances. The commonest exam-
nal contents. Usually additional ports are inserted ple of robotic surgery is radical prostatectomy with
through 5–10 mm incisions in the abdominal wall the robotic reconstruction of the bladder and ure-
and instruments (e.g. scissors, grasping devices, thra in a narrow male pelvis. Other common exam-
retractors, staplers, needle holders, energy devices) ples include partial nephrectomy and thoracic
are introduced and manipulated by the surgeon to surgery. However, nearly all abdominal, thoracic
perform the operation. Procedures such as chole- and some upper aerodigestive and cardiac opera-
cystectomy, gastric fundoplication, hiatus hernia tions have been described using robotic techniques.
repair, division of adhesions, appendicectomy, Recently, transaxillary breast, thyroid and parathy-
splenectomy, adrenalectomy, nephrectomy, oopho- roid surgery have also been described.
rectomy, tubal ligation, bariatric surgery and her-
nia repair can be undertaken laparoscopically
with less morbidity than if undertaken as an open Surgical methods
or conventional operation. Endoscopic surgery
has allowed some procedures to be undertaken as Surgical operations are performed by well worked
day cases, whereas the same procedure performed out, standardised steps which progress in logical
as an open operation would require an inpatient sequence. An operative plan is determined by the
stay of several days (e.g. cholecystectomy, hernia surgeon for every operation.
repair).
Surgical instruments
Thoracic surgery
There are literally thousands of surgical instru-
Thorascopy involves inserting a camera with a ments, some simple and others extremely complex,
light source and instruments into the thoracic cav- but each designed for a specific function. The sur-
ity. The technique is used diagnostically and thera- gical incision is made with a scalpel, which con-
peutically for procedures such as drainage of the sists of a reusable handle and a disposable blade.
thoracic cavity (haemothorax, pleural effusion and Scissors are used to cut other tissues and sutures,
empyema), lung biopsy, pleurodesis and excision of and for blunt dissection with the blades closed.
lung bullae. The mediastinum can be inspected and Diathermy is used for haemostasis and to cut
mediastinal lymph nodes can be biopsied by medi- through tissue layers beneath the skin. Tissues are
astinoscopy, which may prevent the need for an held with dissecting or tissue‐grasping forceps
exploratory thoracotomy. rather than the fingers. Hand‐held forceps either
have teeth for better grasping ability or are non‐ majority of cases of operative and postoperative
toothed for handling delicate tissues. Needle hold- bleeding are due to inadequate surgical haemostasis
ers are used to hold needles for suturing and rather than disorders of clotting and coagulation.
eliminate the need for hand‐held needles, and are Haemostasis is essential in order to prevent blood
therefore safer. They have a ratchet so that the nee- loss during surgery and haematoma formation
dle can be contained securely in the holder while postoperatively. Methods of surgical haemostasis
not in the surgeon’s hand. Retractors allow the include the following.
surgeon to operate in an adequately exposed field. • Application of a haemostatic clamp to a blood
Self‐retaining retractors keep the wound edges vessel and then ligation with a surgical ligature.
apart without the aid of an assistant. Retractors • Suture ligation of a vessel: under‐running a
held by the assistant provide tissue retraction in bleeding vessel with a figure‐of‐eight suture
awkward parts of the wound and in situations which is tied firmly.
where retraction of specific tissues is required so • Application around a blood vessel of small metal
that intricate parts of the operation can be per- U‐shaped clips that are then squeezed closed.
formed. A sucker is used to aspirate blood and • Diathermy coagulation.
body fluids from the operative field and to remove • Localised pressure for several minutes to allow
smoke created by the diathermy. There are many coagulation to occur naturally.
instruments designed specifically for surgical spe- • Application of surgical materials (e.g. oxidised
cialties and procedures. cellulose, Surgicel) which promote coagulation.
• Application of topical agents to promote vaso-
Incisions constriction (e.g. adrenaline) or coagulation (e.g.
thrombin).
Surgical incisions are made so that:
• Packing of a bleeding cavity with gauze packs as
• the operation can be undertaken with adequate
a temporary measure until definitive haemostasis
exposure of the area or structure of interest
can be achieved.
• the procedure can be performed and completed
safely and expeditiously
Sutures and wound closure
• the wound heals satisfactorily with a cosmeti-
cally acceptable scar. Sutures have been used to close surgical wounds for
Thus, incisions are to be of adequate but not exces- thousands of years, and initially were made from
sive length and, if possible, placed in skin creases, human or animal hair, animal sinews and plant
particularly when operating on exposed areas of material. Today, a wide variety of material is avail-
the body such as the face, neck and breast. Parallel able for suturing and ligating tissues (Box 5.3).
skin incisions (‘tram tracking’) and V‐ or T‐shaped Sutures are selected for use according to the
incisions are avoided because of ischaemia of inter- required function. For example, arteries are sutured
vening tissue and pointed flaps. together with non‐absorbable polypropylene or
polytetrafluoroethylene (PTFE) sutures, which are
Tissue dissection non‐thrombogenic, cause virtually no tissue reac-
tion and maintain their intrinsic strength indefi-
Ideally, surgical dissection should be performed
nitely so that the anastomotic scar (which is under
along tissue planes, which tend to be relatively
constant arterial pressure) does not stretch and
avascular. The aim is to isolate (mobilise) the
become aneurysmal. Skin wounds, for example, are
structure(s) of interest from surrounding connec-
sutured with either non‐absorbable sutures, which
tive tissue and other structures with the least
are removed after several days, or absorbable
amount of trauma and bleeding. Tissues should be
sutures hidden within the skin (subcuticular sutures)
handled with great care and respect and as little as
and which are not removed surgically but are
possible. Dissection is undertaken by using a scalpel
absorbed after several weeks.
or scissor (sharp dissection), a finger, closed scissor,
Sutures are available in diameters ranging from
gauze pledget or scalpel handle (blunt dissection),
0.02 to 0.50 mm. The minimum calibre of suture
or the diathermy. Gentle counter‐traction on tissues
should be used, compatible with its function. Non‐
by the assistant facilitates the dissection.
absorbable sutures are avoided for suturing the
luminal aspects of the gastrointestinal and urinary
Haemostasis
tracts because substances within the contained flu-
Surgical haemostasis refers to stopping bleeding ids (e.g. bile, urine) may precipitate on persisting
which occurs with transection of blood vessels. The sutures and produce calculi.
Box 5.3 Sutures
Substance Description* Duration† Trade name Uses
Plain catgut Nat, Multi, Ab 1–2 weeks — Subcutaneous fat

Chromic catgut Nat, Multi, Ab 2–3 weeks — Subcutaneous fat, gastrointestinal
and urinary tract anastomoses
Silk and linen Nat, Multi, Non Prolonged — Skin and cardiac sutures, ligatures
Stainless steel Nat, Mono, Non Prolonged — Sternum, skin and gastrointestinal
staples, orthopaedic wire
Polyglycolic acid Syn, Multi, Ab 3–4 weeks Dexon Gastrointestinal and urinary tracts,
muscle, fascia, subcutaneous fat
Polyglactin Syn, Multi, Ab 4–6 weeks Vicryl Gastrointestinal and urinary tracts,
muscle, fascia, subcutaneous fat
Polypropylene Syn, Mono, Non Indefinite Prolene Ophthalmology, vascular sutures,
abdominal closure, neurosurgery,
fascia, skin
Polyamide Syn, Mono, Non Years Nylon Abdominal and skin closure, hernia
repair
Polytetrafluoroethylene Syn, Mono, Non Indefinite Gore‐Tex Vascular anastomoses, hernia repair
(PTFE)
* Ab, absorbable; Mono, monofilament; Multi, multifilament; Nat, natural; Non, non‐absorbable; Syn, synthetic.
†
Time during which tensile strength is maintained.
The requirements of suture material are as • Monofilament or multifilament: monofilament

follows. sutures pass through tissues easily, are generally
• Tensile strength: the suture must be strong less reactive, and are more difficult to handle and
enough to hold tissues in apposition for as long knot securely. Multifilament sutures are braided
as required. or twisted thread, and are easier to handle and
• Durability: the suture must remain until either knot, but are more likely to harbour microorgan-
healing is advanced or indefinitely if the healed isms within the suture.
tissue is under constant pressure. Recently, cyanoacrylate adhesives (‘superglue’)
• Reactivity: tissue reaction (i.e. an inflammatory have been used to seal small leaks in blood vessels
response) allows absorbable sutures to be and vascular suture lines, and for closure of small
removed by phagocytosis but results in chronic superficial skin wounds. The adhesive polymerises
inflammation if non‐absorbable sutures remain and hardens rapidly on contact with tissues.
in situ.
• Handling characteristics: sutures must be easy to
grasp, handle and tie.
Surgical knots
• Knot security: sutures must be able to be tied effec-
tively so that knots do not come undone or slip. Knots are tied to ensure that ligatures and sutures
Sutures are classified as follows. remain in place and do not slip or unravel. The
• Absorbable or non‐absorbable: the rate of absorp- ability to tie a secure knot is a fundamental tech-
tion of absorbable sutures depends on their com- nique in surgery, and patients’ lives literally
position and their thickness. Disappearance of the depend on knot security (e.g. the knot in a ligature
suture occurs through inflammatory reaction, used to tie off an artery). Knot security depends on
hydrolysis or enzymatic degradation. friction between the throws of the ligature mate-
• Synthetic or natural material: sutures of natural rial, the number of throws used to tie the knot, the
(animal) origin are being phased out of surgical strength of the ligature material and the tightness
practice because of the very minimal risk of dis- of the knot. Usually, multiple throws are used to
ease transmission. A wide variety of synthetic secure the knot (e.g. two reef knots, one on the
suture materials are available. other).
Suturing Surgical drains

The technique of suturing depends on the tissue Drains are used widely in surgical practice to:
and wound being sutured. Sutures may be either • Remove blood or serous fluid, which would
continuous (e.g. subcuticular skin sutures, abdomi- otherwise accumulate in the operative area (e.g.
nal closure, vascular anastomosis) or interrupted wound drain)
(e.g. skin sutures, sternal wires). The function of • Provide a track or line of minimal resistance so
sutures is to hold the adjacent edges of sutured tis- that potentially harmful fluids can drain away
sues in apposition and to immobilise them in that from a particular site (e.g. drain placed into an
position so that wound healing (i.e. neovascularisa- intra‐abdominal abscess cavity).
tion, connective tissue ingrowth and collagen for- Several different methods of drainage may be used
mation) is facilitated. It is essential that sutures are depending on the required function.
not tied so tightly that the tissues encompassed by • Open drainage: a drain tube or strip of soft flex-
them become ischaemic. Skin sutures may be sup- ible latex rubber is placed so secretions or pus
ported by adhesive paper tapes. can drain along the track of the drain into gauze
Retention sutures (incorrectly referred to as ten- or other dressing covering the external end of
sion sutures) are used to close abdominal incisions the drain tube (e.g. drain placed in an abscess
that are thought to be at increased risk of dehiscence, cavity, drain placed prophylactically near a
and are inserted to encompass a large amount of fas- bowel anastomosis in case of subsequent anasto-
cial tissue and are placed 3–5 cm apart. Retention motic leak).
sutures have now been replaced by techniques using • Closed drainage: a tube is placed into an area or
lateral incisions of the abdominal wall, mesh recon- viscus to drain fluid contents into a collecting
struction and negative pressure wound devices. bag so that there is no contamination of the
Within the last two decades, stainless steel staples drained area from outside the system (e.g. chest
have been used to close skin wounds and to per- drain, urinary catheter, cholecystostomy drain).
form gastrointestinal anastomoses. Staples are • Closed suction drain: the drain tube is connected
quicker to use than sutures, but are relatively to a bottle at negative atmospheric pressure so
expensive and produce a worse cosmetic result for that fluid is sucked out of the area (e.g. wound
skin closure than subcuticular absorbable sutures. drain, drain under skin flaps).
It is important to note both the amount and the
type of fluid that drains. Large volumes of fluid
Suture removal drainage may need to be replaced as intravenous
fluids (e.g. duodenal fistula fluid). Depending on
Sutures are removed as early as possible to minimise
the particular situation, it may be necessary to cul-
the risk of infection and scarring, so long as tissue
ture drain fluid or send it for estimation of haemo-
healing is sufficiently advanced that the wound will
globin, creatinine, electrolytes, amylase or protein.
not open when the sutures are removed. Sutures are
A radiological contrast study may be performed
therefore removed at different times, depending on
along the drain tube, for example to estimate the
tissue and general patient factors (Box 5.4). For
size of a cavity being drained.
example, sutures are left in situ for a longer time in
Drain tubes are removed when they are no
patients who are immunosuppressed, malnourished,
longer required, for example when there is mini-
jaundiced or undergoing chemotherapy; in those
mal fluid being drained, or when a cavity being
who have renal failure; and in tissues judged to be
drained has contracted and is small. Drains are
relatively ischaemic, subject to increased stress and
removed simply by cutting the suture which
tension, and which have been irradiated.
anchors them to the skin and withdrawing the tube
from the patient.
Box 5.4 Timing of suture removal at
various sites
Venepuncture
Face 3–5 days Venepuncture involves removing blood from a super-
Neck (skin crease) 5–7 days ficial vein, usually in the antecubital fossa or dorsum
Scalp 7–10 days
of the hand, by inserting a needle attached to a
Abdomen 10 days
syringe or collection tube at negative pressure
Extremity 10–14 days
(Vacutainer system). A venous tourniquet is applied
Amputation stump 21 days
around the arm, which is hung in a dependent
position; the patient vigorously opens and closes the • Short‐term monitoring of central venous pressure.
hand, and the vein is gently patted to encourage A central venous catheter (CVC) may be inserted
venous dilatation. The skin is cleansed with antisep- into the internal or external jugular vein or the sub-
tic and the needle is inserted through the skin into the clavian vein. Temporary CVCs are made of semi‐
dilated vein at an angle of 30–45°. Once the required rigid Teflon, are approximately 25 cm in length
volume is aspirated, the tourniquet is released, the and, depending on their function, are between 1
needle withdrawn, the puncture site immediately and 4 mm in diameter and have one, two or three
covered with a cotton wool swab, and light pressure lumens. Long‐term CVCs are made of barium‐
applied for 1–2 minutes. The site is covered with an impregnated silastic and are quite flexible. They
adhesive dressing. Complications include bruising, have a Dacron cuff bonded to the part of the cath-
haematoma and, rarely, infection and damage to eter which lies subcutaneously and becomes incor-
deeper structures. Inadvertent needlestick injury to porated by fibrous tissue after several weeks so that
the venepuncturist is avoided by careful technique. organisms cannot track along the catheter from the
skin into the circulation.
Intravenous cannulation Some long‐term single‐lumen CVCs are availa-
ble with a small‐volume chamber attached to
Intravenous (i.v.) cannulation is used commonly for
the extravenous end of the catheter (Portacath,
administration of fluids and drugs. Superficial veins
Infusaport). The catheter and chamber are implanted
on the forearms and dorsum of the hands are used
subcutaneously after the vein is catheterised and can
for i.v. cannulation. Antecubital fossa veins are best
be accessed for chemotherapy or blood sampling by
avoided for cannulation because the elbow has to
inserting a needle into it through the skin.
be kept extended to avoid kinking of the cannula.
CVC insertion is best performed in an operating
Leg veins may have to be used in the absence of use-
theatre, under local or general anaesthesia, and
able upper limb veins. Cannulas have a soft outer
with ultrasound localisation of the central vein.
Teflon sheath attached to a hub, and a central hol-
The patient is placed in a supine, slightly head‐
low needle attached to a small chamber.
down position, and the surface anatomy of the
A suitable vein is identified as for venepuncture.
vein is marked. Aseptic technique is essential. A
Local anaesthetic cream is applied to the skin over-
hollow wide‐bore needle is inserted into the vein, a
lying the vein or local anaesthetic (1% lidocaine
guidewire is passed down the needle and the needle
without adrenaline) is injected intradermally next
is removed. The guidewire position is checked
to the vein after cleansing the skin with antiseptic.
radiologically. A plastic dilator is passed over the
The cannula (needle and sheath) is inserted through
guidewire to dilate a track for the catheter and is
the skin into the vein at an angle of 10–30°. The
then removed, and the CVC is passed over the
small chamber fills with blood when the needle is in
guidewire which is removed after the CVC is in
the lumen of the vein. The cannula is then advanced
place. A chest X‐ray is performed to check the final
into the vein. The needle is removed from the sheath
position of the CVC and also to ensure that a
and a closed three‐way tap or i.v. giving set is joined
pneumothorax or haemothorax has not occurred
to the hub of the sheath. The cannula is secured to
due to inadvertent puncture of the pleura or lung.
the skin with adhesive tape.
The catheter is sutured to the skin to prevent dis-
Intravenous infusion is painful when the infusate
lodgement and the exit site is dressed with an
is cold or contains irritants (e.g. potassium, calcium,
adhesive dressing.
drugs of low or high pH), or if the cannula pierces
Peripherally inserted central catheters are now
the vein wall and fluid extravasates subcutaneously.
placed under radiological guidance for the majority
Thrombophlebitis develops at the insertion site
of patients who require long‐term venous access for
after about 3 days, and i.v. cannulas should be re‐
parenteral nutrition or antibiotics, or for those
sited if infusions are required for longer periods.
patients with difficult peripheral venous access.
Central venous catheterisation

Percutaneous catheterisation of a central vein is
Further reading
used for:
• Short‐ or long‐term venous access when periph- Cochran A, Braga R (eds) Introduction to the Operating
eral veins are unsuitable or cannot be used Room. New York: McGraw‐Hill, 2017.
(e.g. prolonged fluid infusion, total parenteral Keen G, Farndon JR (eds) Operative Surgery and
nutrition, ultrafiltration, haemodialysis, plasma Management, 3rd edn. Oxford: Butterworth‐
exchange, chemotherapy) Heinemann, 1994.
d enables cholecystectomy to be performed as

MCQs day‐case surgery in some patients
e can only be used for part of an operation
Select the single correct answer to each question. The
correct answers can be found in the Answers section
3 Sutures:
at the end of the book.
a should be left in the skin for a minimum of 1 week
1 Universal precautions: b often need to be removed with local anaesthetic
a protect operating theatre staff from electric c must be tied tightly so that arterial inflow into
shocks tissues is not possible
b prevent polluted air from entering the operating d made of Prolene will dissolve
theatre e of all types must eventually be removed
c impose a physical barrier between patients and
carers 4 Surgical drains:
d are only to be used when operating on patients a are removed when they are no longer necessary
e protect only against bacterial pathogens b should always be removed the day after surgery
c are removed under general anaesthesia
2 Laparoscopic surgery: d are not necessary with modern surgical
a has a very limited role in general surgical practice techniques
b is inherently unsafe because the surgeon cannot e are required after the majority of general surgery
touch the structures being operated on procedures
c is associated with greater postoperative pain and
immobility
6 Management of surgical
wounds
Rodney T. Judson
University of Melbourne and Royal Melbourne Hospital, Melbourne, Victoria, Australia
seroma formation; and (iv) providing wound sur

Introduction veillance to detect and intervene if any signs of
complications develop. To achieve this aim a care
Surgery entails gaining access to deeper body struc
ful preoperative assessment is made based on clini
tures usually necessitating a surgical incision, which
cal history and examination supported by special
may be performed by a scalpel or the use of dia
tests as indicated. Intraoperative assessment as to
thermy. The final step in the surgical procedure is
the health and perfusion of the wound edges and
closure of the surgical incision (wound). Rapid
the extent of bacterial contamination informs deci
complication‐free healing is anticipated. Unfor
sions regarding the best wound closure technique.
tunately, infection of the wound, described as surgi
Decisions regarding the wound dressing are usually
cal site infection (SSI), remains the most common
made based on whether the wound is closed and
healthcare‐associated infection among surgical
appears dry or whether the wound is to be left
patients. While advances have been achieved in
open. Postoperative care is centred on continuing to
infection control practices, operating room design,
address those risks identified in the preoperative
sterilisation techniques and appropriate use of anti
assessment that are likely to affect wound healing.
biotics preoperatively and perioperatively, SSI
remains a common cause of morbidity and even
mortality. The development of an SSI increases hos Preoperative assessment
pital length of stay by approximately 7–8 days. SSIs
account for up to 16% of healthcare infections, of A number of important factors affect wound
which most are related to bowel surgery (10%) healing and these should be assessed and corrected
with fewer than 1% from orthopaedic procedures. preoperatively if possible.
Other wound complications that affect patient • Poor glycaemic control in diabetics is associated
recovery include haematoma formation and devel with a twofold increase in SSI.
opment of seromas, both of which increase the like • Smoking, with its effect on the cutaneous circula
lihood of wound infection. An SSI is also a common tion, increases the likelihood of SSI.
precursor to wound dehiscence or separation, • Obesity, with increased dead space in the wound,
which if involving the full thickness of the wound favours seroma formation and SSI.
may lead to evisceration of the abdominal contents • Malnutrition delays wound healing.
requiring urgent surgical intervention. Minimisation • Medications such as corticosteroids and immu
of these complications is achieved by (i) preopera nosuppressive drugs increase infection risk.
tive minimisation of any patient factors that might • Systemic anticoagulants increase haematoma for
impede wound healing; (ii) choosing the most mation and subsequent SSI.
appropriate wound closure technique, be that pri • Serious comorbidities, especially cardiorespira
mary wound closure or a method of delayed clo tory disease and decrease in oxygen saturation.
sure; (iii) selection of a wound dressing that will Steps should be taken to address any reversible
protect and support the wound while removing adverse factors if possible. In emergency situations
excessive fluid exudate and potentially reducing time may preclude any meaningful intervention,
45
which is reflected in an increased risk of SSI follow

ing urgent surgery. Persistent risk factors need to be
Preoperative wound preparation
considered when deciding on the best method of
wound management. Primary closure of wounds in
Skin care
the presence of adverse patient factors and bacterial Bathing or showering using soap the day before
contamination is associated with a high incidence surgery is recommended. Preoperative bathing or
of SSI, which delays healing and possibly results in showering using antiseptics has not shown any con
severe systemic sepsis. clusive reduction in postoperative SSI. Preoperative
hair removal such as shaving the day before surgery
may increase infection risk due to colonisation of
Classification of surgical wounds the resulting minor abrasions. If hair removal is
deemed necessary, this should occur immediately
Simple or complex prior to surgery.
The commonest surgical wounds are linear inci
sions involving the skin, subcutaneous tissue and Antibiotic prophylaxis
deeper fascial layers. These incisions are performed An important preoperative decision is the need for
using a sharp scalpel to gain access to deeper struc perioperative antibiotic coverage to reduce the like
tures which are the focus of the surgical procedure. lihood of development of an SSI. This decision is
Operations, especially for malignant disease, occa based on an assessment of the potential wound,
sionally require excision of the skin and subcutane whether any prosthetic material is to be implanted
ous tissues overlying the tumour. These complex at the time of surgery and the burden of patient
wounds may require complicated surgical tech risks factors.
niques to achieve wound closure. The consensus of opinion is that a clean incised
wound in a healthy patient performed in a well‐vas
Clean cularised area does not require antibiotic prophy
laxis. For all other wounds, when prosthetic
If the procedure is performed under sterile condi material is implanted and in patients with risk fac
tions and no contamination of the wound occurs, tors for SSI, preoperative antibiotics should be
the wound is described as a clean incised wound. used.
Such wounds have minimal bacterial contamina For greatest effectiveness antibiotics should be
tion and under ideal circumstances would be administered parenterally approximately 1 hour
expected to have a low SSI rate of 1–2%. prior to surgery to allow appropriate wound con
centration of the antibiotic at the time of the
Clean contaminated incision.
If the respiratory, alimentary, genital or urinary The choice of antibiotic depends on the suspected
tracts are entered under surgically controlled condi or anticipated nature of bacterial contamination.
tions and without unusual contamination, the Most hospitals have agreed antibiotic guidelines
wound is classified as a clean contaminated wound. based on local known bacterial risks. If in doubt
Such wounds would result from procedures includ regarding antibiotic choice it is wise to seek the
ing appendicectomy and cholecystectomy where no opinion of an infectious diseases clinician. For the
major break in technique was encountered. These majority of wounds a single dose of antibiotic is
wounds have a higher rate of SSI. indicated, but in the presence of significant contam
ination or in lengthy operations a supplementary
dose may be indicated. Prolonged prophylactic use
Contaminated
of antibiotics has not been proven to reduce the risk
Operations involving gross spillage of intestinal of SSI and is associated with an increased risk of
contents or where major breaks in sterile technique development of antibiotic‐resistant bacteria.
have occurred are described as contaminated.
Dirty or infected Intraoperative management

Wounds with signs of clinical infection such as
Skin preparation
neglected traumatic wounds or wounds in associa
tion with perforated viscera are described as dirty To minimise contamination of the wound from
wounds. skin flora, an antiseptic skin preparation is used.
6: Management of surgical wounds 47
A solution of chlorhexidine in alcohol is more open using a vacuum dressing to control the result
effective in reducing SSI than aqueous solutions. ing laparostomy. Patients are transferred to an
Care must be taken to prevent pooling of alcohol‐ intensive care unit for resuscitation, including vas
containing skin preparations especially when dia cular filling, correction of any metabolic or clotting
thermy is used to avoid ignition of the flammable abnormality and warming to normal temperature.
solution. Alcoholic solutions should not be used The patient is subsequently returned to the operat
around the eyes or in the external auditory canal to ing theatre in 24–48 hours for closure of the wound.
avoid corneal damage or the potential for the alco
hol to affect the inner ear.
Postoperative management
Choice of wound closure technique
General patient care
The method of wound management is finally
To support wound healing the patient’s general con
decided at the completion of the operation, taking
dition should be optimised. Adequate fluid resusci
into account the preoperative risk assessment, the
tation to maintain wound perfusion, ensuring
conduct of the surgery and the patient’s physiologi
oxygen saturation is above 95% if possible, avoid
cal state. The surgical choices are to manage the
ing hypothermia and providing nutritional support
wound open, to partially close the wound or, as in
will ensure the best conditions for wound healing.
most instances, to close all layers of the wound.
In a well patient with a clean or clean contaminated
Local wound care
wound, primary wound closure is recommended. This
is achieved by closure of any deeper layers of the The care of the wound will depend on the chosen
wound such as the fibrofacial layer of the abdomen method of wound healing.
with a strong, usually slowly absorbed, non‐irritant Wounds closed at the end of the operation with
monofilament suture. In thin patients where no the expectation of healing by primary intention
undermining of the wound edges has occurred, the require a protective supportive dry dressing which
subcutaneous layer does not require any suturing. The only needs attention for the first few days if there
skin edges are then opposed accurately, avoiding any are concerns about the possible onset of infection or
gaps using sutures or staples. Both techniques produce if there is soiling or exudation visible. Wounds with
comparable results with no significant difference in well‐opposed skin edges undergoing normal healing
SSI between continuous or interrupted suture tech should achieve re‐epithelialisation between the skin
niques. In general, low tension sutures are more con edges within 24–48 hours. While it is safe to allow
ducive to healing while excessive tension can produce showering once the wound is sealed, most patients
pressure injury to the wound edge. Retention sutures prefer a protective dressing over the wound to mini
in abdominal wall closure have not been found to pre mise the chances of abrasion from clothing or inad
vent wound dehiscence or evisceration or lessen SSI or vertent tension on the wound causing separation of
postoperative wound pain. the edges. For these reasons, dressings are usually
For wounds with significant contamination or in left intact for 5–7 days, after which the wound may
patients with major continuing risk factors for SSI, be left open. A number of waterproof dressing are
the surgeon may decide to close only the deeper lay available to allow normal showering during this
ers of the wound, leaving the superficial layers open healing phase. Closed wounds at greater risk of
to allow free drainage of any inflammatory exu healing problems may benefit from the use of nega
date. A subsequent wound management plan is tive pressure wound therapy. These dressing are
developed postoperatively based on assessment of designed to stay on for 5–7 days. The potential ben
the state and progress of the wound. If no signs of efits of these dressings are the removal of exudate,
infection appear to be developing, the edges of the reduction in lateral wound tension and a decreased
wound appear healthy and exudation is minimal, chance of seroma or haematoma formation. The use
delayed primary closure is usually performed. If the of these expensive dressing techniques is currently
wound is slow to progress and separation of the being investigated in randomised controlled trials.
edges occurs, the resulting unhealed wound may be Open surgical wounds require a dressing tech
suitable for split skin grafting. This is referred to as nique that controls wound discharge, minimises
healing by tertiary intention. bacterial contamination, provides a moist wound
In patients who are very unstable at the comple environment and is comfortable for the patient. For
tion of surgery, particularly with abdominal opera small wounds hydroscopic gels covered by a semi‐
tions, a decision may be made to leave the wound occlusive absorbent layer may be suitable. For
larger open wounds negative pressure wound ther of Surgical Wound Complications. Canadian
apy has revolutionised patient and wound care. Association of Wound Care, 2018. Available at www.
These devices are utilised until a healthy granulat woundscanada.ca
ing wound base is achieved, following which skin
grafting or vascularised flaps are contemplated to
provide permanent epithelial cover. MCQs
Wound packing and the frequent use of hypochlo
rite‐soaked dressings are becoming treatments of
the past as rapid advances in dressing technology
evolve. Chronic slow to heal wounds are best cared
for by wound care specialists who possess the skills 1 Regarding antibiotic wound prophylaxis:
and understanding necessary to select the most a broad‐spectrum antibiotics should be used
appropriate management plan for these difficult following wound closure until there are signs of
and distressing clinical situations. epithelial closure
b antibiotic prophylaxis must be used prior to
Wound follow‐up closure of all wounds
c antibiotic prophylaxis should be used when
All surgical wounds should be reviewed in 7–10 days
prosthetics are implanted at surgery
to ensure infection‐free healing is occurring. Any
d prophylactic antibiotics should be used for at
signs of infection should prompt action, with antibi
least 48 hours
otic therapy for mild cellulitis or wound drainage if
e antibiotic wound prophylaxis should include
there are signs of suppuration (pus formation). In
coverage of anaerobic organisms
small wounds drainage may be accomplished, using
an aseptic no‐touch technique, by gently opening the
2 Which of the following factors has not been proven
wound using artery forceps at the site of swelling.
to delay wound healing?
Any fluid drained should be sent for microbiological
a uncontrolled diabetes
testing to direct antibiotic therapy if indicated.
b malnutrition
SSI surveillance should extend for 30 days for
c corticosteroids
superficial incisional and deep incisional wounds;
d anxiety
90‐day follow‐up is recommended for surgery
e smoking
involving prostheses. Some deep SSIs may not be
clinically apparent for many months or even years
3 Wound infection is more common following:
following surgery, for example the newly recog
a the use of a continuous skin closure technique
nised slow‐growing mycobacterial infections fol
b primary closure of contaminated wounds
lowing surgery involving cardiopulmonary bypass.
c delayed closure of contaminated wounds
d removal of the sterile wound dressing in less than
5 days
Further reading
e the use of sterile saline rather than antiseptic
Harris CL, Kuhnke J, Haley J et al. Best Practice solutions for wound cleansing
Recommendations for the Prevention and Management
7 Nutrition and the surgical
patient
William R.G. Perry1 and Andrew G. Hill2
1
Department of Colorectal Surgery, Oxford University Hospitals NHS Foundation Trust, Oxford, UK
2
University of Auckland and Middlemore Hospital, Auckland, New Zealand
malnutrition, response to stress and injury, and

Introduction nutritional interventions.
The last 10 years have been exciting times for sur-

geons. Along with advances in surgical techniques Nutrition
and perioperative care, there has been significant
improvement in understanding nutrition and the Nutritional requirements
nutritional management of surgical patients.
There are six components of adequate nutrition: pro-
Such advances in nutrition have developed in par-
tein, water, energy, electrolytes, minerals and vitamins
allel with a growing understanding of metabolic
(Table 7.1). The requirements for these different com-
responses to injury and sepsis. This field has been
ponents vary according to the patient and the clinical
energised by discoveries in molecular biology, includ-
condition. Daily energy requirements are approxi-
ing the role of proinflammatory and anti‐inflamma-
mately 25–30 kcal/kg. This energy is the result of the
tory cytokines as biological response modifiers, the
breakdown of carbohydrates, fats and proteins.
putative role of oxygen free radicals, and the identi-
Proteins are required for maintenance of normal cel-
fication of other mediators of the inflammatory
lular function and are an essential component of
response. Knowledge of metabolism and expertise in
dietary intake. Daily recommended intake is 0.8 g/kg.
nutrition are now fundamental for all surgeons.
Proteins themselves are made up of smaller
Nutrition features low in the body’s homeostatic
amino acid units held together by peptide bonds.
economy. Its priorities are oxygen delivery, regula-
Amino acids can be divided into essential and non‐
tion of acid–base balance and maintenance of fluid
essential, the latter so‐named because we are able to
compartments. Threats to oxygen delivery are dealt
synthesise them ourselves. Correspondingly, we rely
with almost instantaneously by changes in minute
on dietary intake of essential amino acids.
ventilatory volume, alterations of cardiac output,
Finally, several other elements are required for
and improved efficiency of oxygen uptake and
metabolism and growth. These include water‐solu-
extraction by tissues. Acid–base abnormalities take
ble vitamins (B and C), fat‐soluble vitamins (A, D, E
longer to adjust, with both acute buffering and
and K), and trace elements such as copper, iron,
chronic excretion mechanisms. Changes in extra-
selenium and zinc.
cellular and intracellular compartment volumes
occur even more slowly.
Body composition
The body’s adjustments to malnutrition are slower
still, because they are not immediately life‐threaten- The energy stores and body composition of an
ing. Nevertheless, these changes are profound and average 40‐year‐old man weighing 73 kg are shown
critical. Nutritional deprivation and inappropriate in Table 7.2. Of note, women have lower total body
response to the deprived state are a major cause of water, less muscle mass and higher total body fat.
morbidity and mortality in the surgical setting, par- Composition also varies by ethnicity.
ticularly in the context of sepsis and injury. Fat can be hydrolysed to free fatty acids and glyc-
This chapter explores this paradigm by review- erol, representing a high‐energy source producing
ing body composition, nutritional requirements, 9.4 kcal of energy per gram (Box 7.1). The body’s
49
Table 7.1 Nutrition requirements in 25–55 year olds.
Component Requirement in health Requirement after major surgery
Protein 1.0–1.5 g/kg 1.5–2.0 g/kg

Water 40 mL/kg Variable per losses
Energy 40 kcal/kg 40 kcal/kg
Electrolytes 75 mmol sodium Variable per losses
15 mmol potassium
Minerals 15 mEq calcium Variable per losses
40 mmol potassium
10 mEq magnesium
Vitamins B group, C, fat soluble Additional vitamins may benefit during surgical illness
<17 kg/m2 in males). Severe malnutrition can be

Table 7.2 Energy stores and body composition
defined as measured weight being greater than 20%
in a 40‐year‐old 73‐kg man.
less than ‘well’ weight. Approximately 5% of patients
Mass (kg) Available energy (kcal) coming to surgery are severely malnourished, and
malnutrition is present to varying degrees in up to
Water 42 0 50% of patients who have undergone surgery.
Fat 15 110 000 Studies of malnourished children, particularly in
Protein 12 25 000
the context of low‐ and middle‐income countries,
Glycogen 0.6 2 500
have recognised two broad syndromes of malnutri-
Minerals 3.4 0
tion that can be usefully transposed to the adult sur-
gical setting. The first is marasmus, due to inadequate
intake of an otherwise balanced diet (Table 7.3). In
Box 7.1 Energy availability the adult this is commonly termed protein–energy
malnutrition (PEM). Marasmus can result from
• Fat 9.3 kcal/g
anorexia, a decrease in appetite. However, depres-
• Glucose 4.1 kcal/g
• Protein 4.1 kcal/g
sion, medications, dementia and illness are more
common causes in hospitalised patients.
The second entity is kwashiorkor, which results
stores of carbohydrate are low and act as a rapid‐ from an inadequate as well as unbalanced diet con-
response provider of glucose, particularly in stress taining relatively more calories than protein. There
situations. Of the body protein, 45% is structural is characteristic fluid retention, which may mask
and not available for metabolic interchange, while the commonly seen and often rapid erosion of mus-
the remaining 55% is circulating proteins or con- cle and fat stores. In the adult patient, this is often
tained in cells. If this protein is lost it leads to loss seen with sepsis and after trauma.
of function, including muscle weakness and immune It also useful to know of two further subsets of
deficiency. The ratio of the fat‐free mass (total body malnutrition, cachexia and sarcopenia. Cachexia is
weight minus fat) to total body water (fat‐free body characterised by profound loss of adipose and
hydration) is remarkably constant in a healthy per- skeletal muscle mass with associated haematologi-
son, but varies markedly in the unwell patient. cal derangement and deconditioning. It usually
results from an interplay of altered metabolism
and inflammation. Common causes include meta-
Malnutrition bolic disease, cancer, acquired immunodeficiency
syndrome (AIDS) or end‐stage organ disease states.
Malnutrition is the inability to match both meta- Sarcopenia is the loss of muscle mass and quality
bolic and nutrient requirements. The European and manifests as frailty. It is associated with
Society for Clinical Nutrition and Metabolism decreased strength, and results from reductions in
(ESPEN) has defined it as either (i) BMI below 18.5 androgenic hormones, increasing resistance to
kg/m2 or (ii) weight loss over 10% (or 5% over 3 insulin, decreased exercise and decreased protein
months) and reduced BMI (<20 kg/m2 if <70 years intake that is seen with ageing.
old, <22 kg/m2 if >70 years old) or a low fat‐ Diseases also play an important role in malnutri-
free mass index (FFMI, <15 kg/m2 in females and tion syndromes. Gastrointestinal disease can produce
7: Nutrition and the surgical patient 51
Table 7.3 Comparisons between marasmus and kwashiorkor
Marasmus Kwashiorkor
Nutritional defect Impaired delivery Impaired utilisation

Protein catabolism Compensated Uncompensated
Aetiology No food Sepsis
No appetite Major trauma
Gastrointestinal dysfunction Burns
Metabolic rate Normal or reduced Increased
Prognosis if untreated Months Weeks
Principles of treatment Replenish with standard nutrition Resuscitate and support
Use simplest available route Control sepsis
Treat underlying illnesses, if any Provide non‐standard nutritional regimens
Clinical course Straightforward Complicated
obstruction, malabsorption and fistulas resulting in marasmus the body undergoes an important
gastrointestinal dysfunction. Inflammatory media- change, over several days, to using ketone bodies
tors associated with the inflammatory phlegmon (keto‐adaptation) from fat as brain fuel. This adap-
may secondarily lead to PEM and worsen fluid tation preserves muscle protein.
and electrolyte disturbances. AIDS leads to severe In sepsis and trauma, however, this does not
cachexia, similar to that seen in cancer. This is prob- occur. Surgery, injury or infection induces a sys-
ably mediated by cytokines such as tumour necrosis temic inflammatory response – a complex inter-
factor (TNF)‐α and is complicated by chronic infec- play of proinflammatory and anti‐inflammatory
tion and malignancies. In cancer there is a rise in rest- responses – and modification of immunological
ing energy expenditure and the tumour avidly retains and non‐immunological pathways. The metabolic
nitrogen as well as operating at a glucose‐wasteful, response to systemic inflammation is shown in
high rate of anaerobic metabolism. Unlike the situa- Figure 7.1. Glycogen, fat and protein are catabo-
tion in experimental animal models, these tumour lised to increase glucose, free fatty acids and amino
effects are unlikely to explain the degree of cachexia acids in the circulation that are integral to the
often seen in humans. Cancer‐induced anorexia and immune response and phases of healing. As a result,
host cytokine production are probably involved. there is a decrease of these substrates in the periph-
eries for maintenance of protein with a resultant
loss in muscle mass, which ultimately impacts on
Response to stress and injury functional recovery.
With severe sepsis and in burns, this protein
In starvation, glycogen is initially broken down to catabolism is even more marked and energy
produce glucose in order to maintain brain func- expenditure massively increases, fuelled by intense
tion. However, glycogen is rapidly exhausted and in free fatty acid oxidation. All the while, there is a
Systemic inflammatory response
Increase glucose, FFA, AA Decrease glucose, FFA, AA

in circulation in peripheries for maintenance of protein
Rx nutrition
Decrease muscles mass and exercise
Healing Immune response
Immunonutrition
Decrease functional recovery
Fig. 7.1 Metabolic response to systemic inflammation. AA, amino acid; FFA, free fatty acid.
blunted systemic inflammatory response which can

Box 7.2 Markers for nutritional
lead to hypothermia, leucopenia and impaired heal-
assessment
ing amongst other sequelae.
The body’s response to surgery is now known to • Anthropometric measures: skinfold thickness
last well beyond the initial postoperative period. (biceps, triceps, subscapular), BMI
Within a few minutes of beginning an operation the • Biochemical measures: albumin, lymphocyte count,
level of counter‐regulatory hormones (cortisol, gluca- skin recall antigens
gon and catecholamines) rises. In uncomplicated sur- • Clinical history
gery these act only to initiate protein catabolism, as • Dietary history
the endocrine response is relatively short‐lived (lasting
24–48 hours). However, protein catabolism continues
for up to 1 month after major surgery as a result of much remains. Most screening tools therefore
proinflammatory cytokines such as TNF‐α, interleu- address four main principles.
kin (IL)‐1, IL‐6 and IL‐8. These probably act locally, 1 What is the patient’s current condition? For
at the site of injury, and indirectly (via the blood- example, what is their BMI?
stream and in the central nervous system). Imbalances 2 Is their condition stable? Do they have more than
between proinflammatory and anti‐inflammatory 5% involuntary weight loss over 3 months?
cytokines also probably play a role in anorexia, 3 Will the condition get worse? Have they recently
pyrexia, fatigue and fat catabolism. reduced intake for example?
4 Will the disease process accelerate nutritional
Consequences of injury and malnutrition deterioration?
Nutritional assessment begins with a careful clini-
Malnutrition is associated with increased postop- cal evaluation. Important features of the history are
erative complications, mortality, increased length of weight loss greater than 5% during the past 3
stay and decreased quality of life. It is complicated months and a change in exercise tolerance. Physical
by immune incompetence and decreased wound examination may reveal non‐healing wounds,
healing ability. Protein–energy metabolism may oedema and fistulas.
be accompanied by physiological changes such as Body composition is assessed by simple clinical
poor muscle function, manifest as physical weak- tests and a standard blood test. Loss of body fat is
ness and poor respiratory muscle function. Such often apparent from observations of the patient but
changes increase postoperative complications such is also assessed by palpating the triceps’ and biceps’
as pneumonia and prolong length of stay. skinfolds. If the dermis can be felt between finger
Furthermore, oncological outcomes can also be and thumb, then it is likely that the body mass is
compromised by poor perioperative nutrition. composed of less than 10% fat.
Fatigue is a common concomitant of surgical ill- Protein stores are assessed by observation and
ness and is characterised by prolonged mental and palpation of the temporalis, deltoids, suprascapular
physical exhaustion. After surgery it is most pro- and infrascapular muscles, the bellies of biceps and
nounced at 1 week, and slowly improves for up to 3 triceps and the interossei of the hands. If the ten-
months. It is worse in the elderly, in patients who were dons are palpable or the bony shoulder girdle is
tired prior to surgery and in patients with cancer. sharply outlined (tendon–bone test), then the
patient is likely to have lost more than 30% of total
body protein stores.
Nutritional assessment Plasma albumin levels are of assistance in deter-
mining the type of PEM. In kwashiorkor, the albumin
Some 30% of all patients presenting to hospital are may be low, reflecting the expansion of the extracel-
malnourished. It is thus important to screen patients lular fluid space, and this may manifest clinically as
to help predict outcomes and enable nutritional pitting oedema. It is a good prognostic indicator,
intervention. However, there is only one prospec- with values less than 30 g/L associated with poorer
tively validated scoring system, the Nutritional surgical outcomes. However, it is a poor nutritional
Risk Screening (NRS‐2002) (Figure 7.2), and no marker, since those suffering from starvation may in
single clinical or laboratory test defines nutritional fact have a normal serum albumin. Furthermore, it is
status (Box 7.2). a negative acute‐phase protein. As such, albumin val-
The aim of nutritional assessment is to define ues must be interpreted with caution.
how much the patient has lost from his or her body Assessment of physiological function is of vital
stores of protein and fat and, as a corollary, how importance because weight loss without evidence
Part A: Initial screening

1. Is BMI <20.5?
2. Has patient lost weight within last 3 months?
3. Has patient had a reduced dietary intake in the last week?
4. Is the patient severely ill? (e.g. in intensive care)
If yes to any of these questions, proceed to Part B. If no, rescreen weekly.
Part B: Final screening

Impaired nutritional status Severity of disease (= increase requirements)
Absent Normal nutritional status Absent Normal nutritional requirements
Score 0 Score 0
Mild Wt loss >5% in 3 mths or food intake Mild Hip fracture; Chronic patients, in
Score 1 below 50-75% of normal requirement Score 1 particular with acute complications:
in preceding week cirrhosis, COPD
Chronic hemodialysis, diabetes,
oncology
Moderate Wt loss >5% in 2 mths or BMI 18.5– Moderate Major abdominal surgery; Stroke
Score 2 20.5 & impaired general condition or Score 2 Severe pneumonia, hematologic
food intake 25-60% of normal Malignancy
requirement in preceding week
Severe Wt loss >5% in 1 mth (>15% in 3 Severe Head injury; Bone marrow
Score 3 mths) or BMI <18.5 & impaired Score 3 Transplantation
general condition or food intake Intensive care
0-25% of normal requirement patients (APACHE410).
in preceding week
Score + Score = TOTAL SCORE
Age If age >70 add 1 to give “Age-adjusted total score”
Score 3+: the patient is nutritionally at-risk and a nutritional care plan is initiated.
Score <3: weekly rescreening of the patient. If the patient e.g. is scheduled for a major operation, a
preventive nutritional care plan is considered to avoid the associated risk status.
Diagnoses shown in italics are based on the prototypes for severity of disease:
Score= 1: a patient with chronic disease, admitted to hospital due to complications. The patient is weak
but out of bed regularly. Protein requirement is increased, but can be covered by oral diet or supplements
in most cases.
Score= 2: a patient confined to bed due to illness, e.g. following major abdominal surgery. Protein
requirement is substantially increased, but can be covered, although artificial feeding is required in many
cases.
Score= 3: a patient in intensive care with assisted ventilation etc. Protein requirement is increased and
cannot be covered even by artificial feeding. Protein breakdown and nitrogen loss can be significantly
attenuated.
Fig. 7.2 Nutritional Risk Screening (NRS 2002). Source: Kondrup J, Allison SP, Elia M, Vellas B, Plauth M. ESPEN
guidelines for nutrition screening. Clin Nutr 2003;22:415–21. Reproduced with permission of Elsevier.
of physiological abnormality is probably of limited major surgery or trauma in the preceding week and
consequence. Function is observed while perform- where there is evidence of sepsis or ongoing inflam-
ing a physical examination and then by watching mation, such as inflammatory bowel disease.
the patient’s activity on the ward. Grip strength is Determining the intensity and type of malnutrition
assessed, and respiratory muscle strength is assessed is of great importance in setting nutritional goals.
by asking the patient to blow hard holding a strip When PEM is severe and affects physiological func-
of paper 10 cm from the lips. Severe impairment is tion, postoperative complications are more common
present when the paper fails to move. and postoperative stay is prolonged. The identifica-
Metabolic stress will be revealed by history and tion of metabolic stress is also important: because
examination. It is present if the patient has had the extracellular water is expanded, the response to
standard nutritional intervention is impaired and the

Box 7.3 Principles of nutritional
type of malnutrition is predictable.
intervention
• Preoperative nutrition is indicated in severely

Perioperative nutrition malnourished patients.
• Postoperative early tube feeding within 24 hours
Patients often face prolonged preoperative fasting should be initiated in those where early oral
and oral restriction postoperatively. This paradigm nutrition cannot be started and in whom oral
has changed with greater understanding of anaes- intake will be inadequate for more than 7 days.
thetic risk profiles and postoperative metabolic • Postoperative total parenteral nutrition is provided
requirements respectively. Patients are now encour- if a normal intake has not been established within
aged to maintain solid intake up to 6 hours, and 5–7 days for a depleted patient and 7–10 days for
clear fluids up to 2 hours, preoperatively. Some sur- a normal patient.
geons encourage carbohydrate drinks in the preop- • When possible, enteral nutrition is preferred over
erative period, although the evidence is mixed. It parenteral nutrition.
certainly does not increase the risk of aspiration,
and may reduce anxiety and decrease length of stay
for those undergoing major surgery. Box 7.4 Indications for nutritional
Postoperatively, early oral nutrition is encour- intervention in surgical patients
aged, and is a key component in enhanced recovery
after surgery (ERAS) programs. ERAS involves a Indications for preoperative nutrition
combination of interventions that aim to minimise • Severe malnutrition with physiological impairment
stress and accelerate return to function. It includes Indications for total parenteral nutrition
preoperative and postoperative nutrition and fluid • Gut is obstructed
balance guidelines, perhaps the most important of • Gut is short
which is early implementation of postoperative oral • Gut is fistulated
feeding rather than the once traditional ‘gut rest’. It • Gut is inflamed
was initially developed for colorectal surgery but • Gut cannot cope
has now been promoted across several specialties.
Indications for enteral nutrition
In fact, its nutritional principles have been adopted
• Malnutrition with a functioning gut
in non‐operative patients as well. The guidelines for
• Postoperative feeding
acute pancreatitis published by the International
Association of Pancreatology (IAP) and the
American Pancreatic Association (APA) include
importance in laboratory models. Enteral nutrition
early oral feeding for mild pancreatitis and consid-
is administered by mouth if possible (as high‐energy
eration of tube feeding within 48 hours in severe
nutritional supplements), but may also be delivered
pancreatitis, a move away from what again used to
by a fine‐bore feeding tube introduced under fluor-
be the more traditional nil‐by‐mouth approach.
oscopic control or using an endoscope. Fine tubes
can also be placed into the jejunum at surgery and
Indications for nutritional intervention
feeding can begin in the recovery room after the
The principles of nutritional intervention are sum- operation is complete. If prolonged enteral feeding
marised in Box 7.3. Nutritional intervention is indi- is anticipated, a gastrostomy should be created,
cated prior to surgery only in severely malnourished usually via the percutaneous endoscopic route.
patients with physiological impairment. Nutritional
support is required in patients who cannot eat, in Intravenous nutrition
whom intake is insufficient for their needs, in whom
Intravenous nutrition or total parenteral nutrition
the gastrointestinal tract cannot be used and in
(TPN) is useful if the gut is obstructed, too short,
those with accelerated losses (Box 7.4).
fistulated, inflamed or simply cannot cope, such as
in prolonged postoperative ileus. TPN formulations
Enteral nutrition
generally comprise 60–70% dextrose and 10–20%
In circumstances where the gut is functional, enteral amino acids, with lipid emulsion, vitamins and min-
nutrition should be preferentially used. Enteral erals added as required. It is administered by a dedi-
nutrition may be important in maintaining gut cated central venous catheter inserted under sterile
barrier function, demonstrated to be of critical
conditions.
Approximately 50 kcal/kg body weight per day It should be given for approximately 7 days preop-
and 0.3 g/kg of nitrogen as amino acids per day is eratively and postoperatively.
required to achieve gain in body protein. Use of
nutritional intervention must be preceded by cor- Other adjuncts
rection of anaemia, hypoalbuminaemia, fluid and
Epidural anaesthesia blocks much of the early stress
electrolyte abnormalities, and deficits in trace met-
response to surgery and this has been postulated to
als. Vitamins must be dealt with by appropriate
be of critical importance in slowing protein loss.
infusions so that administered nutrients will be
What may be of more importance is the mobility
used efficiently.
that epidural anaesthesia permits the surgical
TPN is not without complications. Central venous
patient in the immediate postoperative period and
catheter infection is potentially life‐threatening and
the ability of the epidural block to limit postopera-
therefore care must be meticulous. Implementation
tive ileus, at least partially due to an opiate‐sparing
of the Centers for Disease Control’s Checklist for
ability.
Prevention of Central Line Associated Blood
Non‐steroidal anti‐inflammatory drugs (NSAIDs)
Stream Infections (https://www.cdc.gov/hai/pdfs/bsi/
may be important in preventing arachidonic acid‐
checklist‐for‐CLABSI.pdf) has seen a significant
mediated tissue damage, as may nitric oxide inhibi-
reduction in infection rates worldwide. TPN has
tion and antioxidants in limiting free oxygen radical
been associated with increased gastrointestinal
damage. These await further evaluation in clinically
bacterial translocation, a heightened proinflamma-
relevant models.
tory state and increased pulmonary dysfunction.
Minimal access surgical interventions have led, in
Overfeeding in particular can lead to respiration dif-
many cases, to earlier recovery from surgery and
ficulties, and excess carbohydrate or fat can lead to
faster return to work. When these techniques are
fatty liver. Excess protein replacement can lead to
combined with other modulators, the improve-
elevations in blood urea nitrogen. Long‐term TPN
ments in postoperative outcome are likely to be
users can also suffer from osteoporosis, although the
quite profound.
aetiology is unclear.
Immunonutrition
Conclusion
Immunonutrition is the supplementation of nutri-
ents that are thought to impact both immune Short‐term preoperative nutritional intervention in
and inflammatory response to injury. These include severely compromised patients decreases postoper-
arginine, omega‐3 fatty acids and glutamine ative complications. The effect is not nearly as
(Table 7.4). Studies investigating the utility of apparent in patients with mild to moderate malnu-
immunonutrition have varied in quality and indeed trition. Postoperative nutritional support is one of
outcome. Consensus is still building, but it is likely the most important developments in modern sur-
that it may have a role in severely malnourished gery and has allowed surgeons much greater leeway
patients with severe trauma, sepsis, acute respira- in the management of surgical complications such
tory distress syndrome and head and neck cancers. as fistulas and bowel obstruction.
Table 7.4 Components of immunonutrition.
Biological function Outcome
Arginine Stimulates immune cells, precursor May decrease infection, reduce

Conditional amino acid to nitric oxide which may improve length of stay
microvascular perfusion
Omega‐3 fatty acids Maintain cell membranes and Some evidence of decreased
Polyunsaturated fatty acids, e.g. modulate inflammatory response mortality, clinically safe
docosahexaenoic acid (DHA) and
eicosapentaenoic acid (EPA)
Glutamine Antioxidant, precursor to May decrease infection, reduce
Conditional amino acid, 70% of glutathione providing energy for length of stay, improve quality of
amino acid mobilised during enterocytes, component of protein life, improve nitrogen balance,
stress response synthesis improve sugar control
3 The average requirement for intravenous nutrition

Further reading per day is:
a 20 kcal/kg body weight
Gustafsson U, Scott M, Hubner M et al. Guidelines for
b 30 kcal/kg body weight
perioperative care in elective colorectal surgery:
enhanced recovery after surgery (ERAS) society recom- c 40 kcal/kg body weight
mendations: 2018. World J Surg 2019;43:659–95. d 50 kcal/kg body weight
Kondrup J, Allison SP, Elia M, Vellas B, Plauth M. ESPEN e 60 kcal/kg body weight
guidelines for nutrition screening. Clin Nutr 2003;22:
415–21. 4 What percentage of patients being admitted to
Weimann A, Brago M, Carli F et al. ESPEN guideline: clini- hospital are malnourished?
cal nutrition in surgery. Clin Nutr 2017;36:623–50. a 10%
b 15%
MCQs c 30%
d 50%
Select the single correct answer to each question. The e 60%
at the end of the book. 5 Which of the following is not true?
a perioperative nutrition is only indicated in
1 Marasmus is characterised by the following
severely malnourished patients
characteristics except:
b postoperative early tube feeding within
a inadequate intake of an otherwise balanced
24 hours should be initiated in those where
diet
early oral nutrition cannot be started and in
b cachexia in the adult
whom oral intake will be inadequate for more
c fluid retention
than 7 days
d decreased metabolic rate
c postoperative total parenteral nutrition is
e easy correction with standard nutrition
provided if a normal intake has not been
established within 5–7 days for a depleted
2 Nutritional markers include the following except:
patient and 7–10 days for a normal patient
a skinfold thickness
d when possible, enteral nutrition is preferred over
b mid‐arm muscle circumference
parenteral nutrition
c total leucocyte count
d serum albumin
e skin recall antigens
8 Care of the critically ill patient
Jeffrey J. Presneill1,2, Christopher MacIsaac2
and John F. Cade1,2
1
University of Melbourne, Melbourne, Victoria, Australia
2
Intensive Care Unit, Royal Melbourne Hospital, Melbourne, Victoria, Australia
A wide variety of comorbidities may adversely

Introduction to critical illness influence the prognosis for recovery following
critical illness, including ischaemic heart disease,

Intensive care for complex and potentially life‐
diabetes, peripheral vascular disease, severe chronic
threatening critical illness is currently provided to
obstructive airways disease or malignancy. In the
about 150 000 patients annually across Australia
absence of these comorbidities, selected patients of
and New Zealand. In Australia, at least 1.7% of
advanced age may benefit from short‐term ICU
acute hospital care episodes involved time in an
admission. Reliable prediction of patient outcome
intensive care unit (ICU), with the average ICU
would greatly assist patient selection, clinical man-
admission almost 4 days in duration, at an average
agement and resource allocation. Several regression
daily cost approaching A$5000.
model‐based systems for critical illness mortality
The concept of ICUs developed over 60 years ago,
prediction are in common use internationally. Such
initially for prolonged mechanical ventilation sup-
models define average effects rather than individual
port. Expanding demand for critical care services has
variation, making them suitable for group compari-
led to there being over 200 ICUs in Australia and
sons but not as arbiters of individual patient care.
New Zealand, with many classified as level 3 or ter-
tiary, meaning hospital facilities capable of support-
ing patients with complex multisystem organ Causes of critical illness
dysfunction for an indefinite period using methods
such as mechanical ventilation, extracorporeal renal The chief categories of causes of critical illness and
support services and invasive cardiovascular moni- thus admission to ICU are shown in Figure 8.1.
toring. Such intensive care has permitted many Severe infection remains the most common and
patients to survive hitherto fatal illness or injury, with concerning problem in the care of seriously ill
the interesting consequence that complex pathophys- patients in hospitals worldwide. The rapid diagno-
iological responses are now seen which could never sis of sepsis is an urgent medical priority, as early
have originally been adaptive, which could be help- identification and appropriate immediate manage-
ful, harmful or neutral and which in turn have led to ment in the initial hours after development of sepsis
new therapeutic opportunities and challenges. is likely to improve patient outcomes. Severe infec-
Overall slightly more than 90% of patients sur- tion provides an important link between either
vive admission to ICU in Australia and New underlying or complicating illness and serious con-
Zealand (Figure 8.1). However, an adverse post‐ ditions such as circulatory, respiratory and other
ICU syndrome of prolonged physical, cognitive and organ dysfunction. Some common definitions of
mental health dysfunction is well described interna- infection and related phenomena such as sepsis
tionally in some survivors of critical illness and and septic shock are shown in Box 8.1. Clinically
their caregivers. A substantial proportion of these suspected sepsis occurs in approximately 1% of
declines may be explained by patient age and Australian hospital admissions, 10% of ICU admis-
comorbidities prior to ICU admission rather than sions, and has a hospital mortality ranging from less
the episode of critical illness itself, and recent than 5% (in the absence of comorbidities and older
Australian data suggest ICU survivors experience a age) to 20%. Septic shock may have a mortality of
quality of life they find acceptable. approximately 40%, despite early antimicrobial
57
Circulatory Respiratory Severe Organ Metabolic

dysfunction dysfunction Trauma Surgery dysfunction dysfunction
infection
ICU
Resuscitation Specific
Diagnosis
therapy (if any)
10–20%
≥75% ≤5%
Persistent
Early cure Early death
critical illness
Isolated ARDS MODS

Low mortality Variable mortality
Fig. 8.1 Pathways of critical illness.
therapy and intensive life support; however, delayed necessarily involve microbial infection. The
recognition of sepsis and administration of relevant constellation of clinical, haematological, and

antibiotics may substantially worsen patient out- biochemical signs typically found in the presence
come. Survivors of severe sepsis commonly exhibit a of infection can often be observed at least tran-
complex post‐sepsis immune dysfunction with both siently in the absence of any identifiable infection,
innate immune dysregulation and adaptive immune as with pancreatitis, trauma, burns, rhabdomyoly-
suppression featuring simultaneous inflammatory sis, necrotic tissue and cardiopulmonary bypass.
and anti‐inflammatory responses that may persist Patients who are critically ill due to suspected sep-
to hospital discharge after clinical recovery. sis or septic shock should receive empirical antimi-
An expanding global problem is the continually crobial therapy as soon as possible, ideally once
emerging antibiotic resistance of microorganisms, cultures of blood and urine samples have been
which challenges the success of the complex and obtained. Attempts are ongoing to develop spe-
invasive procedures that characterise modern hospi- cific and sensitive diagnostic tests for sepsis using
tal practice. The most commonly isolated organisms biomarkers such as procalcitonin or numerous
are Staphylococcus aureus, Staphylococcus epider- others that may improve on the current non‐spe-
midis, Streptococcus pneumoniae, Streptococcus cific clinical signs and long‐standing laboratory
pyogenes, various enterococci, Gram‐negative tools (e.g. white cell count, C‐reactive protein)
bacilli and Candida spp. When sepsis is suspected used to diagnose infection.
but the site remains unknown despite an appropri- Over the last 10 years, multiple randomised trials
ately thorough clinical investigation, potential have investigated therapeutic approaches used in
sources include lungs, urinary tract, abdomen, skin the clinical support of patients with sepsis and sep-
or soft tissue, musculoskeletal system, central nerv- tic shock. An initial report of improved survival
ous system and intravascular devices. with a protocol‐based approach to sepsis manage-
The bodily responses to severe infection may be ment involving a ‘bundle’ of specified interventions
indistinguishable from those due to non‐infective termed early goal‐directed therapy (EGDT) was not
inflammation or indeed to severe injury itself. The confirmed by a meta‐analysis of individual patient
systemic response to injury in general is referred data from three subsequent large multicentre trials
to as the systemic inflammatory response syn- testing the EGDT approach.
drome (SIRS; Table 8.1). The definition of SIRS For those patients with sepsis who remain hypo-
describes a widespread inflammatory response to tensive despite adequate fluid resuscitation, two
a variety of clinical insults, not all of which common choices of vasopressor agents used by
8: Care of the critically ill patient 59
Box 8.1 Definitions relevant to the evaluation of sepsis
Infection
A microbial phenomenon characterised by an inflammatory response to the presence of microorganisms or the
invasion of normally sterile host tissue by those organisms.
Bacteraemia
The presence of viable bacteria in the blood. Similarly, for other classes of microorganisms including fungi, viruses,
parasites and protozoa.
Systemic inflammatory response syndrome (SIRS)

Consists of two or more of the following:
• temperature >38°C or <36°C
• heart rate >90 beats/min
• respiratory rate >20 breaths/min or Paco2 <32 mmHg
• leucocyte count >12 × 109/L, <4 × 109/L, or >10% immature (band) forms.
Sepsis
Sepsis is life‐threatening organ dysfunction caused by a dysregulated host response to infection. It is a syndrome of
physiological, pathological and biochemical abnormalities induced by clinically diagnosed infection, where the
absence of positive cultures does not exclude the diagnosis. Sepsis is a syndrome without, at present, a validated
standard diagnostic test. Any unexplained organ dysfunction should thus raise the possibility of underlying
infection. The clinical and biological phenotype of sepsis can be modified by pre‐existing acute illness, long‐standing
comorbidities, medication and interventions. Specific infections may result in local organ dysfunction without
generating a dysregulated systemic host response.
For clinical operationalisation, organ dysfunction can be represented by an increase in the sequential (sepsis‐
related) organ failure assessment (SOFA) score of 2 points or more.
SOFA score
The score summarises (range 0–24) organ system abnormalities, and accounts for clinical interventions. Laboratory
variables, namely Pao2, platelet count, creatinine and bilirubin, are needed for full completion. Organ dysfunction
can be identified as an acute change in total SOFA score ≥2 points consequent to the infection. The baseline SOFA
score can be assumed to be zero in patients not known to have pre‐existing organ dysfunction.
Septic shock
Sepsis with persistent hypotension requiring vasopressors to maintain mean arterial blood pressure ≥65 mmHg and
with a serum lactate level >2 mmol/L despite adequate volume resuscitation. Adequate volume resuscitation remains
poorly defined. Many studies have specified an intravenous infusion of isotonic fluid, colloid or blood products to
restore the effective circulating blood volume. Other studies nominate a volume of 500 mL. Patients who are
receiving inotropic or vasopressor agents may not be hypotensive at the time that perfusion abnormalities are
measured. Septic shock is a subset of sepsis in which underlying circulatory and cellular/metabolic abnormalities are
sufficiently profound to substantially increase mortality.
These designations are based on 2016 international definitions that have deleted the previous term ‘severe
sepsis’, meaning sepsis complicated by organ dysfunction (Singer et al. 2016). However, multiple older definitions
and terminologies remain in widespread clinical use, including the systemic inflammatory response syndrome,
severe sepsis, septic shock and various definitions of organ dysfunction/failure (Abraham et al. 2000; Kaukonen
et al. 2014).
Abraham E, Matthay MA, Dinarello CA et al. Consensus conference definitions for sepsis, septic shock, acute lung injury, and acute
respiratory distress syndrome: time for a reevaluation. Crit Care Med 2000;28:232–5.
Kaukonen KM, Bailey M, Suzuki S, Pilcher D, Bellomo R. Mortality related to severe sepsis and septic shock among critically ill
patients in Australia and New Zealand, 2000–2012. JAMA 2014;311:1308–16.
Singer M, Deutschman CS, Seymour CW et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis‐3).
JAMA 2016;315:801–10.
intravenous infusion to elevate arterial blood pres- the use of 0.9% sodium chloride with its supra-
sure are noradrenaline and vasopressin, which have physiological chloride content has been associated
similar efficacy and toxicity. Beyond appropriate with the development of metabolic acidosis and
antibiotics, fluid and vasopressor resuscitation and also possibly acute kidney injury. In specific clinical
other critical care support, the role of adjunctive circumstances (e.g. raised intracranial pressure)
glucocorticoids in septic shock has been debated various hypertonic saline crystalloid solutions (e.g.
for several decades. In a recent large multicentre 3%) are used without strong clinical evidence of
randomised trial, hydrocortisone by infusion at 200 improved patient‐centred outcomes. Two recent
mg/day did not influence the risk of death at 90 large open label trials have reported a small advan-
days (which was the trial primary outcome) overall tage for balanced salt solutions (lactated Ringer’s
or in six pre‐specified subgroups. Faster resolution solution or PlasmaLyte A) compared with normal
of shock, from a median of 4 to 3 days, was noted saline with respect to renal function in hospitalised
but this may have been a chance observation. In a non‐critically ill patients, and also in critically ill
separate multicentre trial, the addition of fludro- patients where balanced crystalloid use was associ-
cortisone to hydrocortisone in severe septic shock ated with fewer occurrences of a composite adverse
was associated with some decrease in the risk of outcome (death from any cause, new renal replace-
death at 90 days from 49% to 43%, with a relative ment therapy, or persistent renal dysfunction).
risk of death in the hydrocortisone‐plus‐fludrocor- The prototypical colloid is human albumin solu-
tisone group of 0.88 (95% confidence interval, tion (e.g. 4% albumin in saline). Associated with
0.78–0.99). It remains to be determined if these the elevated cost and potentially limited interna-
contrasting trial results will change clinical practice tional availability of albumin solutions, several
with respect to adjunctive corticosteroid use in varieties of semi‐synthetic colloids were developed,
severe infection. comprising most commonly a form of hydroxyethyl
starch (HES), or succinylated gelatin, urea‐linked
gelatin–polygeline preparations and, least com-
Resuscitation monly, a dextran solution. While use of saline 0.9%
compared with albumin 4% in saline 0.9% in a
There is a potential but unproven role for limited large randomised trial resulted in equivalent patient
pre‐hospital fluid administration with permissive outcomes from critical illness, the overall ratio of
hypotension in adult trauma patients with haemor- the volume of albumin 4% to the volume of saline
rhagic shock during rapid transport to a suitable 0.9% administered was approximately 1 : 1.4 to
surgical facility for definitive haemostasis. In most achieve equivalent hemodynamic resuscitation end
other circumstances, conventional resuscitation points, such as mean arterial pressure or heart rate.
aims to be prompt and complete, with restoration Potential disadvantages of semi‐synthetic colloids
and maintenance of an adequate circulating blood compared to crystalloids have been reported. Use of
volume (that is, treatment of hypovolaemia). This is 6% HES as compared with saline in ICU patients
a fundamental requirement in all seriously ill was associated with increased need for renal
patients. Without adequate blood volume expan- replacement therapy, while in ICU patients with
sion, inotropes and other therapies are less likely to severe sepsis HES was associated with increased
be effective and organ function is likely to be com- mortality compared with the use of the balanced
promised. There is no universal ideal resuscitation crystalloid Ringer’s acetate.
fluid, although it is reasonable that replacement of The volume of acute fluid resuscitation required
losses should usually reflect the major deficit caused in critically ill patients may be a substantial number
by the underlying disease process. Non‐blood of litres. In addition to obvious losses and to antici-
resuscitation fluids are broadly categorised into pated third‐space needs, there is often extra volume
crystalloids and colloids. Crystalloids are further required due to vasodilatation, capillary leak and
described as ‘balanced’ if their chemical composi- blood flow maldistribution. Fluid resuscitation is
tion, especially their chloride content, approxi- complete if blood flow is restored (that is, the
mates extracellular fluid (e.g. Hartmann’s, Ringer’s haemodynamic goal) or if cardiac filling pressures
and PlasmaLyte solutions). In global clinical prac- are optimised, whichever is first. If a satisfactory
tice, the most commonly used crystalloid has been haemodynamic goal has not been achieved despite
the isotonic but ‘unbalanced’ 0.9% sodium chlo- suitable cardiac filling pressures and thus repair of
ride (so‐called normal saline), with 200 million hypovolaemia, inotrope therapy is required if myo-
litres per year administered in the USA. However, cardial contractility is impaired and/or vasopressor
therapy is required if blood pressure is inadequate organ systems: lungs, blood, liver, kidneys, brain
(e.g. in states of low systemic vascular resistance and circulation. With organ system dysfunction val-
due to vasodilatation). In hyperdynamic vasodi- ues from 0 (normal) to 4 (high degree of dysfunc-
lated septic shock, hypotension has been treated tion) based on the worst physiological disturbance
for many years by infusion of agents from one or in each 24 hours of a patient’s admission, the total
both of two major classes of vasopressors: (i) the SOFA score ranges from 0 to 24. Emphasis has
sympathomimetic amines/catecholamines such as shifted in the latest international sepsis and septic
noradrenaline or (ii) vasopressin or its longer‐act- shock definitions from SIRS to quantification of
ing analogue terlipressin. Very recently, a third class organ dysfunction using the SOFA score.
of natural vasopressor, angiotensin II, has emerged There are numerous other scores measuring the
in preliminary clinical trials after difficulty in its severity of illness, trauma or organ dysfunction that
manufacture were eventually solved. While adrena- may be used in the study of critical illness or to
line is the inotrope of choice specifically for ana- benchmark ICU performance. Among those more
phylactic shock, other agents may be used in shock commonly encountered are two versions of the
due to myocardial impairment, such as dopamine, Acute Physiology and Chronic Health Evaluation
or dobutamine often with low‐dose noradrenaline, score (e.g. APACHE II and III), the related Simplified
with such choices guided by clinical practice rather Acute Physiology Score (e.g. SAPS II) and more
than randomised evidence. recently the Australian and New Zealand Risk of
Death (ANZROD) model. As already mentioned,
all these regression‐based outcome prediction mod-
Organ dysfunction and severity of illness els return ‘population average’ estimates that do
not substitute for informed clinical experience in
Functional assessment of organ damage emphasises the proper management of individual patients.
a continuum of progressively worsening organ dys- The current overall mortality of all patients
function rather than an arbitrary dichotomy admitted to ICU in Australia and New Zealand is
between normality and organ failure. Thus, the 8–9%. While development of any substantial organ
older term ‘multiple organ failure’ is often replaced dysfunction, especially if multiple organ systems
by the broader term multiple organ dysfunction are involved (MODS), may increase the probability
syndrome (MODS). Except for the acute respira- of ICU or hospital mortality, the incidence of
tory distress syndrome (ARDS), which is the pul- MODS varies greatly with the patient group under
monary manifestation of MODS and which has consideration. In uncomplicated surgery, it is rare.
precise (though still arbitrary) definitions set by In serious and complicated surgical conditions,
international consensus, MODS has no universally such as trauma, haemorrhage or shock, it may
agreed set of definitions. These definitional difficul- occur in 20%. In uncontrolled sepsis, it may be sub-
ties arise primarily because of incomplete under- stantially higher. For patients with organ dysfunc-
standing of the complex interaction between tion, the time to recovery has been arbitrarily
inflammatory, genetic and potentially other influ- categorised as uncomplicated (<4 days), intermedi-
ences underlying the development of MODS, which ate (4–14 days) or complicated (>14 days).
may be observed following a wide range of human The pathogenesis of MODS remains unclear, and
injury, ranging from pancreatitis to severe trauma several models have been proposed, such as exces-
or most commonly in association with severe infec- sive inflammation, a second‐hit insult, or a complex
tion (septic shock). These complexities are further disturbance of proinflammatory and anti‐inflam-
reflected in the observation that different individu- matory pathways. Management of MODS contin-
als may have quite different responses to seemingly ues to be entirely supportive. While available
similar insults. clinical care and resuscitation practices reduce but
While criteria for individual organ dysfunction do not completely prevent its incidence in the
vary, overall patient mortality tends to increase patient groups at risk, there is evidence of a slow
with the number and severity of dysfunctional reduction over time in the mortality risk with
organ systems present. One widely accepted organ MODS that may be related to overall improve-
dysfunction score, used alone or in combination ments in resuscitation, surgery and critical care sup-
with other scores to predict ICU patient outcome port. However, ICU patients who survive severe
within a research or quality assurance context, is MODS may have reduced long‐term survival com-
the sequential organ failure assessment (SOFA) pared with those ICU patients who manifest less
severity of illness score. This score assesses six severe MODS.
Management of the critically ill Further reading
The detailed management of the critically ill patient Bersten AD, Handy J (eds) Oh’s Intensive Care Manual,
is the subject of a vast literature and of many sub- 8th edn. Elsevier, 2019.
Kelley MA. Predictive scoring systems in the intensive care
stantial textbooks. While this management requires
unit. UpToDate. https://www.uptodate.com/contents/
clinical experience, the general principles are
predictive‐scoring‐systems‐in‐the‐intensive‐care‐unit
straightforward, though their implementation can (accessed 28 April 2018).
be complex, sophisticated and multidisciplinary. Marino PL. Marino’s The ICU Book, 4th edn. Philadelphia:
• Resuscitation and maintenance of an optimal Wolters Kluwer Health, 2014.
blood volume is just as much a continuing prior-
ity as it is an initial goal in the treatment of the
critically ill. However, the optimal fluid status of
individual patients may be difficult to quantify.
• Treatment of respiratory impairment, together MCQs
with circulatory management, comprise the twin
pillars of life support in ICU. Abnormalities of
gas exchange and of pulmonary mechanics are
common and are often severe. Specialised and
sophisticated mechanical ventilation is the main- 1 Treatment of critically ill patients in an intensive
stay of respiratory support. care unit:
• After initial resuscitation, and while circulatory a increases the cost of care but does not improve
and respiratory support are in train, early diag- the prognosis
nosis and specific therapy (if any) are required. b is associated with an approximately 50% survival
• Optimal intensive care aims to balance simultane- rate overall
ous resuscitation, appropriate diagnostic algorithms c is associated with approximately a 5–10% death
and the provision of definitive management. rate overall
• There is much emphasis on the early treatment of d is required for 25% of all hospital patients at
sepsis and on the prevention and treatment of some point in their illness
complicating infections. e is not indicated for any patient over 80 years of age
• Metabolic support is essential, because malnutri-
tion may develop rapidly and is a covariable in 2 Infection in critical illness is:
mortality and because adequate nutrition is a almost always followed by dysfunction in
required for tissue repair. Enteral nutrition is pre- multiple organ systems
ferred if technically feasible. b only able to be diagnosed in the presence of
• Renal support may require renal replacement septic shock
therapy (most commonly with continuous veno- c rarely associated with septic shock
venous haemofiltration techniques). d rarely caused by common bacteria
• Psychosocial support is important for both the e often found in the lungs or abdomen
patient and the family. The patient requires analge-
sia, anxiolysis, comfort and dignity, and the family 3 The sequential organ failure assessment (SOFA)
requires access, information and support. Humanity score:
of care in ICU extends to end‐of‐life care in those a quantifies the overall amount of dysfunction
patients with unsurvivable conditions. across six organ systems
• Intensive care requires continuous patient man- b scores above zero nearly always imply the
agement by a skilled multidisciplinary team in a presence of invasive bacterial or fungal infection
specialised environment. Attention to detail is c rarely exceeds zero after cardiopulmonary bypass
necessary to identify problems and therapeutic procedures
opportunities as early as possible. In general, d helps in the clinical differential diagnosis between
much of the care of the critically ill is founded on infection types
complex physiological support which buys time e is based on the worst physiological disturbance in
for healing to occur. each 8 hours of a patient’s admission
4 Intravenous fluid resuscitation of hypotensive, 5 Commonly applied critical care organ support
hypovolaemic critically ill patients in hospital should involves all of the following except:
be in most cases: a mechanical ventilation for hypercarbia
a slow and gentle using only colloids b vasopressor infusions for low cardiac output
b rapid and partial using crystalloids only states
c slow and complete using colloids only c hemodiafiltration for uraemia
d rapid and complete using crystalloids or colloids d platelet transfusion for thrombocytopenia
or both e inotropic infusions for low cardiac output
e composed mostly of a solution of 4% albumin states
9 Surgical infection
Marcos V. Perini and Vijayaragavan Muralidharan
University of Melbourne and Austin Health, Melbourne, Victoria, Australia
of prophylactic antibiotics, are important factors in

Introduction reducing surgical infections.
Surgical infection refers to infections that require

surgical treatment or those occurring in the after-
math of surgery. They may occur de novo in healthy Natural barriers to infection
patients or as complications of surgical proce-
dures (postoperative infections). Most postopera- The inflammatory and immune response to a break
tive infections do not require surgical intervention. in the natural barriers in the body starts early after
However, it is important for the surgical team to be the insult. When natural barriers such as the epithe-
aware of the prevention, diagnosis and manage- lium of the skin, respiratory system, gastrointestinal
ment of such infections after a surgical proce- tract and urinary system are breached, microorgan-
dure. Surgical site infection (SSI) should always be isms are able to enter tissues locally and start the
considered high amongst the myriad of possible
process of infection. In some circumstances bacte-
postoperative infections and active management raemia may result in distal spread leading to infec-
instituted to reduce its morbidity. tive endocarditis, abscesses in solid organs (liver,
Postoperative infections occur in up to 5% of the spleen) and osteomyelitis. The protection afforded
patients undergoing a surgical procedure. The inci- against infections by the mechanical barrier (integu-
dence and severity depends on patient‐related (host) ment, mucosa) is supplemented by the immune sys-
risk factors and situational risk factors (surgeon, tem. Impairment of the immune system due to
type of surgery). Some risk factors that cannot be disease (diabetes, cancer, chronic illness), patient
avoided, such as immunosuppressed patients and factors (advanced age, malnutrition) or direct sup-
contaminated emergency procedures, increase the pression (chemotherapy, organ transplantation)
risk of postoperative complications. Some medical leads to a blunted and delayed response to infection.
conditions are associated with a high risk of post- This may also result in unusual clinical presenta-
operative infection. These include malnutrition, tions and uncommon microbes, including infections
diabetes mellitus, obesity, chronic inflammation, by commensal organisms. Imbalance of one or more
previous irradiation, advanced age, steroid therapy, components of these defences may have substantial
re‐operations and coexisting infection remote to negative impact on resistance to infection.
the surgical site. Awareness and prevention are the The skin is the most extensive physical barrier in
key factors in achieving optimum outcomes, par- the body preventing infections. In addition to the
ticularly in elective operations. mechanical barrier, local skin flora also play major
General principles and detailed evidence‐based a role in limiting the population of non‐commensal
guidelines for prevention of SSI, central line‐associ- microorganisms. The respiratory system has addi-
ated bloodstream infection and ventilator‐associ- tional defensive mechanisms against sepsis. In the
ated pneumonia have been published. Attention to upper respiratory tract, respiratory mucus traps
detail in postoperative management, with strict larger particles and microorganisms while smaller
adherence to hand hygiene and universal body fluid particles arriving in the lower respiratory tract are
precautions and avoiding under‐ and over‐resusci- phagocytosed by pulmonary alveolar macrophages.
tation, central line insertion under suboptimal con- Impairment of these mechanisms increases the risk
ditions, early removal of abdominal drains and use of respiratory infections.
65
The pancreato‐biliary ductal system, urogenital The interaction of microorganisms with the first‐
and distal respiratory tracts do not possess resident line host defences leads to microbial opsonisation
microflora in healthy individuals. Microorganisms (C1q, C3b), phagocytosis, and extracellular and
may be present if these barriers are impaired by intracellular microbial destruction. The classical and
disease or if they are introduced from an external alternate complement pathways are activated both
source. In contrast the gastrointestinal tract in a by direct contact with, and by IgM and IgG binding
normal individual teems with microorganisms, to, surface cell proteins. This releases a number of
especially in the colon. The highly acidic, low‐ different complement protein fragments (C3a, C4a
motility environment of the stomach significantly and C5a) that enhance vascular permeability.
reduces the concentration of microorganisms Bacterial cell wall components and a variety of
entering the stomach from the oropharynx during enzymes expelled from leucocyte phagocytic vacu-
the initial phases of digestion. This explains the oles during phagocytosis act in this capacity as well.
small number of microorganisms present in the The simultaneous release of substances chemotac-
gastric mucosa, amounting to approximately 102– tic to polymorphonuclear leucocytes (PMNs) in the
103 colony‐forming units (CFU)/mL. Patients bloodstream takes place. These consist of C5a,
receiving proton pump inhibitors have higher microbial cell wall peptides containing N‐formylme-
number of bacteria likely due to diminished gastric thionine, and macrophage cytokines such as IL‐8.
acidity. Microorganisms that are not destroyed in This process of host defence recruitment leads to fur-
the stomach may proliferate in the small intestine, ther influx of inflammatory fluid and PMNs into the
reaching up to 105–108 CFU/mL in the terminal area of incipient infection, a process that begins
ileum. within several minutes and may peak within hours or
In the colon, due to its low‐level oxygen status, days. The magnitude of the response is related to sev-
there is a steady growth in the number of anaerobic eral factors: (i) the initial number of microorganisms,
microorganisms and approximately 1011–1012 (ii) the rate of microbial proliferation in relation to
CFU/g are present in faeces. Large numbers of fac- containment and killing by host defences, (iii) micro-
ultative and strict anaerobes (Bacteroides and other bial virulence, and (iv) the potency of host defences.
species) and several orders of magnitude fewer aer- The inflammatory and immune response leads to
obic microbes (Escherichia coli and other signs and symptoms that will depend on the amount
Enterobacteriaceae, Enterococcus and Candida of cytokine expression and the geographical area in
species) are present. which they are released (local tissue or bloodstream).
Signs of local inflammation include pain (dolor),
warmth (calor), redness (rubor) and swelling/oedema
Pathogenesis of infection (tumor) which may progress locally to abscess for-
mation or spread to cause a systemic response.
When microorganisms enter a sterile environment Sepsis is defined as the presence of at least two
in the host (e.g. subcutaneous tissue, peritoneal or of four SIRS criteria in the setting of confirmed
pleural cavity), a non‐specific general inflammatory infection (Box 9.1). Severe sepsis is defined as sepsis
response is activated by local immune cells (resident resulting in tissue hypoperfusion or end‐organ
macrophages), complement (C) proteins and immu-
noglobulins (non‐specific antibodies). Resident
macrophages secrete a wide variety of cytokines Box 9.1 Systemic inflammatory response
that regulate the cellular components of immune syndrome (SIRS)
response. Macrophage cytokine synthesis is upreg-
ulated and includes secretion of tumour necrosis An inflammatory response that may or may not be
factor (TNF)‐α, interleukin (IL)‐1, IL‐6, IL‐8 and associated with infection. The presence of two or
interferon (IFN)‐γ within the tissue. These are pro- more of the following criteria, one of which must
inflammatory cytokines which cause vasodilata- be abnormal temperature or leucocyte count,
tion, increased vascular permeability and oedema. defines SIRS:
• Core temperature (measured by rectal, bladder,
These cytokines may sometimes initiate a cascade
oral or central probe) >38.5°C or <36°C
of inflammatory responses leading to widespread
• Tachycardia >90 beats/min
systemic effects described as systemic inflammatory
• Hyperventilation demonstrated by respiratory rate
response syndrome (SIRS). Simultaneously, a coun-
>20 breaths/min or Paco2 <32 mm Hg
ter‐regulatory response is initiated consisting of
• White blood cell count >12 × 109/L, <4 × 109/L, or
anti‐inflammatory cytokines (IL‐4 and IL‐10) in an consisting of >10% immature forms (bands)
attempt to limit the extent of the response.
9: Surgical infection 67
ysfunction. Septic shock is defined as sepsis with

d
Box 9.2 Classification of surgical wounds
persistent hypotension despite adequate fluid resus-
citation. Sepsis‐induced hypotension is defined as a Wound classification is based on the degree of
systolic blood pressure lower than 90 mmHg or a expected contamination during the surgery.
mean arterial pressure lower than 70 mmHg.
Clean
Uninfected operative wounds in which no inflamma-
tion is encountered, and the wound is closed
Surgical site infection primarily. By definition, a viscus (respiratory,
alimentary, genital or urinary tract) is not entered
Definition during a clean procedure.
SSI is the most common complication after surgery Risk of infection: 1.3–2.9%
with an overall incidence of 2–5%. It is defined as Clean‐contaminated
an infection related to an operative procedure that A viscus is entered under controlled conditions and
occurs at or near the surgical incision within 30 without unusual contamination.
days of the procedure (or within 90 days if an Risk of infection: 2.4–7.7%
implant is left in place). Clinical criteria for defining
Contaminated
SSI include one or more of the following: (i) puru-
Open fresh accidental wounds, operations with major
lent exudate draining from a surgical site; (ii) posi-
breaks in sterile technique, or gross spillage from a
tive fluid culture obtained from a surgical site that
viscus.
was closed primarily; (iii) surgical site that was reo-
Risk of infection: 6.4–15.2%
pened in the setting of at least one clinical sign of
infection and is culture positive or not cultured; Dirty
and (iv) the surgeon makes the diagnosis of infec- Old traumatic wounds with retained devitalised
tion. SSIs increase the risk of death by 2–11 times, tissue, foreign bodies or faecal contamination.
which is directly related to the infection, and have Risk of infection: 7.1–40%
an overall mortality of 3%. It is estimated that
40–60% of SSIs are preventable.
measures include cessation of smoking, nutritional
Classification (Box 9.2) supplementation and good glycaemic control in
patients with diabetes. Intraoperative measures
SSIs can be classified as incisional (in the wound)
include prophylactic antibiotics, appropriate skin
and organ/space (any part of the anatomy that was
hair removal at the surgical site, sound surgical
opened or manipulated during the operative proce-
technique, hand hygiene and selective use of drains.
dure including anastomotic leaks). The latter account
More recently, the prophylactic use of intraopera-
for one‐third of SSIs but are responsible for more
tive wound irrigation devices has shown decreased
than 90% of the deaths related to SSI. Wound infec-
infection rates compared with non‐irrigated
tions may occur at any time after the procedure and
wounds in the setting of clean‐contaminated inci-
will depend on patient status and aggressiveness of
sions. Irrigation of the surgical wound has been
the pathogen. Most wound infections will be clini-
found to offer benefits by hydrating the tissues,
cally evident between 5 and 10 days after surgery.
allowing better visualisation and removing contam-
inated material. These lower the microbiological
Pathogens
burden and expedite the healing process. However,
The most common organisms causing SSI after a no benefits have been seen when antibiotics are
clean procedure are skin flora including streptococ- added to the irrigation solution. In the postopera-
cal and staphylococcal species. In clean‐contami- tive period maintaining normoglycaemia and nor-
nated procedures, Gram‐negative bacilli and mothermia are important factors.
enterococci are predominant. When a viscus is
entered, the pathogens usually reflect the endoge- Antibiotic prophylaxis
nous flora of the viscus.
The goal of antimicrobial prophylaxis is to prevent
SSI by reducing the burden of microorganisms at
Prevention
the surgical site and to control any bacteraemia
A number of perioperative preventive measures that may occur during the operative procedure.
have been demonstrated to reduce SSI especially Repeat intraoperative doses are warranted for pro-
in major and complex operations. Preoperative cedures that exceed two half‐lives of the drug or for
procedures in which there is excessive blood loss oedema, facilitates bacterial clearance and improves
(>1500 mL). Patients receiving prophylactic antibi- management of the exudate. It promotes wound
otics 1 or 2 hours before the surgical procedure contraction to cover the defect and may trigger
have less SSIs than patients receiving earlier or later. intracellular signalling that increases cellular prolif-
There is no role for postoperative prophylactic eration. The clinical usefulness has been demon-
antimicrobial therapy in routine surgery. In selected strated in treatment of SSI (skin, subcutaneous and
cases where prophylaxis beyond the period of sur- muscular infection) and has also been applied in the
gery is considered, discussion with the infectious management of patients not amenable to abdominal
disease team should be undertaken and prophylaxis closure (laparostomy) in the emergency situation.
extended to no more than 24 hours. A multidiscipli-
nary approach including infectious disease and
cardiology teams should be adopted in patients
Central line‐associated bloodstream
with a prosthetic valve, cardiac pacemaker device infection
or previous infective endocarditis. Staphylococci
and β‐haemolytic Streptococcus species are of Central venous catheters (CVCs) are essential to
prime concern with regard to infective endocarditis. intraoperative and postoperative management of
The main oral pathogen associated with this type of sick patients and in healthy patients undergoing
infection is S. viridans. major operations. They are used widely and for
prolonged duration in patients in intensive care
Early drain removal units (ICUs) for the delivery of vasoactive drugs
and hypertonic solutions and for monitoring and
Drains are often used after major elective abdomi-
management. Central line‐associated bloodstream
nal operations, emergency surgery and thoracic
infection (CLABSI) is defined as a bloodstream
surgery (pancreas resection, total gastrectomy,
infection in a patient who had a central line in place
oesophagectomy, low anterior resections and car-
within 48 hours before the development of the
diothoracic surgery). In elective surgery, drains are
infection and in whom no other source of infection
used to remove the accumulation of inflammatory
is found. It is a significant burden on healthcare sys-
fluid and haematoma while identifying surgical
tems and is associated with increased length of stay
complications. Early drain removal policies have
in both ICU and the hospital.
been adopted in many institutions in order to
The majority (50–70%) of CLABSI cases are
expedite recovery and reduce hospital length of
thought to be preventable by using current evi-
stay. Increasingly, the use of drains is being
dence‐based guidelines. Hand hygiene has been
eschewed in many major elective operations based
shown to be a simple and safe method of preven-
on accumulating evidence (liver resections, colec-
tion but some studies show lack of compliance
tomies, large hernia repairs, partial gastrectomy
rates of up to 30%. Aseptic technique, involving
and splenectomy).
skin preparation with alcohol‐based solution and
the use of full barrier precautions (gloves, masks,
Wound breakdown
gowns), are also essentials. Choosing the ideal site
Simple surgical wound infections presenting as cel- of insertion to minimise sepsis is also important.
lulitis may be managed with antibiotic therapy. The site with the lowest infection rate for CVC
The presence of underlying collections or actual insertion is the subclavian vein, although the inter-
breakdown of part or whole of the wound requires nal jugular vein remains the most widely used site.
additional intervention. This may be radiological Patients with neutropenia, severe burns, malnutri-
or open surgical drainage of purulent material and tion and chronic inflammatory conditions are at
mechanical debridement of devitalised tissue. great risk of CLABSI. Duration of catheterisation,
Wounds opened in such a manner are managed by catheter material, insertion conditions and quality
packing and programmed dressing changes sup- of site care also affect the incidence of CLABSI.
ported by antibiotics. The source of infection in CLABSI may include
Where more intense and continuous aspiration of contamination from surrounding skin, contamina-
the exudate is warranted, negative pressure therapy tion of the CVC, colonisation of the CVC from a
(NPT) may be applied using vacuum‐assisted clo- concomitant bloodstream infection and contami-
sure wound management devices. Sealed suction is nation of the infusions. The skin flora (coagulase‐
applied continuously over the infected area in order negative staphylococci and Staphylococcus aureus)
to aspirate the purulent tissue and to avoid the crea- is the most common type of bacteria seen in blood-
tion of abscess. NPT optimises blood flow, decreases stream infection.
Treatment involves initially sampling the blood hospital‐acquired pathogens are involved. Such
peripherally, changing the catheter with the assis- widespread sepsis may require multiple laparoto-
tance of a guidewire (if there are no signs of skin mies to control the source of sepsis and can lead to
infection) and sampling the catheter tip. Broad‐ abdominal compartment syndrome, which may
spectrum antibiotics should be commenced empiri- require open abdominal wound management.
cally and modified depending on blood culture
results and clinical progress. Patients with positive
peripheral blood culture should be treated with Hospital‐acquired pneumonia
long‐term antibiotics and change of the CVC.
Hospital acquired pneumonia (HAP) is one that
occurs 48 hours or more after admission and did
Intra‐abdominal collections not appear to be incubating at the time of admis-
sion. Pneumonia is the leading cause of infectious
Most SSIs occur in the skin, subcutaneous space mortality in hospitalised patients. Surgery and pro-
and muscle close to the incision. However, organ or longed intubation are the main predisposing fac-
space‐occupying infections such as intra‐abdomi- tors. Surgical patients who undergo thoracic and
nal, intrapleural and intracranial (intracavitary) upper abdominal surgery, those requiring postop-
infections are life‐threatening events due to delayed erative mechanical ventilation and those with pre-
diagnosis and the underlying aetiology. These vious lung conditions are particularly susceptible to
include inflammatory fluid collections and haema- pneumonia. The risk of HAP increases 6 to 20‐fold
tomas that subsequently become infected and in mechanically ventilated patients, denoting that
develop into an internal abscess. Alternatively, there airway intubation itself is a major risk factor for
may be leakage of fluid from the cut surface of an postoperative mortality.
organ or an anastomosis which develops into an Ventilator‐associated pneumonia (VAP) is a sub-
infected collection. These deep infections may type of HAP that develops more than 48–72 hours
remain occult or manifest with few symptoms, after endotracheal intubation. Risk factors for VAP
mimicking superficial SSI and possibly delaying are listed in Box 9.3. The diagnosis of VAP requires
diagnosis and initial treatment. Such complications one or more of the following: fever, leucocytosis or
then become evident when major signs of a sys- leucopenia, purulent sputum, hypoxaemia, or a
temic infection become apparent (e.g. leucocytosis, new or evolving chest radiograph infiltrate. A path-
fever, hypotension, sepsis, elevated lactate and ogen does not need to be identified. Defining the
C‐reactive protein). Diagnosis often requires radio- aetiology of postoperative pneumonia is difficult,
logical evaluation. CT is the most practical choice as most patients are unable to produce an adequate
for intra‐abdominal, pelvic and thoracic collec- sputum sample.
tions. Affected patients should be resuscitated and The pathogenesis of HAP and VAP is related to
broad‐spectrum antibiotics commenced based on the numbers and virulence of microorganisms
the most likely pathogens to be found. entering the lower respiratory tract and the response
Intra‐abdominal collections are one of the most of the host. The primary route of infection of the
common complications that surgeons will face in lungs is through micro‐aspiration of organisms
clinical practice. Treatment depends on the size, which have colonised the oropharynx.
cause, underlying medical condition and systemic
status of the patient. Small collections (<4 cm) may
be treated successfully with systemic antibiotics. Box 9.3 Risk factors for VAP
Radiologically guided percutaneous aspiration and
drainage are indicated for larger localised collec- • Acute respiratory distress syndrome
tions within solid organs or the peritoneal cavity • Advanced age
with a high rate of success. For those collections • Large‐volume gastric aspiration
that are not amenable to radiological intervention, • Blood transfusion
those associated with widespread intra‐abdominal • Immunosuppression
sepsis and where a surgical procedure is warranted • Organ failure
• Coma
for other reasons, open surgical drainage is per-
• Chronic obstructive pulmonary disease
formed. This also allows high‐volume lavage of the
• Trauma
peritoneal cavity. Widespread intra‐abdominal sep-
• Burns
sis in the postoperative period has a high mortality
• Prolonged ventilation
rate of 25–30%, but may exceed 70% where
Prevention strategies for intubated patients are are recent hospitalisation, age more than 65 years
well defined and their cost–benefit proven world- and immunosuppression.
wide. The strategy involves (i) elevating the bed Symptoms of C. difficile infection (CDI) are
head to between 30 and 45°; (ii) actively lightening abdominal pain, fever, diarrhoea, blood in the stool
sedation on a daily basis; (iii) actively assessing the and leucocytosis. It is classified as severe and non‐
potential to wean or extubate on a daily basis; (iv) severe colitis. Non‐severe CDI results in watery
avoiding antacids and histamine H2 blockers unless diarrhoea (three or more loose stools in 24 hours)
clearly indicated; and (v) prophylaxis of deep vein with lower abdominal pain and cramping, low‐
thrombosis. grade fever and leucocytosis (≤15 × 109 cells/L).
The choice of the antibiotic treatment regimen Severe CDI presents with diarrhoea, severe lower
for HAP or VAP should be tailored to the patient’s quadrant or diffuse abdominal pain, abdominal
recent antibiotic therapy, resident flora in the hospi- distension, fever, hypovolaemia, lactic acidosis,
tal/ICU, degree of underlying diseases, severity of hypoalbuminaemia and marked leucocytosis (>15
illness, available blood and sputum cultures, and × 109 cells/L). Fulminant colitis is a severe episode
risk for multidrug‐resistant pathogens. Generally, that is complicated by hypotension, shock, ileus or
initial antibiotic treatment for HAP targets S. megacolon.
aureus, Pseudomonas aeruginosa and Gram‐nega- The diagnosis of CDI is established by a positive
tive bacilli. stool test for C. difficile toxin. Laboratory testing
should be pursued only in patients with clinically
significant diarrhoea, since testing cannot differen-
Catheter‐associated urinary tract tiate CDI from asymptomatic carriage that does not
infection warrant treatment. Radiographic imaging, usually
with contrast CT of the abdomen and pelvis, is
Catheter‐associated urinary tract infection (CAUTI) advised for patients with clinical manifestations of
is a common hospital‐acquired infection. The most severe illness or fulminant colitis to exclude the
important risk factors are the duration of catheteri- presence of toxic megacolon or any condition that
sation followed by errors in catheter insertion and requires surgical intervention. Colonoscopy is not
management. Classic symptoms include flank pain, needed in patients with classic symptoms, positive
suprapubic discomfort, urinary discoloration and laboratory tests and improvement after antibiotic
catheter obstruction. However, in the elderly these therapy. For non‐severe cases oral vancomycin is
often present with non‐specific findings such as the initial treatment, with metronidazole as the sec-
delirium, leucocytosis, malaise or general signs of ond choice. Surgical evaluation should be consid-
sepsis. In the presence of CAUTI the urinary cathe- ered for patients with peritoneal signs, severe ileus,
ter should be removed or (if required) replaced, a toxic megacolon, white blood cell count of 15 ×
urine sample acquired for culture, and empirical 109/L or more and/or elevated plasma lactate (≥2.2
antibiotic therapy commenced and subsequently mmol/L). The rational use of antibiotics is the
tailored based on culture results. mainstay of prevention of CDI. Faecal microbiota
Avoidance of unnecessary catheterisation, use of transplantation is currently emerging as an effective
sterile technique for insertion, and removal as soon therapy for recurrent CDI.
as possible are essential in the prevention of CAUTI.
There is no role for antibiotic prophylaxis in
patients with a urinary catheter. Necrotising fasciitis
Necrotising fasciitis (NF) (Figure 9.1) is a serious

Pseudomembranous colitis and devastating infection that can evolve rapidly
without showing any superficial physical evidence
Pseudomembranous colitis is an inflammation of of spread. NF is characterised clinically by fulmi-
the colon caused by Clostridium difficile overgrowth nant tissue destruction, systemic signs of toxicity
in the colon. It is characterised by elevated yellow‐ and high mortality. Risk factors for NF include skin
white plaques that coalesce to form pseudomem- or mucosal breach, traumatic wounds, diabetes and
branes on the mucosa. It is also known as other immunosuppressive conditions. Fournier’s
antibiotic‐related colitis due to the relationship to gangrene (Figure 9.2) is a subtype of NF originating
previous use of antibiotics. The most common anti- in the perineal area and spreading through the fas-
biotics implicated are fluoroquinolones, clindamy- cia, leading to extensive muscle necrosis. The diag-
cin and cephalosporins. Other risk factors associated nosis can sometimes be difficult, so a low threshold
bullae, necrosis or ecchymosis in the skin. Systemic

toxicity may be observed. NF usually presents
acutely and most commonly involves the extremi-
ties, with the lower extremity more commonly
involved than upper extremity. It should be sus-
pected in patients with soft tissue infection and
signs of systemic illness (fever, haemodynamic
instability) in association with crepitus, rapid pro-
gression of clinical manifestations and/or severe
Fig. 9.1 Necrotising fasciitis of the right thigh. Note that pain (out of proportion to clinical signs).
the subtle mottling and erythema of the surrounding skin The best initial radiological examiation is CT of
vastly underestimates the underlying muscle necrosis of the affected region. Presence of gas in the tissues is
subcutaneous fat and muscle. highly specific for NF and surgical exploration
should be expedited. The diagnosis of necrotising
for suspicion of this condition in patients present- infection is established via surgical exploration of
ing with perineal problems is advised, mainly when the soft tissues in the operating room, with physical
they have signs of sepsis and marked leucocytosis. examination of the skin, subcutaneous tissue, fas-
NF occurs when the bacteria enter the subcuta- cial planes and muscle.
neous layers in regions with relatively poor blood Aggressive surgical debridement and broad‐spec-
flow and hypoxia. These conditions delay the trum antibiotic therapy accompanied by intensive
immune system response and allow bacterial over- care for haemodynamic support should be offered
growth and production of toxins. These toxins promptly. Factors associated with increased mortal-
cause vasoconstriction and vascular thrombosis of ity include white cell count in excess of 30 × 109/L,
the perforating vessels, increasing hypoxia and tis- creatinine above 177 mmol/L, age over 60 years,
sue necrosis and starting a vicious cycle of hypoxia, Clostridium infection, delay of more than 24 hours
necrosis, bacterial growth and more hypoxia. NF in surgical intervention, and infection involving
may be polymicrobial (type 1) or monomicrobial head, neck, thorax and abdomen.
(type 2). The former is caused by aerobic and anaer-
obic bacteria, usually occurring in older adults or
Antimicrobial resistance and antibiotic
diabetic patients. Type 2 NF is most commonly
stewardship in surgery
caused by group A Streptococcus and other
β‐haemolytic streptococci. It may occur in any age
The ever‐increasing number of multidrug‐resistant
group and in individuals with no underlying
microorganisms has been recognised as a grave and
comorbidities.
emergent threat to global public health (Box 9.4).
On physical examination, patients may show
There is an increasing risk of life‐threatening thera-
signs of erythema, oedema extending beyond the
peutic failures due to many drug‐resistant microbial
visible erythema, severe pain which may be out of
proportion to clinical findings, fever, crepitus, and
Box 9.4 Serious threats identified by
the Centers for Disease Control
and Prevention
• Pan‐drug‐resistant (PDR) or extended‐spectrum

drug‐resistant (XDR) Acinetobacter species
• Drug‐resistant Campylobacter species
• Fluconazole‐resistant Candida species
• Extended‐spectrum lactamase‐producing
Enterobacteriaceae (ESBLs)
• Vancomycin‐resistant enterococci (VRE)
• Multidrug‐resistant Pseudomonas aeruginosa
• Drug‐resistant non‐typhoidal Salmonella species
• Drug‐resistant Salmonella
• Meticillin‐resistant Staphylococcus aureus (MRSA)
• Drug‐resistant Streptococcus pneumoniae
Fig. 9.2 Fournier’s gangrene involving the scrotum and • Total drug‐resistant Mycobacterium tuberculosis
right buttock
infections. These result in prolonged hospital stay, Leaper DJ, Edmiston CE. World Health Organization:
higher cost of alternative therapy and increased global guidelines for the prevention of surgical site
mortality. infection. J Hosp Infect 2017;95:135–6.
Although much of the effort on responsible antibi- Mazuski JE, Tessier JM, May AK et al. The Surgical
Infection Society revised guidelines on the management
otic stewardship has focused on primary care provid-
of intra‐abdominal infection. Surg Infect (Larchmt)
ers, there is a significant opportunity for surgeons to
2017;18:1–76.
contribute, as antibiotic misuse appears to be quite Rhodes A, Evans LE, Alhazzani W et al. Surviving sepsis
common. Potential areas for surgical antimicrobial campaign: international guidelines for management of
stewardship supported by evidence are as follows. sepsis and septic shock: 2016. Intensive Care Med
• Discontinuation of antibiotics after routine elec- 2017;43:304–7.
tive surgical cases. Prolonged postoperative use
does not prevent SSI.
• No role for topical wound site antibiotics when MCQs
systemic preoperative antibiotic prophylaxis is
administered. Select the single correct answer to each question. The
• Limited, fixed courses of antibiotics are adequate correct answers can be found in the Answers section
for treating complex intra‐abdominal infections at the end of the book.
after the source control has been achieved. 1 Which of the following statements is true?
• Antibiotics are not required after incision and a use of alcohol‐based solutions on surgical site
drainage of superficial skin abscesses and open- skin does not change the SSI rate
ing of infected superficial SSIs. b hand wash has poor compliance in most of the
• Uncomplicated diverticulitis does not require studies
antibiotic therapy. c sterile technique is not warranted to insert a
• Bacteriuria in patients without frequency, urgency, central venous catheter
dysuria or unspecified suprapubic pain (asympto- d use of prophylactic antibiotics during elective
matic) does not constitute a urinary tract infec- surgery is not necessary
tion and should not be treated with antibiotics. e for most skin infection, cefazolin‐based
• Presence of C. difficile in stool samples in the antibiotics are warranted as they target the
absence of clinical symptoms should not be Gram‐negative skin flora
treated with antibiotics.
2 Regarding the immune response to infection, which
statement is true?
Summary a resident inflammatory cells do not play a role in
the development of infection
Infection is a major cause of surgical morbidity and
b proinflammatory cytokines such as IL6‐ and
is multifactorial. Hand washing, universal body
IL‐10 are produced locally
fluid precautions and attention to surgical tech-
c anti‐inflammatory cytokines are produced in
nique are the factors that surgeons may implement
response to infection and can lead to chronic
to reduce the infection rate. Attention to patient
infection when overproduced
(host) factors that may be improved (nutritional
d alternative complement cascade is activated by
status, anaemia, sarcopenia) prior to surgery,
direct contact with type 2 antigen‐presenting cells
awareness of high‐risk patients and strict imple-
e all of the above are correct
mentation of perioperative preventive strategies
will help reduce the incidence, morbidity and mor-
3 Which of the following is a true statement?
tality of surgical infections.
a sepsis may occur in the absence of SIRS
b surgical infection is diagnosed only when
bacterial overgrowth is documented
Further reading c SSI occurs only in the first 7 days after an
operation
Adamina M, Kehlet H, Tomlinson GA, Senagore AJ,
Delaney CP. Enhanced recovery pathways optimise d SSI only applies to infections that occur in the
health outcomes and resource utilization: a meta‐analysis skin and subcutaneous tissue
of randomised controlled trials in colorectal surgery. e intra‐abdominal abscess after an abdominal
Surgery 2011;149:830–40. operation is classified as SSI
4 Regarding surgical infections, which of the e catheter‐associated infection is more common

following is true? when the central line is inserted in the jugular
a necrotising fasciitis is called Fournier’s gangrene area than the subclavian area
when the infection dissects the deep neck fascia
towards the upper mediastinum 5 Perforated appendicectomy wounds are classified
b necrotising fasciitis is easily diagnosed with as being:
ultrasound scan a clean
c pseudomembranous colitis is an infection b clean‐contaminated
characterised by diffuse involvement of the colon c contaminated
d pseudomembranous colitis is diagnosed by stool d contaminated‐dirty
samples that are incubated for 24–48 hours and e none
show Clostridium difficile overgrowth
10 Transplantation surgery
Michael A. Fink
often used as a bridge to transplantation. The artifi-

Introduction cial pancreas is under development but is not yet
used in standard practice.
Transplantation is the implantation of an organ,
Assessment of the benefit of transplantation
part of an organ or tissue derived from one indi-
needs to take into account the survival of the
vidual into another individual. The indication is
potential recipient with and without transplanta-
most commonly chronic or acute organ failure, but
tion. Modelling of survival of patients with organ
liver transplantation is also performed for meta-
failure can be helpful in making these assessments.
bolic diseases and some forms of malignancy.
For example, the model for end‐stage liver disease
Transplantation of all organs has been shown to
(MELD) score, which was originally developed to
improve survival and quality of life of recipients.
assess the mortality risk of patients with cirrhosis
Aspects that have elements common to transplanta-
undergoing TIPS, has been validated as a prognos-
tion of all organs include recipient assessment,
tic indicator for patients with end‐stage liver dis-
organ donation, recipient selection, transplantation
ease on the liver transplant waiting list. It has
surgery, post‐transplant management including
been shown that the risk of liver transplantation is
immunosuppression, and complications.
not justified for patients with a MELD score less
than 15, but that the benefit of transplantation
increases for patients with increasing MELD
Recipient assessment scores above this.
Recipient selection should take account of the
Recipient assessment takes into account the need for expected utility of transplantation. Transplantation
transplantation, and thus the natural history of the requires either using the precious resource of
disease for which transplantation is contemplated, deceased donor organs or putting a living donor at
and the expected outcome, or utility of transplanta- risk of morbidity and mortality and therefore it is
tion. Without transplantation, some forms of organ important that the expected outcome of transplan-
failure can only be managed in a supportive fashion. tation justifies this. Potential transplant recipients
For example, liver failure is managed by endoscopic therefore undergo a process of evaluation that
surveillance and ligation of oesophageal varices, includes assessment of factors that might impact
antibiotics to minimise the development of encepha- on post‐transplant outcomes. This includes assess-
lopathy, and diuretics, ascitic drainage procedures ment of fitness for the transplant operation, such
and sometimes transjugular intrahepatic portosys- as assessment of cardiac and respiratory function.
temic shunts (TIPS) to manage ascites. None of these In addition, psychological and social factors that
interventions actually reverses the underlying pro- might impact on post‐transplant outcomes, such as
cess of liver failure. There is no reliable method of adherence to immunosuppression medications,
organ support for liver failure. Likewise, respiratory investigations and clinic follow‐up, are assessed.
failure can be managed by oxygen therapy, but there The decision to list a patient for transplantation is
is no viable long‐term mechanical alternative. On made in the context of a multidisciplinary assess-
the other hand, in the case of chronic renal failure, ment. In the setting of acute organ failure, where
organ support is available in the form of haemodi- the patient’s life is at imminent risk, the assessment
alysis and peritoneal dialysis. Ventricular assist process needs to be undertaken in a more urgent
devices are available for cardiac failure and are fashion.
75
of transplants that can be performed. Therefore,

Organ donation organising networks of paired exchange across
large populations can be beneficial. The Australian
There are two main sources of organs for trans-
Paired Kidney Exchange program oversaw a total
plantation: deceased and living donors.
of 154 paired kidney transplants across 22 centres
throughout Australia to the end of 2015.
Living donors Whilst transplantation of all organs (other than
The process of living donor transplantation includes heart, for obvious reasons) has been undertaken
careful assessment of the potential living donor. from living donors, the relative proportion of trans-
Living organ donation is a unique surgical proce- plantation undertaken from living donors varies by
dure, in that, unlike other forms of surgery, the per- organ and geographic region. Kidney transplanta-
son undergoing the procedure is not expected to tion is commonly performed using living donor
derive any physical benefit from it, although they organs. In 2017, 24% of kidney transplants in
might obtain a psychological benefit from the act of Australia and 37% of kidney transplants in New
giving a precious gift to a loved one that should Zealand were performed using grafts from living
help to prolong their life and/or improve their qual- donors. Previously, donor nephrectomy was per-
ity of life. In this situation, the risk borne by the formed as an open operation, but it is now routinely
organ donor is balanced against the expected ben- performed either laparoscopically or retroperito-
efit to the recipient. The process of assessment of a neoscopically. The steps of donor nephrectomy
potential living organ donor includes assessment of surgery include surgical access (laparoscopic or ret-
the quality of the organ, to ensure that there is a roperitoneoscopic), mobilisation of the renal artery
strong likelihood of successful transplantation and (or arteries) and vein, mobilisation, clipping and
long‐term good graft function, and assessment of transection of the ureter, mobilisation of the kidney,
the safety of organ donation for the recipient, in placing the kidney in a bag in preparation for
terms of both the perioperative risk and long‐term extraction, preparation of the wound for extrac-
risk of morbidity and mortality. Living donor tion but without opening the peritoneum (e.g.
assessment should include independent review by a Pfannenstiel incision), securing the renal artery and
physician who will not be caring for the transplant vein with staples or clips, transecting the renal
recipient and who can therefore advocate on behalf artery and vein, removal of the kidney, placing the
of the donor. kidney in saline slush, and cannulation of the renal
The living donor may be genetically related to artery and flushing the kidney with a suitable cold
the recipient (e.g. parent, sibling, child) or unrelated preservation solution (e.g. Ross solution, Soltran or
(e.g. spouse, friend). Some living donor transplanta- histidine–tryptophan–ketoglutarate).
tion is performed using the organ of an altruistic, or Liver transplantation can be performed by
‘good Samaritan’ donor. In this situation, the donor removing a portion of the liver from a living donor.
donates their organ to a stranger. Most commonly, Living donor liver transplantation is relatively
living donor transplantation occurs in a simple one‐ uncommon in Australia and New Zealand; between
to‐one fashion; that is, one donor donates to one 1985 and 2016, 100 living donor liver transplants
recipient. However, in some circumstances, such as were performed in the countries out of a total of
ABO incompatibility between donor and recipient, 5553 transplants (1.8%). In other parts of the
or recipient antibodies against donor antigens, this world, particularly Asia, where deceased organ
is not possible. In this situation, ‘paired exchange’ donation rates are lower, living donors are a more
can be a solution to the problem. The simplest frequent source for liver transplantation. Adult‐to‐
example occurs when donor A is incompatible with child living liver transplantation most commonly
recipient A and donor B is incompatible with recipi- involves removal of segments 2 and 3 (usually
ent B. If donor A is compatible with recipient B and approximately 25% of liver volume) or the left
donor B is compatible with recipient A, a paired hemi‐liver (segments 2, 3 and 4, usually approxi-
exchange can be undertaken whereby donor A mately 40% of liver volume). Adult‐to‐adult liver
donates an organ to recipient B and donor B transplantation most commonly involved removal
donates an organ to recipient A. More complex of the right hemi‐liver. The steps in living donor
chains of donation and transplantation involving hepatectomy include surgical access (open or lapa-
multiple donor and recipient pairs can be under- roscopic); parenchymal transection, which can be
taken. These chains will sometimes involve an undertaken by cavitron ultrasonic aspirator or a
altruistic donor. The greater the number of poten- variety of energy devices; securing and transecting
tial donors and recipients, the greater the number the appropriate hepatic artery, portal vein, hepatic
10: Transplantation surgery 77
duct and hepatic vein; removal of the portion of confirmation of brain death can be made either on
liver to a saline slush bath; and cannulation of the clinical grounds or based on imaging. The clinical
hepatic artery and portal vein and flushing with a criteria are:
suitable cold preservation solution. • the absence of response to noxious stimuli in the
cranial nerve distribution and all four limbs and
Deceased donors trunk, and
• the absence of all the following brainstem reflexes:
Deceased organ donation is usually considered in
–– pupillary light reflex
the setting of patients with a severe neurological
–– corneal reflex
injury in the intensive care unit (ICU) or emergency
–– reflex response to pain in the trigeminal nerve
department. Between 2014 and 2018 in Australia,
distribution
38% of donors died of intracranial (intracerebral
–– vestibulo‐ocular reflex
or extra‐axial, i.e. extradural, subdural or suba-
–– gag reflex
rachnoid) haemorrhage, 36% from cerebral
–– cough/tracheal reflex and
hypoxia or ischaemia, 16% from traumatic brain
• the absence of respiratory effort on an apnoea
injury, 6% from cerebral infarct, 1% from other
test (disconnection of the endotracheal or trache-
neurological conditions and 0% from non-
ostomy tube from the ventilator).
neurological conditions.
The imaging criterion is the demonstration of the
Work‐up for organ donation is a complex multi-
absence of intracranial blood flow, which can be
step process.
assessed by angiography, contrast‐enhanced CT or
• Information regarding the process is provided to
MRI or a nuclear perfusion scan. In all Australian
the potential donor’s family.
jurisdictions, declaration of brain death requires per-
• Assessment for suitability for organ donation is
formance of the assessment by two medical practi-
undertaken. This includes obtaining information
tioners, although the required experience and training
from the family, the general practitioner and the
of the doctors varies slightly between jurisdictions.
medical records in order to determine the likely
organ quality and to assess risks of transplanta-
tion of the donor organs, such as transmission of Donation after circulatory death
infection and cancer.
In the early days of transplantation, the majority of
• Death is confirmed (this step may occur later
deceased donor transplants were performed by the
in the process, as outlined in the following
DCD (also known as donation after cardiac death
section).
and non‐heart beating donation) pathway. With
• Informed consent for donation is obtained from
the enactment of the legal definition of brain death
the donor’s family.
in the 1980s, DBD became the predominant path-
• Communication with recipient units regarding
way of deceased organ donation. However, the rec-
organ offers occurs.
ognition of the imbalance between supply of
• Coordination of the donor procurement opera-
suitable deceased donor organs and the demand
tion is undertaken.
for these organs and the consequent prolonged
There are two main pathways of deceased organ
period of waiting for transplantation and risk of
donation: donation after brain death (DBD) and
death on the waiting list has resulted in a resur-
donation after circulatory death (DCD). These
gence of DCD transplantation in recent years. In
pathways are based on the two definitions of death
2018 in Australia and New Zealand, 163 of 616
that are enshrined in legislation in all jurisdictions
donors (26%) were DCD donors. The rate of DCD
across Australia and New Zealand and most juris-
donors varied by jurisdiction; Victoria had the
dictions in the rest of the world: the irreversible ces-
highest rate at 33%.
sation of all functions of the brain in the person and
There are several ways that potential DCD
the irreversible cessation of circulation of blood in
donors can present, and these are defined as the
the body of the person.
Maastricht categories:
1 dead on arrival
Donation after brain death
2 unsuccessful resuscitation after cardiac arrest
In Australia, declaration of brain death requires that outside hospital
a severe brain injury sufficient to cause death has 3 awaiting cardiac arrest after withdrawal of car-
occurred and that other causes of deep coma, such diorespiratory support
as metabolic, electrolyte and endocrine derange- 4 cardiac arrest in a brain dead donor
ments and sedative drugs, have been excluded. The 5 unexpected cardiac arrest in hospital.
The vast majority of DCD donors in Australia and of circulation and then the donor must be trans-
New Zealand are Maastricht 3 (as outlined in ferred to the operating theatre (unless withdrawal
the following discussion), though occasionally has occurred in the operating theatre), the chest and
Maastricht 4 donation may occur if the donor team abdomen opened, the relevant vessels cannulated
is in the donor hospital at the time that the cardiac and cold perfusion commenced.
arrest occurs. Other categories of donors have The period of warm ischaemia (whose exact defi-
occurred in some parts of the world (notably Spain). nition varies depending on the organ) can have a
Organ donation by the DCD pathway occurs in detrimental impact on the outcome of transplanta-
donors with similar underlying brain injury to tion. The kidneys and lungs, which are relatively
those who donate via the DBD pathway: stroke, resilient to this period of hypoxia, can function
trauma and hypoxia. Occasionally, DCD donation well, with transplantation outcomes similar to
occurs in the setting of other conditions with a poor those of DBD transplantation; however, the results
expected outcome, such as a high spinal cord injury. of heart and liver transplantation using DCD dona-
The patient must be confirmed to have a poor tion are inferior to those using DBD donation. In
expected outcome. Once consent for donation has addition, not all potential DCD donors progress to
been obtained and the organ procurement team has circulatory death within the time required for organ
indicated that they are ready to perform the organ donation. In 2018 in Australia, 111 of 265 (42%)
procurement procedure, cardiorespiratory support intended DCD donors did not proceed to organ
is withdrawn. This usually comprises extubation donation; 64 of these died outside the required time
and cessation of inotropic support. The vital signs frame for organ donation. In contrast, only 49 of
are recorded at frequent intervals following with- 400 (11%) of intended DBD donors did not pro-
drawal of cardiorespiratory support. Once circula- ceed to organ donation. Therefore, any potential
tion has ceased and a sufficient period after this has donor should be given a period of observation to
elapsed to ensure that the process is irreversible, the determine the likelihood of progression to brain
patient is declared dead and organ donation can death and the DCD pathway used only if it is antici-
occur. The exact time between asystole and certifi- pated that progression to brain death will not occur.
cation of death varies between jurisdictions and
even between hospitals in some jurisdictions but is
Deceased organ procurement operation
usually between 2 and 5 minutes.
The DBD and DCD organ procurement pathways The aims of the deceased donor organ procurement
are summarised in Figure 10.1. In DBD donors, operation are to assess the quality and anatomy of
there is usually no period of warm ischaemia (unless the organs, to replace the blood in the organs with
a cardiac arrest occurs during the procedure). In a cold organ preservation solution, to remove the
contrast, in DCD donors, following withdrawal of organs from the body without injury to the organs
cardiorespiratory support, there will usually be a or the vasculature of the organs, to package the
period of reduced organ perfusion prior to cardiac organs appropriately and to place them in an
arrest. Following this, a period of observation is appropriate cold (usually ice‐filled) transport con-
required, in order to ensure irreversibility of the loss tainer. The concept of organ preservation fluids is
Donation after brain death (DBD) Donation after circulatory death (DCD)
Brain death Withdrawal of
cardiorespiratory support Reduced
perfusion
Transfer to operating theatre Warm Cardiac arrest
ischaemia Transfer to operating theatre No
Laparotomy, sternotomy, cannulation perfusion
Laparotomy, sternotomy, cannulation
Cold perfusion Cold perfusion

Cold Cold storage Cold
ischaemia ischaemia
Organ removed from ice

Warm Warm
ischaemia Vascular anastomoses
ischaemia
Reperfusion
Fig. 10.1 Comparison of the donation after brain death and donation after circulatory death pathways.
that they enable the organ to survive outside the After cold perfusion, the organs are removed with
body and without circulation for an extended care to avoid injury to the organs, the vasculature
period (the time varies between organs). Most and associated structures (bile duct, ureters, trachea
organ preservation fluids have a composition simi- and bronchi).
lar to intracellular fluid, in order to minimise move- The organs are placed in a saline slush bath on
ment of solutes across cell membranes, and also the donor back table. The organs are assessed for
contain energy substrates, buffers and osmotic quality and injuries and this information is docu-
agents. Some also contain membrane stabilisers and mented and communicated to the recipient teams.
antioxidants. Cooling of the organs both by perfu- It is preferable to remove the liver and pancreas en
sion with a cold solution and the application of ice bloc, in order to minimise warming of the pancreas,
saline slush results in reduction of the metabolic and these organs are separated on the back table.
requirements that assists the preservation process. Further perfusion on the back table is performed
The operation starts out with a time‐out proce- for the abdominal organs. The organs are triple
dure that includes confirmation of the information bagged, labelled and placed on ice in insulated con-
regarding the donor, including the documentation tainers ready for subsequent transport to the recipi-
confirming death, the donor blood group and serol- ent teams. It is also routine to procure iliac artery
ogy, and confirmation of donor identity comparing and vein grafts for use as extension grafts. These are
the donor identification bracelet with the donor sent in the transport container with the liver and
documentation. The details in the timing of this the pancreas. The chest and abdomen are then
process vary slightly between DBD and DCD donor closed in routine fashion.
procedures. An alternative to this method of organ preserva-
For a DBD donor, intravenous broad‐spectrum tion, which is known as static cold storage, is
antibiotics and methylprednisolone 1 g are given. machine perfusion, which can be hypothermic,
The organ procurement teams consist of an abdom- subnormothermic or normothermic (at body tem-
inal and/or thoracic team. After prepping and drap- perature). In the latter case, oxygenated blood is
ing, a midline laparotomy and median sternotomy generally circulated through the organ using pumps
are performed. A Cattell–Braasch manoeuvre (com- and a membrane oxygenator. Machine perfusion
plete mobilisation of the bowel from the retroperi- can allow (i) assessment of suitability for transplant
toneum) is performed and the aorta and inferior (whether to use or discard the organ) and (ii) resus-
vena cava are exposed. Slings (usually heavy silk citation of the organ with or without modification
ties) are placed around the infrarenal aorta and the of the organ. Machine perfusion systems are becom-
inferior vena cava can also be slung. The quality ing commercially available and it is likely that this
and vascular anatomy of the organs to be procured technology will have an increasingly important role
are assessed. In particular, the porta hepatis is pal- in organ preservation.
pated to determine whether there is a replaced (or
accessory) right hepatic artery arising from the
superior mesenteric artery and the gastrohepatic Recipient selection
(lesser) omentum is examined for the presence of a
replaced (or accessory) left hepatic artery arising Selection of the appropriate recipient of a donor
from the left gastric artery. Further dissection organ offer is based on the ethical principles of
may be required, particularly mobilisation of the equity, which is characterised by equal distribution
pancreas if this is to be procured. The crura of the of risk and benefit, and therefore fairness, and util-
diaphragm are split and divided, exposing the ity, which in this context is characterised by the best
supracoeliac aorta. outcome for donated organs. The relative contribu-
The thoracic team undertakes a preliminary dis- tion of these principles to recipient selection varies
section. After heparinisation (heparin 300 units/kg between organs mainly in relation to the risk of
i.v.), the aorta and pulmonary artery are cannu- waiting list mortality.
lated. The infrarenal aorta (and inferior vena cava, For those organs whose failure results in a high
if desired) is then cannulated. The superior vena risk of waiting list mortality, such as liver, heart and
cava is ligated. Decompression of the heart and lung, allocation of donor organs is based on the
abdominal organs is ensured by venting the left ‘sickest first’ principle, the primary aim being to
atrium and inferior vena cava, respectively. rescue those on the waiting list who have the great-
Immediately following this, the supracoeliac and est risk of waiting list mortality. Scores that assess
ascending aorta are cross‐clamped and perfusion of the risk of waiting list death, such as MELD score
the thoracic and abdominal organs commences. in the case of liver failure, can help inform recipient
selection and, indeed, MELD score is used in this of the donor vena cava to the recipient vena cava
capacity in many parts of the world. (cava replacement) was previously common but is
In the case of kidney transplantation, in which now rarely performed. Liver transplantation
waiting list mortality is less prominent, utility is a requires the anastomosis of two inflow structures
more prominent principle of organ allocation. (the portal vein and hepatic artery). The donor bile
Aspects of allocation that impact on post‐trans- duct is most commonly anastomosed directly to
plant outcome, such as human leucocyte antigen recipient bile duct, but a Roux‐en‐Y anastomosis is
(HLA) matching, play a role. However, patients on sometimes required (e.g. in the case of biliary atre-
the kidney transplant waiting list who have a sia or primary sclerosing cholangitis).
reduced access to donor organs, such as highly sen- The steps of a transplant operation include the
sitised individuals (those who have multiple HLA following.
antibodies secondary to blood transfusions and • Back table preparation of the donor organ:
previous transplants), are given preferential access removal of extraneous tissue, such as the dia-
to suitable donor organs. phragm in the case of liver transplantation, and
reconstruction of the vasculature, such as anasto-
mosis of an iliac artery Y graft to the superior
Transplantation surgery mesenteric and splenic arteries in the case of pan-
creas transplantation.
Transplantation surgery can be performed as an • Induction of anaesthesia.
orthotopic procedure, in which the organ is • Administration of broad‐spectrum antibiotics.
removed and replaced with a donor organ in the • Prepping and draping.
same position as the original, or as a heterotopic • Surgical access: overwhelmingly by open surgery,
procedure, in which the organ is usually not although kidney transplantation has been per-
removed and the donor organ is implanted in a dif- formed laparoscopically and robotically in some
ferent position to the original. Heart, lung and liver centres.
transplantation are usually performed as orthotopic • Removal of the native organ, if appropriate (liver,
procedures, whilst kidney and pancreas transplan- heart, lung).
tation are performed as heterotopic procedures. • Vascular anastomoses (inflow and outflow).
Kidney transplantation involves placing the graft • Reperfusion: removal of the vascular clamps,
in an extraperitoneal position in the iliac fossa, allowing blood to perfuse the organ.
with anastomosis of the renal artery and vein to the • Anastomosis of associated structures, such as the
iliac artery and vein, respectively, and of the ureter trachea or bronchus, bile duct, duodenum and
to the bladder. ureter in the case of lung, liver, pancreas and kid-
Pancreas transplantation is performed by ini- ney transplantation, respectively.
tially anastomosing a donor iliac artery Y graft to • Haemostatic check.
the superior mesenteric and splenic arteries and • Closure.
then anastomosing the iliac artery graft to the Heart–lung transplantation requires additional
recipient iliac artery, the portal vein to the iliac steps, including cannulation and commencement of
vein (in the past, this was often anastomosed to the cardiopulmonary bypass, removal of ventricular
superior mesenteric vein) and the duodenum to the assist devices if applicable, and weaning of cardio-
small bowel to drain the exocrine fluid (in the past pulmonary bypass and decannulation.
this was often anastomosed to the bladder, but the
irritant effect of the pancreatic enzymes caused
haemorrhagic cystitis). The pancreas is placed in Post‐transplant management
an intraperitoneal position (as is the kidney, which
is anastomosed to the opposite iliac vessels) in The site of initial postoperative management var-
the case of simultaneous pancreas and kidney ies with the organ transplanted and the condition
transplantation. of the patient. Heart, lung and liver transplant
Liver transplantation requires anastomosis of the recipients are routinely initially cared for in the
donor inferior vena cava either to a common open- ICU. Organ function may need to be supported
ing of the recipient left, middle and right hepatic postoperatively, such as by intra‐aortic balloon
veins (the ‘piggyback’ approach) or side‐to‐side to pump or haemofiltration, in some cases. Post‐
the recipient inferior vena cava. The removal of a transplant management includes elements of post-
segment of recipient vena cava with the liver and operative care following any major operation,
two anastomoses of the superior and inferior ends including analgesia, antibiotics when appropriate,
thromboprophylaxis, mobilisation, physiotherapy, the production of T lymphocytes and prevent the

introduction of oral diet and discharge planning. In transition of B lymphocytes into plasma cells. They
addition, careful ongoing evaluation of graft func- have a lower risk of nephrotoxicity than calcineurin
tion is required. This may include assessment of inhibitors and therefore can be used in patients with
routine parameters such as haemodynamic obser- impaired renal function. They also have a degree of
vations or measurements; organ output, such as antitumour activity. They reduce wound healing and
bile or urine production; blood tests, such as urea should therefore be changed to an alternative immu-
and electrolytes, liver function tests, blood glucose nosuppressive agent prior to surgery.
and arterial blood gases; and imaging, such as chest
X‐ray, echocardiography or Doppler ultrasound to
assess the graft vasculature. More invasive investi- Complications of transplantation
gation, including graft biopsy, may be required if
there is concern about graft function. Surgical complications
Surgical complications occur most often in the early
Immunosuppression post‐transplant period and include bleeding, vascu-
lar complications and complications related to out-
Immunosuppression is required to prevent graft
flow structures (such as the ureter and bile duct).
rejection. The first dose is often given intraopera-
Postoperative monitoring of the patient’s observa-
tively during the transplant procedure. The choice
tions, wound and blood tests should allow early
and dose of immunosuppression varies depending
identification of bleeding. Early return to the oper-
on the organ transplanted, the immunological
ating theatre is generally advisable for anything
compatibility of the donor and recipient and the
other than minor bleeding. Potential vascular com-
clinical state of the recipient. Some organs are more
promise should be monitored and this generally
immunogenic than others. The intestine, which is
requires routine use of postoperative Doppler ultra-
accompanied by a large load of donor antigen
sound. Arterial or venous kinking, torsion or
and immunocompetent cells, is particularly immu-
thrombosis will usually result in graft loss unless it
nogenic. In contrast, the liver tends to be less
is dealt with expeditiously, most commonly by
immunogenic and therefore usually requires less
repeat operation. Ureteric or bile duct leakage will
immunosuppression than other organs. The pres-
generally be detected by change in the drain tube
ence of donor‐specific antibodies will necessitate
output. Stricture of these structures is most com-
higher levels of immunosuppression than would be
monly related to ischaemia. Ureteric and biliary
otherwise necessary. There are also special cases,
anastomotic complications can usually be managed
such as ABO incompatible transplantation, that
endoscopically, but revision surgery is sometimes
may require other immunological approaches, such
required. Lymphocele is a collection of lymphatic
as plasmapheresis and T‐cell depletion therapies.
fluid that can complicate kidney transplantation.
Immunosuppression is generally (at least early
Careful ligation of lymphatics at the time of mobi-
post transplant) a combination of medications that
lisation of the iliac vessels in preparation for the
target different aspects of the immune response and
vascular anastomoses can help prevent lymphoceles
are therefore synergistic in their effect. Steroids, such
from occurring. Drainage of lymphoceles can be
as prednisolone, reduce the transcription of inflam-
performed percutaneously or by creating a window
matory proteins such as interleukin‐2 and tumour
into the peritoneal cavity.
necrosis factor α. Side effects include fluid retention,
delirium, obesity, hypertension, diabetes mellitus
Rejection
and osteoporosis. Calcineurin inhibitors, such as
tacrolimus and ciclosporin, reduce interleukin pro- Transplantation involves a complex interplay
duction and inhibit the replication of T cells. Their between the host innate and adaptive immune
side effects include tremor, headache, hypertension, system and the donor antigens. In addition, donor
diabetes mellitus, hyperlipidaemia and nephrotoxic- passenger lymphocytes and dendritic cells often
ity. Antiproliferative drugs, such as mycophenolate accompany the transplanted organ. Recipient anti-
mofetil and azathioprine, reduce the production gen‐presenting cells, such as macrophages and den-
of lymphocytes. They can cause neutropenia. dritic cells, ingest antigenic products of donor cells,
Mycophenolate mofetil also commonly causes gas- process these and present the foreign antigens on
trointestinal side effects, including bloating and the surface in association with the recipient major
diarrhoea. mTOR (mammalian target of rapamycin) histocompatibility complex (MHC). MHCs are
inhibitors, such as sirolimus and everolimus, reduce highly polymorphic and are important in the
recognition of self versus non‐self and therefore in occurs. These processes as well as cold storage and
combating infection and cancer. Class I MHC loci then reperfusion in the recipient result in ischaemia
include HLA‐A, HLA‐B and HLA‐C, while class II reperfusion that can impact on graft function. This
MHC loci include HLA‐DP, HLA‐DQ and HLA‐ is sometimes referred to as ‘harvest injury’. Initial
DR. Foreign antigens presented in association with poor function or delayed graft function may neces-
the MHC on the surface of antigen‐presenting cells sitate supportive measures, such as dialysis in the
bind to the T‐cell receptor of CD8‐positive (cyto- case of kidney transplantation. Complete early fail-
toxic) T cells and CD4‐positive (helper) T cells. ure of the graft is referred to as primary non‐func-
CD8‐positive T cells lyse cells that display the rele- tion and urgent re‐transplantation of non‐renal
vant foreign antigen and CD4‐positive cells have a grafts is required to prevent death.
variety of actions including the production of CD8‐ Chronic transplant dysfunction, which can lead
positive cells and activation of B cells. Increasing to late graft loss, can occur through incompletely
levels of HLA matching between donor and recipi- understood complex immunological and non‐
ent reduce the risk of rejection in kidney and lung immunological mechanisms. The pathology of
transplantation but is less relevant in liver trans- chronic transplant dysfunction varies between dif-
plantation. Microchimerism, in which donor lym- ferent organs and includes interstitial fibrosis and
phocytes become incorporated into the host tubular atrophy in the kidney, graft fibrosis and
immune system, and increased numbers of recipient ductopenia in the liver, bronchiolitis obliterans in
regulatory T cells lead to a greater chance of toler- the lung and arteriosclerosis in the heart.
ance, in which the immune response to the trans-
planted cells is ameliorated and the amount of Infection
immunosuppression can be reduced or, in some
Infection can occur by a variety of means. The oper-
cases, ceased altogether.
ation itself can be associated with infection, such as
Rejection is classified as cell‐mediated or anti-
a wound infection or infection of the pleural space
body‐mediated and acute or chronic. Cell‐mediated
or abdomen. There is a risk of transmission of
rejection is the more common pathway and occurs
organisms from the donor to the recipient. The
by activation of CD8‐positive and CD‐4 positive T
commonest of these are viruses, including cytomeg-
cells, resulting in secretion of proinflammatory
alovirus (CMV) and Epstein–Barr virus. Serology
cytokines and cell lysis and apoptosis. Hyperacute
for these viruses is routinely tested in the donor and
antibody‐mediated rejection results from the inter-
the recipient. In some circumstances, particularly if
action of preformed antibody, such as those pro-
donor CMV serology is positive and recipient CMV
duced due to previous blood transfusion or
serology is negative, pre‐emptive antiviral treat-
transplantation, with donor HLA and occurs imme-
ment (valganciclovir) is commenced. In lower risk
diately on reperfusion of the organ. This is very
situations, polymerase chain reaction (PCR) can be
rare. Antibody‐mediated rejection can also occur
used to monitor for the presence of CMV and treat-
later after transplantation due to antibodies that
ment commenced if the patient becomes PCR posi-
develop in response to damaged endothelial cells
tive. Donors are also routinely tested for the
and occurs in response to activation of the comple-
presence of antibody and (in Australia) nucleic acid
ment cascade. The hallmark of antibody‐mediated
testing (NAT) for hepatitis B virus (HBV), hepatitis
rejection is the presence of C4d deposition, which
C virus (HCV) and HIV. Cases of transmission of
can be identified in allograft biopsies.
these viruses have been reported, but the residual
Rejection is diagnosed based on identification of
risk of transmission of these viruses from a donor
allograft dysfunction, such as a rising creatinine in
who tests negative with NAT is exceedingly small,
the case of kidney transplantation or rising liver
even in donor groups at increased risk of infection.
function tests in the case of liver transplantation,
Bacteria and fungi can also potentially be transmit-
and is confirmed by biopsy of the allograft.
ted from donor to recipient. Latent infections, par-
Treatment is usually a course of intravenous or oral
ticularly viral, can be reactivated in the recipient
steroids and increase in the dose of the calcineurin
upon immunosuppression. Finally, the immunosup-
inhibitor.
pressed patient is at increased risk of transmission
from other people in the post‐transplant period.
Graft dysfunction
The risk is highest in the early post‐transplant
The process of brain death is associated with a period, because immunosuppression is generally
‘cytokine storm’. In DCD donors, warm ischaemia most intensive at that time.
Cancer 97%, 90% and 75%, respectively and the 1‐, 5‐

and 10‐year graft survival rates have been 94%,
The immune system is important in the monitoring
83% and 62%, respectively. Living donor kidney
of and defence against cancer and therefore it is not
transplantation has results that are superior to
surprising that immunosuppression predisposes to
deceased donor kidney transplantation. In recent
the development of cancer. Of patients who have
years for primary living donor kidney transplanta-
undergone liver transplantation in Australia and
tion, the 1‐ and 5‐year patient survival rates were
New Zealand, 20% have developed de novo cancer
99% and 96%, respectively, and the 1‐ and 5‐year
after transplantation. Skin cancer developed in
graft survival rates were 98% and 90%,
13%, including 0.9% of the total transplant popu-
respectively.
lation who developed melanoma, and non‐skin
cancer developed in 7%. Transplanted patients
Liver transplantation
require cancer monitoring, including regular skin
checks as well as standard screening as occurs in Liver transplantation outcomes in Australia and
the general population, prevention, such as sun pro- New Zealand are reported by the Australia and
tection, and treatment as required. New Zealand Liver Transplant Registry. To 31
December 2016, 5553 liver transplants had been
Cardiovascular and cerebrovascular disease performed in the countries, 1012 in children and
4541 in adults. The commonest indications in chil-
Complications of immunosuppression, such as dren are biliary atresia (54%) and metabolic dis-
hypertension, diabetes mellitus, hyperlipidaemia eases (14%). The commonest indications in adults
and obesity, contribute to long‐term risks of meta- are HCV disease (22%), alcoholic liver disease
bolic syndrome, ischaemic heart disease and cere- (10%), malignancy, predominantly hepatocellular
brovascular disease. Monitoring and treatment of carcinoma (11%), primary sclerosing cholangitis
risk factors for these conditions is important in the (10%) and fulminant hepatic failure (9%). It is
management of transplant recipients. likely that the indications will evolve over time. In
particular, the widespread availability of direct‐act-
Disease recurrence ing antiviral therapy for HCV is likely to result in a
Some indications for transplantation can recur. For reduction in the proportion of liver transplants per-
example, in liver transplantation, primary sclerosing formed for this indication and the increasing rate of
cholangitis, hepatocellular carcinoma and viral hep- obesity in the community is likely to result in
atitis are at risk of recurrence. The risk of recurrent an increase in the proportion of liver transplants
viral hepatitis has been greatly reduced by effective performed for non‐alcoholic fatty liver disease
antiviral therapy (resulting in suppression of viral (NAFLD). Indeed, the proportion of liver trans-
replication in the case of HBV and eradication in the plants performed for HCV decreased from 28% in
case of direct‐acting antiviral therapy for HCV). 2010–2014 to 19% in 2015–2016 while the pro-
portion of liver transplants performed for NAFLD
increased from 6% to 8% over the same period.
Liver transplantation has been a highly success-
Results of transplantation
ful treatment for selected patients with end‐stage
liver disease, hepatocellular carcinoma and fulmi-
Kidney transplantation
nant hepatic failure. In recent years, the 1‐, 5‐ and
Kidney transplant outcomes in Australia and 10‐year patient and graft survival rates in Australia
New Zealand are reported by the Australia and and New Zealand have been 95%, 86% and 77%
New Zealand Dialysis and Transplant Registry. In and 91%, 82% and 71%, respectively. Patient sur-
2017, 1109 kidney transplants were performed in vival is superior in children compared with adults
Australia and 187 in New Zealand. The most fre- (10‐year patient survival 83% vs. 72%, respec-
quent indications for listing for kidney transplan- tively; P <0.001). The results of split liver trans-
tation in 2017 were glomerulonephritis (42%), plantation, whereby a deceased donor liver is split
diabetic nephropathy (14%) and polycystic dis- into two grafts, generally one for a child and one
ease (12%). Kidney transplantation in Australia for an adult, have been excellent. In children, the
and New Zealand has excellent results. In recent 5‐year graft survival rates for split and whole liver
years for primary (first) deceased donor grafts, the transplantation are 80% and 82%, respectively,
1‐, 5‐ and 10‐year patient survival rates have been and for adults are 75% and 78%, respectively.
Pancreas and pancreatic islet transplantation includes the pancreas), multivisceral (liver, stomach,
pancreas, intestine) and modified multivisceral (the
Pancreas transplantation can be undertaken as a
same as multivisceral, but without the stomach).
whole, solid organ transplant or as an islet cell
Seven intestinal transplants have been performed at
transplant. Whole pancreas transplantation is
a single centre (Melbourne) between 2010 and
most commonly (97% of pancreas transplants in
2019 in Australia. The 1‐ and 5‐year patient and
Australia and New Zealand) performed simultane-
graft survival rates are 86%.
ously with kidney transplantation, in the situation
of a patient with diabetes mellitus (overwhelmingly
Heart transplantation
type 1) who also has renal failure (most commonly
due to diabetes). However, pancreas transplanta- Heart and lung transplant outcomes in Australia
tion can be performed after kidney transplantation and New Zealand are reported by the Australia and
or, occasionally, without prior or simultaneous kid- New Zealand Cardiothoracic Organ Transplant
ney transplantation. Registry. From 1984 to 2018, 2974 heart and 208
Pancreas transplantation outcomes in Australia heart–lung transplants were performed. The com-
and New Zealand are reported by the Australia and monest indications were idiopathic dilated cardio-
New Zealand Islets and Pancreas Transplant myopathy (42%) and ischaemic heart disease
Registry. From 1984 to 2018, 866 solid organ pan- (31%). In 2018, 39% of patients were supported by
creas transplants were performed in Australia and a ventricular assist device at the time of transplan-
New Zealand. In recent years in Australia and New tation and 1% were supported by an intra‐aortic
Zealand, the 1‐ and 5‐year patient survival rates balloon pump. In recent years in Australia and New
following whole organ pancreas transplantation Zealand, the 1‐, 5‐ and 10‐year patient survival
were 97% and 94%, respectively, and the 1‐ and rates were 89%, 83% and 70%, respectively.
5‐year death censored graft survival rates were
94% and 88%, respectively. Lung transplantation
In islet cell transplantation, the islets of
From 1984 to 2018, in addition to the 208 heart–
Langerhans are separated from the pancreatic
lung transplants, 552 single lung and 2749 bilateral
acinar tissue in a complex process of enzymatic

lung transplants were performed. The commonest
digestion. The resuspended islets are then injected
indications were emphysema (29%), cystic fibrosis
percutaneously into the portal vein, following
(23%) and idiopathic pulmonary fibrosis (1%). In
which the islets can engraft in the liver and produce
recent years in Australia and New Zealand, the 1‐,
insulin. The main indication for islet transplanta-
5‐ and 10‐year patient survival rates for DBD lung
tion is type 1 diabetes mellitus with hypoglycaemic
transplant were 90%, 66% and 50%, respectively,
unawareness, which can be life‐threatening, occur-
while the 1‐, 5‐ and 10‐year patient survival rates
ring in patients who do not require kidney trans-
for DCD bilateral lung transplant were 92%, 68%
plantation. To achieve insulin independence, it may
and 61%, respectively (P = NS).
be necessary to perform islet transplantation from
more than one donor into a recipient. The best
results seem to be achieved in small recipients, who
have a low insulin requirement. A total of 116 islet
Surgical issues that can arise
transplants were performed in 58 patients in
in transplant recipients
Australia (there is no program in New Zealand)
from 2002 to 2018. Of these, 20 (34%) achieved
Considering the success of transplantation, many
insulin independence, two patients after a single
transplant recipients are living in the community
transplant, 11 after their second transplant and
and can present with surgical issues. Some of these
seven after their third transplant.
will be related to the graft, as outlined in the section
on complications of transplantation, but others will
be independent of the graft. If a patient presents to
Intestinal transplantation
a healthcare facility with a problem related to the
Intestinal transplantation is a low‐volume proce- graft, immediate transfer to the transplant centre
dure performed predominantly for patients with should be arranged. However, surgical problems
intestinal failure and life‐threatening complications that arise independently of the graft are often best
of total parenteral nutrition. The major categories dealt with expeditiously at the peripheral centre,
of intestinal failure are short gut syndrome and although the transplant unit should be contacted to
motility disorders. A variety of grafts are used ensure that they are aware of the issue and so that
including intestine only, liver–intestine (which relevant advice, including anatomical information
and advice regarding perioperative management of

immunosuppression, can be given. Indeed, undue
Further reading
delay in management of an urgent surgical problem
Alexander S, Hirst K (eds) 41st Annual ANZDATA Report.
can result in a poor outcome. Adelaide, Australia: Australia and New Zealand Dialysis
The variety of emergency surgical issues that and Transplant Registry, 2018. Available at https://www.
occur in transplanted patients is similar to that in anzdata.org.au/report/anzdata-41st-annual-report-
the general community. The presentation of emer- 2018-anzdata/
gency surgical issues can differ in immunosup- Forsythe JLR (ed.) Transplantation, 5th edn. Philadelphia:
pressed patients compared with the general Saunders Elsevier, 2014.
population in that immunosuppression can mask Keogh A, Williams T, Pettersson R (eds) ANZCOTR Report
the symptoms and signs of diseases, particularly 2018. Sydney, Australia: Australia and New Zealand
Cardiothoracic Organ Transplant Registry, 2018.
those that are infective in nature. In addition, infec-
Available at http://www.anzcotr.org.au/pub/e0cc941a/
tive processes can have a poorer outcome in immu-
PDFS/ANZCOTR2018_text.pdf
nosuppressed patients. Lynch SV, Balderson GA (eds) ANZLT Registry Report
The preoperative work‐up of a transplant patient 2016. Brisbane, Australia: Australia and New Zealand
should occur in similar fashion to any other surgi- Liver Transplant Registry, 2016. Available at https://
cal patient. However, immunosuppression and www3.anzltr.org/wp‐content/uploads/Reports/
indications for transplantation mean that there is 28thReport.pdf
an increased risk of diabetes mellitus, hyperlipidae- Webster AC, Hedley J, Kelly PJ (eds) ANZIPTR Report
mia and cardiovascular disease, including hyper- 2017. Sydney, Australia: Australian and New Zealand
tension and ischaemic heart disease, in transplant Islet and Pancreas Transplant Registry, 2019. Available
recipients which will require appropriate preopera- at http://anziptr.org/wp-content/uploads/2019/06/
ANZIPTR-Annual-Report-2019.pdf
tive assessment, potentially including cardiological
investigations.
There is no evidence to suggest that transplant
recipients have bacterial agents that are different MCQs
to non‐immunosuppressed patients and the antibi-
otic prophylaxis that is appropriate to the case
should be used. However, given the predisposition
to infection in the immunosuppressed population,
prophylactic antibiotics should be given even in 1 A 48‐year‐old man is in the intensive care unit after a
clean cases, in which they would not normally be brainstem stroke. Brainstem reflex testing reveals
used. The choice of prophylactic antibiotic should absence of pain response in the trigeminal distribution
be that which would normally be used for the case. and lack of the pupillary, corneal, vestibulo‐ocular,
As with operations performed in patients who are gag and cough reflexes. An apnoea test is performed,
not immunosuppressed, prophylactic antibiotics with disconnection of the endotracheal tube from the
should be given prior to skin incision. Although ventilator. After 4 minutes, a breath is taken. This
the risk of a perioperative hypotensive crisis in patient could become a deceased organ donor if:
patients who have been on long‐term steroid ther- a he had registered as an organ donor
apy is low (approximately 1%), it is appropriate a his family agrees to proceed
to provide steroid cover over the perioperative a donation occurs following a DCD pathway
period. b there is a patient urgently awaiting transplantation
The position of the transplanted organ and vas- c he has no history of infection or cancer
cular grafts may be of importance in some forms of
surgery. Transplanted kidneys are generally extra- 2 Cell‐mediated rejection following liver
peritoneal and therefore not usually at physical risk transplantation:
in a laparotomy, but transplanted pancreata (and a occurs less frequently in the presence of
the kidneys in the case of pancreas–kidney trans- microchimerism
plantation) are intraperitoneal and consideration b occurs more frequently than following transplan-
will need to be given to this fact in planning intra‐ tation of other organs
abdominal surgery. The transplant unit will be in a c occurs less frequently than antibody‐mediated
position to provide advice in these circumstances. rejection
Conversely, operations involving the abdominal d is characterised by deposition of C4d which can
wall of the iliac fossa or groin, iliac vessels or blad- be demonstrated on a liver biopsy
der will potentially put a transplanted kidney at e does not usually require modification of
risk of physical injury. immunosuppression
3 In Australia and New Zealand, living donor kidney 4 A 52‐year‐old brain‐dead potential donor is known
transplantation: to be a man who has sex with men. Transplantation
a is performed most commonly for diabetic of organs from this donor:
nephropathy a cannot occur under any circumstances
b accounts for approximately 10% of all kidney b can be considered if the donor serology is
transplants negative
c has results that are slightly inferior to deceased c can be considered if the donor nucleic acid
donor kidney transplantation testing is negative
d can only be performed between donors and d can occur if condoms had been used during
recipients who have a close personal or genetic sexual intercourse
relationship e can occur without the need for further testing
e has a 5‐year graft survival of approximately 90%
11 Principles of surgical oncology
G. Bruce Mann1,2 and Robert J.S. Thomas1
1
2
Victorian Comprehensive Cancer Centre, Melbourne, Victoria, Australia
Clinical trials are required to evaluate new treat-

Introduction ments and treatment combinations. There has been
a huge amount of basic cancer research that contin-
Surgical oncology focuses on the surgical manage-
ues to provide new insights. Translating these basic
ment of tumours, especially cancerous tumours.
findings into clinically meaningful management is a
Surgical oncology embraces cancer care in a multi-
major challenge and is a key aspect of the discipline
disciplinary framework, internationally recognised
of surgical oncology.
as the standard of care for patients with cancer.
This relies on coordination of surgery with medical
and radiation oncologists, diagnostic specialties
Multidisciplinary care
such as pathology and radiology, together with
input from cancer nurses, allied health disciplines
All clinical disciplines involved in cancer care must
and palliative care specialists.
understand the principles and practical conse-
Surgical resection of cancers remains the corner-
quences of the treatment offered by surgeons, radi-
stone of treatment for many types of cancer.
ation oncologists, medical oncologists and the
Historically, surgery was the only effective form of
allied health disciplines in order to be able to work
cancer treatment, but developments in radiation
in a team to care for cancer patients.
therapy and systemic therapies mean that optimal
outcomes require multidisciplinary treatment plan-
Radiation oncology
ning and delivery in a team‐based approach.
Surgery plays various key roles in cancer care. Radiation therapy may be delivered alone with
Determining what role surgery has in a particular curative intent in some cancers, as an adjuvant ther-
situation depends on accurate definition of the apy to reduce the risk of recurrence in many situa-
problem via preoperative staging investigations and tions, and frequently as a palliative treatment, for
multidisciplinary treatment planning. It is some- example of painful bony metastases in breast and
times needed for diagnosis, is effective for various prostate cancer. Effective symptom relief is often
premalignant conditions or in situ malignancies achieved with the use of radiation therapy.
and is a central part of treatment for most localised Radiation oncology involves the use of ionising
malignancies. Its role in metastatic disease is lim- radiation to selectively kill tumour cells. Radiation
ited, most often used when surgery can provide kills living cells by both direct DNA damage and
effective palliation by either treating or preventing the formation of free oxygen radicals in the cells.
a specific local problem. Free radical formation is the predominant effect
Communication with the patient and family, the and depends on the level of oxygenation of the
obtaining of informed consent and the careful, hon- tissue.
est, realistic but where possible optimistic explana- Ionising radiation is usually delivered to tumours
tion of the results of surgery are all matters of high as external beam therapy, generated by linear accel-
importance to all surgical practice. However, the erators. When a linear accelerator is used to supply
ability to talk sympathetically to cancer patients external beam therapy to a tumour, the patient goes
and their families is particularly important in the through a series of planning exercises to accurately
field of surgical oncology. delineate the tumour and direct the radiation as
87
accurately as possible to the tumour to minimise is treatment given in the absence of known dissemi-
the impact on normal tissues. nated disease in order to reduce the risk of subse-
An alternative method of administration of radi- quent emergence of metastatic disease. Breast
ation is by using a local radiation source applied cancer and colon cancer are two cancers where
close to the tumour. This is known as brachyther- landmark clinical trials have demonstrated signifi-
apy. It is a highly effective form of therapy in cant improvement in survival with the use of adju-
tumours such as cervical cancer, other gynaecologi- vant systemic therapy. Subsequently, effective
cal cancers and prostate cancer. adjuvant systemic therapy has become available for
Both normal and neoplastic cells are affected by a wide variety of cancers.
radiation, so the dose which can be given in any In cases of disseminated disease where cure is not
situation is limited by the tolerance of the sur- generally possible, systemic therapy usually forms
rounding normal tissues. Tissues particularly at risk the basis of treatment, with surgery and radiother-
include the bone marrow and gastrointestinal tract, apy used to address specific problems.
which contain rapidly dividing cells. The spinal
cord is also at risk as it does not have repair mecha- Supportive care
nisms able to manage radiation‐induced injury.
Normal tissues can recover from radiation pro- The holistic approach to the care of the cancer
vided the dose is not extreme, while malignant cells patient encompasses a range of supportive and
repair such damage less well. Fractionation of radia- coordinating services through the treatment phases.
tion, splitting the total dose into multiple daily low This is often delivered by a range of nursing and
doses, allows normal tissues to recover better allied health professionals. Psychosocial support
between doses than cancerous cells or tissues, allow- includes investigation and treatment of cancer
ing better selectivity of the impact of radiation. patients by suitably trained nursing staff, social
workers, psychologists and psychiatrists. Each dis-
cipline can offer some support depending on the
Medical oncology problem faced by the cancer patient. A nurse coor-
While surgery and radiotherapy are ‘local’ treat- dinator often aids in the management of the patient.
ments – they have their impact by treating the tis- The use of such professionals has been shown to
sues that are removed or radiated – many cancers improve outcomes for cancer patients.
have disseminated around the body at the time of
diagnosis. ‘Systemic’ treatments are needed to Survivorship
address these, and it is improvements in systemic Survivorship is a concept that has become promi-
therapy of cancers that have had the biggest impact nent over recent years. As the incidence of cancer
on outcomes over the last 20 years. has increased along with the ageing population,
Medical oncologists use a variety of agents to and cure rates for common cancers have increased,
modify tumour growth. Many of these are cyto- there is an increasing number of people who have
toxic chemotherapy drugs that are toxic to dividing apparently been cured but are left with uncertainty
cells; others are endocrine therapies that target the regarding the chance that the cancer will recur, and
cellular pathways related to hormones (tamoxifen may be suffering morbidity from the cancer and/or
and the aromatase inhibitors in breast cancer are its treatment. These issues should be directly
the best examples of these), while others are ‘bio- addressed at the end of active treatment, where
logical’ therapies that have been developed to mod- patients are ready to move to a long‐term follow‐up
ify some aspect of cellular function or to modify the phase of care. General practitioners and other pri-
immune response to a cancer. mary care practitioners are well placed to manage
Some cancers can be cured with systemic therapy many of these issues.
alone. Many lymphomas and other haematological
cancers, and some testicular tumours are such
Palliative care
examples. However, these are the exceptions and
for most solid tumours systemic treatment alone Modern palliative care programs are part of the
produces a limited or partial response. services offered to cancer patients in whom cure is
Many randomised controlled clinical trials have not possible. These services include ambulatory and
demonstrated a survival benefit from the use of hospice programs for management of the end stages
chemotherapy and other systemic therapies when of life when attempts to cure or actively treat the
given as either neoadjuvant (preoperatively) or cancer have ceased. Physical and psychological
adjuvant (postoperative) therapy. Adjuvant therapy symptom control is an important part of modern
11: Principles of surgical oncology 89
multidisciplinary care. Palliative care physicians only rarely can treatment be commenced without a
also help in pain control and symptom control in pathological diagnosis. Tissue is obtained by fine‐
the earlier stages of the illness and thus broaden needle aspiration, core biopsy or excisional biopsy.
their influence in the journey of the patient with
cancer. Early involvement of palliative care has Percutaneous biopsy
been shown to improve both the quality and also Fine‐needle aspiration cytology and core biopsy
the length of life of many cancer patients. can be done on an outpatient basis and provides a
rapid diagnosis of accessible lesions such as breast
lumps, head and neck lymph nodes and thyroid
Principles of surgery for malignant swellings. Ultrasound guidance for the biopsy nee-
disease dle is necessary and commonly used; CT or MRI
guidance may also be used. Endoscopic biopsy is
The principles involve screening and diagnosis,
the basis of most diagnoses of upper and lower gas-
assessment of the patient, staging of the extent of
trointestinal cancers and lung cancer.
cancer, decisions about treatment by the multidisci-
All these techniques rely on the expertise of the
plinary team, principles of operative surgical oncol-
pathologist to make a definite diagnosis on the
ogy, rehabilitation and follow‐up. Each of these will
basis of either the cytological or histological char-
be dealt with in turn.
acteristics of the tumour, supplemented by a variety
of immunohistochemical assays to accurately define
Screening and diagnosis of malignant
the tissue of origin and assess its likely natural his-
disease
tory and response to particular treatments.
Screening
Excisional biopsy
Randomised controlled trials of population
Where a local mass or skin lesion can be completely
screening have shown survival benefit in a number
excised without significant morbidity, excisional
of diseases. For screening to be effective, the test
biopsy is the treatment of choice, removing the
must be able to detect a common cancer at a stage
problem at the same time as making the diagnosis.
where treatment is more effective than treatment
This technique is commonly used for skin lesions,
given when a cancer becomes symptomatic. The
particularly suspected squamous cell carcinoma,
test must be sensitive, specific and acceptable to
basal cell carcinoma and melanoma.
the public.
Sometimes excisional biopsy (or incisional, where
The most effective screening program has been
not all the lesion is removed) of a deeper lesion is
cervical screening where, since its introduction,
required when attempts to reach a diagnosis in a
there has been a substantial fall in mortality from
less invasive manner have failed or are too danger-
cervical cancer in all age groups. Recently, the Pap
ous, or when the lesion should be removed for cos-
smear is being replaced by an assay for human pap-
metic or other reasons.
illomavirus (HPV), and this should dramatically
improve the already very good outcomes. Similar
Assessment of the patient
less dramatic effects are seen with breast cancer
screening by mammography and colon cancer An important early part of the assessment of a
screening using faecal occult blood testing and fol- patient with cancer is to determine health and fit-
low‐up colonoscopy. ness and ability to tolerate various treatments with
Population screening for prostate cancer using acceptable risk of complications. Many cancer
prostate‐specific antigen (PSA) testing remains con- treatments are demanding on the physical and psy-
troversial due to the potential morbidity of prostate chological resources of the patient. An idea of
cancer treatment, and the inability to distinguish the ‘health’ of the patient can be gained from a sim-
indolent from aggressive cancers. As these prob- ple clinical assessment, the Eastern Cooperative
lems are addressed, evidence around an optimal Oncology Group (ECOG) performance status, with
approach to prostate cancer screening is likely to more complex assessments needed prior to more
emerge. intense treatments.
Diagnosis Staging of malignant disease

A tissue diagnosis is essential prior to the creation of Accurate staging of the extent of disease is of great
a management plan for a cancer patient. The conse- importance in formulating a treatment plan. Clinical
quences of many cancer treatments are so severe that stage is that defined by clinical examination and
imaging of the patient. High‐quality imaging has led A measure of the adequacy of the oncological
to improved accuracy of clinical staging. Pathological surgical operation is demonstrated by the findings
staging is that defined after excisional surgery. on pathological examination of the specimen.
The most commonly used staging system is the Standards exist for ensuring the adequacy of the
TNM (tumour, nodes, metastases) system. The AJCC surgical excision to be assessed in many tumours.
(American Joint Committee on Cancer) defines the The operative specimens need to be correctly orien-
TNM staging for all cancers. Suffixes to the T, N and tated by the surgeon to allow the pathologist to
M indicate the size of the tumour and extent of nodal carefully examine and interpret the specimen. The
disease or metastases. For example, T2N1M0 indi- key issues are usually:
cates the stage of a tumour, for example carcinoma • the precise histopathology of the cancer, includ-
of the colon where the tumour has spread into the ing relevant tumour markers
muscularis propria but not through the wall of the • whether the margins of the specimen removed
colon (T2) and where there are adjacent lymph nodes are clear of tumour
involved (N1) but no metastases detected (M0). • the total number of lymph nodes excised and the
Combinations of T and N stages are grouped into number of involved nodes.
overall stages with similar prognoses, ranging from A major focus of modern cancer surgery has been
stage 0, indicating premalignant disease (e.g. ductal the preservation of function. Improved surgical
carcinoma in situ of the breast) to stage IV, indicating techniques and effective use of multidisciplinary
metastatic disease. The staging system varies dramat- treatment has resulted in diminished morbidity of
ically according to the primary site of the tumour. major cancer surgery. Examples of this include
larynx‐preserving treatment for head and neck
Recommendations about treatment: cancer, limb‐sparing surgery for soft tissue sar-
the multidisciplinary meeting coma and sphincter‐sparing treatment for rectal
cancer.
Armed with information about the diagnosis of the
cancer, the extent of the disease and the fitness of
Margins of surgical excision
the patient, recommendations and decisions can be
made about the most appropriate treatment pro- The degree to which normal tissues should be
gram. Consultation with a multidisciplinary team removed with the primary tumour is a subject con-
may occur prior to surgery; however, if the decision stantly being researched. A universal rule is not
regarding surgery is straightforward, the multidisci- possible to formulate. The principle of complete
plinary meeting may occur after surgery when full local excision with an adequate margin is para-
pathological information is available. However, mount in surgical oncology and many trials have
many cancers may benefit from down‐staging with helped clarify what ‘adequate’ means. It varies sig-
radiotherapy or chemotherapy prior to surgery, and nificantly according to the cancer, its natural his-
early multidisciplinary consultations are important tory and the availability of effective adjuvant
to facilitate this process. therapies.
Principles of operative surgical oncology Lymph node resection

The technical issues in surgical oncology are no Traditionally, the draining lymph nodes from a
different from other surgical interventions. Open primary tumour were excised with the cancer. The
surgery, laparoscopic surgery, robotic surgery, abla- main benefit of this removal is improved prognostic
tive interventions and other technical interven- information, which may affect the decisions regard-
tions all have a place in modern surgical oncology. ing postoperative adjuvant therapy. In some situa-
However, some important oncological principles tions there may be a local control or survival benefit
exist which must be followed by the surgeon for a from removal of early‐involved lymph nodes.
satisfactory outcome. The extent of lymph node surgery has reduced
over recent decades. This is partly due to the recog-
nition that prophylactic excision of uninvolved
Definition of curative surgery
nodes does not provide a survival advantage to the
So‐called curative surgery generally involves an patient and exposes the patient to increased mor-
apparent total excision of the tumour. The primary bidity from the node removal. It is also due to the
tumour and the associated lymph node drainage introduction of lymphatic mapping and sentinel
fields are often excised where nodal involvement is node biopsy, where the first draining lymph node
known, suspected or reasonably likely. can be identified and removed, giving prognostic
11: Principles of surgical oncology 91
information without a great risk of morbidity, and

allowing better informed decisions regarding fur-
Clinical trials and research
ther nodal surgery.
Clinical research is essential for evaluating new
and previously untested treatments. Surgeons are
Palliative surgery
involved in a number of ways:
Palliative surgery aims to improve quality of life by • Provision of tissue for tissue banking. This is a
either preventing or avoiding some symptom‐pro- fast‐growing program throughout the world. The
ducing consequence of the tumour by resection or provision of fresh tissues for genetic studies is of
bypass. This is done even though a cure is known to paramount importance to the understanding of
be impossible. Examples include the following. malignant disease. Collection of accurate clinical
• In the case of pyloric obstruction from an data to accompany the tissue is valuable.
advanced cancer of the stomach, a gastrojejunos- • Surgeons design, implement and run clinical tri-
tomy may provide good palliation of vomiting. als to assess new surgical approaches to cancer.
• Resection of a bleeding cancer of the colon is jus- The recruiter for randomised clinical trials must
tified even in the presence of metastases. have equipoise in relation to the arms of the
Many other examples exist. ‘Tailoring’ this type of study and be able to assure the patient that there
surgery to the needs of the patient without undue is no reason why he or she should not enter the
morbidity is an important role for an oncological trial, as current knowledge does not suggest that
surgeon. one or other arm is clearly ‘better’.
Follow‐up of patient after initial treatment Conclusion

program
A program of follow‐up is required for cancer The surgeon operating on cancer patients in the
patients after their initial treatment. This is for two twenty‐first century must have a deep understand-
main reasons. The first is to monitor and investigate ing of the malignant process, be prepared to work
when appropriate to detect recurrent disease. In as part of a team and offer multidisciplinary care,
general, early diagnosis of symptomatic recurrence communicate well, operate with a high level of skill,
is appropriate, as it allows the most effective pallia- help the patient rehabilitate from the treatment and
tive treatment. Whether imaging to detect asympto- finally be involved in the advancing area of surgical
matic recurrent disease is appropriate depends on science as applied to cancer care.
whether there is treatment for the recurrence that is
more effective in the asymptomatic phase. Early
detection of liver metastases after colorectal cancer Further reading
treatment is appropriate, as cure may be possible
Cancer Australia. All about multidisciplinary care. https://
when appropriately staged patients with liver
canceraustralia.gov.au/clinical‐best‐practice/multidisciplinary‐
metastases are successfully resected. On the other care/all‐about‐multidisciplinary‐care
hand, detection of asymptomatic breast cancer Feig BW (ed.) The MD Anderson Surgical Oncology
metastases has not been shown to be beneficial, and Handbook, 6th edn. Philadelphia: Wolters Kluwer, 2019.
therefore routine surveillance CT and bone scans Morita SY, Balch CM, Klimberg VS, Pawlik TM, Posner
are not done. However, screening for asymptomatic MC, Tanabe KK (eds) Textbook of Complex General
new primary cancers is performed. Surgical Oncology. New York: McGraw‐Hill Education,
The second reason for follow‐up is that it pro- 2018.
vides an opportunity to identify and manage side
effects of the disease and its treatment and to sup-
port the patient psychologically. Increasingly, it is MCQs
recognised that severe psychological morbidity may
exist in cancer patients who have been treated, even
if the cancer is apparently cured. This has led to a
developing interest in the concept of survivor-
ship – understanding the needs of the ‘cured’ cancer 1 Screening for malignant disease is not effective in
patient. Psychosocial support is essential for many which of the following situations?
cancer patients and is best delivered in the setting of a where a tumour is detected at a stage where it
multidisciplinary care. can be cured by treatment
b screening is undertaken on an individual 3 What is adjuvant therapy in the setting of cancer

patient basis treatment?
c there is high public acceptance of the a treatment given to relieve symptoms of the disease
process b treatment given if a cancer cannot be resected
d specificity of screening is high c treatment given in the absence of known disease
e sensitivity of screening is high to reduce the risk of recurrence
d treatment of non‐cancer conditions in patients
2 Which of the following statements in relation to with cancer
regional lymph node dissection at the time of e treatment that has few side effects
primary tumour excision is incorrect?
a allows more accurate tumour staging 4 What are the objectives of ongoing consultations
b allows provision of appropriate prognosis to once cancer therapy has been delivered?
the patient a to check for the presence of local recurrences
c can be undertaken with little morbidity b to assess for late effects of anticancer treatment
d allows appropriate adjuvant treatment to be c to check for evidence of distance recurrence
undertaken d to provide supportive care
e may confer a survival advantage e all of the above
12 Introduction to the operating
theatre
Andrew Danks1, Alan C. Saunder2
and Julian A. Smith3
1,2,3
Monash University, Victoria, Australia; 1 Department of Neurosurgery, 2 Surgery and
Interventional Services Program, and 3 Department of Cardiothoracic Surgery, Monash Health,
Clayton, Victoria, Australia
Surgery has been made safe for the patient; let us rationally on the perceived risks and benefits of the
now make the patient safe for surgery. operation, but the influence of multiple emotional
Lord Moynihan of Leeds (1865–1936) and experiential factors may be more powerful for
many people. These aspects may be optimised by a
caring and expert assessment and professional
Introduction behaviours by the preoperative team.
From the surgical team’s perspective, there is
The operating theatre is a complex clinical environ- the opportunity to work together to rectify the sur-
ment where the care of the surgical patient is facili- gical problem that the patient is suffering from.
tated by the coordination and coalescence of many Specifically, for surgeons there is the opportunity to
crucial factors. Depending on the healthcare facility practise and employ the full array of skills that they
that the operating theatre is in, the operating theatre have developed during their training, such as those
deals with a broad spectrum of procedures, from the described by the Royal Australasian College of
very simple to extraordinarily complex, multi‐team, Surgeons (RACS) competencies (see Box 12.1).
high‐technology operations, in both planned and From the anaesthetist’s point of view, there is
emergency situations. In order to facilitate this, there the challenge of safely inducing, maintaining and
is effectively an inner sanctum or immediate direct awaking the patient from anaesthesia by applying
operating team that includes the patient, surgeon, sur- the pharmaco‐physiological knowledge and skills
gical assistants, anaesthetists, nursing staff and thea- that they possess.
tre technicians (i.e. those in the operating theatre). Nursing staff are involved in both the anaes-
Supporting the direct operating team, there is a thetic and surgical teams. Their specialised skills
complex network outside the operating theatre but and training are vital to the smooth conduct of all
essential to the conduct and successful completion operative procedures.
of safe surgery. This network includes the central The theatre technical staff are crucial for safe
sterile and supply department (CSSD), the ward patient transport, positioning and ensuring that all
staff preparing the patient for surgery and caring appropriate equipment is available and safely func-
for the patient postoperatively, the suppliers of tional for the planned procedure.
essential equipment, imaging resources and pathol- All these groups must work together as a team,
ogy back‐up, as well as hospital administrators. each bringing their unique skill sets together in a
From the patient’s perspective there is a feeling of coordinated, collaborative and respectful way to
approach–avoidance ambivalence. The ‘approach’ facilitate the patient’s care. Appropriate and effec-
element is the patient’s need to have their clinical tive professional behaviour is essential for creating
problem rectified, whilst the ‘avoidance’ reflects the and maintaining a functional team. Respect for
normal fear of the unknown, possible pain, compli- each member of the theatre team is invaluable and
cations and even mortality. This ambivalence over the common courtesy of saying ‘please’ and ‘thank
whether one should or should not proceed is based you’ is a powerful factor in enhancing respect and
93
during any operative procedure. The creation and

Box 12.1 Royal Australasian College
maintenance of a sterile field is discussed in this sec-
of Surgeons competencies for surgeons
tion, which also describes important factors relat-
• Medical expertise ing to each member of the inner sanctum that
• Technical expertise enhance the chance of a satisfactory outcome from
• Judgement/clinical decision‐making the planned surgery. Professional communication
• Health advocacy and the important issue of occupational safety for
• Communication the theatre team are also covered.
• Collaboration As a general point, it is ideal to have a separate
• Management and leadership preparation room for the scrub team to set up the
• Scholar and teacher instruments on sterile trolleys, and another sepa-
• Professionalism and ethics rate room for the preparation of the patient for
anaesthesia.
developing trust in each other. Despite this, emo-

tions may run high under the pressure of surgery. Patient
This may lead to behaviours which may in turn be
Patient preparation is essential to safe surgery (see
counterproductive rather than improving a tense
also Chapter 1). There are many aspects to this. The
situation. Appropriate training may help practition-
first step is the establishment of the correct diagnosis
ers to adapt to these challenges more effectively.
or diagnostic possibilities, and the choice of the cor-
The operating theatre is an excellent venue for
rect operative strategy. During this process, a thera-
teaching and training in all professional disciplines.
peutic relationship must be established between the
It is important that students and junior staff have
surgeon and/or the surgical team and the patient (and
access to this environment to develop their under-
their relatives). Special tests or preparations may be
standing of surgery and anaesthesia. However,
required to clarify the diagnosis and to further assess
there needs to be careful supervision in order to
the condition. The patient’s overall medical condition
maintain patient safety. Ultimately, the safety of the
must be assessed and optimised. Some patients may
patient is of paramount importance throughout
not be fit enough for the first‐line surgical option, so
any visit to the operating theatre.
alternatives may need to be considered.
In this chapter, we consider an overview of each
Once the surgical plan has been established, it is
component that contributes to the patient’s journey
necessary that the patient understands the diagnosis
in the operating theatre under the broad headings
and its implications, the risks and benefits of the
of the operating theatre and the direct patient care
planned procedure, and alternative treatments includ-
team, followed by the important role of the indirect
ing non‐operative options. It is important that this
support staff and systems to support care in the
information is conveyed in their usual language with
operating theatre.
appropriate support available. This process is termed
achieving informed consent. Consent must be clearly
The operating theatre (the ‘inner documented, both for legal reasons and to facilitate
sanctum’) safe ‘time‐out’ procedures (see section Surgeon). In
the elective situation, it is necessary that this consent
The fundamental goal of the modern operating is achieved prior to attendance at the operating thea-
theatre is the establishment of a safe and appropri- tre. In truly urgent situations, consent may be waived
ate environment for effective and safe surgery. if it is genuinely in the patient’s best interest. However,
Surgery is potentially very dangerous. Key dangers it is always best that the patient and relatives under-
include excessive bleeding, damage to vital organs, stand as much as possible, even in an emergency. The
failure to achieve the goals of the operation, poor comprehensive approach to gaining an informed con-
wound healing, surgical site infection (SSI) or other sent can be achieved by describing the planned proce-
infections, venous thromboembolism, fluid imbal- dure, its goals and expected outcome, and embellishing
ance and other concerns. it along the lines of the mnemonic SCAR:
A central concept is the creation of a sterile field S Side effects
to provide the safest access to the part of the body C Complications
to be operated upon in such a way that the risk of A Alternatives
SSI is minimised. It must be the focus of all con- R Risks
tributors to the inner sanctum that an appropriate A patient information brochure for the specific
sterile field is established, protected and maintained operation (Figure 12.1) may be an invaluable aid to
12: Introduction to the operating theatre 95
Fig. 12.1 Sample pages from a patient information brochure for coronary artery bypass grafting.
Fig. 12.1 (Continued)

the consent process. This can help the patient and as a hand table for surgery of this region or a tour-
their family to understand and discuss the forth- niquet for many orthopaedic limb operations,
coming operative treatment. It may also be valuable through to more complex devices such as cardio-
in providing some standardisation of the discussion pulmonary bypass machines for cardiac surgery,
process, and in avoiding the omission of important the ultrasonic surgical aspirator for hepatic and
information. neurosurgical resections, and operating micro-
For planned elective procedures, the patient’s scopes for the most delicate work.
comorbidities should be identified and corrected as The value of experienced well‐trained theatre
much as possible so that the patient’s general condi- technicians cannot be underestimated in contribut-
tion is optimised prior to surgery. A simple example ing to the care of the patient from the perspective of
of this is the cessation of smoking, ideally for a equipment provision. They also play a key role in
minimum of 4 weeks prior to the operation, which transferring and positioning the patient for surgery.
has been shown to significantly reduce postopera- Patients may be placed in a variety of positions to
tive complications and may lead to the patient stop- facilitate their surgery. The theatre technician’s
ping smoking altogether. Another critical issue is knowledge of how to do this well is crucial for the
the management of antithrombotic and antiplatelet welfare of both the patient and the operating team.
agents perioperatively. A targeted history is required Many patients are operated on in the supine posi-
to identify these and other health issues that may tion. However, prone, lateral and lithotomy posi-
have an impact on the planned surgery and its tions are required for certain surgeries, whilst
conduct. specialised head frames are required for intracra-
Careful synthesis of the operative candidate’s nial procedures. Specialised operating tables and
health and readiness for surgery can be amplified add‐on components allow for patient positions to
by appropriate investigations, especially in the be achieved safely, and even allow for changes or
older patient (>70 years), such as urinalysis, full adjustment of position intraoperatively. There is a
blood examination, electrocardiogram (ECG), elec- real expertise required to do this. The final respon-
trolytes, chest X‐ray and so on. Subsequently, pre- sibility for patient position remains with the sur-
operative assessment may involve other specialties geon, so careful overview of this aspect is required.
such as cardiologists, diabetic specialists, nephrolo- One of the critical aspects of positioning is the
gists and our allied health colleagues, for example avoidance of pressure and traction injuries. Certain
physiotherapists to help with breathing exercises pressure points need particular attention, such as
preoperatively. The concept of training the patient the heels in the supine position or the condyles of
to be ready for elective surgery is becoming more the ankle in the lateral position. The ulnar nerve
popular, so‐called ‘prehabilitation’ that helps to posterior to the medial epicondyle of the elbow is
prepare the patient both physically and mentally particularly vulnerable to pressure, which may
for the forthcoming operative procedure. result in a disabling tardy ulnar palsy. Likewise,
pressure on the head of the fibula may damage the
Operating theatre equipment and technical lateral peroneal nerve.
support An increasing challenge in this domain is the
management of morbidly obese patients who
Modern surgery frequently requires specific spe-
require surgery. Special equipment such as hover
cialised equipment. Good planning and communi-
mats may be required to move these patients safely
cation is essential in order that the right equipment
without risk to the theatre personnel, as well as spe-
is available in good working order for the right
cially designed bariatric operating tables to safely
patient at the right time. This may be challenging to
cope with the loads involved.
coordinate in busy operating suites where similar
procedures are occurring simultaneously, placing
Anaesthetists and anaesthetic care
conflicting demands on certain pieces of specialised
(see also Chapter 3)
equipment. Awareness of what is required for any
particular operation and coordination of theatre Modern anaesthesia is a beautiful blend of knowl-
lists are important for minimising such conflicts. edge of human physiology and complex pharma-
There are certain key items common to all thea- cology and its interaction with a complex spectrum
tres, such as operating lights, anaesthetic machines, of pathology and the challenges created by the sur-
gas supplies, operating tables, suction, electrocau- gical procedure. Chapter 3 deals with many aspects
tery and theatre trolleys. Specific items are required of how anaesthetists assess and manage this com-
for specialty surgery, including simple items such plex myriad of challenges. Underlying this are
essential principles of teamwork within the operat- As well as ensuring that all equipment and instru-
ing theatre where the anaesthetist is vital. ments are sterile and working for the forthcoming
Once again, excellent communication is funda- operation, the scout and scrub ‘count in’ all instru-
mental in achieving exemplary teamwork during ments and disposable items before the operation
the patient’s journey through theatre. This com- and ‘count out’ the same items as the operation
mences with a thorough assessment of the patient’s concludes. It is important that interruptions be
suitability for operation and the associated risks. minimised during this process, as this is one of the
This may be summarised in the universal American key safety checks of all operative procedures.
Society of Anesthesiologists (ASA) scoring system. Obviously, the numbers must match in all catego-
Flowing on from this is the concept of the patient’s ries. An incorrect count at the conclusion of the
potential frailty as judged by their physiological operation warns the team that an object from the
status and whether the planned procedure may scrub nurse’s original count may be still in the
indeed be futile. The anaesthetist can make signifi- patient. This must necessitate a recount, and a
cant contributions to the detailed discussions with search of the operative field and surrounds. If the
the patient, their family, the surgical team and other count is still not correct, the patient must be either
interested parties about proceeding with surgery, re‐explored or imaged radiologically to exclude the
and how this may be done as safely as possible. possibility of a retained instrument or device before
Each operating theatre will have an anaesthetic they leave the theatre. Once again, good communi-
machine with appropriate monitoring equipment, cation is the key to ensuring excellent patient safety.
and an anaesthetic trolley with drugs and other An easy way to summarise the method for the
equipment. Typically, expiratory carbon dioxide and nursing staff to be maximally effective is to practise
tissue oxygen saturation (pulse oximetry) are moni- the PAP principles of Proper Preparation, Astute
tored as well as the ECG and normal observations. Anticipation, and Professional Participation.
Temperature monitoring and warming blankets are An experienced scrub nurse who is well prepared,
also important as intraoperative hypothermia has anticipating the next step in the operation and par-
been linked with increased infection rates, as well as ticipating by timely smooth delivery of instruments
slow wakening from anaesthesia. to the surgical team greatly enhances the efficiency
Drugs of addiction need to be managed specifi- of the procedure and thereby facilitates safe sur-
cally to meet legal requirements, so they are securely gery. The scout is his or her supply line for whatever
stored outside the actual operating theatre. Another is needed in the sterile field and must adopt a simi-
key role of the anaesthetists intraoperatively is the lar attitude of anticipation and participation.
administration of prophylactic medications, such as One of the benefits of this approach is the smooth
antibiotics and thromboprophylaxis as well as ther- and efficient exchange of instruments and equip-
apeutic agents such as heparin or blood products ment between the surgical team and the scrub
for cardiac and vascular surgeries. The lines of com- nurse. For non‐sharps instruments, if the surgeon is
munication between the anaesthetic and surgical clear in his or her request of what is required next,
teams are critical to the smooth administration of then the scrub nurse should be able to place it in the
such agents. correct way into the surgeon’s hand without the
surgeon having to look away from the operative
Surgical (scrub) and scout (circulating) nurse field. Sharp instruments should not be passed hand
to hand, but in an appropriate container such that
For the vast majority of operative procedures, a
the surgeon picks up the sharp item and after use
minimum of two surgical nurses are required. Both
returns it to the container (Figure 12.2), in order to
are specially trained to work within the theatre
minimise the risk of injuries.
environment and must have an exceptional under-
standing of sterility and the process of establishing
Surgeon
a sterile field. The surgical or scrub nurse scrubs,
gowns and gloves according to the established The surgeon is responsible for the decision to oper-
standards and is in charge of the instruments and ate, and the preoperative, operative and postopera-
disposable items that will be used for the planned tive management of the patient. This requires many
operation. The scout or circulating nurse is also a skills, summarised by the nine RACS competencies
trained scrub nurse who opens and provides all the (Box 12.1). Whilst many tasks are delegated to oth-
equipment in a sterile fashion to the scrub nurse. ers, the surgeon is responsible for the overall out-
The two nurses work as a team within the operat- come of the patient and must at all times be an
ing room and require quarantined time and space advocate for that patient. Additionally, the surgeon
to do their essential work. and the anaesthetist are the most highly trained
members of the team. At law, the senior doctors are many ways and idiosyncrasies about how this may
held accountable, in whole or in part, for all aspects occur, which will reflect cultural and societal norms,
of the operation. Therefore, the surgeon must act as as well as individual differences in style. In twenty‐
leader of the cohesive operative team, in partner- first century Australia, a collegiate and relatively
ship with the anaesthetist. democratic style is generally optimal in engaging all
The surgeon, whether in training and being staff in the team.
supervised by a more senior colleague or a special- An important step in team engagement and a
ist, fully trained surgeon, must be able to take critical element in patient safety is the preoperative
charge of the operating team for the commence- team time‐out (TTO). This is now internationally
ment and safe conduct of the operation. There are recognised under the banner of the World Health
Organization (WHO) checklist (Figure 12.3). This
must be overseen by the operating surgeon. At the
simplest level, this aims to ensure that the correct
part of the correct patient is to undergo the correct
operation at the right time. However, the process
extends beyond this to encompass review of critical
elements of patient assessment and theatre equip-
ment. Anticipated critical events are anticipated
and discussed.
All team members in the inner sanctum of the
operating team must participate in the TTO. If any
member has concerns, they must feel empowered to
voice those concerns with the rest of the team
before proceeding to start the operation. Ideally, in
order to involve the patient in this crucial step, the
Fig. 12.2 Scalpel in a plastic bowl in readiness for TTO should be completed with the patient awake,
passing to the surgeon. wherever possible.
Fig. 12.3 WHO Surgical Safety Checklist. Source: https://www.who.int/patientsafety/topics/safe‐surgery/checklist/en/.

Reproduced with permission of WHO.
Surgical assistant Suction must be done carefully, as excessive suc-

tion may traumatise the tissues and cause bleeding
Surgical assisting can be one of the most challeng-
or damage to a vital structure. Start gently and lis-
ing and yet one of the most rewarding activities for
ten to the instructions provided. The assistant must
medical students, surgical aspirants and trainees. It
avoid blocking the light illuminating the surgical
is also part of the role for senior surgeons mentor-
field or obscuring the surgeon’s line of sight to the
ing trainees during their training. It is an art of sorts
operative field at all times.
and requires undivided attention to the operation
It is essential to avoid breaking sterility at any
as well as a mindset of ‘What can I do to make this
time. Hands should be kept above the waist and
operation as straightforward as possible for the
below the shoulders, out in front at all times,
operating surgeon?’ If the assistant is new to thea-
while avoiding contact with anything non‐sterile.
tre or has not seen the operation before, this can be
If this occurs accidentally, the person responsible
very difficult, especially if the procedure is not
should immediately own up and avoid touching
going well (e.g. unexpected bleeding). Timely
the sterile field until the loss of sterility can be
appropriate questioning can help assisting to be a
rectified.
most rewarding educational experience.
As one gains more experience, better anticipation
Retraction may be a challenging task for the inex-
and initiative develop. Opportunities to become
perienced assistant. The goal is to display the anat-
more ‘surgical’ readily present themselves to those
omy in the best possible way for the surgeon. It is
who continue to show interest in the safe conduct
best to maintain the retractor position to the best of
of operative procedures. Preparation of one’s skills
one’s ability until it is adjusted by the surgeon.
at workshops and practice of these at quiet times
Remember that excessive force may cause trauma to
are important in readying oneself for opportunities
the tissues of the patient. It is important to follow the
that may arise to take an important role in surgery.
operation, as the required retraction does change as
Another important role of the more experienced
the operation evolves and of course will ultimately
assistant is that of the co‐pilot, supporting and
be dispensed with as the operation concludes.
backing up the primary surgeon.
Other assisting activities, such as cutting sutures
and deploying electrocautery and suction, should
The medical student in the operating suite
be done at the direction of the operating surgeon. In
general, dissecting scissors are not used to cut Clearly, the work that goes on in the operating suite
sutures. It is important to develop the habit of cut- is central to the care of the surgical patient.
ting with the tips of the scissors to reduce the risk of Therefore, it is essential that students attend the
cutting a vital structure deep to the suture. operating suite to witness a range of surgeries. This
Electrocautery involves closure of bleeding points is also an excellent environment to learn about ster-
by heat from an electrical current. Monopolar dia- ile practice.
thermy involves the flow of current from the instru- There are challenges in achieving access.
ment to the surrounding tissues, then back to the Regrettably, there is a relationship between the
machine via a return plate. Typically, the surgeon number of personnel in an operating room and
will grasp the bleeding point with the tips of a for- infection rates. Therefore, many theatres will limit
ceps and will ask the assistant to touch the monop- the number of observers in the operating room to
olar probe to the forceps and activate the current one or two at any one time. However, most surgical
via a switch. Generally, this contact is best made units perform many surgeries per week, so there are
high on the surgeon’s instrument, avoiding the sur- always opportunities to observe.
geon’s line of sight. It is important to listen carefully In order to gain a patient‐centred understanding
about when to stop in order to prevent charring of of surgery, it is essential that the student under-
the tissues. stands the patient’s illness and indications for sur-
Bipolar diathermy involves the electrical current gery before attending. It is necessary to read the
flowing between the tips of special forceps applied notes, and to meet the patient preoperatively. A
to the bleeding point by the surgeon. The assistant proper history and examination should be per-
may be asked to activate the circuit via a pedal and formed. Medical students must be mindful of the
may be required to keep the tips moist by applica- nursing and other staff needing to prepare the
tion of a small volume of fluid. The goal is to apply patient and also to be respectful of the patient and
enough fluid to allow boiling at the tips of the for- their anxiety about the forthcoming procedure.
ceps, avoiding charring or flooding by under‐ or Nonetheless, opportunities for these interactions
over‐application. are available for the careful and patient student.
Verbal consent for observation should sought from clearance programs instituted preoperatively for
the patient preoperatively. the colonised patients.
In the operating theatre, it is necessary to intro- In surgery of the large bowel, a major cause of
duce oneself to the surgical team, and request per- postoperative SSI is related to contamination from
mission to observe the procedure. A balance needs the bowel flora. Preparation of the bowel with
to be found between being involved as closely as strong osmotic aperients may reduce infection
possible, whilst not interfering with the safe and rates. Sometimes, for certain common procedures
efficient conduct of the procedure. Respect for the (e.g. hysterectomy or colectomy) a so‐called bundle
sterility and safety of the procedure is paramount at of care is initiated as a protocol‐driven way of mini-
all times. It is wise to be prepared to present the mising SSI by commencing preoperative risk reduc-
patient’s clinical details to one’s senior colleagues if tion strategies and continued appropriate strategies
requested. through the operation and into the postoperative
period.
Once intravenous access has been achieved by
Creation and maintenance of a sterile field
the anaesthetist, appropriate antibiotic prophylaxis
The creation and maintenance of a sterile zone for is administered as per guidelines. It has been dem-
the operation is a fundamental tenet of modern sur- onstrated that it is optimal that this be given at least
gery as previously noted. This section covers preop- 30 minutes before skin incision so that adequate
erative preparation, surgical scrubbing, gowning antibiotic levels are achieved at the incision site. It
and gloving, skin preparation, draping and protec- is critical that excessive antibiotic use and duration
tion of the sterile field. These principles apply to all be avoided to minimise the risk of antibiotic resist-
types of wound (see Chapter 6) but may need to be ance developing in the bacteria in the hospital envi-
adapted to the particular circumstances. ronment. After the patient is positioned as per
surgical requirements, the planned operative field
Preoperative preparation and surrounding skin is clipped, not shaved, in
readiness for the operation.
In some surgical procedures (e.g. cardiac, neuro-
logical and prosthetic joint replacement surgeries),
the patient’s skin flora are a major cause of SSI. Theatre dress code and hand hygiene
The skin cannot be completely sterilised because Staff may carry pathogens picked up from other
of the complex adnexal structures (sweat glands, patients or from the hospital environment includ-
hair follicles and sebaceous glands) and the coming some with high levels of antibiotic resistance. It
plex microbiome that inhabits the skin. Normal is important that appropriate clean theatre attire be
commensals include potential ‘weak’ pathogens donned by all staff before entering the operating
such as Propionibacterium, Corynebacterium and suite, and that this be changed when they return to
Staphylococcus epidermidis, whilst colonisation theatre from other environments. It is important
with Staphylococcus aureus may occur in up to that hand hygiene be performed before entering
25% of normal individuals. Colonisation with and leaving the individual theatre, and whenever
multiple serious pathogens is common in hospital- contamination might occur. Each institution will
ised patients, especially when they are sick, receiv- develop specific hand hygiene and dress codes for
ing antibiotics or have diseases or ulceration of the theatre environment.
the skin.
Therefore, it is necessary to achieve the maximal
The operating theatre
possible reduction in the burden of pathogenic skin
flora in the immediate preoperative period. The The operating theatre must be an extremely clean
patient may be asked to use an appropriate skin environment, with appropriate surfaces that pro-
decontaminant before coming to the operating the- vide a high level of cleanliness and specific cleaning
atre. The patient’s operative area must not be protocols to ensure that this is maintained. The
shaved before arriving in theatre, as this practice room must be large enough to accommodate all the
has been proven to increase the risk of postopera- personnel and equipment and to allow sufficient
tive infection. space to create an ideal sterile field. Modern stand-
In many forms of surgery, preoperative carriage ards dictate that the airflow is controlled and spe-
of Staphylococcus aureus in the nose, groin or other cifically filtered to a high standard to minimise
areas is a common risk factor for SSI. In many ser- bacterial contamination by this route. Some thea-
vices, screening for this pathogen is undertaken and tres have laminar flow to optimise this further.
Skin preparation chemical burns may result. Full‐thickness burns

have been reported. Indeed, many cases of so‐
In theatre, the surgeon has a choice between four
called iodine allergy are actually chemical burns
common skin preparation solutions, as well as
because a plastic drape has been placed over wet
some less common alternatives. The principal
alcoholic iodine preparation, keeping it in a liq-
options are aqueous preparations of chlorhexidine
uid state on the skin.
or iodine (typically povidine iodine), or solutions
• Alcoholic preparations must not be used on
of each of these agents in alcohol (typically 70%
mucous membranes, open wounds or recent inci-
ethanol in water). All these options achieve sub-
sions as chemical burns will result, even from
stantial reductions in bacterial counts on the
limited exposure.
treated skin surface. Studies demonstrate a greater
• If an alcoholic preparation is allowed to enter the
effect on pathogenic species than the normal flora.
eye, then blindness is likely to result because of
The alcohol‐based preparations achieve greater
damage to the cornea. Therefore, the surgeon who
reductions over a shorter time period. However, the
uses these alcoholic skin preparations is assuming
organisms tend to reappear over time, and can be
a serious but manageable responsibility.
cultured from the wound in increasing numbers as
Fortunately, the aqueous skin preparations may be
the operation proceeds. Phage typing has demon-
used safely without these concerns. They are clearly
strated that organisms present on the skin preop-
the preparation of choice for eye surgery, opera-
eratively are commonly the cause of postoperative
tions involving the mucous membranes or open
infections.
wounds, or for re‐operations. They may also be
There is a theoretical benefit to chlorhexidine
required for teams that cannot manage the respon-
over iodine, as chlorhexidine is still bactericidal in
sibility of alcoholic preparations.
the dry state. Iodine‐based preparations are no
longer active once they dry. Iodine is also inacti-
vated by blood, whereas chlorhexidine is not. In Surgical scrub
general, infection rates have been demonstrated to
be about 50% lower in patients receiving either of All surgical staff need to perform a surgical scrub
these alcoholic skin preparations, as compared with before gowning and gloving for the procedure. The
the aqueous solutions. Another advantage to alco- process is akin to the skin preparation of the
holic iodine is that it dries the skin and thereby patient. Each operating theatre will have its own
improves the adhesion of adhesive plastic drapes, protocols for this. The first scrub of the day should
which facilitates this style of draping. ensure a high level of cleanliness of the hands and
There are time constants involved in the bacteri- forearms including the fingernails and up to the
cidal effects of these preparations. Typically, at least elbows. The appropriate antiseptic must then be
5 minutes of contact with the wet solution is applied to these regions for the correct time period.
required to achieve optimal decontamination of the Common antiseptics are chlorhexidine 4% or povi-
skin with the alcoholic preparations. Some authori- done iodine 10% diluted in tap water. Generally,
ties advise preparation for as long as 20 minutes for the first scrub should be for 5 minutes, with 3‐min-
aqueous preparations, but this is often deemed to ute scrubs for subsequent cases, unless significant
be impractical. contamination has occurred. Alcohol‐based scrub
Unfortunately, there are serious limitations and solutions achieve a lower bacterial count than
dangers associated with alcoholic skin prepara- water‐based solutions in shorter time periods and
tions. These are real dangers that have caused seri- are therefore preferable; 90 seconds is an accepta-
ous harm to patients. The authors are aware of ble scrub time for these agents.
specific cases of each of the problems listed here.
For this reason, many hospitals have removed these
Gowning and gloving
solutions from the formulary despite their proven
benefits in infection prevention. Meticulous technique and practice are required to
• There is a risk of fire if pools of the solution are effectively utilise the closed technique as shown in
left under the patient allowing alcoholic vapours Figure 12.4. Double gloving is widely recom-
to rise and be ignited by sparks from electrical mended to reduce the risk of bacterial contamina-
cautery. tion from the hands of the staff through micropores
• If an alcoholic skin preparation is left on the or tears in the gloves. This practice also reduces the
skin in a liquid state (in pools or even just a film risk and severity of needlestick injuries to staff
under plastic) during an operation, then serious members.
(a)
(b) (c)
(d) (e)
Fig. 12.4 Closed gloving where the hands remain within the gown sleeves whilst the gloves are applied. Source: Sullivan
EM. Surgery. In: Ballweg R, Sullivan EM, Brown D, Vetrosky DT. Physician Assistant: A Guide to Clinical Practice, 5th
edn. Philadelphia: Elsevier Saunders, 2013:356–409. Reproduced with permission of Elsevier.
Surgical drapes protective layer after skin preparation and draping

has been completed.
After adequate skin preparation of a wider zone
than the anticipated operative field, surgical drapes
Preservation of the sterile field
are applied to define the operative component of
the sterile field and to cover the surrounding area. Once the sterile field is established, it should not be
Sometimes these are extensive enough to exclude left unattended. Scrubbed staff should stay close to
the non‐sterile part of the operating theatre. The the sterile field and movements by non‐scrubbed
drapes are performing a true barrier function, so staff kept to a minimum whilst surgery is in pro-
they need to be resistant to fluid strike‐through gress. This includes traffic in and out of the theatre.
and be robust enough to not tear easily but also There should be an ethos of respect to the patient
flexible enough to conform to the idiosyncrasies of that the sterile zone created for their operative
the human body. Most modern drapes are dispos- treatment is a sacrosanct zone. Indeed, it is impor-
able as opposed to the old‐fashioned linen drapes. tant that any breach of the sterile zone is dealt with
The surgical drapes are usually attached by an and rectified immediately.
adhesive backing but care must be exercised in With the establishment of the sterile field for the
their removal, especially in the elderly and infirm anaesthetised patient, and with all the essential
due to the possibility of fragile skin, which may staff and equipment ready, the operation can com-
tear readily. This includes the adhesive films which mence. Every member of the team confirms that
are often deployed for many surgeries as an extra they are ready to go and the scalpel is passed to the
surgeon in the appropriate way. During the opera- involved in the aftercare, both immediately in the
tion, noise should be kept to a low level as clear recovery room and subsequently on the ward. This
communication within the surgical team is key to includes such information such as the frequency of
safe surgery. The surgical team must be focused on observations, reportable observations using medi-
the task at hand. Some surgeons use background cal emergency team (MET) criteria, fasting status,
music to enhance the ambience of the theatre fluid management, oxygen administration, wound
and optimise their performance, but there is a risk care management, patient positioning, postopera-
that this may act as a distraction or inhibit good tive test ordering and allied health management.
communication. These orders must be enhanced by appropriate pro-
tocols prepared to underpin the teamwork between
Occupational safety in the operating theatre the surgical and postoperative teams.
One critical element is the transmission of infor-
It is essential that everyone in an operating theatre
mation about the patient’s general medical condi-
is aware of the potential occupational hazards and
tion, preoperative assessment of this, and routine
aspires to minimise their impact. The most concern-
medications. Errors of omission involving the
ing hazard is the potential for exposure to bodily
patient’s essential medications may be a significant
fluids, especially blood with the resultant risk of
source of postoperative mishap.
blood‐borne infections. The potential risks include
contracting HIV/AIDS or various forms of viral
hepatitis. The prevention of penetrating injuries by
careful attention to safe handling practices of sharp
The outer network (supporting the inner
instruments is fundamental to reducing this risk of
sanctum)
transmission. Personal protective equipment, such
Holding bay and recovery room
as appropriate eyewear, gowns, gloves and masks,
are of considerable benefit. Most operating suites will have a holding bay
There are also potential risks from X‐ray radia- where patients can be held prior to entering the
tion during intraoperative radiography, which must operating theatre proper. This is an appropriate
be prevented by the use of protective lead clothing environment for a preoperative check to ensure
and lead shielding. Lasers may cause eye damage, identity, site and side of surgery, allergies and a
so specific precautions are required when this tech- number of other basic checks.
nology is employed. The recovery room is a specialised environment
The commonest cause of workplace injuries in the staffed by specially trained nursing staff who are
operating suite are the physical forces involved in skilled in managing patients emerging from anaes-
the handling of the unconscious patient. Injuries to thesia. The first hour after surgery is a risky time,
the lumbar and cervical spine may result. It is impor- when significant medical and surgical issues may
tant that there is proper planning and personnel arise. Skilled observation by a nurse committed
resourcing for patient movement and positioning. one‐on‐one to the individual patient plays a crucial
Four people are typically required for the physical role in shepherding the patient through this chal-
work of rolling a patient to the prone position, as lenging phase. In some hospitals, a high proportion
well as two people to handle the head and the feet of patients are admitted to an intensive care envi-
respectively, and the anaesthetist must also be free to ronment for the first 12–24 hours at least, but
manage the airway during patient movement. this is substantially more expensive and is not the
common practice in Australia.
Operative recording and information
transfer Central sterile and supply department
Accurate recording of the anaesthetic, the opera- The provision of working instruments that are
tive findings and the procedure performed are properly sterilised is one of the most basic require-
essential for the care of the patient, audit of surgi- ments of modern safe surgery. The CSSD is often
cal activity and coding. There are different systems adjacent to operating theatres, and generally shares
to do this, but accuracy and detail must be a linked management structure. It must be efficient
achieved. The example in Figure 12.5 highlights and function at a very high standard.
the basic dataset required for an accurate surgical After being used, non‐disposable surgical instru-
operation note. ments must undergo prompt initial cleaning to
Furthermore, clear postoperative orders must be remove contaminants before they dry and harden.
documented to communicate clearly to the staff This may be performed by the scrub team or in the
NSN 7540-00-634-4156
MEDICAL RECORD OPERATION REPORT

PREOPERATIVE DIAGNOSIS
SURGEON FIRST ASSISTANT SECOND ASSISTANT
ANESTHETIST ANESTHETIC TIME BEGAN:

TIME ENDED:
CIRCULATING NURSE SCRUB NURSE TIME OPERATION BEGAN TIME OPERATION COM-
PLETED
OPERATIVE DIAGNOSES
DRAINS (Kind and number) SPONGE COUNT VERIFIED
MATERIAL FORWARDED TO LABORATORY FOR EXAMINATION
OPERATION PERFORMED
DESCRIPTION OF OPERATION (Type(s) of suture used, gross findings, etc.) PROSTHETIC DEVICES DATE OF OPERATION
(Lot no.)
SIGNATURE OF SURGEON DATE
PATIENT'S IDENTIFICATION (For typed or written entries give: Name - last, first, middle; REGISTER/I.D. NO. WARD NO.
grade; date hospital or medical facility)
OPERATION REPORT
Medical Record
STANDARD FORM 516 (REV. 5-83)
Prescribed by GSA/ICMR
FIRMR (41 CFR) 201-45.505
Fig. 12.5 Example of an operation note template. Source: https://www.gsa.gov/Forms/TrackForm/33055. Reproduced

with permission of General Services Administration.
CSSD. A further clean and inspection under magni- professional manner is important to avoid error,
fication then takes place in the CSSD. Once the and to reassure the patient and their family, who
instruments are clean and confirmed to be in good are likely to be anxious at that time. The postopera-
working order they are sterilised, which is the pro- tive care on the ward must be a real team effort as
cess that kills all forms of life, whether done chemi- it is a truly multidisciplinary activity. The complex-
cally or physically. Modern standards are more ity varies greatly depending on the nature of the
stringent than previously in order to kill prions surgery and the patient’s illness. Once again, the
such as CJD, as well as the standard bacteria, key aspect is good professional skills in all person-
viruses and fungi. nel and good communication in both written and
Typically, the instruments are assembled as sets, verbal formats. Accurate and clear postoperative
defined in a standard way for a variety of standard orders and agreed protocols for patient care set the
procedures. The sets of instruments are wrapped agenda. Regular review, and repeated communica-
and labelled, sterility indicators incorporated and tion between medical and nursing teams must con-
an expiry date determined. Sterilisation is then per- tinue through the postoperative phase.
formed. Stringent quality control is routine in this
process. Appropriate storage is required until the Imaging, radiography and pathology
set is used. When instruments are brought to the
Many operations are planned on the basis of a
theatre, it is essential to check that the packaging is
series of preoperative images, which may range
intact and dry and that the expiry date and the ste-
from plain X‐rays to MRI scans, angiograms or
rility indicator status are acceptable. This safety
nuclear medicine studies. For the safe performance
check of the instruments during set‐up is one of the
of the operation on the correct part of the correct
critical roles of the scout and scrub nurses.
patient, it is essential that there is a system in place
that allows secure and reliable access to imaging for
Ward nursing staff
the patient.
The ward staff, whether in a day surgical facility or In addition, intraoperative radiology using image
an inpatient ward, have a comprehensive checklist intensification (Figure 12.6) is critical to many
to run through to ensure that patients are ready to operative procedures. Examples include cholecys-
go to the operating theatre. This includes the fasting tectomy with intraoperative cholangiography, car-
status of the patient, allergy alerts, definition of the diac pacemaker insertion, spinal surgery and many
planned operation and consent. Rigorous processes orthopaedic procedures. It is essential that there be
are essential, which may be challenging in urgent clear systems of planning and communication to
situations. Conducting these checks in a highly ensure the availability of staff and equipment for
Fig. 12.6 Image intensifier system used in the operating theatre.

these procedures. Everyone in the operating theatre

must take appropriate radiation precautions and
Conclusion
wear the protection as stipulated for their own
Operating theatres are complex systems involving
protection. Similar organisation and appropriate

many staff and sophisticated equipment. The main-
precautions must also be taken with the use of radi-
tenance of the highest standards of performance
oisotopes, such as in the procedure of sentinel node
at all levels is crucial to the ultimate goal of safe
biopsy.
patient care in the operating theatre environment.
Intraoperative histopathology is sometimes
Underpinning the culture of safety must be excel-
required to assist with making a diagnosis or deter-
lent communication at all times by all the partici-
mining if the resection margin around a tumour is
pants, both within the immediate operating theatre
adequate or not. Expert pathological support and
team but also the supporting network.
the necessary communication intraoperatively to
manage and discuss the specimen may be critical to
the patient’s outcome. Again, preoperative planning
and organisation are required to ensure the availa- Further reading
bility of this resource.
The back‐up of blood bank for blood and blood Cochran A, Braga R (eds) Introduction to the Operating
products may be critical in many operations. Room. New York: McGraw‐Hill, 2017.
Furthermore, intraoperative monitoring of the Fuller JK (ed.) Surgical Technology: Principles and
Practice, 7th edn. St. Louis, MO: Elsevier, 2017.
patient’s biochemical, haematological, coagulation
Woodhead K, Fudge L (eds) Manual of Perioperative Care:
and blood gas parameters is important in many
An Essential Guide. Oxford: Wiley Blackwell, 2012.
complex and prolonged procedures. There is an
increasing trend towards so‐called point‐of‐care
testing to simplify much of this and provide imme-
diate information about the patient’s status, effec- MCQs
tively in real time. This facilitates enhanced patient
safety.
Hospital administration
1 John is a normal 19‐year‐old man who presents to
Organising for a patient to have an operation is a the emergency department with right iliac fossa
complex undertaking and requires robust secure pain, and a temperature of 37.5°C. He looks mildly
systems and many personnel. To open and staff a unwell. The surgical diagnosis is acute appendicitis
theatre with no extras costs about A$1000/hour; and appendicectomy is advised. Regarding consent:
adding extra complex equipment increases the costs a consent is not necessary because this is an
dramatically. The role of hospital and surgical emergency
department administration in securing and con- b full surgical consent is obtained from John in the
firming funding, and managing all this cannot be emergency department, with proper discussion
underestimated. of possible complications, alternate treatment
The introduction of new procedures, devices and options, etc.
techniques requires a clear governance process c it is not necessary to disclose who will be doing
overseen by the hospital administration, as it is ulti- the operation because he is a public patient
mately accountable for patient welfare. It is essen- d full surgical consent should be obtained from his
tial that the health service administration works parents, with proper discussion of possible
with the operating theatre teams to maximise the complications, alternate treatment options, etc.
value for the funding dollar. Quality assurance must because he is under 21 years of age
occur through audit of patient outcomes, as well as e full surgical consent is obtained from John when
case reviews at morbidity and mortality meetings. he arrives in theatre, with proper discussion of
Variations in care and outcomes require governance possible complications, alternate treatment
mechanisms to assure everyone, but especially options, etc.
patients and their families, that the highest stand-
ards of surgical care are being pursued and main- 2 The most important aim of the surgical team
tained. The monitoring of SSI rates is a prime but time‐out is:
simple example of measuring how well a system of a financial consent and checking of insurance
surgical care is functioning and being maintained. status
b building teamwork and common goals within the c open the wound immediately to look for the
broader surgical team missing patty
c checking that the patient is fit for surgery and d request an image intensifier to take an X‐ray to
anaesthesia see if the missing patty can be seen in the wound
d checking contact details of the next of kin e close the wound and take the patient for
e verifying the correct patient and procedure with an urgent CT scan, keeping them under
identification of the site and side of surgery anaesthesia to allow return to theatre to find the
missing patty if it can be seen inside the head
3 The risks of aqueous povidine iodine skin
preparations include: 5 The most common cause of surgical site infection
a fire in clean elective orthopaedic surgery in a modern
b chemical burns of the skin operating theatre is:
c blindness a the organisms present in the nostrils of the
d wound infection surgical team
e none of the above b the organisms present on the hands of the
surgical team
4 You have just closed the wound after a long and c the organisms present on the anaesthetists
challenging open craniotomy for removal of a large d the organisms present on the skin of the patient
meningioma. The scrub nurse informs you that prior to surgery
there is a surgical patty missing. What is the e the organisms present on the surgical instruments
optimal response? or prostheses
a inform the nurse that you checked for patties
before closing so it is not possible that one could 6 It is possible to sterilise which of the following:
have been left inside; you then proceed to place a the patient’s skin where the surgical wound will
dressings and ask the anaesthetist to wake the be incised
patient b the surgical assistant
b pause and take a short break while the nurse c the surgical instruments
performs a repeat count to see if an error may d the hands of the surgeon provided that they
have occurred, and then undertake a search of glove correctly
all possible places where a patty could be hidden e all of the above
13 Emergency general surgery
Benjamin N.J. Thomson1,2 and Rose Shakerian2
1
2
Royal Melbourne Hospital, Melbourne, Victoria, Australia
some surgeons would not routinely manage abdom-

Introduction inal conditions. The emergency work was in
competition with elective surgery and endoscopy
In Victoria, Australia, during the year 2010–2011,
lists, as well as outpatient services. Surgical trainees
24% of all surgical admissions were emergency surgi-
in consultation with the on‐call consultant most
cal admissions. In some of the large metropolitan hos-
frequently led the traditional model.
pitals the emergency surgery caseload can be as high
as 38%. This increase in emergency surgery workload
is not limited to Australia, with similar proportions Emergency general surgery models
and increases reported in Europe and the USA.
Emergency general surgery admissions account The main features of emergency general surgical
for over 50% of total admissions in general surgery models of care include the separation of elective
departments in public hospitals in Australia. In the and emergency work, consultant‐led care, robust
year 2015–2016, the Royal Melbourne Hospital handover and trainee supervision. The model is spe-
Department of General Surgical Specialties admit- cific to each hospital and depends on the patient
ted 7298 patients, with 4936 (68%) emergency volume, case mix, complexity and available
general surgery and trauma admissions. An emer- resources. Consultant‐led care is also a critical com-
gency general surgery patient is defined by the ponent, allowing for proven benefits of improved
American Association for the Surgery of Trauma patient care, teaching and better utilisation of radi-
(AAST) as ‘any patient requiring an emergency sur- ological investigations. Various names exist for the
gical evaluation for disease within the realm of gen- models, including emergency general surgery (EGS)
eral surgery’. It has been estimated that emergencies services, acute care surgery (ACS) units and acute
in general surgery account for 80–90% of general surgical units (ASUs). The on‐call period for each
surgical deaths. Furthermore, complication rates in consultant surgeon may be 24 hours up to 7 days.
emergency surgery exceed those of a similar elective The first specialised emergency surgical units
procedure by twofold to fourfold. were designed for trauma care and started at the
Birmingham Accident Hospital in the UK in 1947.
In the USA the first shock trauma centers opened in
Traditional models of emergency general Chicago and Baltimore in 1966. Meta‐analysis of
surgery care the comparison of patient care before and after the
formation of trauma centres and systems demon-
Individual general surgical units who manage both strated a 15% reduction in mortality.
elective and emergency surgery patients without The concept of consultant‐led care for emergency
dedicated resources characterised the traditional general surgical patients originated in the UK, fol-
model of care for emergency general surgery lowing the National Confidential Enquiry in Patient
patients. These resources included dedicated surgi- Outcome and Death (NCEPOD) that demonstrated
cal staff, wards and theatre access. Emergency poor outcomes for emergency surgery patients
admissions were managed by general surgical units undergoing operative procedures by junior surgical
on a rotating on‐call roster. This would result in staff. This in part led to the development of ASUs
patients being admitted to subspecialty units where in the UK.
109
In Australia, trauma centers have been the main- Not all emergency general surgical procedures
stay of trauma care since the late 1990s. The rede- require surgical intervention. The commonest surgi-
sign of emergency general surgery services was led cal intervention remains appendicectomy and along
by a number of bodies that included the relevant with cholecystectomy, laparotomy and perianal
state departments of health, the Royal Australasian surgery these four surgical groups account for more
College of Surgeons and General Surgeons Australia. than 50% of surgical interventions (Table 13.2).
The impact of subspecialty training has also been The overall 30‐day mortality for emergency general
problematic because it has often limited the expo- surgery patients is around 4%, with an increasing
sure to emergency surgery, with many surgeons con- mortality rate with age.
sequently believing that they lack the required skills Laparotomy is a common general surgical opera-
to manage acute general surgical admissions. tion accounting for 12.5% of surgical procedures
There have been many studies from the USA, at the Royal Melbourne Hospital. In the UK, 30
Europe, Australia and New Zealand that report sig- 000–50 000 laparotomies are performed per year. It
nificant improvements in the care of emergency carries a significant risk of morbidity and mortality.
general surgical patients, with a reduction in mor- The initial Emergency Laparotomy Network
tality, morbidity, length of stay, time to surgery,
emergency department length of stay and out‐of‐
hours theatre. From a workforce perspective, the Table 13.2 Common emergency general surgical
impact has included increased access to training operations*.
opportunities for surgical trainees, increased con-
Procedure Percentage
sultant supervision in theatre, a reduction in on‐call
commitments and a reduction in workload. Appendicectomy 29.7
Cholecystectomy 13.2
Laparotomy 12.5
Emergency general surgical disorders Perianal abscess/pilonidal 10.1
abscess/anal fistula
Wound debridement/soft 8.4
The majority of emergency general surgical admis-
tissue abscess
sions are for abdominal complaints (Table 13.1). In
Hernia repair 4.7
comparison to elective surgical admissions, emer- Other 21.3
gency general surgical patients are older with higher
rates of comorbidities, such as hypertension, dys- * These data relate to 1804 emergency general surgical
lipidaemia, type 2 diabetes mellitus and renal operations over a 2‐year period at the Royal
impairment. Melbourne Hospital.
Table 13.1 Emergency general surgical admissions*.
Admission diagnosis Percentage Chapters
Non‐specific abdominal pain 12.5 68

Acute appendicitis 11.9 28
Biliary disease 8.1 19
Perianal/pilonidal disease 4.9 34
Constipation 4.9 63
Acute pancreatitis 4.7 22
Diverticular disease/diverticulitis 4.3 30
Intestinal obstruction 4.0 26, 31, 32
Gastritis/colitis/gastroenteritis 3.7 16, 29
Skin and soft tissue infection 3.4 46
Gastrointestinal bleeding 2.8 16, 17, 65, 66
Gynaecological 2.1 68
Hernia 1.9 43
Urological 1.0 59
Other 32.9
* These data relate to 4468 admissions to the Royal Melbourne Hospital over a
2‐year period, with corresponding references to other chapters in this book.
13: Emergency general surgery 111
prospective study of 1853 patients reported a 30‐ Paterson‐Brown S, Paterson HM (eds) A Companion to
day mortality of 14.9%, whilst the American Specialist Surgical Practice: Core Topics in General and
College of Surgeons National Surgical Quality Emergency Surgery, 6th edn. Edinburgh: Elsevier, 2019.
Improvement Program (NSQIP) database of 37 553 Shakerian R, Thomson BN, Gorelik A, Hayes IP,
Skandarajah AR. Outcomes in emergency general sur-
patients reported a 30‐day mortality of 14% during
gery following the introduction of a consultant‐led unit.
2005–2009. The various surgical pathologies neces-
Br J Surg 2015;102:1726–32.
sitating surgery are wide‐ranging and include pep-
tic ulcer disease, diverticulitis, small bowel
obstruction, large bowel obstruction and trauma. MCQs
Non‐specific abdominal pain comprises the
majority of general surgical emergency admissions, Select the single correct answer to each question. The
accounting for 13–40% of admissions in the UK. correct answers can be found in the Answers section
The diagnosis is made after appropriate assessment at the end of the book.
and investigation of a patient, with a diagnosis
unable to be reached in a small percentage. The 1 Emergency general surgical patients:
majority of patients will settle within 2 weeks of a have a lower rate of morbidity compared with
onset of pain. elective general surgical admissions
Causes of abdominal pain that may be missed b have a higher mortality rate compared with
include intra‐abdominal malignancy and, in par- elective general surgical admissions
ticular, colon cancer. Other diagnoses include irrita- c only account for a small proportion of admissions
ble bowel syndrome, viral infections, gastroenteritis d can be adequately managed without specialised
and acute gynaecological conditions such as pelvic emergency general surgical units
inflammatory disease and ovarian cysts. Far less e all of the above
frequently, medical conditions such as myocardial
infarction, diabetic ketoacidosis and pneumonia 2 Common emergency general surgical procedures
may present with abdominal pain. include:
Abdominal wall pain is also a common cause for a appendicectomy
abdominal pain due to iatrogenic nerve injuries, b laparotomy
occult hernias, myofascial pain syndromes, rib c abscess drainage
pathology, nerve root pain or rectus sheath d cholecystectomy
haematoma. e all of the above
3 Non‐specific abdominal pain is:

Further reading a a failure to make a diagnosis
b usually caused by appendicitis
General Surgeons Australia (GSA). 12 Point Plan for c the commonest reason for admission to an
Emergency General Surgery. GSA, Melbourne, Australia, emergency general surgical unit
2010. Available at https://www.generalsurgeons.com. d best treated with opiate analgesia
au/media/files/Publications/PLN%202010‐09‐19%20 e usually leads to a chronic abdominal pain
GSA%2012%20Point%20Plan.pdf syndrome
Section 2
Upper Gastrointestinal Surgery
14 Gastro‐oesophageal reflux
disease and hiatus hernias
Paul Burton and Geraldine J. Ooi
Monash University and Alfred Health, Melbourne, Victoria, Australia
Introduction Surgical anatomy and physiology
Gastro‐oesophageal reflux disease (GORD) is The oesophagus is an approximately 25‐cm long

defined as ‘symptoms or complications resulting muscular tube that runs from the upper oesopha-
from the reflux of gastric contents into the oesoph- geal sphincter, passing through the thoracic cavity,
agus or beyond, into the oral cavity (including lar- then via the oesophageal hiatus in the diaphragm to
ynx) or lung’.1 GORD is one the most common intersect the gastric cardia. Above the intersection
diseases in Western societies. It is responsible for with the cardia, the intrinsic lower oesophageal
substantial symptoms, impairment in quality of life, sphincter (LOS), a thickening of oesophageal circu-
results in significant healthcare costs as well as lost lar smooth muscle, protects the lower oesophagus
work time and is an important risk factor for from reflux.
oesophageal adenocarcinoma. The LOS can actually be thought of as a com-
It is important to note that some reflux of gastric plex. The smooth muscle component is reinforced
contents into the oesophagus probably occurs by the diaphragmatic crura, hiatal canal and
intermittently in everyone, particularly after eating. phreno‐oesophageal ligament. These components
When this occurs excessively and there is damage work synergistically to provide an optimal barrier
to the mucosa and/or significant symptoms develop, to reflux. The intrinsic LOS remains tonically con-
it is referred to as GORD. Around 10–15% of the tracted, preventing reflux. When food is swallowed
population have significant symptoms and many it opens in a coordinated fashion to allow the food
more have intermittent symptoms. bolus into the stomach.
In practical terms it is when we become aware of
it, usually because of symptoms of burning retros-
ternal pain (heartburn) and/or regurgitation of con- Aetiology/pathogenesis of GORD
tents into the mouth or excessive, intense salivation
(water brash) that we call the condition GORD and The precise reasons why gastro‐oesophageal reflux
think of it as a medical disorder. develops is unknown, but it certainly appears to be
Another important point is to differentiate a hia- a disease associated with the western lifestyle, and
tus hernia from GORD, although these terms are most clinicians believe that overeating, obesity,
frequently confused. Certain types of hiatus hernia alcohol and smoking are important factors.
promote reflux. However, the presence of a hiatus The pathophysiology of reflux predominantly
hernia is by no means representative of reflux dis- relates to events known as transient lower oesopha-
ease. Additionally, hiatus hernias can cause prob- geal sphincter relaxations. Several times every hour
lems, sometimes severe, that are not related to the LOS relaxes, allowing the stomach to vent air.
reflux. This is not consciously controlled and people are
1
Vakil N, van Zanten SV, Kahrilas P, Dent J, Jones R. The Montreal definition and classification of gastroesophageal
reflux disease: a global evidence‐based consensus. Am J Gastroenterol 2006;101:1900–20.
115
116 Upper Gastrointestinal Surgery
unaware of this happening. Reflux of gastric juice

into the oesophagus can occur during these relaxa-
Complications of gastro‐oesophageal
tions. Another factor that favours reflux is separa-
reflux
tion of the LOS from the crural diaphragm as in a
Chronic irritation of the lower oesophageal mucosa
sliding hiatus hernia. Weakness of the intrinsic LOS
due to refluxed gastric juice can lead to severe
can also occur, reducing the barrier function of the
problems. Prior to widespread availability of pow-
sphincter.
erful acid‐suppressing medication, significant com-
Other specific factors that may influence reflux
plications were far more common.
include increased intra‐abdominal pressure (preg-
Severe oesophagitis and oesophageal ulcers rep-
nancy or central obesity). Reflux occurs after meals
resent an advanced form of reflux and can result in
because there is hypersecretion of acid and a thin
chronic blood loss and anaemia. If reflux is severe
layer of concentrated acid appears immediately
and long‐standing, the inflammatory process and
beneath the oesophago‐gastric junction. A delay in
healing is associated with the development of
gastric emptying may also be a factor in increasing
fibrous tissue. If enough fibrous tissue forms, like
reflux.
any scar it will contract, leading to narrowing of
the oesophageal lumen. Patients can have dyspha-
Surgical pathology gia as a result.
Spillover of refluxate can be aspirated via the lar-
Most patients with GORD have normal oesopha- ynx into the lungs. This can result in chronic cough,
geal mucosa. In severe forms of the disease mucosal lung infection and even lung abscess in extreme
erosions can occur. Erosive oesophagitis is thought cases. This is usually associated with specific situa-
to be primarily due to the low pH of gastric fluid tions where there is a large volume of reflux and
contacting oesophageal mucosa. It is also likely at impaired protective reflexes.
times that bile and other enzymes contribute to the
mucosal injury. Barrett’s oesophagus
Oesophagitis is graded according to the Los
Angeles classification (grade A, B, C and D), with A In a small proportion of patients, the oesophageal
representing the presence of damage of the least mucosa responds to reflux by replacing the squa-
severity and D representing disease of the highest mous mucosa with columnar mucosa, a process
severity. Figure 14.1 shows an example of erosive known as intestinal metaplasia or Barrett’s oesoph-
oesophagitis. agus. The significance of Barrett’s oesophagus
relates to its status as a premalignant condition,
thought to be the precursor of oesophageal
adenocarcinoma.
Obesity and reflux
Obesity is a significant risk factor for reflux.
Increased intra‐abdominal fat raises intra‐abdomi-
nal pressure, thereby favouring reflux due to an
increased pressure gradient between the intra‐
abdominal stomach and intrathoracic oesophagus.
Obesity independently increases transient LOS
relaxations. Given the epidemic of obesity, there are
not surprisingly many obese patients with GORD.
Hiatus hernias
Fig. 14.1 Endoscopic photograph of erosive oesophagitis
in the lower oesophagus. The black arrow indicates
gastric mucosa projecting above the level of the
A hiatus hernia is present where there is projection
diaphragm as a sliding (type I) hiatus hernia. The white of the stomach more than 2 cm into the mediastinum,
arrow indicates the diaphragm. Regions of erosive above the diaphragm. In the normal situation there
oesophagitis (LA grade A) can be seen, where the pale is 2–3 cm of oesophagus within the abdominal
oesophageal mucosa has been eroded due to reflux (E). cavity.
14: Gastro-oesophageal reflux disease and hiatus hernias 117
Hiatus hernias are subdivided into three different Common symptoms of para‐oesophageal hernias
types. include pain and discomfort after meals, probably
• Type I hiatus hernias are the most common and associated with intermittent twisting and partial
often asymptomatic. These hernias are present obstruction of the stomach. Patients can have some
when the LOS is located greater than 2 cm above reflux symptoms, but that is usually not the major
the diaphragm. They are also called sliding her- problem. Despite their size, para‐oesophageal hia-
nias, because the LOS has slid vertically up above tus hernias are occasionally asymptomatic. If the
the diaphragm. This predisposes to reflux by dis- hernia is asymptomatic, then it seems reasonable to
rupting the coordinated effect of the LOS com- leave it, instructing the patient to seek urgent medi-
plex. Additionally, it creates a positive pressure cal attention if pain and/or vomiting should
gradient from the higher pressure intra‐abdomi- develop.
nal stomach to the lower pressure intrathoracic Stasis and possibly mechanical trauma in the
LOS, favouring reflux. intrathoracic stomach can result in chronic blood
• Type II hiatus hernias occur when the LOS remains loss due to linear erosions of the stomach at the
within the abdomen and the greater curve of the level of the diaphragm, known as Cameron’s ulcers.
stomach ‘rolls up’ into the mediastinum through Patients sometimes present as an acute emergency,
the oesophageal hiatus. This type of hernia is called with obstruction of the hernia, where the stomach
para‐oesophageal, as the hernia occurs alongside twists and patients are unable to eat because the
the oesophagus. These hernias can sometimes be stomach has twisted. In extreme cases of obstruc-
huge and involve virtually all the stomach. Other tion, the stomach can occlude its own blood supply,
organs such as the transverse colon and spleen can becoming strangulated.
be present in very large hiatus hernias. Figure 14.2
shows a CT image of a type II hiatus hernia.
• Type III hiatus hernias are mixed hernias, with Clinical presentation of GORD
components of both sliding and para‐oesopha-
geal hernia (Figure 14.3). Most hernias, where The majority of patients with GORD present with
there is a significant portion of the stomach in heartburn, a sensation of retrosternal burning pain,
the mediastinum, are type III rather than type II, usually occurring after eating, with particular foods
as the LOS has migrated upwards slightly rather (spicy, rich or fatty food as well as chocolate, wine
than staying fixed within the abdomen. or caffeine) more likely to provoke symptoms.
(a) (b)
Fig. 14.2 Large type II hiatus hernia. Coronal CT scans of the same patient taken 4 weeks apart. (a) A large
uncomplicated hiatus hernia can be seen, with almost all the stomach (S) in the mediastinum, above the diaphragm
(thick arrow). (b) The hernia has become obstructed and grossly distended, with substantial food residue within the
stomach (yellow arrow). Gas is also noted in the gastric wall (white arrow). This patient required emergency surgery
and a total gastrectomy to remove the infarcted stomach.
Fig. 14.3 Barium swallow demonstrating a type III hiatus hernia (mixed sliding and para‐oesophageal components).
The images are in the lateral projection. The oesophagus (O) can be seen above the diaphragm. The lower oesophageal
sphincter (A) is seen above the diaphragm and the stomach (S) has ‘rolled up’ into the mediastinum. Barium (B) can be
seen flowing into the stomach below the diaphragm. In the second frame (right), the lower oesophageal sphincter is
relaxing to allow barium to pass into the stomach (C).
Symptoms are typically episodic and may wax and Endoscopy should be considered in patients
wane over many years. Often, over a period of 6–8 with symptoms that persist despite compliance
weeks symptoms are significant then may gradually with 4–8 weeks of twice‐daily proton‐pump inhib-
recede. itor (PPI) therapy. If patients respond appropri-
Symptoms of reflux can usually be classified into ately to acid suppressive therapy and do not
typical symptoms (those that have a high likelihood manifest alarm symptoms, endoscopic evaluation
of association with reflux) and atypical (those that is not deemed necessary, except for men older than
have a lower likelihood of association with reflux). 50 years with chronic symptoms (>5 years) and
Typical symptoms can be further divided into irri- additional risk factors, such as nocturnal reflux,
tant and volume symptoms. Irritant symptoms are elevated body mass index, tobacco use and family
primarily heartburn. Volume symptoms include history of Barrett’s oesophagus or oesophageal
regurgitation of liquid or semi‐digested food in a adenocarcinoma.
passive manner, which may occur on exertion or If erosive oesophagitis is found, further investiga-
when leaning forward. Nocturnal regurgitation can tion is not usually warranted. If the patient has a
be particularly troublesome and frightening for normal oesophagus on endoscopy, then 24‐hour
patients as they may awake choking. pH monitoring can be performed to obtain a more
Atypical symptoms include chest pain, dyspepsia, specific assessment and diagnosis of reflux.
epigastric pain, nausea, bloating and belching as
well as extra‐oesophageal manifestations such as
chronic cough, a hoarse voice or sore throat. These Oesophageal manometry
symptoms may or may not be attributable to reflux. Oesophageal manometry is performed to evaluate
the function of the oesophagus. In particular, the
strength and coordination of peristalsis and the
Investigation of GORD tone and relaxation of the LOS are measured.
Surgeons very frequently perform manometry prior
The great majority of patients with reflux either to anti‐reflux surgery to exclude a significant prob-
never go to the doctor with their problem, or are lem with contraction of the oesophageal muscle
relatively simply treated with medication and that may impact surgery or to establish an alterna-
changes to their lifestyle. tive diagnosis such as achalasia.
Which patients should be investigated further? Manometry is often performed prior to 24‐
Patients with typical heartburn that can be treated hour pH monitoring to determine the location of
easily do not require further investigation. Some the LOS and thereby guide placement of the
symptoms are so‐called alarm symptoms and when pH probe. Oesophageal manometry involves
a patient presents with dysphagia, haematemesis, placement of a thin tube, via the nose, into the
weight loss or anaemia, urgent investigation with oesophagus and thence into the top of the stom-
endoscopy is usually required. ach. Pressure measurements can then be taken
(a) (b)
Time
Fig. 14.4 High‐resolution manometry trace displayed as a line plot (a) and spatiotemporal plot (b). This manometry
plot was taken from a patient in quiet respiration, aiming to assess the function of the lower oesophageal sphincter over
several respiratory cycles. The line plot displays a series of pressure measurements over time. Each line represents data
from a single pressure sensor. Data presented in this way is very difficult to interpret. In the spatiotemporal plot,
distance from the nares is on the y‐axis, time on the x‐axis and different pressures are represented by different colours
(scale on right of image). The respiratory cycle can be seen, with deeper blue (I) representing lower intrathoracic
pressure during inspiration and lighter blue expiration (E). The yellow and pink colours around a depth of 46–48 cm
represent the lower oesophageal sphincter and diaphragm. The thick black arrow indicates high pressure at the
diaphragm due to inspiration and the thin arrow the intrinsic lower oesophageal sphincter pressure during expiration.
along the tube, which has a series of pressure sen- provided from 24‐hour pH monitoring is very
sors along its length. important in making treatment decisions, particu-
Figure 14.4 demonstrates an oesophageal larly if surgery is being considered.
manometry plot in the resting phase. Manometry This test involves passage of a fine tube through
data are displayed as a spatiotemporal colour plot, the nose into the oesophagus (with the sensor
where pressure, time and depth data (distance located in the oesophagus, 5 cm above the top of
from the nose) are displayed. The spatiotemporal the LOS). The sensor detects changes in pH and,
plot is similar to a topographical map, where col- more frequently now, flow of fluid can be measured
ours may represent different heights of terrain. As using changes in impedance (resistance) along the
often 30–40 sensors (more than 16 sensors repre- tube. The sensor remains in place for 24 hours.
sents high‐resolution manometry) are placed on In most laboratories, over 24 hours, the normal
the manometry catheter, it is very difficult to inter- value for percentage time spent with pH below 4 in
pret the data collectively if they are displayed as the oesophagus is 4% or less. If more than 50% of
individual line traces. Spatiotemporal presentation reported symptoms are correlated with a period of
of data allows an overview to be obtained at a oesophageal acid exposure (pH <4), the symptoms
glance. Computerised algorithms aid greatly in the are considered to be due to reflux and a diagnosis
interpretation of high‐resolution oesophageal of GORD made. A 24‐hour pH trace is shown in
manometry. Figure 14.5.
Twenty‐four‐hour pH monitoring Imaging investigations

Twenty‐four‐hour pH monitoring (now usually Barium swallow is a simple investigation but has a
also incorporating impedance monitoring) is con- limited role in simple reflux, although it is an accu-
sidered the gold standard for assessing and quanti- rate means of assessing hiatus hernias. Radiopaque
fying GORD. This is because it provides an objective barium is swallowed, and the outline of the oesoph-
measure of the amount of reflux and the pattern of agus can be identified using fluoroscopy. Figure 14.3
reflux over a 24‐hour period. Additionally, when shows a barium swallow of a type II hiatus hernia.
patients experience symptoms, they can be recorded Computed topography (see Figure 14.2) provides
and it can then be determined whether that symp- better anatomical delineation, particularly of large
tom correlated with a reflux event. The information hiatus hernias. This allows quantification of the
pH>4.0
pH<4.0
19:50:00 20:06:40
Heartburn
Acid reflux
Fig. 14.5 Recording from a 24‐hour pH monitoring test. The line trace is a simple graph over time, in this case a
25‐minute period. It represents a continuous measure of pH, 5 cm above the top of the lower oesophageal sphincter.
In this snapshot the horizontal line represents a pH of 4. A series of dips in pH below this level represent reflux events.
Importantly, the red and blue coloured vertical lines represent reported symptoms by the patient (heartburn and acid
reflux). Symptoms closely correlated with dips in pH to less than 4, suggesting that reflux is responsible for the
symptoms.
extent of stomach or other organs herniating into A range of medications are commonly used to
the mediastinum and aids in operative planning. treat GORD and many are available over the coun-
Nuclear scintigraphy is a functional test that ter without a prescription. These medications are
involves the patient consuming a radiolabelled more likely to be effective in improving irritant
semi‐solid meal such as porridge. The presence of symptoms of reflux such as heartburn. The three
reflux can be seen over several hours and gastric most common categories of medication are antac-
emptying assessed (as delayed gastric emptying can ids, histamine H2 receptor antagonists and PPIs.
be a precipitating factor of GORD). Antacids are essentially buffers that aim to coat
the lining of the oesophagus and stomach, thereby
Upper gastrointestinal endoscopy protecting the mucosa. They have rapid onset and
offset of action. Antacids contain specific com-
Upper gastrointestinal endoscopy involves passage
pounds such as calcium carbonate.
of a flexible tube via the mouth into the oesophagus
Histamine H2 receptor antagonists are effective
and stomach. Images are then transmitted to a
acid‐suppressing medications. These work via
screen, frequently in high definition. Endoscopy has
inhibition of histamine at H2 receptors, thereby

the advantage of being able to visualise the mucosa
reducing gastric acid secretion. They have a rapid
(see Figure 14.1) and inspect for changes of reflux
onset of action and may work particularly well
oesophagitis as well as identify other mucosal prob-
overnight.
lems such as Barrett’s oesophagus. Endoscopy is
PPIs are the most powerful acid‐suppressing medi-
usually performed in a sedated patient or under
cations available. They work by blocking the parietal
local anaesthesia. It allows direct sampling of the
cell proton pump (H+/K+ exchange pump), prevent-
mucosa with biopsies.
ing secretion of H+ ions into the gastric lumen. Very
effective acid suppression is achieved. These medica-
Treatment of gastro‐oesophageal reflux tions have a slower onset of action and should be
taken daily to maintain acid suppression.
As many people experience reflux, initial advice The advantage of drug therapy is its simplicity
would usually centre around lifestyle change. and efficacy. In severe GORD, medication may be
Changes advocated include improvement in diet, required long term and there are potentially adverse
avoiding trigger foods, not eating immediately prior effects of taking medications for many years. If vol-
to going to bed, obtaining regular exercise or mod- ume or atypical symptoms are the major problem,
est weight loss, smoking cessation and reduction in medications are less effective because they do not
alcohol intake. stop gastro‐oesophageal reflux occurring.
is usually a more significant undertaking. The major

Surgery problem is breakdown of the phreno‐oesophageal
ligament and widening of the oesophageal hiatus.
Surgery is a generally safe and highly effective treat-
The operation aims to reposition the stomach within
ment for chronic GORD. It is usually considered in
the abdominal cavity. Additionally, the oesophageal
patients with more severe disease, affecting health
hiatus needs to be repaired and reduced to a normal
and disrupting quality of life. Indications for sur-
size to prevent recurrent herniation. Repair can be
gery include non‐response to lifestyle change or
performed with sutures or mesh.
medication, volume symptoms, breakthrough
symptoms despite maximal medical therapy and
patient reluctance to take medications longer term.
Bariatric surgery in patients with GORD
Obesity and reflux are closely associated, and
Fundoplication therefore performing a procedure that can control
This is generally a simple laparoscopic procedure reflux and achieve substantial weight loss has con-
with a hospital stay of one to two nights. In a fun- siderable attraction. There are several bariatric
doplication any hiatus hernia (even small) is repaired surgery options available: Roux‐en‐Y gastric
with sutures. The fundus of the stomach is then bypass (RYGB), gastric banding and sleeve gas-
wrapped around the lower oesophagus. Effectively, trectomy. RYGB is a highly effective and durable
this creates a one‐way valve. Physiologically, the LOS option that effectively controls reflux.
resting pressure increases and transient LOS relaxa- Laparoscopic adjustable gastric banding (LAGB)
tions are eliminated. Importantly, surgery almost is an effective anti‐reflux procedure; however, in
completely stops reflux, rather than just reducing situations where there is dilatation above the
symptoms which is achieved with medication. LAGB, reflux may develop. Sleeve gastrectomy is
Over 90% of patients are extremely satisfied the most commonly performed bariatric surgical
with the results of surgery and would be willing to procedure but is considered to have a higher inci-
do it again. Recent data suggest that 20 years fol- dence of reflux following surgery.
lowing surgery most patients have achieved and
sustained an excellent outcome from surgery.
Patients undergoing laparoscopic fundoplication Further reading
should also be aware that there are (uncommon)
perioperative risks, including infections, bleeding Engstrom C, Cai W, Irvine T et al. Twenty years of experi-
splenic injury and oesophageal perforation. There is ence with laparoscopic anti‐reflux surgery. Br J Surg
an approximately 2% conversion rate to open 2012;99:1415–21.
operation because of difficulties that may be Keung C, Hebbard G. The management of gastro‐oesoph-
encountered during the laparoscopic procedure. ageal reflux disease. Aust Prescr 2016;39:6–10. Full
Complications specific to fundoplication are usu- text free online at www.australianprescriber.com
Mikami DJ, Murayama KM. Physiology and pathogenesis
ally related to dysphagia, which occurs if the proce-
of gastroesophageal reflux disease. Surg Clin North Am
dure is made too ‘tight’. In some patients, the wrap
2015;95:515–25.
seems to break down with time and the incidence of
recurrent reflux is about 15% over many years. It is
possible to undertake further surgery in such cir-
cumstances, although it is usually more difficult the MCQs
second time around.
Postoperative management is relatively standard, Select the single correct answer to each question. The
with oral fluids being commenced immediately, and correct answers can be found in the Answers section
a soft diet introduced when the patient can tolerate at the end of the book.
it. Patients are advised to refrain from anything that
1 Which of the following is not considered an alarm
raises their intra‐abdominal pressure to high levels
symptom requiring urgent investigation in a patient
(such as heavy lifting) for about 8 weeks, to allow
presenting with reflux symptoms?
the hiatus to adequately seal with fibrous tissue.
a large hiatus hernia
b dysphagia
Hiatus hernia repair
c haematemesis
This operation is very similar to a fundoplication, d weight loss
but is used to treat a type II or III hiatus hernia and e anaemia
2 Initial assessment and management of a patient b bariatric surgery should not be performed in a
with suspected GORD should not include: patient with a large hiatus hernia
a history and examination c very few patients have type II hiatus hernias
b endoscopy d oesophageal manometry and pH testing are
c lifestyle advice required prior to operative repair of types II and
d evaluation of risk for oesophageal cancer III hiatus hernias
e consideration of treatment with medication e Barrett’s oesophagus is commonly associated
with a hiatus hernia
3 Which of the following is true concerning hiatus
hernias?
a patients with sliding hiatus hernias generally
have reflux
15 Tumours of the oesophagus
Ahmad Aly1,2 and Jonathan Foo2
1
2
Austin Health, Melbourne, Victoria, Australia
subtypes include adenosquamous carcinoma, neu-

Types of tumour roendocrine carcinomas, melanomas, lymphomas,
sarcomas, small cell carcinomas and adenoid cystic
Benign carcinoma.
Benign oesophageal tumours are rare and account The prevalence of squamous cell carcinoma and
for less than 1% of all oesophageal neoplasms. adenocarcinoma depends on the prevailing risk fac-
Leiomyomas account for two‐thirds of these and tors in differing regions of the world. Geographically,
arise from the muscularis propria or muscularis squamous cell carcinoma has a 50‐ to 100‐fold
mucosa. These smooth muscle tumours are often greater incidence in high‐risk areas compared with
solitary, indolent and with an intact overlying the rest of the world. For example, in Henan Province,
mucosa. There are only rare case reports that China the incidence rate is over 160 per 100 000
describe progression to leiomyosarcoma. compared with 2–3 per 100 000 in North America,
Small leiomyomas are often asymptomatic and Australia and Europe. While the most predominant
found on routine imaging or endoscopy. As they histological subtype worldwide is squamous cell car-
increase in size or have an annular configuration cinoma, adenocarcinoma is much more common in
they may cause dysphagia. If symptomatic or large the western world and is increasing in incidence, for
(>5 cm) excision should be considered. Rather than example in the USA the incidence has increased from
a formal oesophageal resection, these firm and 3.6 per million in 1973 to 25.6 per million in 2006.
well‐encapsulated masses can often be surgically Geographical differences and changing distribu-
enucleated via either an open or minimally invasive tion over time relate to changes in risk factors
approach. On occasion, leiomyomas may be very (Box 15.1). Patients with other aerodigestive malig-
large and necessitate formal resection such as nancies have a 5–8% risk of developing synchro-
oesophagectomy (Figure 15.1). nous or metachronous oesophageal squamous
Other rarer entities include schwannomas, tumours, probably because of exposure to the same
epithelial polyps, haemangiomas, granular cell
environmental carcinogens and the phenomenon of
tumours and duplication cysts. While gastrointesti- ‘field change’. While smoking and alcohol induce
nal stromal tumours are found in the oesophagus, chronic oesophageal inflammation, this plays a
their presence in the oeosphagus is rare in compari- much smaller role in the aetiology of adenocarci-
son with other parts of the gastrointestinal system. noma compared with squamous cell carcinoma.
Instead obesity, particularly with an intra‐
abdominal distribution of fat and the associated
Malignant
gastro‐oesophageal reflux‐induced acid and bile
Oesophageal cancer is the ninth most common can- injury to the distal oeosphagus, is a more promi-
cer worldwide; in Australia around 1400 people nent risk factor. The injured oesophageal tissue
per year are diagnosed with oesophageal cancer. adapts, via an unknown mechanism, by changing
The survival outcomes are poor in comparison with from normal stratified squamous epithelium to
other types of cancer and only 16–27% of all metaplastic columnar epithelium with characteris-
patients survive 5 years from the initial diagnosis. tic goblet cells. Known as Barrett’s oeosphagus,
The common histological subtypes are adenocar- this change to intestinal metaplasia is thought to
cinoma and squamous cell carcinoma. Rarer be a precursor to the dysplasia–cancer sequence of
123
(a) (b)
Fig. 15.1 (a) Large oesophageal leiomyoma on coronal CT and (b) resected specimen.
Another factor proposed as being involved in the

Box 15.1 Risk factors for squamous cell
epidemiology of oesophageal cancer may be the
carcinoma and adenocarcinoma
increasing prevalence of Helicobacter pylori infec-
of the oesophagus
tion. Since Helicobacter pylori induces gastritis and
Squamous cell carcinoma decreased acid secretion, this may in turn reduce
Smoking acid reflux, and hence Barrett’s oesophagus and
Alcohol cancer. The treatment of Barrett’s oeosphagus is pri-
Diet rich in nitrosamines marily through the use of proton‐pump inhibitors
Deficiency in trace elements (PPIs) to reduce acid reflux. There is no evidence for
Caustic injury a difference in the incidence of adenocarcinoma in
Low socioeconomic status Barrett’s oesophagus between patients who are
Achalasia treated with a PPI or anti‐reflux surgery.
Hereditary tylosis
Plummer–Vinson syndrome
Adenocarcinoma
Anatomy and clinical features
Barrett’s oeosphagus
Obesity The oeosphagus extends from the cricopharyngeus
GORD muscle in the neck, which is typically 15 cm from
High dietary fat the upper incisor teeth, to the gastro‐oesophageal
Male sex junction. The oeosphagus is divided into a cervical,
Smoking thoracic and abdominal component. The upper
third of the thoracic oesophagus begins at the tho-
racic inlet and extends to the tracheal bifurcation
at 24 cm. The middle third extends from 24 to 32
adenocarcinoma. While most people with Barrett’s cm and the distal oesophagus from 32 cm to the
oesophagus do not progress to oesophageal adeno- diaphragm. The abdominal oeosphagus is a short
carcinoma, further cellular injury from reflux may length of 2 cm as it enters the gastro‐oesopha-
then lead to low‐grade dysplasia, high‐grade dys- geal junction (usually 40 cm from the incisors).
plasia and ultimately oesophageal adenocarcinoma. Anatomically, adenocarcinoma commonly involves
The risk of cancer progression is estimated to be 1 the lower oeosphagus and gastric cardia rather
per 100 patient‐years and surveillance endoscopy than the upper and middle thoracic oesophagus in
with biopsy should be considered in these patients. which squamous cell carcinoma is more common.
Recent developments suggest that molecular bio- Since the bulk of adenocarcinomas occur in the
markers may be employed to identify patients at distal third and near the gastro‐oesophageal junc-
increased risk of progression to oesophageal tion, tumours in proximity to the gastro‐oesopha-
adenocarcinoma. geal junction are categorised using the Siewert
15: Tumours of the oesophagus 125
cm change from involvement of the recurrent laryngeal

5 nerve are less common.
Adenocarcinoma
of the distal I
oesophagus Diagnosis/staging
1
0 Initial upper gastrointestinal endoscopy provides
Cardia cancer II
a histological diagnosis and assesses the tumour’s
2 anatomical dimensions. The tumour must then be
Subcardia III staged accurately to dictate appropriate manage-
cancer 5 ment and provide prognosis. Oesophageal tumours
are staged using the eighth edition of the American
Joint Committee on Cancer (AJCC) TMN staging
system (Table 15.1) published in 2018. Typical
staging investigations include a combination of
upper gastrointestinal endoscopy, computerised
tomography (CT), endoscopic ultrasound and posi-
Fig. 15.2 Classification of adenocarcinomas around the
tron emission tomography (PET). CT of the chest,
gastro‐oesophageal junction. Subcardial tumours
abdomen and pelvis is often the first study per-
(Siewert III) are staged with the stomach cancer TMN.
formed and provides information about potential
resectability and/or presence of metastatic disease.
classification to differentiate between gastric and Endoscopic ultrasound is a useful complement
oesophageal tumours and to guide limits of resec- to detail T staging and mediastinal lymphade-
tion (Figure 15.2). nopathy where it may affect treatment choice.
Around the oeosphagus there is a rich submu-
cosal lymphatic system that drains the mucosal
lymphatics. Lymphatic metastases may spread lon- Table 15.1 American Joint Committee on Cancer
gitudinally along this plexus to the regional lymph TMN Classification for Oesophageal Cancer, 8th
nodes all the way to the neck and abdomen or edition.
through the muscularis mucosa into the thoracic T category
duct and venous system. Tumours may be found TX Tumour cannot be assessed
incidentally on imaging or endoscopy, diagnosed T0 No evidence of primary tumour
during surveillance endoscopy or present with Tis High‐grade dysplasia, defined as malignant
symptoms. cells confined by the basement membrane
Most patients are older than 50 years, with a T1 Tumour invades the lamina propria,
male predominance. Early oesophageal cancer is muscularis mucosae or submucosa
often identified incidentally on surveillance endos- T1a Tumour invades the lamina propria or
copy for Barrett’s oeosphagus or the presence of muscularis mucosae
T1b Tumour invades the submucosa
only non‐specific symptoms. In contrast, the pres-
T2 Tumour invades the muscularis propria
ence of specific symptoms is usually an ominous
T3 Tumour invades adventitia
indicator of at least locally advanced disease. T4 Tumour invades adjacent structures
Progressive dysphagia is common and the patient T4a Tumour invades the pleura, pericardium,
describes difficulty in swallowing solid food and azygos vein, diaphragm, or peritoneum
eventually liquids. The site of the ‘hold‐up’ sensa- T4b Tumour invades other adjacent structures,
tion has only a modest correspondence to the loca- such as aorta, vertebral body or trachea
tion of the tumour; it is usually located above, but N category
not below, the actual site of obstruction. NX Regional lymph nodes cannot be assessed
Other symptoms include odynophagia, melaena, N0 No regional lymph node metastasis
N1 Metastasis in 1–2 regional lymph nodes
regurgitation, substernal pain and weight loss.
N2 Metastasis in 3–6 regional lymph nodes
Acute gastrointestinal haemorrhage is more com-
N3 Metastasis in 7 or more regional lymph nodes
monly associated with adenocarcinoma than squa- M category
mous cell cancer and in rare cases this can be a M0 No distant metastasis
herald bleed from an aorto‐oesophageal fistula. M1 Distant metastasis
Aspiration from an aero‐oesophageal fistula, symp-
tomatic para‐neoplastic syndromes and vocal T, tumour; N, node; M, metastases.
Fluorodeoxyglucose PET with integrated CT is also cancer (T1a) but this does not allow nodal assess-
conducted in the initial staging work‐up to further ment, which is important for prognosis and deci-
corroborate CT findings or identify distant meta- sions about adjuvant therapy. Locally advanced
static disease not initially identified on CT. disease (stage II/III) is considered for multimodal
Further investigations such as staging laparoscopy therapy while metastatic disease is treated with pal-
(particularly for adenocarcinoma), thoracoscopy, liative intent. Without a screening program, oesoph-
bronchoscopy, endoscopic bronchial ultrasound ageal cancers in western countries are normally
and neck ultrasound‐guided fine needle aspiration diagnosed when they are symptomatic and, by
should be considered depending on whether resec- inference, either locally advanced or metastatic.
tion is offered or initial staging investigations are Neoadjuvant therapy is used in locally advanced
insufficient for accurate staging. disease and may involve either chemotherapy or
Staging investigations complement each other. chemoradiotherapy. While previously there has
No single investigation is sufficient and the sequence been controversy about whether surgery alone
of investigations depends on each patient and the should be offered, a Cochrane review has demon-
institution’s oncological multidisciplinary team. strated a 19% relative increase in survival post neo-
adjuvant chemotherapy at 5 years. The choice of
chemotherapy or chemoradiotherapy depends on
Principles of treatment histological subtype and unit preference. The role
of interval PET imaging and biomarkers to assess
Once the tumour is accurately staged, the patient tumour response has the potential to tailor neoad-
and tumour factors are normally reviewed at a can- juvant therapy to the individual.
cer multidisciplinary meeting (Figure 15.3). With Following the publication of the CROSS trial in
the complexity of staging investigations and treat- 2012 (chemoradiotherapy comprising carboplatin
ment decisions, the multidisciplinary meeting pro- and paclitaxel with concurrent radiotherapy of
vides subspecialty review and a pivotal point to 41.4 Gy in 23 fractions) and the MAGIC trial in
offer multidisciplinary consensus on therapy for the 2006 (chemotherapy comprising epirubicin, cispl-
individual patient. In over one‐third of cases the atin and 5‐fluorouracil in three preoperative and
diagnostic and staging information or treatment three postoperative cycles), it has become widely
plan may be altered after review by the multidisci- accepted that locally advanced tumours are best
plinary meeting. treated with a multimodal approach since surgery
Early‐stage disease (defined as stage I/node nega- alone has a 5‐year survival of less than 20%.
tive) may be considered for surgery alone since Neoadjuvant therapy in the form of either chemo-
5‐year survival is 80% or greater. In selected cases, therapy alone or chemoradiotherapy may be offered
endoscopic resection may be considered for early and then surgical resection is undertaken.
Diagnosis
Staging
Potentially resectable disease in fit patient Metastatic disease/the patient unfit

for curative treatment
Stage I Stage II/III Stage IV

Disease
progression
Surgery only Neoadjuvant therapy

Palliative Symptomatic and best
EMR in (chemoradiotherapy/
chemotherapy or supportive care
selected cases chemotherapy)
radiotherapy
Surgery
Fig. 15.3 An example management protocol for oesophageal adenocarcinoma. EMR, endoscopic mucosal resection.
Definitive chemoradiotherapy with resulting the left gastric artery is ligated at its origin. Our
higher doses of radiotherapy is favoured in upper preference is to also perform a pyroclastic to
oesophageal squamous cell cancers or in resectable improve gastric drainage and for a feeding jejunos-
disease where surgery cannot be performed in a tomy tube to be inserted.
comorbid or elderly patient. The supine patient is then repositioned for a right
posterolateral thoracotomy. This allows the expo-
Surgical sure required to perform a radical en‐bloc resection
and lymphadenectomy. Once the tumour specimen
Contraindications to surgery include distant vis- is exenterated then the stomach is delivered via the
ceral or nodal metastases and direct infiltration of diaphragmatic hiatus into the chest. The stomach is
the tracheo‐bronchial tree or aorta. There is no role fashioned into a tube, mobilised up to sit mainly in
for palliative oesophagectomy. Instead, the goals of the thoracic cavity to reduce the risk of reflux and
surgical resection are to completely resect the an oesophago‐gastric anastomosis is performed
tumour with an adequate margin and an ade- high in the thoracic cavity (Figure 15.5).
quate lymphadenectomy of the representative nodal
stations. Most surgeons will perform a lymphad- Mckeown’s procedure (three‐stage subtotal
enectomy of the upper abdomen and mediastinum, oesophagectomy)
which is known as a two‐field dissection. A three‐ This operation is commonly performed for tumours
field dissection (incorporating the cervical nodes) is that involve the upper to middle thoracic oeospha-
sometimes considered in some centres for squa- gus and involves a cervical oesophago‐gastric anas-
mous cell carcinoma. tomosis. A right thoracotomy is first performed to
Careful selection is required to achieve the mobilise the thoracic oesophagus. The patient is
goals of surgery because a curative resection may then placed in a supine position and both a left cer-
involve two or all three of the cervical, thoracic or vical incision and a laparotomy are performed. The
abdominal compartments. Potential surgical candi- stomach is fashioned into a conduit and brought up
dates should have a careful risk assessment, espe- through the posterior mediastinum into the neck
cially with regard to their cardiopulmonary status where an anastomosis is performed.
because of the high postoperative morbidity of
oesophagectomy. Transhiatal oesophagectomy
There are three archetypal procedures for thoracic This procedure involves the ‘shelling out’ of the
and gastro‐oesophageal junction tumours: a two‐ oesophagus by a surgeon’s hand via the diaphrag-
stage subtotal oesophagectomy (Figure 15.4a), a matic hiatus and neck without a thoracotomy. The
three‐stage subtotal oesophagectomy (Figure 15.4b) stomach is brought up into the neck to fashion a
and a transhiatal oesophagectomy. While the three cervical oesophago‐gastric anastomosis. In experi-
differ in the manner of resection, all three preferen- enced hands this partially blind procedure is safe,
tially use the stomach as the conduit to replace the with similar perioperative mortality rates. However,
resected oeosphagus via the posterior mediastinum. the operation is controversial as an oncological
If this route is unavailable because of previous sur- procedure since extensive thoracic lymphadenec-
gery or sepsis, then the retrosternal and subcutane- tomy is not formally performed.
ous routes are possible alternatives.
Laparoscopic, thoracoscopic and robotic
Ivor Lewis oesophagectomy (two‐phase approaches
oesophagectomy) The anatomical boundaries of the oeosphagus
This operation was named after the eminent Welsh mean that open procedures expose the patient
surgeon Ivor Lewis who in 1945 published his to lengthy incisions in the chest and abdomen.
novel approach to the oeosphagus via the right Increasingly, high‐volume centres have introduced
chest, where by simply dividing the azygos vein the minimally invasive oesophagectomies to minimise
oesophagus would be exposed for dissection. the impact of multi‐compartment surgery, such as
It is commonly performed for tumours of the degree of blood loss and time spent in intensive care
lower third of the oeosphagus and Siewert and in hospital. Large‐volume case series in these
I tumours. A laparotomy is first performed to mobi- centres demonstrate comparable cancer outcomes
lise the stomach on its right gastric and right gas- with open surgery but careful case selection is still
troepiploic arterial pedicles. A lymphadenectomy is required.
performed at the coeliac trunk to skeletonise the While there are several approaches for oesopha-
common hepatic and root of the splenic artery and geal resection, the stomach remains the preferred
(a)
(b)
Fig. 15.4 (a) Ivor Lewis oesophagectomy with an intrathoracic oesophago‐gastric anastomosis. (b) Three‐stage
oesophagectomy. In this example, a colonic interposition is depicted in the retrosternal route with an anastomosis in
the neck.
conduit for oesophageal reconstruction because it multidisciplinary approach with a head and neck
is relatively robust and only a single anastomosis is surgical unit. Typically, these tumours are squa-
required. The lesser curvature of the stomach is mous cell type and the survival outcomes of treat-
largely excised, but the right gastroepiploic artery ment with chemoradiation are similar to those of
and right gastric artery are preserved. The high surgery. For this reason, and because of the exten-
point of the fundus is used to anastomose the sive nature of surgery, many of these patients are
oesophagus to the isoperistaltic stomach. Should treated with definitive chemoradiotherapy.
the gastric conduit fail or the stomach is a non‐ Historically, an oesophagectomy was regarded as
viable option, then the colon or jejunum can be a highly morbid procedure with a significant mor-
fashioned into a conduit. tality rate. Perioperative mortality has improved
Tumours of the cervical oesophagus require and now in major centres this is considerably less
resection of the hypopharynx and the larynx as than 5%. The dramatic reduction in mortality
well as the oeosphagus. These often require a is due to increasing referrals to specialised units
Supra-azygos oesophago
gastric anastomosis Box 15.2 Complications after
Azygos vein divided oesophagectomy
Medical
Cardiac
Atrial arrhythmia*
Myocardial infarction
Cardiac failure
Pulmonary
Atelectasis*
Pneumothorax
Bronchopneumonia with or without aspiration*
Sputum retention*
Pleural effusion*
Gastric conduit
Pulmonary embolism
Respiratory failure
Other medical†
Renal failure
Hepatic failure
Stroke
Surgical
Intraoperative or postoperative haemorrhage
Tracheobronchial tree injury
Recurrent laryngeal nerve injury
Anastomotic leakage
Gangrene of conduit
Intrathoracic gastric outlet obstruction or gastric stasis
Herniation of bowel through diaphragmatic hiatus
Chylothorax
Fig. 15.5 Two‐stage oesophagectomy, with the stomach
Empyema
in the posterior mediastinum.
Wound infection
Note that surgical complications are technique‐ and
operator‐dependent, thus incidences can vary
* Relatively common occurrence
in tertiary‐level hospitals, careful patient selec-
tion, multidisciplinary consensus for management, †
Should all be uncommon
enhanced recovery programs and improved postop-
erative management.
The use of early mobilisation, careful fluid
Multi‐compartment surgery increases the likeli-
balance, early nutritional support and adequate

hood of typical post‐surgical conditions such as
thoracic analgesia has served to reduce complica-
pulmonary, cardiac and renal complications. Pain,
tions and the ensuing morbidity and mortality.
fluid balance, blood loss and pre‐existing cardiores-
Unfortunately, there remains a significant risk of
piratory risk factors can all potentiate the risk of
complication following oesophagectomy which
these complications, which can occur in 30–40% of
entails surgery in at least the thoracic and abdomi-
all patients. On occasion, complications such as a
nal compartments.
unilateral pleural effusion or atrial fibrillation are
subtle signs of more significant complications such
Complications of surgery
as an anastomotic leak and a high index of suspi-
Complications exist in all surgeries. Oesophageal cion is required to intervene early. Specific early
resections have a high risk of morbidity with the oesophagectomy complications include anasto-
extensive en‐bloc dissection in both abdominal and motic and conduit leaks, chyle leaks and laryngeal
thoracic cavities. Postoperative complications may nerve injuries.
be categorised into general medical or procedure‐ Historically, the anastomotic leak rate has been
specific complications (Box 15.2). 20–30% but in recent times the incidence of this
has fallen to less than 5% in major units. Leaks

may occur because of excessive conduit tension,
poor vascularity, faulty surgical technique or
patient factors such as malnutrition or underlying
vascular disease. These are diagnosed with cross‐
sectional imaging, fluoroscopy and upper gastroin-
testinal endoscopy. Early anastomotic leaks often
within 72 hours may be investigated with surgical
exploration, whilst late leaks are typically man-
aged with aggressive non‐operative management.
Whether early or late, nutritional support and con-
trol/drainage of mediastinal and thoracic sepsis are
critical components.
The thoracic duct enters the thoracic cavity
through the aortic opening between the aorta and
azygous vein. It is divided as part of the en‐bloc
resection for an oesophagectomy. Occasionally, the
secured duct may leak or there is aberrant anatomy Fig. 15.6 Self‐expanding metallic oesophageal stent
resulting in a chylothorax. The chyle losses are rich in situ.
in free fatty acids and immune complexes, which
can swiftly result in malnutrition. High‐volume
losses require surgical exploration whilst losses of Argon‐beam plasma coagulation and laser treat-
less than about 500 mL may be treated with a ments such as the neodymium yttrium–aluminium–
medium‐chain triglyceride enteral diet. Resistant garnet (Nd:YAG) laser are less frequently used with
leaks may require a lymphangiogram with emboli- the popularity of stents, although they can be con-
sation or shunting procedures. sidered when a stent cannot be deployed, such as in
Laryngeal nerve palsies can occur during an the cervical oesophagus. Less common palliative
oesophagectomy. The long looping path of the treatments also include photodynamic therapy and
recurrent laryngeal vagus nerve is vulnerable the injection of intralesional alcohol.
to injury in the upper thorax and in particular dur-
ing the cervical mobilisation of a three‐stage
oesophagectomy. Prognosis
The postoperative complications of oesophagec-
tomy may quickly become life‐threatening. Often The survival from oesophageal cancer remains
subtle signs and biochemical aberrations are pre- poor in comparison with other cancers, with an
sent in a physiologically well patient. A high index overall survival of 8–16% at 5 years. Two‐thirds of
of suspicion, early investigation and treatment patients are not suitable for resection and with pal-
are required to minimise the rapid physiological liative management they have a median survival
deterioration with chest or abdominal sepsis. of 8 months. The remaining one‐third of patients
have potentially curative disease at the time of
diagnosis. Care should be delivered with a multi-
Symptomatic treatment disciplinary approach in specialised centres. Since
The majority of patients in western countries survival is so dependent on stage, early detection
present with stage IV disease, with dysphagia and and accurate staging is crucial for delivering opti-
significant weight loss. While there are other symp- mal treatment.
toms, dysphagia from malignant obstruction is
extremely debilitating. With careful patient selec-
tion, dilatation and the endoscopic placement of a Further reading
self‐expanding metal oesophageal stent provide
Cunningham D, Allum WH, Stenning SP et al. Perioperative
symptomatic relief and a normal route for nutrition
chemotherapy versus surgery alone for resectable gas-
(Figure 15.6).
troesophageal cancer. N Engl J Med 2006;55:11–20.
Palliative radiotherapy can be delivered via Rice TW, Patil DT, Blackstone EH. 8th edition AJCC/
brachytherapy or external beam. Brachytherapy is an UICC staging of cancers of the esophagus and esoph-
alternative in dysphagia and external beam therapy agogastric junction: application to clinical practice.
can be useful with symptomatic bleeding or pain. Ann Cardiothorac Surg 2017;6:119–30.
Ronellenfitsch U, Schwarzbach M, Hofheinz R et al. b endoscopic ultrasonography

Perioperative chemo(radio)therapy versus primary c positron emission tomography
surgery for resectable adenocarcinoma of the stom-
d ultrasound with or without fine‐needle
ach, gastroesophageal junction, and lower esophagus. aspiration of neck
Cochrane Database Syst Rev 2013;(5):CD008107.
e CT scan
van Hagen P, Hulshof MC, van Lanschot JJ et al.
Preoperative chemoradiotherapy for esophageal or
3 Which of the following is the most likely risk factor
junctional cancer. N Engl J Med 2012;366:2074–84.
for development of a squamous cell cancer of the
oesophagus?
a smoking
MCQs b alcohol intake
c obesity
d history of cancer of the larynx
e achalasia
1 For patients suffering from oesophageal cancer, 4 The most common benign tumour of the
which of the following symptoms indicates the oesophagus is:
worst prognosis? a adenosquamous carcinoma
a hoarseness of voice b fibrovascular polyp
b weight loss of more than 10% of usual body weight c leiomyoma
c dysphagia to solid and semi‐solid food d haemangioma
d regurgitation of swallowed food e neurofibroma
e odynophagia
5 The diagnosis of chylous leak after oesophagectomy
2 A 75‐year‐old man complains of progressive is not helped by:
dysphagia for 2 months. He has lost 4.5 kg in a analysis of chylomicrons in the chest tube
weight and can only tolerate a liquid diet. output
Oesophageal cancer is suspected. Which of the b lymphangiogram
following investigations is most likely to detect c milk challenge
evidence of distant metastases from his cancer? d Gastrografin contrast swallow
a upper endoscopy e test for triglyceride in chest tube output
16 Peptic ulcer disease
Paul A. Cashin1 and S.C. Sydney Chung2
1
Monash University and Monash Health, Melbourne, Victoria, Australia
2
Chinese University of Hong Kong and Union Hospital, Hong Kong
antrum, and is the real culprit in the majority of

Introduction cases. Helicobacter pylori remains one of the most
common bacterial infections in the world. In the
Peptic ulcer is a common condition. Each year, peptic
upper gastrointestinal tract it is considered a hostile
ulcer disease (PUD) affects approximately 4 million
commensal. Its global presence in humans is esti-
people worldwide; 2–10% of these ulcers will perfo-
mated to be up to 50%. Chronic infection with H.
rate. The incidence and severity of PUD has been
pylori is a major aetiological factor in PUD.
decreasing in the western world and has now reached
Individuals colonised with H. pylori have a seven-
a stable incidence. However, as a result of the wide-
fold increase in the risk of developing PUD. The
spread use of freely available non‐steroidal anti‐
organism is found in more than 90% of patients
inflammatory drugs (NSAIDs), the incidence of ulcer
with duodenal ulcers and more than 80% of
disease in the elderly is increasing in many parts of
patients with gastric ulcers. Antibiotic eradication
the world. Complications of the disease such as per-
of the bacterium heals the ulcer and prevents recur-
foration and bleeding can be quite catastrophic.
rence. Such a discovery has completely revolution-
ised the understanding of the pathogenesis and
Aetiology management of peptic ulcers.
Other associated factors have been implicated in
Peptic ulcers occur when the balance between acid the co‐aetiology of PUD. These include age (the old
secretion and the natural defence mechanism of the in developed countries and the young in developing
mucosa is disturbed. Classical sites for peptic ulcers countries), NSAID ingestion, smoking, genetic fac-
are the first part of the duodenum, the angula tors, and those with multiple endocrine neoplasia
incisura and the antrum/pre‐pyloric region of the (MEN)‐1. Many of these act by amplifying the
stomach, the lower end of the oesophagus in effect of H. pylori on the gastric epithelium or by
patients with gastro‐oesophageal reflux, along the leading to pathological acid hypersecretion
edges of a gastroenterostomy (marginal ulcers), and (MEN‐1/gastrinoma in association with this).
inside a Meckel’s diverticulum if there is ectopic Mucosal defence against acid–pepsin digestion
gastric mucosa. consists of the mucous layer on the mucosa, which
Whilst acid hypersecretion has traditionally been serves as a barrier between the lumen and the epi-
thought to be the most important factor in the cau- thelial surface, the secretion of bicarbonate and the
sation of ulcers, in particular duodenal ulcers, this rapid turnover of mucosal cells. Other factors can
is now known not to be the case. The classical acutely damage this barrier, such as reflux of bile
example of the effect of increased acid production into the stomach and by mucosal ischaemia. These
is the infrequently seen Zollinger–Ellison syndrome. are additional factors that can weaken the mucosal
Uncontrolled gastrin production by pancreatic or defence and contribute to the development of
duodenal adenoma causes maximal stimulation of ulcers. ‘Stress’ ulcers are common in severely ill
the parietal cell mass, producing massive amounts patients, particularly those treated in intensive care
of acid and resulting in a particularly aggressive units, when not receiving prophylactic acid sup-
form of PUD. pression. Cushing’s ulcers and Curling’s ulcers are
The most common and important aetiological stress ulcers occurring after head injuries and severe
factor is Helicobacter pylori, a Gram‐negative burns, respectively. These ulcers are caused by
organism that resides in the mucus layer of the increased acid production in stressed patients, and
133
mucosal ischaemia as a result of splanchnic using microscopy or the rapid urease test. The detec-
hypoperfusion. tion of H. pylori proteins and antigens in faecal
specimens has also been used. Culture of organisms
is difficult and rarely performed in clinical practice.
Duodenal ulcer Serology detects past as well as current infection
and is simple to conduct as only a drop of blood is
Practically all duodenal ulcers occur in the first and necessary. The accuracy of the commercially availa-
second parts of the duodenum, being most common ble test kits has improved but their validity must be
in the duodenal bulb. This part of the duodenum is confirmed for each country as there are geographi-
in the direct path of the acid contents of the stomach. cal differences in the genetic make‐up of the bacte-
Alkaline pancreatic juice and bile, which enter the rium. Serology cannot be reliably used to assess the
duodenum in the second part, have not yet had an success of eradication therapy, as antibody levels
opportunity to neutralise the gastric acid. Duodenal can remain raised for prolonged periods even after
ulcers are more common than gastric ulcers. They successful eradication.
tend to occur in younger patients and are more com- In the urea breath test, urea labelled with a non‐
mon in men than women. There is also a genetic pre- radioactive (13C) or radioactive (14C) carbon iso-
disposition; the disease is more common in family tope is given by mouth. Helicobacter produces
members of index cases, patients with blood group urease, which splits the urea into ammonia and car-
O, non‐secretors of blood group antigens in the bon dioxide. If 13C or 14C is detected in the exhaled
saliva, and those with high circulating pepsinogen. breath, the presence of Helicobacter is confirmed.
The urea breath test is a reliable non‐invasive way
Clinical features of confirming the success of eradication therapy,
but care must be used when attempting to use it as
The cardinal symptom of duodenal ulcer is pain.
a primary diagnostic modality as associated gastric
The pain is typically localised to the epigastrium, is
diseases such as gastric cancer may be missed. For
dull or burning in character, starts several hours
this reason, endoscopic examination and biopsy
after a meal, wakes the patient at night and is
remains the most important test.
relieved by food or antacids. Nausea, bloating and
In patients who have undergone endoscopy, a
vomiting may be present during an acute exacerba-
convenient test is the rapid urease test. Antral biop-
tion but are not prominent features. In contrast to
sies are embedded in a gel containing urea and an
patients with non‐ulcer dyspepsia, ulcer patients
indicator dye (neutral red). The ammonia produced
localise the pain to the epigastrium with one finger.
as a result of urease is alkaline and changes the
Apart from mild tenderness in the epigastrium,
indicator dye to a red colour. This gives a rapid
patients with uncomplicated ulcer disease do not
result, often within an hour, and is cheaper than his-
have physical signs.
tology. The use of proton pump inhibitors (PPIs)
The course of duodenal ulcer disease is one of
such as omeprazole lead to a suppression of organ-
relapses and remissions. The patient complains of
ism numbers in the gastric mucosa. This can lead to
episodes of severe pain lasting for weeks, inter-
false‐negative results in patients undergoing the
spersed by months of remission, the pattern repeat-
urea breath test, urease test and even histology. It is
ing itself over several years. The disease may burn
recommended that patients on PPIs have these
itself out after 10–15 years.
ceased at least 2 weeks prior to urea breath testing
or, if testing is to be performed at endoscopy, that
Diagnosis
biopsies are taken for histology from both antrum
It is difficult to clinically differentiate duodenal and body of stomach to increase the yield.
ulcer from other causes of upper abdominal pain
(gastric ulcer, acute gastritis, non‐ulcer dyspepsia,
Treatment
reflux oesophagitis, gastric cancer, gallstones) with
confidence on clinical grounds alone. Upper gastro- The aim of treatment is to alleviate the ulcer pain,
intestinal endoscopy is the most accurate diagnostic to heal the ulcer, to prevent recurrence and to fore-
method, and essential to the diagnosis. The oesoph- stall complications. With powerful acid‐inhibiting
agus, stomach and the first and second part of the drugs (PPIs) and effective regimens to eradicate
duodenum can be clearly seen, and ulcers biopsied Helicobacter, these aims can be achieved by medi-
using this technique. cal therapy in the great majority of patients. Apart
Helicobacter pylori can be demonstrated by serol- from giving up smoking and avoiding, if possible,
ogy, by the urea breath test, or in antral biopsies ulcerogenic drugs, lifestyle modification such as a
16: Peptic ulcer disease 135
change in diet or avoidance of stress is not neces- Eradication of Helicobacter pylori

sary. Such changes are difficult to make and there is Antibiotic eradication of H. pylori is now the cor-
little evidence that they accelerate ulcer healing. nerstone of ulcer treatment, coupled with PPI ther-
Nowadays, elective surgery for uncomplicated apy. It is also the main reason why elective surgery
ulcer disease is rarely, if ever, indicated. Nearly all for PUD is now very rare. The bacteria dwell in,
ulcer surgery is performed as an emergency proce- and are protected by, the mucous layer of the gas-
dure for complications. tric pits and are difficult to eradicate. Multiple
drugs need to be administered simultaneously.
Commonly used drugs Effective combinations should result in eradica-
tion in more than 90% of patients if patient
Antacids compliance is satisfactory. Examples of such com-
Antacids may be in tablet or liquid form. They are binations are 1–2 weeks of triple therapy using a
either magnesium based (liable to cause diarrhoea) PPI, clarithromycin and amoxicillin. Side effects,
or aluminium based (may cause constipation). especially gastrointestinal upsets, are common.
Antacids give rapid temporary relief of ulcer pain Combinations of a PPI and two other antibiotics
but do not heal ulcers unless taken in very high can be used if allergy issues arise. These combina-
doses. This is not recommended. tions have become first‐line therapy in most
countries.
Histamine H2 receptor antagonists In some countries, H. pylori has begun to
Antagonists of the histamine H2 receptor (H2 block- exhibit significant resistance and cause issues
ers) were the first group of drugs to be marketed with both failure of treatment and in recurrent
that effectively block gastric acid secretion. disease. Recurrence may be partly socioeconomic
Examples are cimetidine, ranitidine and famotidine. with repeated infections but may be partly the
Relief of pain occurs after a few days and up to result of treatment leaving resistant organisms in
90% of ulcers heal after a 6‐week course. Once the the upper gastrointestinal tract. Improper and
drug is stopped, however, acid production returns uncontrolled use of antibiotics is also a major
to normal and ulcer recurrence is highly likely. problem in some countries, with a potential
Proton pump inhibitors impact worldwide. In patients with recurrent or
PPIs such as omeprazole, esomeprazole, pantopra- non‐responsive infections, antimicrobial resist-
zole and lansoprazole lead to near complete inhibi- ance should be investigated.
tion of gastric acid production. Symptomatic relief The addition of PPIs to the antibiotics improves
and ulcer healing is even more impressive than with the eradication rate by maintaining a gastric pH
H2 blockers. However, once the drug is stopped close to or above 6 and may also help to reduce the
ulcer recurrence is common. PPIs have been shown development of resistance.
to both prevent and heal ulcers associated with
NSAID use. For this reason, they are used as proph- Surgery
ylaxis in acutely ill patients to prevent ‘stress’ ulcer-
ation, particularly in the intensive care setting. PPIs The classical operations for non‐emergency duode-
are now first‐line treatment for PUD, in conjunc- nal ulcer disease are designed to reduce gastric acid
tion with H. pylori eradication. production (Table 16.1). Nowadays their use is
almost entirely confined to the management of
Sucralfate ulcer complications (non‐healing or obstruction) or
Sucralfate is a drug that is not absorbed but exerts its not done at all. Essentially one can remove the acid‐
action by physically covering the ulcer base. Ulcer producing part of the stomach or sever the vagus
healing rates are similar to those with H2 blockers. nerve, which controls acid secretion. With so many
Table 16.1 Operations for duodenal ulcers.
Mortality (%) Side effects Recurrence rate (%)
Pólya’s gastrectomy 2–5 +++ 5

Vagotomy and drainage 1 + 5–10
Highly selective vagotomy <0.5 ± 15
Vagotomy and antrectomy 2–5 ++ 1
of these operations having been performed in the the disease and are described in a subsequent
past, it remains important to understand them. section.
Billroth II gastrectomy
Acid is secreted by parietal cells in the body and the Gastric ulcer
fundus of the stomach. In order to ensure adequate
reduction of acid output, at least two‐thirds of the Gastric ulcers are less common than duodenal
stomach needs to be resected. Patients who have had ulcers. They affect the older age group. Gastric
this operation are unable to tolerate large meals. ulcers are more common in patients from lower
Weight loss, malnutrition and anaemia are common socioeconomic groups. NSAIDs are a common
unless actively managed. The rapid entry of food cause of gastric ulcers as is H. pylori infection. In
into the intestine leads to ‘dumping’ syndromes – the patients with non‐healing gastric ulcers, malig-
patient feels faint or unwell after a meal. This may nancy or a gastrinoma should be considered.
be due to transudation of fluid in response to an
osmotic load in the gut (early dumping, occurring Clinical features
10 minutes after a meal) or rapid absorption of glu- As in duodenal ulceration the usual presentation is
cose, leading to insulin release and rebound hypo- epigastric pain. The pain is typically exacerbated by
glycaemia (late dumping, occurring 2–3 hours after food. Nausea, unremitting pain and weight loss are
a meal). Although rare these functional complica- common. Any clinical differentiation from duode-
tions can be distressing and difficult to manage. nal ulcer and gastric cancer is unreliable.
Truncal vagotomy and drainage Diagnosis

Gastric acid production may also be decreased by
All suspected gastric ulcers must be investigated by
dividing the vagus nerve, thus removing the nerv-
endoscopy and biopsy. Biopsy is essential as gastric
ous stimulation of the parietal cell mass. If the
cancer is common and sometimes difficult to dif-
whole vagal trunk is cut, delay in gastric emptying
ferentiate from benign ulceration.
occurs in a significant number of patients because
Double‐contrast barium meal X‐ray examina-
the motor supply to the antrum is also severed. A
tions were extensively used in the past and were
drainage operation, either a pyloroplasty or gastro‐
often inaccurate and misleading. Nowadays they
enterostomy, is necessary. These operations are rela-
are largely confined to history.
tively easy to perform and are useful in emergency
As seen through the endoscope a benign gastric
situations. Between 5 and 10% of patients com-
ulcer has smooth regular margins. The most com-
plain of diarrhoea, due to rapid transit of food
mon site is the angular incisura, followed by the
through the gut.
lesser curvature and the antrum. An ulcer seen out-
side these locations should raise the suspicion of
Highly selective vagotomy
malignancy, although all gastric ulcers can be
This operation aims to divide the vagal fibres sup-
malignant or benign. Malignant ulcers are often
plying the parietal cell mass but leave the innerva-
irregular with raised, rolled‐up edges. With potent
tion of the antrum (the nerve of Latarget) intact.
acid suppression, even malignant ulcers may com-
The operation is technically demanding and time‐
pletely heal over temporarily, leaving an area of
consuming. Side effects are almost non‐existent but
mucosal irregularity. All gastric ulcers must be sub-
the recurrence rate is higher than in other
jected to multiple biopsies. After a course of eradi-
procedures.
cation therapy, repeat endoscopy to assess healing
and repeat biopsy are mandatory. This is usually
Vagotomy and antrectomy
performed 6–12 weeks after completion of pharma-
In this operation the vagal trunks are divided to
cological treatment.
remove the vagal stimulation of acid production
and the antrum is resected to remove the source of
Treatment
gastrin, another potent stimulator of gastric acid
secretion. Continuity of the gastrointestinal tract is Although acid output is normal or low in patients
restored by Roux‐en‐Y gastrojejunal anastomosis. with gastric ulcers, ulcer pain is controlled and the
The main attraction of this operation is the very ulcer heals with acid suppression. PPIs are the med-
low ulcer recurrence rate. ications of choice. Because gastric ulcers are often
Most operations for duodenal ulcer disease are larger than duodenal ulcers they generally take
done in an emergency setting for complications of longer to heal. Greater than 80% of gastric ulcers
are associated with positive H. pylori on urease Peptic ulcer bleeding is the most common cause
testing or seen at biopsy. Eradication of the bacte- of upper gastrointestinal haemorrhage and is a fre-
rium is indicated in all patients to reduce the recur- quent cause of emergency hospital admission. The
rence rate. Other gastric ulcers are caused by mortality is up to 10% and has remained constant
NSAIDs, but these medications are so frequently despite advances in diagnosis and treatment. This is
used in the community that it is not indicated to due to an increase in the number of elderly people
simply cease these drugs. Full treatment with PPIs, presenting with this condition.
H. pylori eradication and re‐endoscopy is still best About 85% of bleeding ulcers stop bleeding
practice. If it is not possible for the patient to stop spontaneously and do not require specific measures
taking an NSAID, a PPI taken concurrently confers to stop the haemorrhage. The mortality in those
a degree of protection. who continue to bleed or develop rebleeding while
Gastric cancer may masquerade as a gastric ulcer. in hospital is 10‐fold higher. The likelihood of
If complete healing of the ulcer is not achieved with rebleeding may be predicted on clinical grounds
two courses of medical therapy, surgical resection and the appearance of the ulcer on endoscopy.
of the ulcer may be considered. However, repeat Haematemesis and shock on admission suggest a
biopsies will usually provide the answer, often aided large initial bleed and are associated with a higher
by endoscopic ultrasound in a non‐healing ulcer. risk of recurrent haemorrhage. Ulcers with stigmata
Pre‐resection diagnosis allows the patient with gas- of recent haemorrhage, such as a visible vessel or an
tric cancer to receive optimum cancer care with adherent blood clot seen on endoscopy, are also
neoadjuvant chemotherapy/radiotherapy to achieve more likely to rebleed but, if possible, treated endo-
maximum cure rates. scopically they are less likely to rebleed. On the
Non‐healing benign ulcers should be investigated other hand, if a clean‐based ulcer is seen on endos-
for Zollinger–Ellison syndrome (see the last section copy the risk of rebleeding is very low. Larger ulcers
in this chapter). Poor medication compliance are more likely to rebleed. The risk of rebleeding
should also be considered and these patients often decreases with time after the initial bleed. If rebleed-
have low serum gastrin levels, consistent with them ing does not occur within the first 72 hours on PPI
not taking their PPIs. treatment, it is unlikely to occur. Higher acute
The aim of surgical treatment for benign disease transfusion requirements correlate with higher
is to resect the ulcer‐bearing part of the stomach. rebleeding risk.
The operation of choice for gastric ulcers is Billroth
II style gastrectomy, in which the distal half of the
Clinical features
stomach is removed and intestinal continuity
restored with a Roux‐en‐Y gastrojejunostomy. In The patient may vomit fresh blood and clots (indi-
patients where it is medically indicated not to per- cating torrential bleeding) or coffee‐ground mate-
form major resectional surgery, for example age rial (acid haematin resulting from the action of
and comorbidities, or the ulcer is in the proximal gastric acid on haemoglobin). More commonly the
stomach, local excision of the actual benign ulcer patient passes melaena (semi‐liquid tarry black
has reasonable results, coupled with ongoing PPI stool with a characteristic sickly smell). The consist-
therapy. ency and colour of the melaena may give some clue
to the rapidity of the bleeding: the redder and less
well formed the stool, the brisker the haemorrhage.
Complications of ulcer disease There may be a background of long‐standing PUD,
and history of another episode of bleeding in the
Complications of duodenal ulcers include bleeding, past. In 30% of patients there is a history of recent
perforation and gastric outlet obstruction. intake of NSAIDs or aspirin. The patient may com-
plain of dizziness or faint on getting up from a
supine position or demonstrate a postural drop in
Bleeding
their blood pressure indicating hypovolaemia in
Peptic ulcer bleeds occur when the ulcer erodes a association with the bleed.
vessel in the ulcer base. Classical textbook cases of Patients are sometimes diagnosed with rectal
posterior duodenal ulcers eroding the gastroduode- bleeding if transit is quick enough and the bleeding
nal artery and gastric ulcers eroding the left gastric significant. All patients with semi‐altered blood on
artery are rarely seen in the modern era. Most cases rectal examination should be considered for
of ulcer bleeding result from erosion of medium‐ gastroscopy first to rule out a rapid transit upper
sized arteries in the submucosa. gastrointestinal bleed.
Apart from melaena on rectal examination, bleeding or stigmata of recent haemorrhage predic-
patients with a mild to moderate amount of blood tive of high risks of rebleeding. In the modern era,
loss show little abnormality on examination. rebleeding is usually again treated endoscopically.
Tachycardia, sweaty palms, hypotension, anxiety If immediate control cannot be achieved, in both
and agitation are signs of shock and call for urgent gastric and duodenal ulcers, in a setting where it is
blood volume replacement. Abdominal pain is an available, radiological embolisation of the bleeding
unusual feature. vessel can control the bleeding or delay the need for
acute surgical intervention. All these interventions
Treatment require a multidisciplinary team approach.
If none of these means is able to control the
Resuscitation
bleeding, surgery needs to be considered with at
All patients who have had a significant gastrointes-
least the advantage of almost always knowing the
tinal bleed within the past 48 hours should be
site of bleeding in the upper gastrointestinal tract.
admitted to hospital. Two large‐bore intravenous
Direct suture of the bleeding vessel via a duodenot-
cannulas should be inserted and blood drawn for
omy in bleeding duodenal ulcers is the treatment of
baseline tests and cross‐matching. In the acute
choice in this case. In bleeding gastric ulcers, local
stage, the haemoglobin level is a poor guide to the
excision of the ulcer should be considered to obtain
need for transfusion as haemodilution may not
a definitive biopsy. Rarely is an antrectomy or
have occurred. The decision to replace the blood
vagotomy required given the effectiveness of PPI
volume by plasma expanders or blood should be
therapy and H. pylori eradication therapy.
based on signs of hypovolaemia and the rapidity of
the bleeding. In elderly patients with poor cardiac
reserve, or in patients with massive bleeding, moni- Perforation
toring central venous pressure by a central venous
Perforation occurs when the ulcer erodes through
line gives a more accurate indication of the amount
the full thickness of the gut wall. Gastric and duo-
of fluids needed.
denal contents spill into the peritoneal cavity caus-
ing sudden acute pain and then generalised
Identify the bleeding point peritonitis. The most frequent site of perforation is
If facilities allow, all patients admitted with upper the anterior wall of the first part of the duodenum.
gastrointestinal haemorrhage should undergo Males outnumber females in a ratio of 9 : 1. The
endoscopy within 24 hours of admission. Patients incidence of ulcer perforation in the elderly is
who vomit fresh blood or are in shock may have increasing because of the increased use of NSAIDs.
ongoing massive blood loss and should undergo Often there are few prodromal ulcer symptoms.
endoscopy once they are resuscitated. An accurate
diagnosis forms the basis of logical treatment, and Clinical features
the precise location of bleeding is of paramount
importance should surgery be needed to control The patient presents with sudden onset of severe
bleeding. abdominal pain. The onset of pain is so sudden that
the patient can often accurately pinpoint the exact
moment when the perforation occurred.
Control bleeding Approximately 10% of patients have no preceding
Ulcer bleeding stops spontaneously in about 80% history of classic ulcer symptoms. Meticulous his-
of patients. Only a small percentage require specific tory is important in terms of identifying risk factors
measures to stop bleeding. In recent years endo- and comorbidities such as cirrhosis and portal
scopic procedures have become the first‐line hypertension, immunological diseases requiring
method of controlling ulcer bleeding. The most steroid therapy and renal failure. The physical signs
popular methods are injection therapy using adren- in the abdomen are dramatic. There is generalised
aline solution and/or sclerosants, such as polido- tenderness, guarding and rebound tenderness. The
canol, absolute alcohol or ethanolamine; contact abdominal muscles are held rigid, giving the classi-
thermal methods, such as the heater probe or cal board‐like rigidity. Abdominal respiratory
multipolar electrocoagulation; or direct endoscopic movements and bowel sounds are often absent. The
clipping of a visible vessel in the base of the ulcer. percussion note over the liver may be resonant
Not infrequently, multiple methods need to be used because of free intraperitoneal air. In patients
to achieve control at gastroscopy. Endoscopic hae- in whom the perforations are sealed off by
mostasis should be applied for ulcers with active adjacent organs the signs may be localised to the
epigastrium. In other cases, the spillage from the

perforation may track down the right paracolic
gutter, resulting in maximal tenderness in the right
iliac fossa. This is the so‐called right paracolic gut-
ter syndrome, and may be mistaken for acute
appendicitis. Similar tracking may occur down the
left side of the abdomen to mimic perforated
diverticulitis.
Investigations
A plain chest radiograph with the patient in the
erect position shows free gas under the diaphragm
in 80% of cases. Large volumes of subphrenic free
gas are more indicative of a perforated ulcer,
whereas small volumes may suggest a colonic per-
foration but this is not diagnostic as peptic ulcers
may be walled off by omentum leading to small vol-
umes of gas.
The presence of free gas on plain X‐ray is gener-
ally sufficient information to proceed to definitive
surgical treatment. Further investigation with con-
trast CT scanning may be required if the diagnosis
is not clear.
Treatment
Once an acute abdomen has been recognised or
the diagnosis is made, the patient should be given
parenteral opiates for pain relief, intravenous flu-
ids and antibiotics should be administered and a
nasogastric tube passed as soon as possible to
decompress the stomach to avoid ongoing con-
tamination. Unless there is clear evidence that the
ulcer has been sealed off, an operation should be Fig. 16.1 Patch repair of perforated duodenal ulcer with
performed without delay. In young patients with a vascularised omental plug.
localised signs, trials of conservative management
with intravenous antibiotics, nasogastric drainage
and contrast X‐ray to confirm sealing of the ulcer
within 24 hours have been successful in some closing the defect. The closure of the defect in the
studies. stomach does not narrow the lumen and healing is
The operation of choice for a perforated duode- usually excellent with the well‐vascularised
nal ulcer is a simple patch repair. A piece of well‐ stomach.
vascularised omentum is sutured over the The discovery that PUD can be cured by eradi-
perforation to plug it (Figure 16.1). This is fol- cation of H. pylori has diminished the enthusiasm
lowed by a thorough lavage of the peritoneal cav- for definitive surgery at the same time as the
ity with copious amounts of warm saline to patch repair and it is now rarely performed. For
remove all the exudate and food particles. An patients known to be Helicobacter negative, an
intraperitoneal drain tube may be inserted in the ulcer‐curing operation (e.g. Billroth II gastrec-
vicinity of the repair. In most cases this is now tomy or Pólya gastrectomy) may be considered if
done with laparoscopic surgery, avoiding a painful there has been a long history of troublesome
wound. ulcer disease with complications, provided that
For a perforated gastric ulcer, the preferred repair the condition of the patient is good and the
is done by excising the ulcer, thereby obtaining a degree of contamination of the abdomen not too
biopsy to rule out a malignant ulcer, and primarily severe.
Obstruction decompressed, an endoscopy should be carried out

to confirm the diagnosis and to exclude malignancy.
Long‐standing duodenal or pre‐pyloric ulcers may
If the obstruction is due to oedema around an active
cause gastric outlet obstruction. It may be due
ulcer, such measures may restore patency. In the
either to fibrosis resulting from chronic ulceration
majority of cases, operative management is
and healing or to oedema associated with acute
required. Modern treatment involves a surgical
ulceration.
antrectomy and a Roux‐en‐Y reconstruction. In the
less fit a gastroenterostomy alone may bypass the
Clinical features obstruction but does not address the ulceration. In
elderly patients unfit for surgery, dilatation of the
The cardinal symptom is repeated vomiting of
stenotic area using a balloon catheter under endo-
undigested food that is not stained with bile. A his-
scopic guidance may be considered.
tory of long‐term PUD is frequent, as is long‐term
NSAID use. There may be weight loss and dehydra-
tion. In more indolent forms there may be early
Zollinger–Ellison syndrome
postprandial fullness and bloating. Abdominal
examination shows a dilated distended stomach.
This is a rare disease accounting for less than 1% of
Succussion splash (splashing noise on rocking the
PUD and is caused by over‐production of gastrin by
patient’s abdomen) is present several hours after a
G‐cell tumours of the pancreas or duodenum. This
meal.
is most often associated with the gastrin‐secreting
The inability to take fluids by mouth and vomit-
neuroendocrine tumor gastrinoma. Maximal gas-
ing of gastric juice lead to severe fluid and electro-
trin stimulation of the parietal cells leads to intrac-
lyte problems. The patient rapidly becomes
table peptic ulcerations. The majority (90%) of
dehydrated and salt depleted. Loss of acid and chlo-
gastrinomas occur within the ‘gastrinoma triangle’
ride ions in the gastric juice result in hypochlorae-
bounded by the cystic duct and bile duct, the junc-
mic alkalosis. There may be a large deficit of total
tion of the head and neck of the pancreas, and the
body potassium. Because of the severe sodium
second and third parts of the duodenum. Two‐
depletion, the distal renal tubules secrete potassium
thirds of all gastrinomas occur outside the pan-
and hydrogen ions in exchange for sodium ions in
creas. Approximately 50% of gastrinomas are
the glomerular filtrate. The urine is therefore acidic
malignant and up to one‐third have liver metasta-
in severe cases of gastric outlet obstruction,
ses; 10% of patients with Zollinger–Ellison syn-
although the patient is alkalotic. This is the so‐
drome have multiple lesions of the pancreas rather
called paradoxical aciduria.
than discrete tumours.
A gastric cancer in the antrum or the pyloric
canal causing obstruction may present in an identi-
cal manner. Clinical features
The diagnosis should be suspected when peptic
Treatment ulcers occur at unusual sites, such as the second
part of the duodenum or the jejunum, or ulcers
Fluid and electrolyte losses should be replaced by recur after adequate surgery. One‐third of patients
infusion of normal saline. Large amounts of potas- have watery diarrhoea due to high gastric output.
sium are likely to be required. Administration of Dehydration and acid–base or electrolyte imbal-
potassium supplements should be guided by esti- ance may occur.
mation of the serum level and acid–base balance. It
should only commence when renal failure is
excluded. Correction of alkalosis is not necessary. Diagnosis
Once the fluid and electrolyte deficiencies are cor- Gastrin can be measured by radioimmunoassay.
rected the body’s homeostatic mechanisms will The diagnosis is confirmed by demonstrating a high
restore the acid–base balance. fasting gastrin level. This may be confounded by
The stomach should be decompressed with a high‐dose PPIs, which also elevate gastrin levels but
nasogastric tube. Food particles may block the usually not to the level of a gastrinoma. Nuclear
tube, requiring gentle gastric irrigation. Intravenous medicine studies and MRI are helpful in localising
PPIs are administered. Once the stomach is these tumors in the gastrinoma triangle.
Treatment
MCQs
The aim of treatment of Zollinger–Ellison syn-
drome is twofold: Select the single correct answer to each question. The
• to control the high gastric acid output and sever correct answers can be found in the Answers section
the ulcer diathesis at the end of the book.
• to treat the gastrinoma. 1 With a perforation of a duodenal ulcer which
In the past a total gastrectomy was recommended occurred 6 hours ago, which of the following
to remove gastric acid production. Nowadays, the features is least likely to be present?
ulcer diathesis can usually be controlled by a high a generalised abdominal tenderness and guarding
dose of PPI. If a single discrete tumour can be iden- b the bowel sounds are hyperactive
tified in the pancreas or the duodenum, surgical c percussion over the liver may demonstrate
excision is the treatment of choice. resonance
d the respiration is shallow and the abdominal
muscles are held rigid
Further reading e plain radiograph shows free gas under the
diaphragm
Cirocchi R, Soreide K, Di Saverio S et al. Meta‐analysis of
perioperative outcomes of acute laparoscopic vs open 2 Which of the following factors is most likely to be
repair of perforated gastroduodenal ulcers. J Trauma associated with a significant risk of rebleeding from
Acute Care Surg 2018;85:417–25. a duodenal ulcer?
Debraekeleer A, Remaut H. Future perspective for poten-
a no further bleeding within 72 hours of the initial
tial Helicobacter pylori eradication therapies. Future
bleed
Microbiol 2018;13:671–87.
Lagoo J, Pappas TN, Perez A. A relic or still relevant: the b a clean based ulcer seen on endoscopy
narrowing role for vagotomy in the treatment of peptic c age less than 50 years
ulcer disease. Am J Surg 2014;207:120–6. d a visible vessel with adherent clot seen on endoscopy
Malmi H, Kautiainen H, Virta LJ, Färkkilä N, Koskenpato e the patient is female
J, Färkkilä MA. Incidence and complications of peptic
ulcer disease requiring hospitalisation have markedly 3 Which of the following is the treatment of choice
decreased in Finland. Aliment Pharmacol Ther for a perforated duodenal ulcer in a 56‐year‐old
2014;39:496–506. man with a strong history of ulcer disease and signs
Smith RS, Sundaramurthy SR, Croagh D. Laparoscopic
of peritonitis after 12 hours?
versus open repair of perforated peptic ulcer: A retro-
a conservative management with nasogastric
spective cohort study. Asian J Endosc Surg
2019;12:139–44. suction and intravenous fluids
Spiliopoulos S, Inchingolo R, Lucatelli P et al. b vagotomy and pyloroplasty
Transcatheter arterial embolization for bleeding peptic c omental patch repair and peritoneal lavage
ulcers: a multicenter study. Cardiovasc Intervent Radiol d highly selective vagotomy
2018;41:1333–9. e partial gastrectomy
17 Gastric neoplasms
John Spillane
University of Melbourne and Division of Cancer Surgery, Peter MacCallum Cancer Centre, Melbourne,
Victoria, Australia
cancers although its role in pathogenesis is

Gastric adenocarcinoma unclear.
Approximately 10% of gastric cancers are heredi-
Gastric cancer is the fourth most common cancer
tary, with 30–40% of hereditary diffuse gastric cancer
and the second most common cause of cancer‐
due to a germline mutation in the E‐cadherin CDH1
related deaths worldwide. It is a tumour that in the
gene. This was initially diagnosed in New Zealand
western world is often diagnosed late, with almost
Maori families with a high penetrance (70–80%) and
50% of patients having locally advanced or meta-
a lifetime risk of approximately 67% in men and
static disease at the time of diagnosis. High‐inci-
83% in women, who also have an increased risk of
dence areas occur in eastern Asia, particularly
breast cancer (mostly lobular) of 20–40%. It is recom-
Korea and Japan, as well as central and eastern
mended that at‐risk patients over the age of 20 years
Europe. It is more common in men. Over the last 40
with a CDH1 mutation or patients of any age with a
years the worldwide incidence of gastric cancer has
positive biopsy have a total gastrectomy. Patient under
been decreasing with an associated fall in the mor-
the age of 20 or over the age of 20 and who have
tality. The majority of the fall has been associated
declined prophylactic surgery should be placed in an
with tumours within the middle and distal stomach
endoscopic surveillance program.
as well as tumours involving the entire stomach.
Gastric cancer is also associated with other
The incidence of proximal gastric cancer has
genetic conditions, such as hereditary non‐polypo-
remained unchanged, making up approximately
sis colorectal cancer syndrome and, less commonly,
30% of all gastric cancers. Gastric cancers can be
with familial adenomatous polyposis coli and
classified anatomically into gastro‐oesophageal
Li–Fraumeni and Peutz–Jeghers syndromes.
junction tumours and true gastric cancers.
Symptoms include dyspepsia, upper abdominal
Histology
pain, anorexia and in more advanced stages weight
loss, vomiting and anaemia. The majority of gastric cancers are adenocarcino-
mas. The remainder are a mixture of lymphomas,
Epidemiology gastrointestinal stromal tumours and uncommon
malignancies such as neuroendocrine tumours.
Risk factors in areas with high incidence are
Adenocarcinomas are divided histologically
thought to be due to a combination of poor nutri-
using the Lauren classification into two main types,
tion, sanitation, obesity, smoking and alcohol
diffuse and intestinal, plus mixed and indetermi-
consumption. Diet, particularly foods that are
nate. Another classification is the World Health
salted, smoked, pickled or preserved foods rich in
Organization (WHO) system, which defines
salt and nitrites, increase the risk of gastric cancer.
tumours based on the histological pattern (tubular,
Helicobacter pylori is also directly associated
papillary, mucinous, poorly cohesive and rare).
with the development of gastric cancer; particular
strains, for example those positive for cytoxin‐
Staging
associated gene (cagA) and vacuolating cytotoxin
gene (vacA), are implicated. In western countries, The eighth edition of the American Joint Committee
approximately 60% of H. pylori are cagA positive on Cancer (AJCC) staging system has defined
but in Japan almost 90% of strains are positive. tumours crossing the oesophago‐gastric junction
Epstein–Barr virus has been detected in gastric (OGJ) with their epicentre in the proximal 2 cm of
143
the stomach as oesophageal cancers. Cancers cross- which increases with advancing T stage (T1a, ~3%;
ing the OGJ with the epicentre in the proximal 2–5 T1b, ~20%; T2, ~40%; T3, 50–60%; T4, ~70%).
cm of the stomach are stomach cancers.
Staging is based on the T (tumour), N (node) and
Regional lymph nodes
M (metastases) system and is now subdivided into
different categories. Clinical staging (cTNM) is a Regional nodes are defined as perigastric nodes
clinical assessment of the patient usually with stag- along the greater and lesser curvature, and the
ing investigations completed but no pathological supra‐ and infra‐pyloric and right and left pericar-
specimen. Pathological staging (pTNM) occurs dial regions, plus regional nodes along the left gas-
after assessment of the pathological specimen. tric, coeliac, common hepatic and splenic arteries,
Assessment post neoadjuvant therapy and patho- the hilum and hepatoduodenal nodes. The Japanese
logical specimen analysis is now termed ypTNM. Research Society categorises this into 16 lymph
This assesses the response of the cancer to therapy node stations, six perigastric and 10 regional sta-
and assesses if viable tumour cells are still present tions. Lymph node resections are then designated
within the resected stomach and lymph nodes. D1 (removing only perigastric nodes) or D2 (includ-
Depending on which system is used, the stage of the ing D1 nodes plus the other regional nodes).
tumour can be different (Table 17.1). Staging cor- Routine removal of the spleen is no longer per-
relates with survival and varies according to which formed as it increases the morbidity without
of the three systems are used. improving survival, although is still resected in
T staging is based on the depth of penetration of selected cases. Nodes around the porta hepatis or
the primary tumour (Table 17.2). Gastric cancer adjacent to the aorta are classified as D3. A D2 lym-
has a higher incidence of metastasis to lymph nodes, phadenectomy is considered the standard of care
Table 17.1 AJCC staging system for gastric cancer (8th edition) including clinical staging (cTNM), pathology
staging (pTNM) and post‐neoadjuvant therapy (ypTNM).
T N M cTNM pTNM ypTNM
Tis N0 M0 0 0
T1 N0 M0 I IA I
T1 N1 M0 IIA IB I
T2 N0 M0 I IB I
T1 N2 M0 IIA IIA II
T2 N1 M0 IIA IIA II
T3 N0 M0 IIB IIA II
T1 N3a M0 IIA IIB II
T2 N2 M0 IIA IIB II
T3 N1 M0 III IIB II
T4a N0 M0 IIB IIB II
T2 N3a M0 IIA IIIA III
T3 N2 M0 III IIIA III
T4a N1 M0 III IIIA III
T4a N2 M0 III IIIA III
T4b N0 M0 IVA IIIA III
T1 N3b M0 IIA IIIB II
T2 N3b M0 IIA IIIB III
T3 N3a M0 III IIIB III
T4a N3a M0 III IIIB III
T4b N1 M0 IVA IIIB III
T4b N2 M0 IVA IIIB III
T3 N3b M0 III IIIC III
T4a N3b M0 III IIIC III
T4b N3a M0 IVA IIIC III
T4b N3b M0 IVA IIIC III
Any T Any N M1 IVB IV IV
17: Gastric neoplasms 145
Investigation
Table 17.2 Definition of gastric TNM staging.
The diagnosis is made by gastroscopy and biopsy of
T stage the tumour. Tumours are further evaluated with
TX Primary tumour not assessable
endoscopic ultrasound (EUS) which assesses the T
T0 No primary tumour
and N staging. It can discriminate between superfi-
Tis Intraepithelial tumour without invasion of
lamina propria cial (T1–T2) and advanced (T3–T4) tumours as
T1a Invasion of lamina propria or muscularis well as assess lymph node positivity.
mucosae Computed tomography (CT) can assess nodal
T1b Invasion of submucosa and metastatic disease sites. Positron emission
T2 Invasion of muscularis propria tomography (PET) is less useful because signet
T3 Invasion of subserosal connective tissue ring tumours and poorly differentiated or diffuse
without invasion of visceral peritoneum or adenocarcinomas often lack fluorodeoxyglucose
adjacent structures (FDG) uptake that can lead to under‐staging of
T4a Invasion of serosa/visceral peritoneum
the disease. A diagnostic laparoscopy with
T4b Invasion of adjacent organs/structures
peritoneal washings and biopsy of any atypical
N stage
NX Regional lymph nodes unable to be assessed
peritoneal nodules will detect low‐grade meta-
N0 No regional metastatic nodes static disease not assessed by conventional imag-
N1 1 or 2 positive regional nodes ing. The risk of peritoneal spread increases with
N2 3–6 positive regional nodes advancing T stage and is highest with T4 and lini-
N3 7 or more positive regional nodes tis plastica tumours.
N3a 7–15 positive regional nodes Molecular testing for over‐expression of human
N3b 16 or more positive regional nodes epidermal growth factor receptor (HER2) should
M stage be performed. HER2 is a transmembrane tyrosine
M0 No distant metastases kinase receptor that regulates cell proliferation and
M1 Distant metastases
suppresses apoptosis. Approximately 12–20% of
gastric adenocarcinomas are HER2 positive.
Early gastric cancer

Box 17.1 Paris classification of
Early gastric cancer is gastric cancer confined to
microscopic morphology of early
the mucosa or submucosa (T1) regardless of
gastric cancer
lymph node status. The microscopic morphology
Type 0‐I Protruded type (0‐Ip, pedunculated of the lesions is defined by the Paris classification
or 0‐Is, sessile) (Box 17.1). More than 65% of cases are type
Type 0‐IIa Superficial and elevated type 0‐IIc.
Type 0‐IIb Flat type In countries with high levels of gastric cancer,
Type 0‐IIc Superficial and depressed type screening programs have been introduced. In Japan,
Type 0‐III Excavated type approximately 50% of gastric cancers are diag-
nosed at an early stage compared with approxi-
mately 20% in western countries. The frequency of
gastric cancer is significantly lower in western
throughout most of the world. At least 16 lymph
countries, making mass screening programs not
nodes must be assessed pathologically, with the
cost‐efficient. However, they can be considered for
removal of more than 30 nodes felt to be desirable.
high‐risk groups such as CDH1 carriers.
Nodal involvement outside these areas is consid-
The diagnosis of early gastric cancers can be
ered metastatic disease. The nodal staging is based
difficult. In addition to conventional endoscopy

on the total number of positive nodes removed (see
with white light imaging, chromoendoscopy uses
Box 17.1).
dye‐based enhancing agents such as acetic acid and
indigo carmine that are sprayed across the surface
of suspicious lesions to aid diagnosis and identify
Metastatic sites
the margins of the lesion. Other techniques include
The most common sites of metastatic disease are narrow‐band imaging technology and magnifying
the liver, peritoneum and non‐regional lymph endoscopes that allow near‐focus imaging of the
nodes. Pulmonary and central nervous system gastric mucosa and are built into modern
metastases occur but are less common. gastroscopes.
Surgery other arteries supplying the stomach (left and right

gastric, left and right gastroepiploic arcade) will be
Complete surgical resection with or without neo-
resected with the surgical specimen. In both cases a
adjuvant and adjuvant therapy is still the only
reconstruction is performed with the proximal
curative modality for gastric adenocarcinoma.
jejunum in a Roux‐en‐Y fashion or Billroth II
The type of operation varies depending on the
anastomosis that can be used for distal gastrecto-
position of the tumour, stage of disease and type
mies. Complications include anastomotic leakage,
of cancer.
fluid collections, abscesses and issues related to
ileus, bowel obstructions or poor motility. Late
Endoscopic therapy complications include gastritis, oesophagitis,
The treatment of early gastric cancer with endo- dumping, weight loss, and vitamin B12 and folate
scopic resection has become more common over the deficiencies.
last decade. The two main techniques are endo- There has been increasing use in recent years of
scopic mucosal resection (EMR) and endoscopic minimally invasive surgery, laparoscopic and, more
submucosal dissection (ESD). EMR involves the recently, robotic surgery to perform distal and total
separation of mucosa from submucosa by an injec- gastrectomies. The advantages of these approaches
tion of fluid. A variety of different techniques are are a shorter length of stay, less intraoperative
then used to resect the mucosa, including injection‐ blood loss, decreased pain, less use of intensive care
assisted, cap‐assisted and ligation‐assisted tech- services and quicker return to full function. The
niques. ESD involves resecting the mucosa around lymph node resection numbers are equivalent to
the lesion using an electrosurgical knife followed by open surgery, although the operating time is longer.
resection of the submucosa. The advantages of ESD The morbidity and mortality of laparoscopic sur-
over EMR are a higher en bloc and histological gery is equivalent in most studies to open surgery.
complete resection rate and lower local recurrence. Both robotic and laparoscopic gastrectomies have a
The disadvantage is a higher perforation rate considerable learning curve, with a significant early
(1–4.5%). Bleeding, both intraoperative and conversion rate.
delayed (~15%), is similar between the two meth-
ods. Recurrence rate following ESD is up to 1.1%.
The 5‐year overall survival is 92%. Chemotherapy and radiation therapy
This technique is used on tumours that are less As many patients present with advanced disease at
than 2 cm in diameter, well differentiated and the time of initial diagnosis, combined with the
without ulcerative features. Attempts to expand poor overall outcomes, particularly in the West for
these criteria are being investigated and well‐dif- all but the most early disease, a concerted effort has
ferentiated non‐ulcerated tumours of 3 cm or less been made in the last two decades to investigate the
could be considered for endoscopic resection. benefits of chemotherapy and radiotherapy in the
This relies on knowing that the risk of lymph treatment of gastric cancer. Treatments have used
node metastases is less than 3% for a T1a tumour. combinations of neoadjuvant (treatment prior to
T1b–T4 tumours should undergo standard surgi- surgical resection), adjuvant (commencing after
cal resection. If complete endoscopic resection is surgical resection) and perioperative (both neoad-
not possible, patients should undergo surgical juvant and adjuvant) therapies. The type of chemo-
resection. Ongoing endoscopic follow‐up is therapy also varies between studies. This can make
required due to the risk of metachronous gastric data interpretation confusing as to which regimen
cancer. is best. Additionally, studies within Asia have excel-
lent results but sometimes use treatments that are
Surgical resection not available in the West. The following sections
summarise general information regarding the use of
A total gastrectomy is indicated if the tumour
these therapies, which should be considered for any
involves the entire stomach or proximal stomach or
patient with nodal involvement or stage II–IV.
if the patient is a carrier of the CDH1 mutation. A
distal gastrectomy is indicated for tumours in the
Neoadjuvant chemotherapy
body or antrum, where a 4–6 cm proximal margin
can be obtained and leave a sufficient proximal Neoadjuvant chemotherapy down‐stages disease
stomach (minimum of 2 cm margin to the OGJ) for before surgical resection. A number of trials have
good functional capacity. For a distal gastrectomy examined this issue, the largest being MAGIC
the short gastric vessels must be preserved as the (Medical Research Council Adjuvant Gastric
Infusional Chemotherapy). This British study used for gastric cancer) had an improved disease‐free
three cycles of neoadjuvant and adjuvant chemo- and overall survival, although it required patients
therapy in addition to surgery for patients with to use a chemotherapy drug called S‐1 which is not
stage II or higher disease versus surgery alone. The available outside of Asia. The CLASSIC
trial showed a significantly improved overall and (Capecitabine and Oxaliplatin Adjuvant Study in
progression‐free survival for perioperative chemo- Stomach Cancer) used more conventionally avail-
therapy. However, 34% did not commence postop- able chemotherapy, again showing an improved
erative chemotherapy and only 42% received the disease‐free survival and an estimated improved
planned dose. The study included patients with dis- overall survival at the 5‐year follow‐up analysis.
tal oesophageal and gastro‐oesophageal junction Further studies are ongoing in this area, predomi-
tumours in addition to gastric cancers and used nantly in Asia.
what is now considered slightly older chemother-
apy regimens. However, a meta‐analysis of this Adjuvant chemoradiation
study and a number of other smaller studies has
The first trial to show a benefit of adjuvant chemo-
shown a statistically improved overall and progres-
radiotherapy was the Intergroup 0116 trial, which
sion‐free survival plus R0 resection rates in patients
investigated surgery plus adjuvant chemoradiother-
receiving neoadjuvant chemotherapy. Despite the
apy versus surgery alone. Although there was an
limitations of all these studies, neoadjuvant therapy
improved overall and disease‐free survival, which
became one standard of care approach. Ongoing
persisted at 10 years, there were some significant
studies are investigating the best type of chemother-
criticisms of the study. The surgery was not con-
apy regimen.
trolled, with 36% of patients receiving a D1 resec-
tion and only 10% receiving a D2 resection. Only
Neoadjuvant chemoradiation 65% completed the chemoradiotherapy as planned,
the majority due to toxicity. However, this study
Chemotherapy is known to be radiosensitising – it
changed the treatment approach for gastric cancer
makes tumour cells more responsive to radiation
and was adopted in many countries. The Korean
therapy. However, very few studies have investi-
ARTIST trial, comparing chemotherapy with chem-
gated this with regard to gastric cancer and there
oradiotherapy following a D2 resection, showed no
are no published randomised controlled trials.
difference in overall survival at 7 years of follow‐
There have been a number of studies investigating
up; however, it did show an improvement in sub‐
this treatment for oesophageal cancer, and have
analysis of patients who were lymph node positive.
included patients with gastro‐oesophageal junc-
A few other smaller trials have shown similar
tion and gastric cardia tumours. Studies such as
results, namely no survival difference between
CROSS (ChemoRadiotherapy for Oesophageal
chemotherapy and chemoradiotherapy. It is not
Cancer followed by Surgery versus Surgery alone)
clear if chemoradiotherapy adds a significant ben-
have shown an improved overall survival. Whether
efit to a D2 resection.
this can be extrapolated to gastric cancers is not
clear but is the subject of ongoing investigations
such as the TOPGEAR trial, an international pre-
Molecular therapy
dominantly western trial that has randomised
patients to neoadjuvant chemotherapy or chemo- The ToGA trial (Trastuzumab for Gastric Cancer)
radiotherapy prior to surgery with adjuvant showed an improved overall and progression‐free
chemotherapy. survival for HER2‐positive advanced gastric cancer
treated with trastuzumab plus chemotherapy with
no increase in adverse advents. Herceptin‐based
Adjuvant chemotherapy
therapies have now been incorporated into the
A number of older small studies have investigated chemotherapy treatments for patients with gastro‐
adjuvant chemotherapy. They used old chemother- oesophageal junction and gastric cancers that are
apy regimens that failed to show an improvement HER2 positive.
in survival. Two recent trials have investigated A number of ongoing studies are investigating
adjuvant chemotherapy, both conducted in Asia, the use of targeted therapies as well as immune sys-
but it is not clear if the results can be transferred tem modulating agents in the treatment of gastric
to western populations. Both studies used a D2 cancer. The results of these trials may significantly
gastrectomy as an entry criterion. The Japanese alter the management of gastric cancer in the
ACTS‐GC (Adjuvant Chemotherapy Trial of S1 coming years.
histopathological diagnosis. They comprise 2% of

Gastrointestinal stromal tumours all gastric malignancies.
Gastric neuroendocrine tumours have been clas-
Gastrointestinal stromal tumours (GIST) can arise
sified into well‐differentiated (types I–III) and a
anywhere within the gastrointestinal tract but are
poorly differentiated neuroendocrine carcinoma
most commonly found within the stomach (50–
(type IV). Tumours are graded according to the
60%). One‐third of tumours are asymptomatic
number of mitoses per 10 high‐power fields and
with the rest presenting with symptoms related to
percentage of tumour cells labelling positive for
mass effect such as dysphagia, early satiety, abdom-
Ki‐67 antigen.
inal discomfort, obstruction plus perforation and
These tumours are diagnosed by endoscopy and
anaemia. The median age at diagnosis is 60 years,
staged with EUS, CT, FDG and 68Ga DOTA‐TATE
with most having a mutation of C‐Kit or less com-
PET. Serum chromogranin A, which is expressed in
monly PDGFRA, succinate dehydrogenase defi-
secretory granules of the ECL cells, may be elevated
ciency and BRAF mutations.
and is a useful marker of response to treatment and
Up to 50% of patients present with metastatic
recurrence.
disease, most commonly to the omentum, perito-
• Type I tumours (70–80%): occur more com-
neum or liver. It is unusual, except in paediatric
monly in women, and are associated with chronic
cases, to have lymph node metastases. GIST push
atrophic gastritis, pernicious anaemia, elevated
onto surrounding structures without invading
plasma gastrin and low gastric acid levels. They
them.
are usually asymptomatic, with small (5–8 mm)
Surgical resection is recommended for primary
frequently multiple lesions found predominantly
tumours greater than 2 cm or for smaller tumours
within the fundus or gastric body. They are usu-
that are either symptomatic or increasing in size.
ally benign, with a 96% 5‐year survival.
Tumours of less than 2 cm often do not progress
Histology: grade 1, exhibits mitoses of less than 2
and can be conservatively managed with follow‐up
and Ki‐67 of less than 3%. Management is con-
CT scans. Tumours with high‐risk features on EUS
servative, with endoscopic follow‐up to detect
(irregular borders, ulceration, echogenic foci, het-
the rare event of malignant transformation.
erogeneity and cystic spaces) should be resected.
Surgery is reserved for high‐risk cases (six lesions,
Surgery involves segmental resection of only the
with three to four lesions larger than 1 cm or one
tumour to achieve negative resection margins
lesion larger than 2 cm).
allowing stomach preservation. Recurrence is high,
• Type II tumours (5–10%): caused by autologous
particularly in cases of increased size and high
gastrin secretion from a gastrinoma and associ-
mitotic rate. Intermediate and high‐risk tumours
ated with the Zollinger–Ellison syndrome, with
are treated with tyrosine kinase inhibitors
92% having multiple endocrine neoplasia type I
(imatinib). Current recommendations are for 3
syndrome. Up to 35% have metastatic disease at
years of adjuvant therapy.
diagnosis. The tumours are usually less than 1
For unresectable or metastatic disease, tyrosine
cm, have a low pH (<2), and may be multiple and
kinase inhibitors can achieve partial response
located in the proximal stomach. Histology:
rates of 50% and in stable disease of 30%. It is
grade 2, exhibits mitoses of 2–20 and Ki‐67 of
sometimes possible for tumours to subsequently
3–20%. Treatment is surgical resection along
become surgically resectable. Although response
with the gastrinoma. If the gastrinoma cannot be
rates are good, drug resistance occurs within
resected, acid hypersecretion needs controlling
2–2.5 years. Initial treatment is dose escalation
with proton pump inhibitors or serotonin
with imatinib. If further progression occurs,
antagonists.
second‐line therapy with sunitinib or third‐line

• Type III tumours (5–25%): occur predominantly
therapy with regorafenib can improve progres-
in males (~80%), and are usually large solitary
sion‐free survival.
tumours (1–2 cm) found in the fundus and body
but can occur within the antrum. Histology:
grade 3, exhibits mitoses of greater than 24 and
Gastric neuroendocrine tumours Ki‐67 of greater than 20%. More than 50% have
metastatic disease at the time of diagnosis.
Gastric neuroendocrine tumours arise from the Tumours are often poorly differentiated, with a
enterochromaffin‐like (ECL) cells located within high mitotic rate and Ki‐67. They are not
the gastric fundal mucosa. They are rare but have associated with hypergastrinaemia.
been increasing in incidence over the last 50 years • Type IV tumours: poorly differentiated, also
due to increased use of endoscopy and improved known as anaplastic high‐grade neuroendocrine
tumour or small cell carcinoma of the stomach. Olino KL, Tyler DS. Gastric neoplasms. Surg Clin North
The tumours are large (>2 cm), solitary and occur Am 2017;97:xv–xvi.
throughout the stomach. Approximately one‐ Van Cutsem E, Sagaert X, Topal B et al. Gastric cancer.
third have a concurrent gastric adenocarcinoma. Lancet 2016;388:2654–64.
There may be a reduced chromogranin A level
due to loss of ECL cell secretory function.
Types III and IV are treated with a radical partial or MCQs
total gastrectomy and an extended lymph node dis-
section. Metastatic disease is treated with somato-
statin analogues or peptide receptor radionuclide
therapy with lutetium‐177 or yttrium‐90 and
chemotherapy. 1 A 55‐year‐old male has been diagnosed with a
T2N1M0 gastric cancer in the upper body of the
stomach on staging investigations. Which of the
Gastric lymphoma following is the correct management plan?
a radical total gastrectomy and D2
Gastric lymphoma arises from lymphoid tissue in lymphadenectomy
the lamina propria. It is rare, comprising 3% of gas- b perioperative chemotherapy, total gastrectomy
tric tumours and 10% of lymphomas. More than and D2 lymphadenectomy
90% belong to two histological subtypes, low‐grade c radical distal gastrectomy and adjuvant
mucosa‐associated lymphoid tissue (MALT) lym- chemoradiotherapy
phoma (40%) and diffuse large B‐cell lymphoma d neoadjuvant chemoradiotherapy then total
(DLBL; 55%). The remainder comprise Burkitt’s gastrectomy
lymphoma and low‐grade non‐MALT lymphomas.
Most present with symptoms of epigastric pain, 2 A 60‐year‐old female is diagnosed with a GIST
anorexia, weight loss, bleeding and vomiting. B tumour in the proximal stomach invading the
symptoms (fever, night sweats and weight loss) are diaphragm and spleen. Which of the following is
not common in gastric lymphoma. At endoscopy, the correct management?
multiple superficial and deep biopsies are needed to a imatinib
aid the diagnosis and test for H. pylori. Staging is b radical total gastrectomy
completed with CT, PET, bone marrow biopsies c resection of proximal stomach, diaphragm and
and blood films. Chemotherapy and occasionally spleen
radiotherapy are the mainstay of treatment, with d sunitinib
surgery for complications (bleeding or perforation).
Eradication of H. pylori is important in the treat- 3 A 22‐year‐old female with CDH1 mutation had a
ment of MALT but also for DLBL disease. This can recent endoscopy with biopsies showing no
result in remission in up to 80% of cases with local- evidence of gastric cancer. She is reluctant to
ised disease. undergo a prophylactic gastrectomy. The manage-
ment options include:
a insist she undergo a total gastrectomy
Further reading b regular endoscopic follow‐up
c treatment with trastuzumab
Ajani JA, In H, Sano T et al. Stomach. In: Amin MB, Edge d EUS to better assess the stomach
SB, Greene FL et al. (eds) AJCC Cancer Staging Manual,
8th edn. New York: Springer, 2017:203–20.
18 Obesity and bariatric surgery
Yazmin Johari1 and Wendy A. Brown2
1
General Surgery Registrar, Alfred Health, Melbourne, Victoria, Australia
2
Department of Surgery and Centre for Obesity Research and Education, Monash University and Alfred
Health, Melbourne, Victoria, Australia
theory weight loss should be easy, a simple reversal

Introduction of the energy equation. In practice it is very hard to
achieve. Only 3% of obese persons can lose a sub-
Obesity is a rapidly growing problem in today’s soci-
stantial amount of weight and keep it off. This is
ety. The prevalence of obesity worldwide has nearly
because the body defends its fat mass vigorously, a
tripled since 1965. According to the World Health
concept known as the fat homeostat. Once an obese
Organization (WHO), in 2016 there were over 1.9
person loses weight, hormones that promote hun-
billion overweight or obese adults and 41 million
ger are produced, hormones that produce satiety
overweight or obese children under five. Over two‐
are decreased and the metabolic rate slows down.
thirds of adults in the USA are overweight or obese.
Weight loss is a powerful health improvement
In 2015, 63% of adults in Australia were considered
tool: the loss of just 5% of total body weight leads to
overweight or obese, compared with 56% in 1995.
impressive improvements in cardiovascular and met-
The WHO defines overweight and obesity as
abolic health. This means that once an obese person
follows.
loses weight, they can only consume around 1200
• Overweight: body mass index (BMI) greater than
kcal per day to maintain that weight loss for the rest
or equal to 25 kg/m2
of their life, and they are hungry. Hunger is very dif-
• Obese class I: BMI 30–34.99 kg/m2
ficult to control in the long term, and the character-
• Obese class II: BMI 35–39.99 kg/m2
istics of those persons who do manage to sustain
• Obese class III: BMI greater than or equal to 40
weight loss are that they weigh themselves daily, they
kg/m2.
severely caloric restrict on days that they have gained
The significance of obesity is considerable. It is well
even 0.5 kg and they exercise vigorously.
known to be closely related to a wide variety of dis-
Bariatric surgery refers to surgical management
eases, including type 2 diabetes, heart disease, stroke,
aimed to promote weight loss. All bariatric proce-
cancers, hepatic steatosis, osteoarthritis of the spine
dures aim to help a patient control their hunger,
and weight‐bearing joints, and obstructive sleep
allowing them to consume that small amount of
apnoea. The American Obesity Association has stated
1200 kcal/day and maintain their weight loss. On
that obesity increases the risk of death by at least
average, all bariatric procedures enable patients to
50%, making obesity the second leading cause of
lose and maintain around 50% of their excess weight,
preventable death in the USA. In addition to health
where excess weight is defined as the weight above a
consequences, the economic impact of obesity is sign-
BMI of 25 kg/m2. This translates to around 25–30%
ficant. The cost of treatment of obesity and its com-
total body weight loss, which is much higher than
plications in the USA is over US$200 billion.
what may be achieved with conservative programs.
Furthermore, obesity may lead to other indirect costs,
such as absenteeism or loss of productivity at work. Prevalence
It is estimated that 220 000 people underwent bari-
Baiatric surgery and its role atric surgery in the USA in 2008. Between 2014 and
in weight loss 2015, 22 700 bariatric surgeries were performed in
Australia, compared with 9300 procedures between
Fundamentally, obesity is caused by consumption 2005 and 2006. The number of procedures world-
of energy in excess of expenditure of energy. In wide has relatively plateaued since 2008, with the
151
USA being the most prolific, followed by Brazil, • Improvement in psychosocial status: improvement
France, Mexico, Australia and New Zealand. in depression, body image and quality of life.
The most common procedures performed are:
• sleeve gastrectomy Mechanisms of weight loss
• laparoscopic adjustable gastric band (LAGB)
• Early induction of satiety and sustained satia-
• Roux‐en‐Y gastric bypass (RYGB)
tion: these procedures alter the normal hormonal
• biliopancreatic diversion with duodenal switch
milieu or change the neural signals to cause early
(BPD/DS).
cessation of feeding and sustained satiation so
Indications that the person does not seek more than two to
three meals per day.
• BMI of greater than or equal to 40 kg/m2 • Malabsorption: procedure decreases the effective
• BMI of 35–39.9 kg/m2 with an obesity‐related absorption of nutrients by shortening the length
comorbidity of functional small bowel, for example in bilio-
• BMI of 30–34.9 kg/m2 with uncontrollable type pancreatic diversion.
2 diabetes mellitus or metabolic syndrome • Combination of restriction and malabsorption,
such as RYGB and BPD/DS.
Contraindications
• Untreated depression or psychosis
• Untreated eating disorder Laparoscopic adjustable gastric band
• Current drug and alcohol abuse
• Severe cardiac disease prohibiting anaesthesia LAGB is a satiety‐inducing procedure whereby a
• Inability to comply with nutritional changes and saline‐filled adjustable silicone band is placed near
requirements the gastro‐oesophageal junction to create a small
stomach pouch with a capacity of 15–20 mL. The
Benefits band is then connected to a port that is placed sub-
cutaneously. The port can be easily accessed in the
• Sustained weight loss: bariatric surgery has been
clinic to increase or decrease the amount of saline
proven to be more effective than behavioural or
in the band to adjust the stoma (opening) of the
medical management of obesity in morbidly
band, thus controlling the food intake (Figure 18.1).
obese patients. In the 10‐year prospective con-
When the band contains the appropriate amount
trolled Swedish Obese Subjects Study, bariatric
of saline, patients describe feeling satisfied after a
surgery successfully reduced patients’ weight by
small amount of food. They then do not seek fur-
16.1% compared with an increase in weight of
ther food for several hours as they are not hungry.
1.6% in the control group who underwent
Typically, patients will eat two to three small meals
behaviour modification.
a day, meaning they are consuming around 1200
• Increased physical function.
kcal/day.
• Improvement in medical comorbidities:
Patient compliance and regular long‐term fol-
◦◦ Type 2 diabetes: better glycaemic control con-
low‐up are vital for monitoring satiety, food intake
tributes to remission and improvement in dis-
and weight. This information is used to frequently
tal peripheral neuropathy.
adjust the amount of saline in the gastric band sys-
◦◦ Hypertension: improves obesity‐related
tem to individualise therapy. A multidisciplinary
hypertension.
team involving the surgical team, nutritionist and
◦◦ Dyslipidaemia: improves lipid profiles with
general practitioner is important for providing edu-
reduction in low‐density lipoprotein, triglycer-
cation about food choice and eating style, band
ide and total cholesterol, and increase in high‐
adjustment and monitoring for complications, as
density lipoprotein.
the foreign body in situ may potentially fail or
◦◦ Obstructive sleep apnoea: decreased apnoea–
develop late complications (see Table 18.1).
hypopnoea index (AHI, the number of apnoea
and hypopnoea events per hour of sleep),
Advantages
reduced daytime sleepiness.
◦◦ Joint pain: decreased load on weight‐bearing • The expected weight loss (EWL) achieved by
joints such as the spine, hips and knees. LAGB is 50% over 1–2 years, at a rate of 0.5–1.0
◦◦ Polycystic ovarian syndrome: restored menstrual kg/week. Results have been demonstrated to be
cycles, lessened hirsutism and hyperandrogenic durable beyond 10 years.
symptoms, and increased ability to conceive. • It is a reversible procedure.
18: Obesity and bariatric surgery 153
Gastric pouch
Tube
Band
Port (positioned
subcutaneously)
Fig. 18.1 Laparoscopic adjustable gastric band.
• The adjustability of the band offers advantages Complications

when addressing various nutritional needs, such as
See Table 18.1.
increased nutrient and caloric intake in pregnancy.
• It is a relatively simple procedure, with a lower
perioperative complication rate compared with a
more involved procedure such as RYGB. Sleeve gastrectomy
• Several conversion options are available: sleeve
gastrectomy, RYGB, BPD/DS. Laparoscopic sleeve gastrectomy is currently the
most common procedure in Australia, accounting
for 52.5% of total bariatric procedures between
Disadvantages
2014 and 2015. It involves removing the fundus
• Rate of weight loss is slower (0.5–1.0 kg/ week) and greater curvature of the stomach and reduc-
compared with sleeve gastrectomy until it stabi- ing stomach volume from 2 L to 100–150 mL.
lises 2 years postoperatively The new tubular stomach is resistant to stretch-
• Strict follow‐up is required to adjust caloric ing due to the removal of fundus. It was first
intake and maintain weight loss especially in the described in 1998 as a part of biliopancreatic
first year. diversion but is now considered a stand‐alone
• There is a 10–30% risk of re‐operation or revi- procedure due to its efficacy and minimal inva-
sion in 10 years. siveness (Figure 18.2).
Table 18.1 Complications of laparoscopic adjustable gastric band.
Symptoms/signs Investigations Management
Acute
Acute stomal obstruction
• Acute postoperative period Inability to tolerate Barium swallow Expectant management
secondary to postoperative oral fluids until oedema reduced
oedema or inadequate removal postoperatively May require revisional
of perigastric fat surgery
• Post‐adjustment excessive Inability to tolerate — Remove excess fluid from
fluid inserted into the system oral fluids post port
adjustment
• Acute food bolus obstruction Vomiting — Drink carbonated fluids
after eating difficult textured undigested food to dislodge the food bolus
food in excess and too quickly and saliva Remove fluid from the
system
Acute band slippage and Epigastric pain Abdominal X‐ray Nil orally
stomach herniation Haematemesis Barium swallow Remove all fluid from the
Dehydration system
Vomiting Prompt band revision
Unable to tolerate
solid food
Port infection (can be associated Cellulitis/collection Gastroscopy should be Antibiotics
with band erosion) over port site considered to assess Drainage of infective
gastric integrity in collection
suspected band erosion Removal with or without
replacement of port
Chronic
Band erosion Loss of satiety Gastroscopy Nil orally
Weight gain Intravenous antibiotics
Spontaneous port Band removal and
infection drainage or omental
patch
Chronic band slippage and Vomiting Barium swallow Remove all fluid from the
stomach herniation Regurgitation system
Volume reflux May require revisional
(especially with surgery
recumbency)
Inability to tolerate
a solid diet
Pouch dilatation Vomiting Barium swallow Remove fluid from the
Regurgitation system
Volume reflux Introduce small amounts
Weight gain of fluid into the system
Decreased satiety gradually
Increased need for May require revisional
adjustment surgery
Port flipped Difficulty in Abdominal X‐ray Port revision
accessing port
Port leaking. Tubing Decreased satiety Repeatedly checking the Port/band revision
disconnected, kinked or leaked Increased need for amount of fluid within
adjustment the system
Fluoroscopy
Advantages gastroscopy is recommended for assessing reflux

in patients with symptoms of reflux but which
• EWL is approximately 60–66% at 2 years. There
remains undiagnosed.
are only three series describing results beyond 8
• Weight regain: there are only three studies published
years at this time. All have a weight loss of 50%
beyond 8 years and all report around a 30% con-
EWL at the later time points.
version rate to RYGB for weight regain or reflux.
• It is technically easier to perform than RYGB or
• Nutritional problems: patients must be vigilant
BPD as it does not require multiple anastomoses.
with multivitamin supplementation. There are
• It does not require strict and close follow‐up as
case reports of beri‐beri in patients who were
for LAGB.
vomiting after this procedure. There a risk of
iron, calcium, B‐group vitamin and protein defi-
Disadvantages ciencies (see Table 18.2).
• Conversion from sleeve gastrectomy usually
involves more difficult operation such as RYGB Complications
or BPD/DS. See Table 18.2.
• Gastro‐oesophageal reflux: sleeve gastrectomy
has been shown to increase pre‐existing symp-
toms of reflux or encourage the development of Roux‐en‐Y gastric bypass
symptoms of reflux if the patient is asympto-
matic preoperatively. There have been recent RYGB, developed with the intention of creating
reports of a 15–20% incidence of de novo restriction and malabsorption, has been the gold
Barrett’s oesophagus at 5 years post surgery. This standard of weight loss operations since the 1980s.
procedure is not suitable for patient with pre‐ Alan Wittgrove and Wesley Clark first described
existing symptomatic reflux. Preoperative the laparoscopic approach in 1994. There has been
Gastric sleeve
Resected
stomach
Fig. 18.2 Sleeve gastrectomy.

Table 18.2 Complications of laparoscopic sleeve gastrectomy.
Symptoms/signs Investigations Management
Acute
Bleeding/haematoma Symptoms of blood loss and Full blood examination May require return to
at staple line intra‐abdominal bleeding theatre
Gastric leak Abdominal pain Inflammatory markers Nil orally and parenteral
Symptoms of sepsis CT (on‐table oral nutrition
contrast to assess for leak Intravenous antibiotics
and associated collection) Drainage of intra‐
Gastroscopy abdominal collection
Endoscopic/ surgical
intervention
Chronic
Gastro‐oesophageal Heartburn Barium swallow Proton pump inhibitors
reflux disease and Volume reflux Gastroscopy Conversion to RYGB
Barrett’s oesophagus Effortless regurgitation
Stenosis (commonly Dysphagia Barium swallow Endoscopic balloon
at the incisura) Vomiting dilatation
Inability to tolerate oral diet Revisional surgery/
conversion to RYGB
Expansion of gastric Loss of restriction Barium swallow Revisional surgery/
sleeve Weight gain conversion to RYGB
Gastric pouch
Proximal gastro-jejunostomy
Biliopancreatic
limb Roux (alimentary)
limb
Distal jejuno-jejunostomy
Common channel
Fig. 18.3 Roux‐en‐Y gastric bypass.

a gradual decline in its use globally, with the discov- of functional small bowel for nutrient absorption
ery of more minimally invasive options such as (Figure 18.3).
sleeve gastrectomy and other bariatric procedures.
It involves creating a small gastric pouch of 15–30 Advantages
mL isolated from the distal stomach, the jejunum is
• EWL after RYGB at 2 years is around 70% and
divided and the distal end attached to the stomach
50% at 5 years.
pouch (alimentary or Roux limb), whilst the other end
• Improves gastro‐oesophageal reflux symptoms.
(biliopancreatic limb with output from duodenum,
liver and pancreas) is attached to the alimentary limb
Disadvantages
about 1 m distal to the stomach, so that the remainder
of the stomach and duodenum are bypassed. Most • It is a more complex procedure with higher intra-
nutritional absorption occurs in the common channel. operative risk of complications such as anasto-
The small gastric pouch serves to restrict caloric mosis leak (see Table 18.3).
intake. Dividing the small bowel reduces the length • It is a permanent procedure.
Table 18.3 Complications of Roux‐en‐Y gastric bypass.
Description Symptoms/signs
Acute
Anastomotic Can occur at either anastomosis Abdominal pain
leak Revision of previous bariatric procedures carries higher risk Symptoms of sepsis and vascular
compromise
Gastric The blind end pouch becomes distended secondary to distal Abdominal pain, hiccups, shoulder
remnant obstruction or paralytic ileus postoperatively, and may lead to pain, abdominal distension,
distension rupture, spillage of gastric content and severe peritonitis shortness of breath
Internal Secondary to mesenteric defects that are not closed Abdominal pain
herniation intraoperatively Symptoms of small bowel
• Mesenteric defect at jejuno‐jejunostomy obstruction
• Space between the transverse mesocolon and Roux‐limb
mesentery (Petersen’s defect)
• Defect in the transverse mesocolon in retrocolic Roux limb
(when Roux limb positioned posterior to transverse colon)
Chronic
Dumping Secondary to rapid transit of food into small bowel Nausea, diaphoresis, abdominal pain,
syndrome diarrhoea after high sugar meals
Malnutrition Occurs due to reduced intake and absorption of Symptoms of micronutrient
micronutrients, particularly iron, calcium, vitamin B12, deficiencies
thiamine, folate
Pouch Can also occur with dilatation of the anastomosis between Loss of restriction, weight gain
dilatation gastric pouch and Roux limb
Anastomosis/ Usually occurs at the gastro‐jejunal anastomosis typically Vomiting, volume reflux,
stomal several weeks after surgery dysphagia, and inability to tolerate
stenosis Presents clinically when the stoma narrows to <10 mm in oral intake
diameter
Marginal Occur commonly near gastro‐jejunal anastomosis due to Abdominal pain, symptoms of
ulcers gastric acid injuring the jejunum gastrointestinal bleeding, stomal
Can occur in association with gastro‐gastric or gastro‐colic fistula stenosis or perforation
Candy cane Occurs due to excessive long blind afferent Roux limb that Postprandial epigastric pain often
Roux distends with food relieved by vomiting, reflux, food
syndrome Can present as early as 3 months postoperatively or as late as regurgitation
10 years
Cholelithiasis Secondary to rapid weight loss causing changes in bile Symptoms of biliary colic or other
constituents complications of cholelithiasis
Develops in 38% of patients within 6 months postoperatively
Gastro‐ Connection between the gastric pouch and the excluded Weight gain
gastric fistula stomach remnant Symptoms of marginal ulcers
Commonly causes marginal ulcers
• Revision is complicated and incurs higher opera- and lowers the incidence of anastomostic ulcers
tive risk. and diarrhoea.
• There is a higher risk of nutritional deficiency. Because of its technical difficulty and risks, BPD/
DS is relatively uncommon, accounting for 1%
of bariatric procedures performed in the USA and
Complications
only 0.2% in Australia in 2017.
See Table 18.3.
Advantages
• Rapid and substantial weight loss: EWL at 2
Biliopancreatic diversion with duodenal years is 70–80%.
switch
Disadvantages
BPD/DS is both restrictive and malabsorptive. It • This is a more complex procedure with higher
involves creating a gastric sleeve and preserving the mortality and intraoperative and postoperative
pylorus. The ileum is then divided with the distal risks such as anastomosis leak.
end attached to the remaining stomach, creating an • Malnutrition: protein malnutrition, anaemia, met-
alimentary/Roux limb with a short common chan- abolic bone disease, fat‐soluble vitamin deficiency.
nel. The proximal ileum, which contains the output
from the duodenum, liver and pancreas, is attached
to the terminal ileum 50–100 cm away from the
ileocaecal valve (Figure 18.4). Conclusions
This procedure differs from the original biliopan-
creatic diversion that involves the division of the Bariatric surgery plays a key role in the treatment
duodenum from the pylorus and removal of the of obesity. It has been shown to be an effective
pylorus. This is to avoid the complication of stasis adjunct in achieving and maintaining substantial
Gastric sleeve
Gastro-ileal
anastomosis
Biliopancreatic limb
Alimentary limb
lleo-ileal anastomosis
Common
channel
Fig. 18.4 Biliopancreatic diversion with duodenal switch.

weight loss, as well as treating obesity‐related dis- 2 Which of the following is not a contraindication for
ease. Whilst procedures differ in their weight loss bariatric surgery?
trajectories, by 5 years it appears that weight a severe cardiac disease
loss is similar for all procedures. Patient selection b untreated major depressive disorder
and compliance with follow‐up and dietary recom- c inability to comply with nutritional changes and
mendations are crucial in the success of these requirements
procedures. d obstructive sleep apnoea
Severe complications from bariatric surgery are e current alcohol dependence
uncommon, but high suspicion is warranted when
patients with a history of bariatric surgery present 3 Lucy underwent a bariatric procedure that involves
to the clinic or emergency department. Long‐term dividing the jejunum and attaching the distal end to
follow‐up is pertinent for ensuring the success of a small gastric pouch that is disconnected from the
surgery, maintaining adequate nutrition and moni- remaining stomach. Which procedure did she have
toring for complications as these may present many done?
years after the initial operation. a Roux‐en‐Y gastric bypass
b sleeve gastrectomy
c biliopancreatic diversion with duodenal switch
d laparoscopic adjustable gastric band
Further reading e jejunoileal bypass
O’Brien PE. Bariatric surgery: mechanism, indications, and 4 Jon presented to the emergency department 5 days
outcomes. J Gastroenterol Hepatol 2010;25:1358–65. after laparoscopic sleeve gastrectomy. He has not
O’Brien PE, Dixon JB, Brown W. Obesity is a surgical dis- been quite well since, with epigastric pain, nausea,
ease: overview of obesity and bariatric surgery. ANZ J intermittent fevers and chills, and is unable to
Surg 2004;74:200–4.
tolerate much oral intake. What investigation
Sjostrom L, Lindroos A, Peltonen M et al. Lifestyle, diabe-
would be most helpful in the emergency depart-
tes, and cardiovascular risk factors 10 years after bari-
atric surgery. N Engl J Med 2004;351:2683–93. ment to diagnose his problem?
Telem D, Greenstein AJ, Wolfe B. Late complications of a gastroscopy
bariatric surgery operations. https://www.uptodate. b barium swallow
com/contents/late‐complications‐of‐bariatric‐surgical‐ c computed tomography
operations?search=bariatric%20surgery&source=search_ d abdominal ultrasound
result&selectedTitle=12~150&usage_type=default& e magnetic resonance cholangiopancreatography
display_rank=12 (accessed 9 February 2018).
5 Sookyung underwent laparoscopic adjustable
gastric banding 6 months ago and was doing well
with regular small increments of saline inserted into
MCQs her band system up to 7 mL. At her 6‐month
outpatient review, she had a further 0.5 mL of
saline inserted into her band, but 2 hours later she
noticed she was unable to tolerate her smoothie.
What is the most likely cause of Sookyung’s
1 Which of the following procedures is most likely to problem?
increase gastro‐oesophageal reflux? a acute prolapse of proximal stomach
a Roux‐en‐Y gastric bypass b acute stomal obstruction from excessive fluid in
b sleeve gastrectomy system
c biliopancreatic diversion with duodenal switch c band erosion
d laparoscopic adjustable gastric band d port leaking
e all of the above e acute food bolus obstruction
Section 3
Hepatopancreaticobiliary Surgery
19 Gallstones
University of Sydney and Westmead Hospital, Sydney, New South Wales, Australia
Incidence: an overview Types
In most western countries, and certainly in Gallstones are essentially crystals that develop in
Australia, gallstones are the most frequent gastroin- the gallbladder; however, in some circumstances
testinal surgical cause for admission to hospital. In they may develop outside the gallbladder, primarily
Australia, the gallbladder is the most frequently in the bile duct. In 80% of cases in western coun-
removed organ and approximately 50 000 chole- tries the gallstones will be cholesterol or mixed
cystectomies are done each year. stones which contain calcium. Pigmented stones are
The incidence of gallstones varies widely depend- black or brown in colour. Black stones are generally
ing on the demographic group. In Australia, the associated with haemolytic conditions and are
incidence of gallstones is estimated to be 10–15% small and composed predominantly of calcium bili-
and most of these patients are asymptomatic. In rubinate and mucin glycoproteins. Brown stones
comparison, the incidence of gallstones amongst are more commonly seen in Asian populations and
black sub‐Saharan Africans is less than 5%. In are associated with parasitic or bacterial infections.
Asian populations, the incidence may be lower Unlike black stones they more commonly form in
(5–10%) but as more Asians are exposed to high‐ the biliary passages.
fat western diets this incidence is on the increase.
The incidence of gallstones amongst the indigenous
peoples of Chile is 49% in women and 12% in Bile production and the enterohepatic
men, whereas the indigenous peoples in North circulation
America may have the highest reported rates with
up to 29% of men and 64% of women developing Bile acids are formed by two pathways. The classic
gallstones. Gallstones are the chief risk factor for pathway occurs only in the liver as it requires the
the development of gallbladder cancer. This is enzyme cholesterol 7α‐hydroxylase (CYP7A1),
important: gallbladder cancer is rare in western which is found in the hepatocytes, to hydroxylate a
countries (less than two cases per 100 000 popula- sterol nucleus. The alternate pathway occurs in
tion per year) but more common in Chile (15.6 extrahepatic tissue such as the kidney, macrophages
cases per 100 000 women per year). and vascular endothelium where the enzyme oxys-
Importantly, the incidence of gallstones increases terol 7α‐hydroxylase oxidises cholesterol to oxys-
with age and this is a significant issue, especially in terols, which are then transported to the liver where
western countries with ageing populations. In par- the primary bile acids, cholic and deoxycholic acid,
ticular, gallstones are much more frequent over the are formed. In healthy individuals without liver dis-
age of 40. A British autopsy study showed that the ease the alternate pathway only contributes 10% of
incidence of gallstones in women aged 50–59 years overall bile acid synthesis.
was 24% and this increased to 30% in the ninth After the bile acids are synthesised in the liver
decade. The same study showed that amongst men they are conjugated with either glycine (75%) or
the incidence increased from 18% in those aged taurine (25%) and are then secreted into the bile
50–59 years to 29% in the ninth decade. ducts and stored in the gallbladder where
163
164 Hepatopancreaticobiliary Surgery
concentration of the bile occurs. When a meal is • Obesity and dietary factors: obese individuals
eaten the gallbladder is stimulated by cholecysto- have a higher risk of gallstones compared with
kinin (CCK) and the gallbladder empties 70–80% lean individuals. It has been estimated that the
of its contents into the bile duct and subsequently relative risk of gallstones is increased by a factor
into the duodenum and small bowel. Once in the of at least two in both men and women who are
intestine the bile forms micelles and is responsible obese. Morbidly obese women (BMI >32 kg/m2)
for digesting fats, fat‐soluble vitamins and some have an even higher risk of gallstone formation
drugs. It is thought that the primary cause of cho- with an age‐adjusted relative risk of 6. A diet
lesterol gallstones is the presence of cholesterol‐ which leads to increased obesity increases the
supersaturated bile, which is lithogenic. This risk of gallstone formation. It does appear that
lithogenicity may be modified by factors within the any diet which is high in fats and cholesterol
bile such as excess cholesterol, changes in the bil- increases the risk of gallstone formation.
iary and bowel microbiome, low bile salt levels, Conversely, the risk of gallstones may be reduced
abnormal lipid transport, mucus secretion and by a low‐fat diet, legumes and a moderate intake
impaired gallbladder emptying. The production of of alcohol. Certainly, it does appear that some
bile acids is the main pathway for the excretion of ethnic groups who have a low risk of gallstone
cholesterol, accounting for about 50% of daily formation such as Native Americans may form
excretion. In a healthy adult the liver produces gallstones at an increased rate with exposure to a
600–750 mL of bile per day. western diet, which is usually low in fibre and
Once primary bile acids are secreted into the high in refined carbohydrates and fat. Rapid
bowel, some are deconjugated to secondary bile weight loss is also associated with an increased
acids by intestinal bacteria. In the ileum some of the risk of gallstone formation.
secondary bile acids are reabsorbed passively, • Genetic predisposition: gallstones often run in
whereas the conjugated bile acids are reabsorbed families, with an increased risk of gallstone for-
by an active transport system. In most individuals mation related to family history.
95% of bile acids are reabsorbed in the ileum and • Ethnicity: as noted earlier, the incidence of gall-
transported back to the liver and only 5% are stone formation varies for different ethnic
excreted via the large bowel. If there is increased groups.
secretion via the large bowel, due to a variety of • Total parenteral nutrition (TPN) is a known risk
causes such as ileal resection, previous cholecystec- factor for cholelithiasis. It was recognised some
tomy, inflammatory bowel disease or radiation time ago that seriously ill patients in intensive
therapy, this may be associated with the develop- care on TPN were at increased risk of acalculous
ment of chronic diarrhoea. cholecystitis. However, more recently it has been
recognised that many of these patients do in fact
have microlithiasis. It has been shown that for
Risk factors seriously ill patients in intensive care that biliary
sludge may appear after a few days of fasting.
In the majority of patients who develop gallstones the Biliary sludge will appear ultrasonographically
causes are multifactorial. However, there are many after 4 weeks of TPN in up to 50% of patients
factors that predispose to gallstones that are modifi- and this may increase the longer the TPN is con-
able. The causes of gallstones include the following. tinued. After cessation of TPN many instances of
• Age: as previously noted the incidence of gall- microlithiasis will resolve rather than progress to
stones increase with age. gallstone formation. The mechanism of gallstone
• Gender: females are at least twice as likely to formation may be related to ileal atrophy due to
develop gallstones as men, at least up to meno- TPN.
pause. This is probably related to both endoge- • Haemolytic diseases: particularly in sickle cell
nous oestrogen and the oral contraceptive. disease, hereditary spherocytosis and hereditary
• Pregnancy: this is an independent risk factor for elliptocytosis where there is chronic haemolysis,
the development of gallstones. It is common for this leads to increased bilirubin secretion with
women to develop symptoms during pregnancy the formation of black pigment gallstones.
and this is because of increased oestrogen secre- • Other chronic diseases: ileal Crohn’s disease is asso-
tion, which results in increased biliary sludge for- ciated with an increased incidence of gallstones.
mation. This may resolve after childbirth but Likewise, cystic fibrosis is associated with an
may result in definitive persistent gallstones in increased prevalence of gallstones. Cirrhosis is
about 5% of women. associated with an increased prevalence of
19: Gallstones 165
gallstone formation. Spinal cord injury is associated

Table 19.1 Tokyo diagnostic criteria for acute
with a significant increase in the risk of formation
cholecystitis.
of gallstones possibly due to gallbladder stasis.
• Drugs: those which may increase the risk of gall- A Local signs of inflammation, etc.
stone formation include thiazide diuretics, ceftri- 1 Murphy’s sign
axone and octreotide. Conversely, statins may 2 RUQ mass/pain/tenderness
decrease the risk of gallstone formation. B Systemic signs of inflammation, etc.
1 Fever
2 Elevated CRP
Presentation 3 Elevated WBC count
C Imaging findings
Biliary colic and acute cholecystitis Imaging findings characteristic of acute cholecystitis
Definite diagnosis
It is estimated that 10–15% of the population in 1 One item in A and one item in B are positive
Australia and the USA will have gallstones. 2 C confirms the diagnosis when acute cholecystitis
However, most people with gallstones are asympto- is suspected clinically
matic. It is estimated that each year 2–4% of people
with gallstones will develop symptoms and, gener- CRP, C‐reactive protein; RUQ, right upper quadrant;
ally, once symptoms develop they will continue, WBC, white blood cell count.
although this is unpredictable and may be modified Source: Yokoe M, Takada T, Strasberg SM et al. New
by a change in diet and other factors. Most patients diagnostic criteria and severity assessment of acute
cholecystitis in revised Tokyo Guidelines. J
who develop symptoms related to gallstones will
Hepatobiliary Sci 2012;19:578–85. © 2012 Japanese
develop biliary colic. This usually manifests as epi-
Society of Hepato‐Biliary‐Pancreatic Surgery.
gastric and right upper quadrant pain that may Reproduced with permission of John Wiley and Sons.
radiate to the back and often follows a fatty meal.
This is often associated with nausea or vomiting
cholecystitis is highly variable and influences the
and there may be a history of fatty food intoler-
choice of treatment. The Tokyo guidelines are an
ance. The pain may vary from relatively mild to
attempt to grade the severity of acute cholecystitis
excruciating. The pain is caused by a stone lodging
and are widely used by clinicians (Table 19.2).
in the outlet of the gallbladder and the pain may
resolve suddenly with dislodgement of the stone.
If the stone does not dislodge, the blockage of the
Gallstone pancreatitis
gallbladder outlet or cystic duct causes increased Gallstones are the most common cause of pancrea-
pressure within the gallbladder. The bile is then titis in western countries and account for 60–70%
forced into the wall of the gallbladder, resulting in of cases. In the majority the pancreatitis is mild and
oedema and inflammation. As the pressure increases self‐limiting. It may be severe in 20% and in such
this causes venous ischaemia, which can lead ulti- cases mortality may approach 20–30%. Gallstone
mately to necrosis of the wall of the gallbladder if pancreatitis is increasing in incidence in western
the process is not arrested. Pathophysiologically, countries and has an estimated incidence of about
this can result in an empyema of the gallbladder 40 per 100 000 population per year. It is most com-
where the gallbladder is full of pus or indeed perfo- mon in women in their sixties.
rates. This infection may result in translocation of Although the association between gallstones and
bacteria, resulting in bacteraemia or indeed septi- pancreatitis was first described in the nineteenth
caemia. The most common organisms involved in century, the mechanism was not well understood. It
this process are Gram‐negative organisms such as is now believed that a stone passing through the
Escherichia coli, Klebsiella or Pseudomonas. Other sphincter of Oddi causes irritation, oedema and
organisms that may be present include Clostridium, temporary obstruction to the pancreatic duct,
Staphylococcus or Salmonella. resulting in outflow obstruction to the pancreatic
Acute cholecystitis is associated with persistent duct and a raised intraluminal pressure. This causes
right upper quadrant pain and tenderness. Nausea a cascade of biochemical reactions that result in
or vomiting is frequently present and the patients release of pancreatic enzymes and oedema of the
are often febrile. Murphy’s sign, when an examiner pancreas resulting in inflammation. If the process
notes that a patient stops breathing due to pain continues unabated this results in further inflam-
over the inflamed gallbladder, is helpful in diagnos- mation, release of inflammatory cytokines and a
ing acute cholecystitis but its absence does not systemic inflammatory response syndrome (SIRS).
exclude it (Table 19.1). The severity of acute The severity of the pancreatitis is unpredictable but
Table 19.2 Tokyo guidelines for severity of acute Table 19.3 Causes of acute cholangitis.
cholecystitis.
Cholelithiasis
Grade III (severe) acute cholecystitis Benign biliary stricture
Associated with dysfunction of any of the following Congenital factors
organs/systems: Postoperative factors (damaged bile duct, strictured
• Cardiovascular dysfunction: hypotension requiring choledojejunostomy, etc.)
treatment with dopamine ≥5 μg/kg per min or any Inflammatory factors (oriental cholangitis, etc.)
dose of noradrenaline Malignant occlusion
• Neurological dysfunction: decreased level of Bile duct tumour
consciousness Gallbladder tumour
• Respiratory dysfunction: Pao2/Fio2 ratio <300 Ampullary tumour
• Renal dysfunction: oliguria, creatinine >2.0 mg/dL Pancreatic tumour
• Hepatic dysfunction: PT‐INR >1.5 Duodenal tumour
• Haematological dysfunction: platelet count Pancreatitis
<100 × 109/L Entry of parasites into the bile ducts
External pressure including Mirizzi syndrome and
Grade II (moderate) acute cholecystitis
Lemmel syndrome
Associated with any of the following conditions:
Fibrosis of the papilla
• Elevated white cell count >18 × 109/L
Duodenal diverticulum
• Palpable tender mass in right upper quadrant
Blood clot (haemobilia)
• Duration of complaints >72 hours
Sump syndrome after biliary enteric anastomosis
• Marked local inflammation (gangrenous
Iatrogenic factors
cholecystitis, pericholecystic abscess, hepatic abscess,
biliary peritonitis, emphysematous cholecystitis)
Grade I (mild) acute cholecystitis present in this way. It may or may not be associated
Does not meet the criteria of grade II or grade III acute with pancreatitis or cholangitis.
cholecystitis. Grade I can also be defined as acute
cholecystitis in a healthy patient with no organ Cholangitis
dysfunction and mild inflammatory changes in the
gallbladder, making cholecystectomy a safe and low‐ Cholangitis was first described by Charcot in 1887
risk operative procedure and was termed ‘hepatic fever’. Charcot’s triad con-
sists of fever accompanied by rigors, jaundice and
PT‐INR, prothrombin‐international normalised ratio. right upper quadrant abdominal pain. It can be
Source: Yokoe M, Takada T, Strasberg SM et al. New defined as acute inflammation and infection in the
diagnostic criteria and severity assessment of acute biliary tract. It requires elevated bile duct pressure
cholecystitis in revised Tokyo Guidelines. J usually due to some form of obstruction and the
Hepatobiliary Sci 2012;19:578–85. © 2012 Japanese
presence of increased bacteria in the bile duct. The
Society of Hepato‐Biliary‐Pancreatic Surgery.
causes of cholangitis are summarised in Table 19.3.
Reproduced with permission of John Wiley and Sons.
Cholangitis is a medical emergency that requires
prompt treatment. The mortality may approach
10% overall and is higher in elderly patients with
it may be that increased time of obstruction of the significant comorbidities. Charcot’s triad as diag-
pancreatic duct is associated with more severe cases. nostic criteria for cholangitis is not adequate.
Risk factors for gallstone pancreatitis include Although the specificity is probably greater than
multiple small stones and a dilated cystic duct. 90%, the sensitivity is low at about 25%. As such,
Gallstones are found in the faeces of up to 90% of the Tokyo guidelines are a better method of diag-
patients with gallstone pancreatitis. A minority of nosis in acute cholangitis and these are set out in
patients with choledocholithiasis develop gallstone Table 19.4. Likewise, there is a severity assessment
pancreatitis. Of those patients with symptomatic (Table 19.5).
gallstones, the annual risk of developing gallstone
pancreatitis is about 1%. Fistulisation of gallstones into the bowel
This is uncommon but may be seen rarely but more
Choledocholithiais and jaundice
commonly in elderly patients. A large gallstone may
Gallstones present in the biliary tracts are common. obstruct the bowel if this occurs. The obstruction
The elderly are at highest risk and jaundice or will more commonly occur at the ileo‐caecal valve
abnormal liver function tests may be the presenta- (Barnard’s syndrome) but may occasionally
tion. Up to 20% of patients with gallstones may obstruct the duodenum (Bouveret’s syndrome).
19: Gallstones 167
Table 19.4 Diagnostic criteria for acute cholangitis. Table 19.5 Severity assessment criteria for acute
cholangitis.
A Systemic inflammation
A‐1 Fever and/or shaking chills Grade III (severe) acute cholangitis
A‐2 Laboratory data: evidence of inflammatory Defined as acute cholangitis associated with the onset
response of dysfunction in at least one of any of the following
B Cholestasis organs/systems:
B‐1 Jaundice • Cardiovascular dysfunction: hypotension requiring
B‐2 Laboratory data: abnormal liver function tests dopamine >5 μg/kg per min, or any dose of
C Imaging noradrenaline
C‐1 Biliary dilatation • Neurological dysfunction: disturbance of
C‐2 Evidence of the aetiology on imaging (stricture, consciousness
stone, stent, etc.) • Respiratory dysfunction: Pao2/Fio2 ratio <300
• Renal dysfunction: oliguria, serum creatinine >2 mg/dL
Suspected diagnosis: one item in A plus one item in
• Hepatic dysfunction: PT‐INR >1.5
either B or C
• Haematological dysfunction: platelet count <100 × 109/L
Definite diagnosis: one item in A, one item in B and
one item in C Grade II (moderate) acute cholangitis
Associated with any two of the following conditions:
Definitions
• Abnormal WBC count: >12 × 109/L, <4 × 109/L
A‐2 Abnormal white blood cell counts, increase in
• High fever: ≥39°C
serum CRP levels, and other changes indicating
• Age: >75 years old
inflammation
• Hyperbilirubinaemia: total bilirubin >5 mg/dL
B‐2 Increased serum ALP, GTP (GGT), AST and ALT
• Hypoalbuminaemia: <STD ×0.7
levels
Other factors which are helpful in diagnosis of acute Grade I (mild) acute cholangitis
cholangitis include abdominal pain (RUQ or upper Grade I acute cholangitis does not meet the criteria of
abdominal) and a history of biliary disease such as grade III (severe) or grade II (moderate) acute
gallstones, previous biliary procedures and placement cholangitis at initial diagnosis
of a biliary stent. In acute hepatitis, marked systematic Notes
inflammatory response is observed infrequently. Early diagnosis, early biliary drainage and/or treatment
Virological and serological tests are required when for aetiology, and antimicrobial administration are
differential diagnosis is difficult fundamental treatments for acute cholangitis classified
Thresholds not only as grade III (severe) and grade II (moderate)
A‐1 Fever: temperature >38°C but also grade I (mild). Therefore, it is recommended
A‐2 Evidence of inflammatory response: white cell that patients with acute cholangitis who do not
count <4 or >10 × 109/L, CRP >5 mg/L respond to the initial medical treatment (general
B‐1 Jaundice: bilirubin >2× normal limit supportive care and antimicrobial therapy) undergo
B‐2 Abnormal liver function tests early biliary drainage or treatment for aetiology
ALP >2× upper limit of normal
GTP >2× upper limit of normal PT‐INR, prothrombin‐international normalised ratio;
AST >2× upper limit of normal STD, lower limit of normal; WBC, white blood cell count.
ALT >2× upper limit of normal Source: Kiriyama S, et al. New diagnostic criteria and
severity assessment of acute cholangitis in revised
ALP, alkaline phosphatase; ALT, alanine Tokyo Guidelines. J Hepatobiliary Pancreat Sci.
aminotransferase; AST, aspartate aminotransferase; 2012;19:548–56. © 2012 Japanese Society of
CRP, C‐reactive protein; GTP (GGT), Hepato‐Biliary‐Pancreatic Surgery. Reproduced with
γ‐glutamyltransferase; RUQ, right upper quadrant. permission of John Wiley and Sons.
Source: Kiriyama S, et al. New diagnostic criteria and
severity assessment of acute cholangitis in revised significant risk factor for gallbladder cancer, with more
Tokyo Guidelines. J Hepatobiliary Pancreat Sci. than 75% of patients having gallstones. The relative
2012;19:548–56. © 2012 Japanese Society of risk of gallstones causing gallbladder cancer is 4.9.
Hepato‐Biliary‐Pancreatic Surgery. Reproduced with
permission of John Wiley and Sons.
Diagnosis
Gallbladder cancer Baseline haematological and biochemical

Gallbladder cancer is rare in western countries but
investigations
highly lethal. In Australia the incidence is less than 2 Elective investigation of a patient with gallstones
per 100 000 population per year. Gallstones are a should include a routine full blood count,
electrolytes and liver function tests. Up to 10% of associated with thickening of the gallbladder wall
patients who present electively may have choledo- (>4 mm) and sometimes fluid collections. It is accu-
cholithiasis, the presence of which may be sug- rate in demonstrating masses or polyps within the
gested by abnormal liver function tests. If there is a gallbladder and will show if there is abnormal bil-
history of jaundice it is important to determine bili- iary dilatation (>7 mm).
rubin and alkaline phosphatase concentrations and
INR (international normalised ratio). In the patient Abdominal CT
who presents acutely with abdominal pain, meas-
An abdominal CT scan is not recommended in the
urement of C‐reactive protein to estimate the degree
routine diagnosis of gallstones. It may have a place in
of inflammation is helpful and amylase and lipase
imaging for severe complicated cholecystitis but has a
levels should be done to exclude pancreatitis.
lower sensitivity and specificity for diagnosing gall-
stones in the gallbladder than ultrasound. It also car-
Plain abdominal X‐ray
ries the risk of exposure to ionising radiation and a
This has limited usefulness. Only 15% of gallstones higher cost than ultrasound. Abdominal CT scanning
will have enough calcium to be seen on a plain in the diagnosis of choledocholithiasis has a sensitivity
abdominal X‐ray. of 60–80% with a specificity in excess of 95%. CT
cholangiography is infrequently performed because of
Ultrasound the risk of allergic reactions but does increase the sen-
sitivity for the diagnosis of choledocholithiasis to
This is the investigation of choice for gallstones and
85–95% and the specificity to 88–98%.
avoids ionising radiation, which is particularly
important in young people. Good‐quality ultra-
Endoscopic ultrasound
sonography has a sensitivity and specificity in
excess of 95% in uncomplicated cases. Obesity, In Australia, this technique is becoming more
previous surgery and bowel gas may impede the widely available and although not a first‐line
accuracy of the test in diagnosing gallstones. The investigation for the diagnosis of gallbladder

stones are shown by a bright echogenic appearance gallstones is very accurate. In the diagnosis of

with posterior shadowing (Figure 19.1). Ultrasound choledocholithiasis it is even more accurate, with a
has variable accuracy in diagnosing choledocho- sensitivity reported as 89–94% and a specificity of
lithiasis, with a sensitivity of 50–80% but a speci- about 95%. The disadvantage is that it requires
ficity of over 90%. specialised equipment and training and cannot be
Ultrasound is also useful in diagnosing cholecysti- done on an outpatient basis. It is most useful in
tis by demonstrating tenderness over the gallbladder patients where the diagnosis is uncertain.
Fig. 19.1 Ultrasound of gallbladder containing gallstones, showing an echo with acoustic shadowing.
19: Gallstones 169
Magnetic resonance imaging Symptomatic gallstones

cholangiopancreatography
Non‐operative measures
Magnetic resonance cholangiopancreatography is
Some patients are able to control their symptoms
the diagnostic modality of choice for choledocho-
for a significant period of time with a low‐fat diet.
lithiasis. It does not involve ionising radiation.
Unfortunately, most patients find that they are
The disadvantages of the modality relate to its
unable to stay on the diet and recurrence of symp-
cost, limited availability, patient claustrophobia
toms is common. There are a variety of herbal and
and previous procedures such as pacemakers
naturopathic treatments and diets which are
which may contraindicate it. However, the tech-
reputed to dissolve gallstones or alleviate symp-
nique is highly accurate in diagnosing choledo-
toms but there is little evidence to support this
cholithiasis, with a sensitivity of 92–94% and a
approach.
specificity of 99%.
Dissolution therapy with ursodeoxycholic has
been shown to have a low rate of cure, with only
Endoscopic retrograde 27% of patients exhibiting dissolution of stones
cholangiopancreatography after treatment and a high rate of recurrence.
Endoscopic retrograde cholangiopancreatography Extracorporeal shock wave therapy (lithotripsy)
(ERCP) is uncommonly used as a diagnostic test and is highly successful for renal tract stones and has
is a therapeutic tool to clear the bile duct of stones. also been tried for gallstones. One of the major
There are rare but serious complications, such as issues is that breaking up gallstones results in mul-
bleeding, bowel perforation and pancreatitis. tiple small stones that may be more likely to pass
into the biliary tract and cause pancreatitis and
Laparoscopic ultrasound other complications. Lithotripsy may cause dissolu-
tion of stones in up to 55% of patients but more
This is sometimes used at the time of laparoscopic than 40% of patients will develop recurrent gall-
cholecystectomy to diagnose common bile duct stones within 4 years. This treatment is also limited
stones. by expense and availability.
Technetium‐labelled hepato‐
iminodiacetic acid Cholecystectomy
This test has little use in the diagnosis of gallstones Removal of the gallbladder in patients who are fit
but may be useful in diagnosing acute cholecystitis for surgery is the treatment of choice in sympto-
or chronic acalculous cholecystitis. matic gallstones. This is usually performed by a
laparoscopic (keyhole) technique due to shorter
length of hospital stay, less pain, shorter return to
work and better cosmesis. It usually involves four
Treatment
or five small incisions of 1 cm in length. The major-
ity of elective procedures can be done with an over-
Asymptomatic gallstones
night stay, although there is now good evidence that
There is little evidence to justify treating asympto- a majority of elective procedures can be done as
matic gallstones. Likewise, there is little evidence day‐only admissions. In many centres in Australia
that lifestyle modifications will lower the risk of the procedure is accompanied by an operative chol-
developing symptoms related to gallstones if they angiogram to check the anatomy and exclude
are found incidentally. There are situations where a choledocholithiasis.
discussion with a patient with asymptomatic gall- In elective cases, the 30‐day mortality is under
stones is important. For example, in a patient who 0.5% and the majority of patients will have recov-
requires a heart transplant where the risk of biliary ered fully within 2 weeks. However, there are risks
sepsis is significant, where a patient is going to associated with the procedure, including infection,
spend a significant period in a remote area such as need to convert to an open procedure (normally
Antarctica or with a patient whose ethnic group <2%), bile leaks, pneumonia and deep venous
has a high risk of gallbladder cancer. There may thrombosis. The most feared risk is a bile duct
also be occasional circumstances where a patient injury (BDI). This will usually be a result of misi-
has to undergo surgery for another reason and dentification of the anatomy. When laparoscopic
it may be reasonable to consider removal of the cholecystectomy was introduced there was an
gallbladder at the same time. increase in the incidence of this complication. This
risk now appears to have stabilised and a major gallbladder within 4 weeks is regarded as best prac-
transection of the bile duct probably occurs at a tice to avoid the risk of repeated episodes in the
rate of about one in 800–1000 cases in Australia. patient with mild uncomplicated pancreatitis.
Emergency procedures carry a higher risk of com-
plications. An emergency laparoscopic cholecys-
tectomy can be an extremely difficult procedure Burden of disease on Australian society
due to the difficulty in identifying the anatomy.
Occasionally, it may be impossible to perform a In Australia, approximately 50 000 laparoscopic
complete cholecystectomy and the surgeon may cholecystectomies are performed each year. It is one
consider a cholecystostomy where the gallbladder of the most common surgical procedures performed
is drained or a subtotal cholecystectomy. In the in Australia and represents a significant expenditure
acute situation where the patient is extremely ill of public resources. The demand for the procedure
and not fit for operation, a percutaneous cholecys- appears to be on the increase. Patient outcomes indi-
tostomy performed radiologically may be an option cate wide variability in the cost, hospital stay and
to allow the condition to settle followed by a lapa- complications and there is no evidence that this situ-
roscopic cholecystectomy when the patient has ation is different in other western countries. A recent
recovered. study in private hospitals in Australia showed that
Most patients will not notice significant digestive 98% of patients stayed at least one night in hospital,
problems after removal of the gallbladder. A small despite evidence that a majority can be done as true
proportion will develop fatty food intolerance that day cases. Furthermore, amongst 320 surgeons who
may be quite individualistic and there is also an performed five or more procedures per year the total
incidence of bile salt‐induced diarrhoea. hospital cost varied from A$4543 to A$21 419, with
an average cost of A$7235. The average 30‐day
readmission rate was 7.8%. This suggests that for a
Timing of surgery common procedure, there are significant variations
In the patient who does not require hospital admis- in outcome and cost and that there is a substantial
sion for biliary colic the procedure can be planned opportunity for efficiency gains and savings.
electively. However, this does depend on the
resources available. If the procedure is likely to be
Further reading
delayed for some months, then there is a high like-
lihood of re‐presentation to the hospital and a Cremer A, Arvanitakis M. Diagnosis and management of
higher risk of prolonged hospital stay and other bile stone disease and its complications. Minerva
complications. Gastroenterol Dietol 2016;62:103–29.
In the patient who presents with acute chole- Gurusamy KS, Davidson BR. Gallstones. BMJ 2014;348:
cystitis and requires hospital admission for intrave- g2669.
nous antibiotics, the timing of surgery is Knab LM, Boller AM, Mahvi DM. Cholecystitis. Surg
controversial. The concern is that earlier surgery in Clin North Am 2014;94:455–70.
Mayumi T, Okamoto K, Takada T et al. Tokyo Guidelines
this group may be associated with a higher risk of
2018: management bundles for acute cholangitis and
conversion to an open procedure and an increased
cholecystitis. J Hepatobiliary Pancreat Sci 2018;25:
risk of BDI and other complications. However, 96–100.
there is now good evidence from meta‐analyses Miura F, Okamoto K, Takada T et al. Tokyo Guidelines
that early operation is associated with a more 2018: initial management of acute biliary infection
rapid recovery with no increase in complications and flowchart for acute cholangitis. J Hepatobiliary
than delayed operation after the cholecystitis has Pancreat Sci 2018;25:31–40.
settled. Portincasa P, Di Ciaula A, de Bari O, Garruti G, Palmieri
Likewise, in the patient who presents with acute VO, Wang DQ. Management of gallstones and its
pancreatitis related to gallstones the timing of sur- related complications. Expert Rev Gastroenterol
gery is controversial. There is an argument that Hepatol 2016;10:93–112.
Royal Australasian College of Surgeons and Medibank.
some delay in removing the gallbladder is appropri-
Surgical Variance Report 2017 General Surgery.
ate because there is a risk that the pancreatitis may
Available at https://www.surgeons.org/media/25242159/
worsen, particularly in the first 48 hours. This is a surgical‐variance‐report‐2017‐general‐surgery.pdf
clinical decision as to when operation should be Shabanzadeh DM, Sorensen LT, Jorgensen T. Determinants
performed and there is a move to performing chol- for gallstone formation: a new data cohort study and a
ecystectomy on the index admission depending on systematic review with meta‐analysis. Scand J
resources available. In any case removal of the Gastroenterol 2016;51:1239–48.
19: Gallstones 171
b ERCP and sphincterotomy with stone extraction

MCQs c antibiotic therapy followed by laparoscopic
cholecystectomy
d choledocholithotomy
e ERCP, sphincterotomy with stone extraction and
later consideration of cholecystectomy
1 An 80‐year‐old woman presents with biliary pain
and stones are seen in the gallbladder on ultra- 3 Which of the following is the appropriate
sound. The probability of the pain being due to a investigation in a patient presenting with a recent
stone in the common bile duct is approximately: episode of right upper quadrant pain and a normal
a 5% physical examination?
b 10% a abdominal CT scan
c 20% b ERCP
d 30% c plain X‐ray of the abdomen
e 50% d upper abdominal ultrasound
e cholescintigraphy
2 A 73‐year‐old man presents with cholangitis.
He has had no previous abdominal operation.
The definitive treatment should be:
a cholecystectomy and choledocholithotomy
20 Malignant diseases of the
hepatobiliary system
Thomas J. Hugh1 and Nigel B. Jamieson2
1
University of Sydney and Royal North Shore Hospital, Sydney, New South Wales, Australia
2
University of Glasgow and Glasgow Royal Infirmary, Glasgow, UK
provide an assessment of whole liver function. The

Introduction Child–Pugh score has been the gold standard for
decades but does not discriminate well between
The most common primary malignant tumours
mild and moderate liver dysfunction. Similarly, the
arise from either hepatocytes (hepatocellular can-
model for end‐stage liver disease (MELD) score is
cer) or the epithelial cells of the bile duct (cholangio-
mostly only helpful in patients with severe liver
carcinoma). Secondary tumours (liver metastases)
disease.
can spread from many different primary tumour
Dynamic quantitative liver function assessment
types.
tests have been used to predict the safe limits of the
extent of hepatic parenchymal resection. The most
frequently employed modality in patients with pri-
Assessment of liver function mary liver tumours is the indocyanine green reten-
preoperatively (Box 20.1) tion test. This can be done using a simple
non‐invasive pulse dye densitometry measurement
Preoperative assessment of liver function is impor- (a bedside test).
tant for determining the risk of hepatic failure and Sophisticated computed tomography (CT) with
mortality after liver resection. Conventional labo- three‐dimensional reconstruction helps measure
ratory testing (liver function tests, platelet count, the likely functional liver remnant (FLR) volume
coagulation studies) should reflect the extent of after resection. In general, an FLR of 25% or
underlying liver function. Unfortunately, these tests more is considered safe in patients with preopera-
alone have a low sensitivity for predicting the risk tive normal liver function, whereas a value in
of remnant liver dysfunction following a major excess of 30–40% is necessary in patients with
resection and need to be considered preoperatively underlying liver disease. Portal vein embolisation
in the context of organ imaging studies. may be used preoperatively to stimulate liver
In patients with primary malignant liver tumours, hypertrophy.
the presence of underlying chronic liver disease Emerging important tools of liver function
may limit the extent of hepatic resection. In patients assessment before liver resection include molecular
with colorectal liver metastases a particular hazard imaging techniques using either 99mTc‐diethylenetri-
is the possible effect of prior systemic chemother- aminepentaacetic acid (DTPA)‐galactosyl human
apy, which may cause either steato‐hepatitis or serum albumin or 99mTc‐mebrofenin hepatobiliary
sinusoidal dilatation, both of which increase mor- scintigraphy. These tests may be used to provide an
bidity after resection. indication of functional hepatocyte mass and are
Clinical risk scores are based on selected clini- particularly helpful if done in conjunction with CT
cal symptoms and conventional test results and volumetry.
173
temporary or permanent palliation for malignant

Box 20.1 Investigations of hepatobiliary
tumours.
malignancy
Liver function assessment Computed tomography

Biochemical
CT scans play a critical role in the diagnosis, stag-
Clinical risk scores (e.g. Child–Pugh)
ing and characterisation of primary and secondary
Dynamic quantitative tests (e.g. indocyanine green
liver tumours. In most cases, the diagnosis can be
retention)
Molecular imaging (e.g. mebrofenin test)
made without the need for tissue sampling confir-
mation. This modality is readily available and can
Radiology be performed with faster scan times than magnetic
Ultrasound resonance imaging (MRI). Generally, it is well toler-
CT (contrast‐enhanced, volumetry, CT ated especially by elderly patients or those with
cholangiography) multiple morbidities who often have difficulty
MRI (contrast‐enhanced, volumetry, MRCP)
cooperating with the breath‐hold requirements of
PET (FDG, 68Ga‐DOTA‐TATE)
an MRI scan. Contrast‐enhanced multidetector CT
ERCP
provides fast, high‐quality, thin‐section imaging of
both intrahepatic and extrahepatic disease.
The characteristic feature of hepatocellular carci-
Ultrasound noma (HCC) is late arterial enhancement with rela-
tive washout compared with the liver parenchyma
Ultrasound is a widely available, cheap and non‐ during the venous or delayed phases. In contrast,
invasive investigation. The detection of space‐occu- liver metastases are typically hypo‐attenuating dur-
pying lesions in the liver, porta hepatis or pancreas ing the non‐contrast phase, and enhance less than
is dependent on body habitus and may be affected surrounding liver following contrast. In the pres-
by the amount of surrounding intestinal gas. ence of hepatic steatosis, liver metastases may be
iso‐attenuating or even slightly hyper‐attenuating.
Endoscopic retrograde The enhancement pattern is typically peripheral,
cholangiopancreatography and while there may be central filling in during the
Endoscopic injection of contrast directly into the portal venous phase, the contrast usually washes
bile ducts is an accurate method of demonstrating out in the delayed phase. Some primary tumours
biliary obstruction and determining cause. produce hyper‐enhancing (hypervascular) liver
Endoscopic retrograde cholangiopancreatography metastases including renal cell, thyroid and neu-
(ERCP) can be combined with cytological brush- roendocrine tumours.
ings or biopsy for diagnosis, as well as insertion of
plastic or partially covered self‐expanding metal CT cholangiography
stents for temporary or permanent relief of malig-
nant biliary obstruction. Before requesting an ERCP CT after intravenous drip infusion of Biliscopin
for potential hilar or intrahepatic ductal obstruc- (meglumine iotroxate) provides non‐invasive visu-
tion, it is important to consider the risk and man- alisation of the biliary tree by excretion of contrast
agement options in the likely event of contamination into bile. It may help evaluate the extent of involve-
of the obstructed liver segments. ment of the biliary tree by a malignant tumour
(Figure 20.1). This modality cannot be used in
Percutaneous transhepatic cholangiography patients with an iodinated‐contrast hypersensitiv-
ity, and is ineffective and hazardous in those with a
Radiological injection of contrast directly into the serum bilirubin level above 30 mmol/L.
intrahepatic bile ducts may be preferable to ERCP
in some circumstances to relieve jaundice without
Magnetic resonance imaging
contaminating obstructed liver segments. In fact, it
may be the only option when the ampulla is MRI provides useful imaging of the liver without
inaccessible endoscopically due to a large distal
exposure to radiation. There have been rapid
cholangiocarcinoma or when there has been previ- advances in MRI technology over the past decade
ous foregut surgery. Complex interventional tech- and this modality is emerging as a critical investiga-
niques including biliary stricture dilatation, stent tion for diagnosing and staging malignant hepato-
placement or ‘rendezvous’ procedures in conjunc- biliary tumours. Use of the hepatobiliary‐specific
tion with an endoscopic approach may provide contrast agent Gd‐EOB‐DTPA (Primovist) produces
20: Malignant diseases of the hepatobiliary system 175
Fig. 20.1 CT cholangiogram of a malignant biliary Fig. 20.2 Magnetic resonance cholangiogram of a benign
stricture in the left duct due to an iCCA. biliary stricture mimicking a Klatskin tumour.
both dynamic and liver‐specific images and is more serum bilirubin levels secondary to obstruction
sensitive than MRI without contrast or with non‐ (Figure 20.2).
specific contrast agents. Advantages of MRI over
CT include the capacity to evaluate a greater vari- CT or MRI for investigating malignant
ety of tissue properties, including fat content, hepatobiliary tumours?
restriction of diffusion and T2‐weighted signalling,
There have been many comparative studies of the
all of which improve lesion detection and charac-
two techniques over the past 20 years with demon-
terisation. However, disadvantages include the lim-
strated advantages and disadvantages for each
ited availability of this modality in some countries,
modality. In practical terms, both modalities may
slower scan times compared with CT, and poor tol-
be necessary and helpful but ultimately the decision
erance in some patients because of claustrophobia
to perform one over the other will depend on insti-
and the need for prolonged breath‐holding.
tutional preferences, specific patient needs and
The characteristic diagnostic features of HCC on
accessibility. In general, CT scans are more widely
Gd‐EOB‐DTPA enhanced MRI are arterial phase
available, and possibly need less expertise to per-
hyper‐enhancement followed by portal venous or
form and to interpret than MRI scans. MRI is cer-
delayed phase washout. In contrast, liver metasta-
tainly more prone to artefacts than CT, and detailed
ses typically demonstrate a peripheral rim enhance-
and specialised interpretation of the images may
ment and lack of central enhancement in the
not be available outside of specialist centres.
dynamic phase, especially when central tumour
In relation to HCC, both modalities have similar
necrosis is present. During the hepatobiliary phase,
sensitivity and specificity when considered on a
liver metastases usually become hypointense.
per‐patient basis, and most clinical practice guide-
lines recommend either multiphase CT and MRI
Magnetic resonance
with extracellular contrast agents as the first‐line
cholangiopancreatography
investigation for diagnosis and staging. However,
Magnetic resonance cholangiopancreatography MRI may have superior per‐lesion sensitivity in dif-
(MRCP) enables rapid non‐invasive evaluation of ferentiating tumour from non‐tumour tissue, par-
both the biliary and pancreatic ducts without the ticularly in patients with chronic liver disease. As
use of intravenous contrast agents. Significant with all malignant hepatobiliary tumours both
improvements in spatial and temporal resolution techniques are limited in detecting lesions of less
over the past decade make MRCP an ideal non‐ than 10 mm in diameter.
invasive investigation of the intrahepatic and extra- In patients with perihilar cholangiocarcinoma,
hepatic biliary tree in patients with malignant both multiphase CT and Gd‐EOB‐DTPA enhanced
biliary tumours. This modality is used instead of MRI (including MRCP) yield similar staging accu-
CT cholangiography in patients with elevated racy. To determine resectability it is critical to
obtain detailed imaging of the porta hepatis to the diagnosis without the need for tissue confirma-
examine the extent of disease spread along the bil- tion. When there is doubt, referral for a specialist
iary tree and into adjacent vascular structures. This hepatobiliary opinion is preferable to biopsy. Of
can be achieved with three‐dimensional computer‐ course, there are some situations in patients who
assisted reconstruction of the portal structures are eligible for resection where a tissue diagnosis is
obtained from a standard multiphase CT scan with needed to help guide neoadjuvant treatment. This
the aid of commercially available software. can be done percutaneously under radiological
However, MRI may have an advantage over CT guidance or alternatively as a controlled core nee-
because of better soft‐tissue contrast resolution, dle biopsy under laparoscopic vision.
which is particularly helpful for evaluation of infil-
trating tumours and peripheral ductal
involvement. Primary malignant tumours (Box 20.2)
Numerous clinical guidelines recommend that a
multiphase CT scan of the chest and abdomen as
well as an MRI scan should be done at the begin- Cholangiocarcinoma
ning of the management process in all patients with
Cholangiocarcinoma (CCA) is a relatively rare
colorectal liver metastases. Contrast‐enhanced MRI
tumour but the second most common primary
is certainly better than CT for detecting lesions of
hepatobiliary malignancy after HCC. The overall
less than 10 mm and when there is known steatosis.
incidence rate is 0.4–4 per 100 000, and in 2013
It is also more sensitive than CT for detecting resid-
Australia had an incidence rate of 2.9 per 100
ual disease in the post‐chemotherapy liver.
000. The disease is more prevalent in certain parts
of Southeast Asia such as northeast Thailand
Positron emission tomography
where rates in men are as high as 96 per 100 000.
Positron emission tomography with fluorodeoxy- Overall men are more frequently affected than
glucose (FDG‐PET) is widely used in clinical oncol- women, and most cases occur over the age of 65
ogy. In patients with colorectal liver metastases, this years. Over the past three decades there has been a
investigation may identify otherwise radiologically steady increase in the incidence of CCA in western
occult disease beyond the liver, thereby improving populations, although the reasons for this are
selection of patients for resection. Although a recent unknown.
meta‐analysis of retrospective data did not show Cholangiocarcinoma is anatomically classified as
any improvement in disease‐free or overall survival intrahepatic (iCCA, 10–15%), perihilar (pCCA,
in patients with colorectal liver metastases, most 50–70%, Klatskin tumour) and distal (dCCA,
clinical guidelines recommend routine use in the 20–30%). Inflammation and cholestasis are known
assessment of patients with potentially resectable to be key factors in carcinogenesis but there are
disease. There should be a 3–4 week delay between
the end of chemotherapy and the PET/CT examina-
tion to prevent false‐negative findings.
Box 20.2 Classification of malignant
In contrast, the sensitivity of FDG‐PET in pri- hepatobiliary tumours
mary malignant tumours is low because of wide
variations in glucose 6‐phosphatase activity in the Primary
liver. Accordingly, this investigation is not com- Hepatocellular origin
monly used for the diagnosis and staging of patients Hepatocellular cancer
with either HCC or cholangiocarcinoma outside of Hepatoblastoma
high‐volume specialist centres. Biliary origin
Cholangiocarcinoma
Role of percutaneous biopsy for malignant Gallbladder carcinoma
hepatobiliary tumours Biliary cystadenocarcinoma
Other rare tumours
Percutaneous biopsy should not be done in patients Haemangiosarcoma
with possible malignant hepatobiliary tumours Hepatic epithelioid haemangioendothelioma
who might be suitable for a potentially curative Primary hepatic lymphoma
resection. This is because of the risk of needle track Primary hepatic neuroendocrine tumours
seeding after transperitoneal procedures and the
Secondary
potential negative impact of this on survival. In
Liver metastases
most cases modern multimodal imaging can make
Management
Box 20.3 Risk factors for
cholangiocarcinoma The prognosis following diagnosis of CCA depends
on the location and stage of the tumour as well as
Definite patient comorbidity. Overall, iCCAs have a worse
Primary sclerosing cholangitis prognosis than cancers in extrahepatic sites (pCCA
Biliary parasites (Opisthorchis viverrini, Clonorchis and dCCA). Median survival for unresectable
sinensis)
tumours is 5–12 months, and palliative chemora-
Hepatolithiasis
diotherapy can provide a modest survival advan-
Caroli’s disease
tage over best supportive care. In Australia in 2014,
Choledochal cysts (types I and IV)
the overall 5‐year relative survival after diagnosis
Exposure to the radiocontrast agent Thorotrast
of CCA was 19%. Only radical resection offers the
Possible chance of cure. However, the extent of lymphovas-
Cirrhosis cular spread and the ability to achieve an R0 mar-
Diabetes mellitus gin clearance are critical factors impacting
Obesity long‐term outcome.
Chronic hepatitis B/C infection Contraindications to resection include bilateral
Excessive alcohol intake (>80 g/day) multifocal disease, distant metastases and comor-
bidities that outweigh the operative risks. Regional
lymph node metastases are not an absolute con-
traindication to resection, although N1 disease is
distinct genetic mutational changes associated with
an independent prognostic factor for a poor
each of the different tumour locations (Box 20.3).
outcome.
Whole‐genome expression profiling has confirmed
After adequate staging and concluding that the
activation of pathways driving proliferation (e.g.
tumour can be resected, it is important to thor-
EGF, K‐Ras, AKT/mTOR/PI3K and MET), angio-
oughly assess for any comorbidity that might limit
genesis (e.g. vascular endothelial growth factor
a major surgical procedure. Depending on the size
receptor) and inflammation (e.g. interleukin 6).
and stage of the disease, these operations can be a
Morphologically, these tumours are classified as
formidable undertaking due to local infiltration of
mass‐forming, periductal‐infiltrating or intraductal
adjacent structures and the frequency of underly-
papillary. Most iCCAs are mass‐forming while
ing chronic liver disease. A preoperative cardiac
pCCAs and dCCAs are typically periductal‐infil-
and respiratory assessment is often helpful. Relief
trating. Histopathologically, up to 95% of CCAs
of jaundice, control of sepsis, minimisation of
are adenocarcinomas.
alcohol intake and strict diabetic control in the
The clinical presentation of CCA depends on the
weeks leading up to the operation are also
location of the tumour and varies from an inciden-
important.
tal finding or vague abdominal symptoms for intra-
hepatic mass‐forming tumours to painless
Treatment options
obstructive jaundice for extrahepatic tumours.
Often, local invasion into surrounding blood ves- Intrahepatic cholangiocarcinoma
sels and nerves is found at presentation, and in the Although resection is usually only possible in less
case of iCCAs tumour growth may infiltrate exten- than 30% of cases, this can result in a median sur-
sively into adjacent liver parenchyma. Vascular vival of up to 39 months and a 5‐year survival rate
compression or occlusion occurs in advanced dis- of up to 40%. Adjuvant chemoradiotherapy after
ease and may contribute to segmental or hemilobar resection does not improve outcomes. Systemic
liver atrophy. chemotherapy and/or best supportive care may be
Several staging systems for CCA have been pro- offered to patients with unresectable iCCA or to
posed but the most widely adopted is the American those who are unable to tolerate a major resection.
Joint Committee on Cancer/Union for International However, the results are often disappointing in rela-
Cancer Control (AJCC/UICC) system. This has tion to toxicity, oncological benefit and overall sur-
shown stage‐survival correlation for the different vival. Other palliative treatment options for
tumour types but is limited by the need to include liver‐only or liver‐dominant disease include locore-
histology to determine T and N status. gional treatments such as radiofrequency ablation
Serum tumour markers such as carcinoembry- (RFA) or microwave ablation (MWA), transarterial
onic antigen (CEA) and CA19-9 are often used in chemoembolisation (TACE) or selective internal
patients with cholangiocarcinoma. radiation therapy (SIRT).
Perihilar cholangiocarcinoma (Klatskin tumour) South America (Chile, Ecuador and Bolivia) and in
A multidisciplinary approach and multimodal northern India, Pakistan, Japan and Korea. The
treatment is needed for this complex disease. Biliary most important risk factor for the development of
drainage for hilar CCA may be warranted and can gallbladder cancer is gallstones but the presence of
be done by either ERCP or percutaneous transhe- primary sclerosing cholangitis or an anomalous
patic cholangiography, and the choice is usually pancreatobiliary junction also increase the risk.
institution dependent. Gallbladder cancer occurs mostly in patients
Resection offers the only chance of long‐term over 50 years old and there is a marked female pre-
survival for pCCA. This involves removal of the ponderance in the order of 6 : 1. It is found in the
extrahepatic bile duct in conjunction with a hepa- fundus of the gallbladder in approximately 60% of
tectomy and radical porta hepatis lymphadenec- cases. Adenocarcinoma accounts for 98% of cases
tomy. Concomitant vascular resection increases the but other rarer variants include papillary, muci-
potential for morbidity but may be necessary to nous, squamous and adenosquamous subtypes. A
achieve a negative (R0) resection margin. In con- range of genetic alterations have been implicated,
trast to portal vein resection, hepatic artery exci- including oncogene activation, tumour suppressor
sion causes more morbidity and does not improve gene inhibition, microsatellite instability and meth-
long‐term survival. Overall morbidity and mortal- ylation of gene promoter areas.
ity rates after major resection are 40–70% and The three most common ways that gallbladder
5–15%, respectively. The 5‐year survival after cancer may present are as follows:
resection of a Klatskin tumour ranges from 10 to • an unsuspected discovery at the time of cholecys-
40%. Patients with primary sclerosing cholangitis tectomy for presumed benign disease
complicated by pCCA should be considered for • incidentally at histopathology after routine
liver transplantation if they meet the appropriate cholecystectomy
criteria. • less commonly with abdominal symptoms due to
Surgical palliation in the form of cholecystec- advanced disease.
tomy and biliary–enteric anastomosis for biliary The presence of abdominal pain, a mass, weight
drainage is sometimes undertaken but is associated loss or jaundice are ominous signs usually indicat-
with increased morbidity and mortality compared ing either local invasion or metastatic spread. Most
with endoscopic management. Other palliative of these patients have unresectable disease. The
treatment options include stereotactic radiotherapy clinical presentation may be like benign gallbladder
and photodynamic therapy. disease and the radiological findings may be con-
fused with acute or chronic cholecystitis. A preop-
Distal cholangiocarcinoma erative diagnosis of Mirizzi syndrome (extrinsic
Cancer of the distal common bile duct (dCCA) compression of the extrahepatic bile duct due to
often presents clinically just like a pancreatic can- pressure and inflammatory change from an
cer. When imaging and endoscopic findings demon- impacted stone in the neck of the gallbladder)
strate locoregional disease only, patients with an proves to be due to a cancer of the gallbladder in a
adequate performance status should be offered small proportion of patients.
pancreaticoduodenectomy. Median survival after a
potentially curative resection is approximately 24
months, with 5‐year survival rates ranging from 20 Diagnosis and staging
to 40% depending on the extent of disease. As with Transabdominal ultrasound allows accurate
hilar tumours, placement of a covered metal biliary assessment of the features of a gallbladder
stent by ERCP provides excellent relief of jaundice polyp, including size and depth of invasion.
in most patients. Dynamic contrast‐enhanced CT of the abdomen
Palliative systemic chemotherapy for unresecta- and chest document the extent of local and dis-
ble or metastatic disease is usually based on gemcit- tant spread. For large tumours, Gd‐EOB‐DTPA
abine and cisplatin. Unfortunately, median survival (Primovist)‐enhanced MRI may provide addi-
is usually less than 12 months in most patients. tional evaluation of possible involvement of the
biliary tree or infiltration into liver parenchyma.
Gallbladder cancer
Lymph node metastases from gallbladder cancer
Gallbladder cancer is rare, with a worldwide varia- are not easily detected by either CT or MRI. 18F‐
tion in incidence of 1–25 per 100 000. The promi- FDG‐PET, if available, may identify distant
nent geographic variation correlates with the occult disease, which would preclude radical
prevalence of gallstones. High rates are seen in surgical intervention.
Diagnostic laparoscopy to identify peritoneal location is most predictive of long‐term outcome,

dissemination may be helpful in patients with radi- and this in turn is influenced by the depth of inva-
ologically detected advanced tumours. In patients sion of the primary tumour.
with an incidental gallbladder cancer found at his- Gallbladder cancer is the most aggressive of the
topathology after laparoscopic cholecystectomy, biliary tract cancers and has the shortest median
repeat staging laparoscopy before undertaking a overall survival duration. Complete resection offers
radical resection may exclude disseminated disease. the only chance of cure but unfortunately recur-
However, the yield from laparoscopy is generally rence rates are high. Positive resection margins,
low except in patients with poorly differentiated, lymph node metastasis and poorly differentiated
large cancers or when there has been a positive tumours are independent risk factors for poor
resection margin. prognosis after ‘curative’ resection. Laparoscopic
The histopathology report from the original cholecystectomy is contraindicated when gallblad-
cholecystectomy should be carefully reviewed for der cancer is known or suspected preoperatively
the exact tumour location, the depth of invasion unless there is clear radiological evidence of local-
and the extent of lymphovascular spread. The pres- ised mucosal disease only.
ence of involved resection margins will determine
the need for radical resection of adjacent structures Incidentally discovered gallbladder cancer
including the bile duct. following cholecystectomy
Serum tumour markers such as CEA and CA19‐9 Cholecystectomy alone is sufficient treatment for
may be elevated and will help confirm the diagnosis tumours confined to the mucosa (Tis) or lamina
in patients with suspicious gallbladder polyps. propria (T1a). Surgical options for tumours that
However, the sensitivity and specificity of these invade the muscular layer of the gallbladder (≥T1b)
tests is too low to warrant routine use for screening are more controversial. Although there is ongoing
purposes. debate, a consensus statement of experts in 2014
The most common staging system for gallbladder recommended en‐bloc resection of adjacent liver
cancer is the AJCC/UICC TNM staging system. (Couinaud segments 4b and 5) and complete portal
This identifies five different stages depending on lymphadenectomy for patients with T1b tumours
the extent of disease and incorporates histological (Figure 20.3). Regional lymph node metastases (N1
information about T and N status. In Japan, where or N2) are found in 18–60% of patients with T2
gallbladder cancer is relatively common, the tumours (invasion of the muscularis layer of the
Japanese Society of Biliary Surgery staging system gallbladder). Accordingly, there is consensus that
is more often used. This system differs slightly by these patients should undergo similar radical resec-
expanding on both the T and N stage definitions. It tion to reduce the risk of local and distant
may provide slightly better prognostication after recurrence.
resection compared with the AJCC/UICC system, Resection of the extrahepatic bile duct should
especially in patients with more advanced disease. only be undertaken when there is direct extension
Incorporation of the histological subtype and grade or microscopic involvement of the cystic duct mar-
of the gallbladder cancer has been advocated to gin. Addition of a biliary anastomosis in the pres-
improve the prognostic value of these staging sys- ence of non‐dilated ducts is associated with a
tems further. significant risk of bile leak and stenosis. Similarly,
port‐site excision should not be carried out rou-
tinely as this is not associated with improved long‐
term outcome.
Management
The 5‐year survival rates in patients with T1b–2
The prognosis for patients with gallbladder can- cancers range from 10 to 60% after cholecystec-
cer depends on the location and stage of the tomy alone compared with 59–90% following
tumour as well as patient comorbidity. The lack of more radical resection. Given the propensity for
a submucosa in the gallbladder wall and the prox- recurrence after R0 resection of T2–4 disease in N1
imity to the liver predisposes this malignancy to gallbladder cancer, patients with nodal metastases
direct spread into the adjacent hepatic segments should be considered for adjuvant systemic chemo-
(4 and 5), the bile duct and nearby abdominal therapy and/or chemoradiotherapy.
viscera. Lymphatic dissemination occurs com-
Treatment of patients with a large gallbladder
monly, and the cystic and peri‐choledochal lymph mass due to malignancy may also involve a radical
nodes are often the initial site of spread. However, resection, but this often provides only marginal
the number of involved nodes rather than the benefit particularly in the presence of jaundice.
Fig. 20.3 Gallbladder cancer (T2bN0M0) immediately after resection and at 4 years follow‐up.
Instead, staging laparoscopy may be warranted to procedures are likely to be limited to a few special-
exclude disseminated disease, which might prevent ist centres.
an unhelpful resection. Direct invasion of either the Many patients present with advanced disease
duodenum or colon does not necessarily indicate and are therefore not resectable and have a poor
nodal involvement and in carefully selected patients prognosis. Palliative options include biliary drain-
en‐bloc resection may still be appropriate. age (endoscopic or by surgical bypass), systemic
Several Japanese groups have reported the feasi- chemotherapy and radiotherapy. Gemcitabine
bility of radical resection for advanced gallbladder alone or in combination with 5‐fluorouracil (5‐FU),
cancer including the addition of extended hepatec- capecitabine or cisplatin is well tolerated in most
tomy or pancreaticoduodenectomy, with accepta- patients and provides marginal improvement in
ble morbidity and mortality and an apparent survival compared with best supportive care.
improvement in patient survival. The 5‐year sur-
vival rates vary from 29 to 87% but this is at the
Hepatocellular carcinoma
expense of significant morbidity (40–50%) and
mortality (up to 60%). It is worth stating that Hepatocellular carcinoma is a malignant tumour of
these results come out of highly experienced cen- hepatocytes that often arises in the context of end‐
tres and may not necessarily be transferable to stage chronic inflammation (cirrhosis). It is the most
non‐Japanese centres. In most western series, radi- common primary liver tumour (worldwide age‐
cal treatment of locally advanced tumours by standardised rate is 15.3 per 100 000), and the fifth
resection of adjacent organs, extended hepatec- most common malignancy in men and the ninth in
tomy or vascular reconstruction has not been women. For both sexes, HCC is the second highest
associated with prolonged disease‐free or overall cause of cancer‐related deaths. It occurs more often
survival, and so this cannot be recommended. in men than women, and the incidence rates peak
Instead, these patients should be considered for after age 60 years. There are significant variations of
clinical trials of neoadjuvant chemotherapy. disease burden across the world, with the highest
Laparoscopic, robotic‐assisted and total robotic age‐standardised rates per 100 000 occurring in
radical resection of gallbladder cancer have been underdeveloped regions in eastern Asia (31.9),
performed at specialised centres. Small cases series Southeast Asia (22.2), western Africa (16.4) and
have reported safety and feasibility outcome data Melanesia (14.8). In 2012 the age‐standardised rate
for T1b, T2 and even T3 tumours that are equiva- per 100 000 in Australia/New Zealand was 6.4.
lent to outcomes following an open procedure. Incidence and mortality rates are rising in some
However, there are significant technical challenges western countries, which traditionally have had a
related to the adequacy of the lymphadenectomy low disease burden. Although the reasons for this
and the difficulty of a bile duct reconstruction that are not fully understood, it may be due to a combi-
will need to be overcome before these approaches nation of factors including changing migration
are adopted more widely. For now, these patterns, an increased prevalence of hepatitis

C infection from intravenous drug abuse, and Diagnosis

because of rising rates of obesity and type 2 diabe-
Several different imaging modalities including
tes. A curative treatment for hepatitis C has been
ultrasound, CT and MRI may be used to either
available since 2013 and although this reduces the
evaluate patients with chronic liver disease or
risk of developing HCC, the risks are not eliminated
diagnose and characterise a suspected HCC.
and these patients require ongoing surveillance.
Screening programs in high‐risk patients usually
HCC is a complex disease with multiple possible
involve 6‐monthly ultrasound scans. The addition
aetiologies. The main risks are chronic hepatitis B
of serum alpha-fetoprotein (AFP) levels improves
virus (HBV) infection, chronic hepatitis C virus
the sensitivity of these programs for detecting
(HCV) infection and dietary exposure to the car-
small tumours and worldwide this has led to a
cinogen aflatoxin B1. Other risks include non‐alco-
decrease in late‐stage presentations.
holic fatty liver disease, alcohol‐induced cirrhosis,
Dynamic, multiphase, contrast‐enhanced CT or
obesity, dietary iron overload, metabolic disorders
MRI is the current standard for the imaging diag-
such as antitrypsin deficiency, and inherited condi-
nosis of HCC. The use of hepatobiliary contrast
tions such as haemochromatosis and Wilson’s dis-
agents and the inclusion of diffusion‐weighted
ease. However, approximately 15–20% of patients
sequences during MRI have improved detection
in ‘western’ countries have no obvious predisposing
rates and may be particularly helpful in differenti-
risk factors.
ating regenerative nodules from early HCC. Except
Various underlying gene and protein expression
in specific circumstances these imaging modalities
patterns have been described in hepatocellular can-
have largely replaced tissue biopsy for the diagnosis
cer. These include point mutations of the c‐KRAS
of HCC. Chest CT is important to assess for meta-
gene, co‐amplification of the cyclin D1 gene, muta-
static disease, particularly before undertaking radi-
tion of the β‐catenin gene, reduction of expression
cal surgical intervention.
of p21WAF/Cip1 and p16, and increased expres-
The yield from routine diagnostic laparoscopy
sion of transforming growth factor (TGF)‐β and
prior to undertaking resection of HCC is low
DNA methyltransferase (DNMT1) mRNA.
except in patients with cirrhosis, multifocal
The clinical presentation of HCC varies depend-
tumours and radiological evidence of major vascu-
ing on whether patients are in a high‐ or low‐risk
lar invasion.
group. In those with compensated chronic liver dis-
ease, most liver cancers are detected during screen-
Staging and predictive models
ing or surveillance. A progressively rising serum
AFP level should raise suspicion of a new hepato- Several clinical models focus on the impact of the
cellular cancer. Malignant change should also be underlying liver function. These include the Child–
suspected when there is a sudden deterioration in Pugh classification, the MELD score and the albu-
liver function. Frequently, this is due to either min–bilirubin (ALBI) grading system.
hepatic or portal vein thrombosis. Spontaneous Child–Pugh grade A patients do well following
rupture of HCC occasionally occurs in patients surgical intervention, but the classification is not
with large exophytic tumours, and this is associated particularly helpful for predicting outcomes in
with significant risk of mortality from peritonitis more advanced disease. The MELD score is helpful
and shock. In patients with no risks for chronic in cirrhotic patients only, and is derived from three
liver disease, mild to moderate abdominal pain, laboratory values (international normalised ratio,
weight loss, early satiety or a palpable mass in the serum total bilirubin and serum creatinine). Patients
upper abdomen are the most frequent presenta- with a MELD score of 10 or less are suitable for
tions. These symptoms often signify locally surgical intervention. Those with a score of 10–15
advanced disease. have a moderate risk of complications, while
The overall prognosis after a diagnosis of HCC is patients with a MELD score above 15 should not
poor, with a median survival of approximately 3–5 undergo surgical intervention. The ALBI grade is
months for untreated symptomatic patients. based on assessment of the serum albumin and bili-
Outcome is dependent on the tumour biology, the rubin and can be used in patients with or without
stage of the disease, the patient’s underlying comor- cirrhosis. This may be a better prognostic discrimi-
bidity and liver function, and optimal therapy. The nator for early‐stage disease than either the Child–
fibrolamellar variant that usually occurs in non‐cir- Pugh classification or the MELD score.
rhotic young adults is less aggressive than more Other clinical decision models combine liver
common subtypes, and prolonged survival may be function parameters with markers of disease biol-
possible even in advanced disease. ogy (e.g. size, number of tumours, the presence of
vascular invasion). The two most commonly used Therefore, ablation is the preferred option for
are the Barcelona Clinic Liver Cancer (BCLC) stag- patients with underlying liver dysfunction (Child–
ing system and the Cancer of the Liver Italian Pugh B–C). Of course, RFA or MWA are only pos-
Program (CLIP) score. sible for tumours that are anatomically accessible
The two main staging systems that include a his- and not adjacent to major vascular or biliary struc-
topathological assessment of disease are the AJCC/ tures. A reasonable approach in patients with early‐
UICC staging system (8th edition) and the Japan stage HCC and good liver reserve is to offer upfront
Integrated Staging (JIS) score. The AJCC/UICC percutaneous ablation followed by close post‐treat-
staging system is the most commonly used classifi- ment radiological surveillance. If local recurrence
cation in patients who undergo resection or trans- does occur, the tumour and surrounding ablated
plantation. However, the JIS score is simpler to use area can then be resected.
and may be better at discriminating outcome in Although liver transplantation is associated with
early HCC. Of all the histopathological factors, the significant perioperative risk and requires long‐
most consistently identified predictor of poor long‐ term immunosuppression, it is appealing because it
term survival after both resection and liver trans- eliminates the tumour and underlying chronic liver
plantation is the presence of microvascular invasion disease, as well as the risk of new intrahepatic can-
(MVI). This is difficult to determine preoperatively cers. Overall, liver transplantation provides the
and while several clinical predictive models have best long‐term survival for early‐stage HCC com-
been proposed none of these have been widely pared with other treatment options. Only patients
validated. aged under 70 years are considered, and selection
is determined by the Milan criteria (one lesion <5
cm or up to three lesions, each <3 cm, no extrahe-
Management
patic disease, and no evidence of gross vascular
Hepatocellular carcinoma is a complex disease that invasion). The 5‐year overall survival rates after
is best managed within a multidisciplinary environ- liver transplantation for HCC range from 52 to
ment. Management of the chronic liver disease is 81%. Selection beyond the Milan criteria has been
just as important in many of these patients as man- advocated (one lesion <6.5 cm or up to three
agement of the HCC. Curative intent treatments lesions, each <4 cm with a cumulative diameter <8
should be offered to all eligible patients with early‐ cm) to treat patients with more advanced tumours.
stage disease. Although patients with more Critics of this more liberal approach argue this is
advanced disease may still be offered curative treat- associated with higher rates of post‐transplant
ment, this will depend on the tumour staging and recurrence and lower long‐term survival. Patients
the underlying liver reserve. may be offered locoregional therapy such as
Early‐stage HCC is defined both clinically and ablation or TACE while waiting for their liver
pathologically, and this leads to difficulty inter- transplant.
preting the literature regarding treatment algo- Living‐donor liver transplantation (LDLT) has
rithms. Clinically, early‐stage HCC usually refers theoretical advantages of shorter waiting times,
to tumours of 3 cm or less in size and three or higher‐quality grafts and shorter ischaemic times
fewer in number, and with underlying good liver compared with traditional deceased donor liver
reserve (Child–Pugh A). Some groups classify transplantation. Disadvantages include the poten-
tumours of 2 cm or less as ‘very’ early stage dis- tial for perioperative risks in the donors, and ongo-
ease. Confusingly, tumours described by the Milan ing concerns that this approach may increase
criteria (which includes solitary lesions up to 5 recurrence rates in recipients. Generally, the criteria
cm) are also sometimes considered early‐stage for transplantation for HCC are more liberal for
HCC. ‘eastern’ countries than ‘western’ countries. This
There is ongoing controversy about the best may be because LDLT is performed more often
management of patients with early‐stage tumours than deceased donor transplantation because of a
(≤2 cm). Several meta‐analyses of both non‐ran- shortage of deceased donor organs. Worldwide,
domised and randomised studies have concluded HCC accounts for approximately 20–40% of liver
that percutaneous RFA may be inferior to liver transplantations, although in Australia and New
resection, but that MWA may have an advantage Zealand the figure is closer to 10%.
when comparing overall and recurrence‐free sur- Many patients with early‐stage HCC and good
vival. Regardless, both ablation techniques are less liver reserve are treated by liver resection because of
invasive and associated with fewer complications the shortage of donors for liver transplantation.
and shorter hospitalisation than liver resection. Specialist surgical expertise is now widely available
in most countries, and a potentially curative liver and 20.5). Careful preoperative assessment is
resection results in comparable 5‐year and 10‐year required to determine adequate remnant liver
survival outcomes to liver transplantation. reserve and to exclude the presence of extrahe-
Unfortunately, only 10–40% of patients with HCC patic disease. In general, liver resection is con-
are suitable for resection at the time of diagnosis. In traindicated in patients with extensively multifocal
the absence of underlying parenchymal disease, up or bilateral tumours, or when there is involve-
to 65–75% of the liver can be resected provided ment of the main portal vein or the inferior vena
that vascular inflow/outflow and biliary drainage cava.
are maintained. Minor resections can be under- Palliative options for patients with inoperable
taken in patients with early Child B disease without disease include locoregional therapy such as TACE
portal hypertension, but this is often associated or SIRT. Although these patients may have
with significant morbidity. improved quality of life and survival compared
Complications after hepatectomy are common, with best supportive treatment, overall they have a
with morbidity rates of 31–50%. Reported 5‐year poor prognosis with a median survival of only
overall survival rates after liver resection range 11–20 months. TACE is the best option for patients
from 37 to 61%, while 5‐year disease‐free survival with large or multifocal HCC without macrovascu-
rates range from 23 to 32%. Unfortunately, recur- lar invasion or extrahepatic metastasis. Objective
rence occurs commonly and to date there are no tumour responses are achieved in 35–50% of
universally accepted adjuvant treatments to reduce patients, and TACE can be repeated if necessary
this risk. Variables most frequently found to pre- depending on tumour response and the patient’s
dict long‐term outcome include tumour size, underlying liver reserve.
tumour number and severity of the underlying Oral administration of the multi‐kinase inhibitor
liver disease. Other important prognostic factors sorafenib may also prolong survival in patients
are untreated HBV and HCV infection, and the with advanced‐stage HCC who are unsuitable for
histological finding of MVI in the tumour speci- either resection or locoregional treatment. SIRT
men. To reduce recurrence and improve survival does not provide a survival advantage over
TACE is sometimes used as neoadjuvant therapy sorafenib but may be associated with better tumour
in patients with resectable HCC. However, a response rates and less side effects.
recent systematic review of the literature con-
cluded that this does not improve disease‐free
Ruptured HCC
survival.
To date, laparoscopic resection of HCC has Spontaneous rupture of HCC is a rare and life‐
mostly involved minor resections. This approach is threatening complication. The exact mechanism
associated with less blood loss and transfusion of rupture is not fully understood, and while this
requirements, less overall morbidity and a shorter complication can happen anywhere in the liver it
length of stay compared with open resections. occurs most frequently in large exophytic
Importantly, there appears to be no difference in tumours. Urgent fluid resuscitation is required,
short‐ or long‐term oncological outcomes. and subsequent transarterial embolisation (TAE)
Laparoscopic and robotic major liver resections for for haemostasis has a high success rate (53–
HCC have also been done and early reports suggest 100%). Overall 30‐day mortality rates after TAE
that oncological outcomes are also comparable are lower than after urgent open surgical haemo-
with open techniques. stasis. Furthermore, emergency liver resection is
also associated with poor long‐term outcomes
because the tumour stage and functional liver
Intermediate or advanced stage HCC
reserve are unknown, and disseminated malignant
Unfortunately, more than 50% of all HCCs are cells increase the risk of peritoneal and distant
diagnosed at an intermediate or advanced stage, metastases. Tumour re‐rupture after TAE has an
and in those who do not satisfy the Milan criteria extremely poor prognosis.
the only hope of cure is liver resection. These In patients who remain stable after the initial
patients have a high risk of recurrence, and out- TAE, laparoscopy and washout of the haemoperi-
comes following resection must be weighed toneum several days later may speed up recovery
against the lack of other potentially curative from the inevitable ileus that follows such a cata-
options. Certainly, long‐term disease‐free survival strophic event. Most groups advocate re‐imaging
is possible in some patients, even those with large later to reassess the role of a staged liver resection
(>10 cm) or multinodular tumours (Figures 20.4 in patients who have non‐progressive disease.
42 months post central hepatectomy
Fig. 20.4 Large central hepatocellular carcinoma secondary to haemochromatosis in a patient with Child–Pugh A
disease.
Colorectal liver metastases

Secondary tumours (liver metastases)
Colorectal cancer is the third most common cancer
Liver metastases are a major cause of death in worldwide and ranks as the second leading cause of
advanced malignant disease. Untreated metastases cancer‐related deaths in developed countries. In
are associated with short survival especially when patients who undergo preoperative imaging, liver
derived from oesophageal, stomach, pancreas or metastases are found in 35% of newly diagnosed
breast primary neoplasms. The most common pri- patients and another 8–30% of patients develop
mary sites for liver metastases are, in order of fre- metastatic spread to the liver during subsequent
quency, the bronchus, breast, colon and rectum, follow‐up. Synchronous colorectal liver metastases
and uterus. The predilection for metastases to (CRLM) are detected at or before the diagnosis of
develop in the liver is because of direct portal the primary cancer; metachronous CRLM are
venous blood flow from the intra‐abdominal vis- detected at any time 3 months after the diagnosis of
cera. However, other biological factors are also the primary cancer. The exact cut‐off for diagnosing
involved given that tumours such as melanoma, metachronous CRLM is arbitrary (and controver-
breast and testicular carcinoma which have no por- sial) and depends on the thoroughness of investiga-
tal venous drainage also spread frequently to this tions at the original presentation.
site. Management decisions in patients with liver Following the introduction of effective chemo-
metastases are difficult and relatively undefined therapeutic agents in the mid 1990s (oxaliplatin
except in those with colorectal liver metastases. and irinotecan) and targeted biological agents in
2yrs post central hepatectomy
Fig. 20.5 Large central hepatocellular carcinoma in a patient with Child–Pugh B disease.
the late 2000s (bevacizumab and cetuximab), there and for excluding residual disease in the post‐chem-
have been dramatic improvements in outcomes for otherapy liver (Figure 20.6). PET/CT scans detect
patients with CRLM. Treatment strategies are extrahepatic disease including local recurrence at
evolving rapidly because of the development of new the site of the primary tumour excision. Although
therapeutic agents and improvements in our under- numerous clinical guidelines recommend routine
standing of the molecular heterogeneity of colorec- PET/CT for all patients with CRLM, there is ongo-
tal cancer. Ideally, patients should be managed in a ing debate about the value of this investigation.
multidisciplinary environment which includes sur- Meta‐analyses demonstrate that PET findings can
geons, medical and radiation oncologists, radiolo- alter management decisions in up to 24% of
gists and nuclear medicine physicians. At present, it patients but this is mainly in patients at high risk of
is not routine to have geneticists and molecular sci- extrahepatic disease. Ideally, PET/CT should not be
entists involved in multidisciplinary team discus- done within 6–8 weeks after completion of chemo-
sions, although this may be helpful and necessary as therapy to avoid false‐positive results. However,
personalised treatment options become more read- this may not always be practical.
ily available. Elevated levels of serum carcinoembryonic anti-
gen (CEA) may be used to support the diagnosis
Investigations and to monitor progress after treatment.
Contrast‐enhanced abdominal/pelvic and thoracic
Staging
CT is the investigation of first choice. A second
modality such as ultrasound or MRI should be used The original Dukes staging system for colorectal
when further clarification is needed. Gd‐EOB‐ cancer does not include a classification for liver
DTPA enhanced MRI is more sensitive than CT for metastases and therefore is not applicable. The
detecting liver metastases under 10 mm in diameter AJCC TNM system designates patients with CRLM
Fig. 20.6 MRI scan showing multifocal colorectal liver metastases (arrows) not seen on CT.
as stage IV disease. This is further subdivided into

Box 20.4 Treatment options for patients
STAGE IVa (spread to the liver only), stage IVb
with colorectal liver metastases
(spread to more than one distant organ) or stage
IVc (spread to distant parts of the peritoneum). Systemic treatment
Chemotherapy (5‐FU, oxaliplatin, irinotecan)
Biologics (cetuximab, panitumumab, bevacizumab)
Clinical risk models Liver resection
Liver ablation (microwave ablation, radiofrequency
Several clinical risk scoring systems have been devel-
ablation, cryotherapy)
oped that stratify patient prognosis based on preop-
Regional arterial treatments
eratively identifiable clinicopathological factors.
Irinotecan DC‐beads
Variables that consistently relate to survival include
Selective internal radiation therapy
the number and size of liver metastases, the nodal Direct chemotherapy infusion (5‐FU, oxaliplatin)
status of the primary tumour and the preoperative Stereotactic body radiation therapy
serum CEA level. Externally validated systems Best supportive care
include the Nordlinger score, MSKCC score,
Basingstoke index, Iwatsuki score and Mayo scor-
ing system. Although these stratification systems
help predict overall survival, they do not accurately (other than in ‘high‐risk’ disease) is not strong.
select patients who might benefit from adjuvant Regardless, the pros and cons of systemic treatment
treatment. This is likely to be improved by incorpo- must be discussed in detail and this is time‐consum-
ration of proteomic and genomic biomarkers into ing and can be confusing for the patient with newly
the models (e.g. KRAS and BRAF mutation status). diagnosed CRLM.
At the initial diagnosis, it is important to deter-
mine whether the liver metastases are resectable,
Chemotherapy and biologics in the potentially resectable or not resectable, and if
management of patients with CRLM patients are fit for surgical intervention. In practical
(Box 20.4) terms this provides a guide for the use of systemic
treatment, although there are numerous other fac-
Adjuvant chemotherapy is considered standard of tors that contribute to this decision.
care for patients with high‐risk primary colorectal In patients with otherwise ‘low‐risk’ resectable
cancers without distant metastases. Although liver metastases, and where an R0 resection margin
chemotherapy is frequently given, the evidence for (microscopically clear) can be achieved, upfront
a benefit in patients with resectable liver metastases liver resection or preoperative chemotherapy
followed by resection are equally appropriate Biomarkers and molecular signatures in CRLM

treatment options. Treatment usually consists of a
Colorectal cancer is a heterogeneous disease associ-
doublet regimen of 5‐FU and oxaliplatin limited to
ated with multiple different gene mutations.
six cycles (FOLFOX). Overall 5‐year survival rates
Assessment for KRAS and BRAF mutations is now
of 48–51% are equivalent for these two approaches.
routine before treatment with EGFR‐targeted mon-
Adjuvant therapy post liver resection is not routine
oclonal antibodies (cetuximab or panitumumab).
but may be warranted based on pathological assess-
Only patients with KRAS wild‐type disease should
ment of the resected specimen.
be offered these therapies. However, there is mount-
In contrast, patients with resectable but ‘high‐
ing evidence that ‘expanded RAS’ analysis may be
risk’ liver metastases (e.g. multiple or large metasta-
needed to identify tumour subtypes with varying
ses, synchronous disease, suspicion of low‐volume
response rates due to different codon mutations.
extrahepatic disease) should be offered periopera-
Recently, a classification was proposed that iden-
tive doublet chemotherapy (FOLFOX) for 3 months
tified four molecular genotypes of tumour associ-
before and after liver resection. This may or may
ated with distinct prognoses:
not be combined with monoclonal antibody ther-
• CMS1 (immunogenic and hypermutated)
apy (either bevacizumab or cetuximab depending
• CMS2 (epithelial, marked WNT and MYC sig-
on KRAS status). More aggressive triplet regimens
nalling activation, best prognosis)
combining 5‐FU, oxaliplatin and irinotecan
• CMS3 (metabolic dysregulation)
(FOLFOXIRI) have been advocated but this
• CMS4 (mesenchymal features, worst prognosis).
requires careful selection of patients because of the
These classifications represent a breakthrough in
toxicity of this treatment.
our understanding of the underlying molecular
Patients with potentially resectable CRLM may
mechanisms of this disease and may help individu-
be down‐staged with aggressive systemic treatment.
alise treatment regimens including the role of hepa-
The best combination in this situation is unknown
tectomy. Numerous new biomarkers are emerging
and is the subject of ongoing study. In patients with
but are not yet in routine clinical practice. Ideally,
KRAS wild‐type disease, doublet chemotherapy
these will enhance further our ability to predict
plus an anti‐EGFR (epidermal growth factor recep-
response to treatment.
tor) antibody may be the best option, although tri-
plet therapy (FOLFOXIRI) plus bevacizumab (a
vascular endothelial growth factor inhibitor) may
Liver resection: postoperative outcomes
also be considered. In patients with RAS‐mutant
and long‐term survival
disease, a cytotoxic doublet plus bevacizumab or
FOLFOXIRI plus bevacizumab is recommended. Resection offers the best chance of cure for patients
Maximum response is usually seen after 12–16 with isolated CRLM. The first step in a multidisci-
weeks of treatment. These patients need to be re‐ plinary team‐managed treatment strategy is to
evaluated regularly to identify non‐responders and determine whether the patient has resectable dis-
to prevent over‐treatment of patients who respond ease, and whether they are fit enough to undergo an
and then become candidates for liver resection. operation. Classical indications for liver resection
Some patients achieve a complete radiological are based on the number and size of the metastases
response after treatment and this poses a clinical and whether there is extrahepatic disease or not.
dilemma about whether to resect or watch these More recently, there is consensus that all patients
original sites of tumour in the liver. Despite evi- should be considered for potentially curative resec-
dence that up to 40% of these treated tumours have tion if there is enough liver remnant and adequate
pathological evidence of microscopic residual dis- vascular inflow/outflow and biliary drainage can be
ease, most surgeons prefer a watch‐and‐wait obtained. This radical surgical approach has
approach rather than performing a blind resection resulted in a shift of thinking towards the contrain-
of the tumour site based on the original imaging. dications rather than the indications for liver resec-
Patients with non‐resectable CRLM and who are tion (Figure 20.7).
unlikely ever to be offered liver resection because of Refinements of surgical technique have contrib-
local factors or extrahepatic metastases may be con- uted to the increased safety of liver resection over
sidered for locoregional treatments combined with the past two decades. These include the use of low
systemic therapy. Locoregional treatments include central venous pressure anaesthesia, intermittent
thermal ablation (RFA or MWA), TACE (with DC portal inflow occlusion (Pringle manoeuvre), pre-
beads), SIRT using yttrium‐90 radiolabelled parti- cise tumour localisation using intraoperative ultra-
cles, or stereotactic body radiation therapy. sound, and improved transection instruments
Fig. 20.7 Multifocal colorectal liver metastases requiring an extended right hepatectomy. IVC, inferior vena cava.
including the Cavitron ultrasonic surgical aspirator resection may be particularly beneficial in apical
(CUSA), stapling devices and energy‐based surgical and dorsal segment resections which are difficult to
vessel sealing tools. resect laparoscopically. To date most reports involve
Major morbidity after liver resection (defined as a small case series undertaken by highly specialised
complication of Clavien–Dindo grades III or IV) units. Barriers to more widespread adoption include
occurs in up to 20% of patients and depends on the limited access to robots in many hospitals, higher
extent of resection. Specific complications of liver costs compared with open or laparoscopic
resection include post‐hepatectomy liver failure, bile approaches, and lack of a suitable robotic liver‐dis-
leakage, haemorrhage and intra‐abdominal sepsis. secting device.
Laparoscopic operations are associated with less Overall, in‐hospital and 90‐day mortality rates
overall morbidity, lower transfusion rates and after liver resection are usually less than 5%.
shorter length of hospital stay than open proce- Regardless of the approach, patients with advanced
dures. Furthermore, several meta‐analyses have age, comorbid disease and who undergo synchro-
shown that oncological outcomes are not compro- nous hepatic and colon resection have the highest
mised by a laparoscopic approach and in fact may procedure‐related mortality following major liver
allow patients to return to adjuvant treatment resection.
faster than after an open procedure. After liver resection, overall 5‐year survival rates
There is growing interest in robotics for the man- range from 25 to 63% (mean 40%) and 5‐year dis-
agement of patients with liver metastases because ease‐free survival rates range from 4 to 47% (mean
of the advantages of three‐dimensional imaging 25%). Overall 10‐year survival rates as high as
and multi‐degree operative freedom. Robotic liver 36% have been reported in some series.
Strategies to increase resection rates • colonoscopy 12 months after liver resection; if

no adenomatous polyps are identified, repeat
Upfront liver resection is feasible in only 15–25%
every 3–5 years; if advanced adenomatous pol-
of patients, although systemic chemotherapy is
yps are identified, repeat in 1 year.
effective in down‐staging some patients with ini-
tially unresectable disease. There are several other
options that are used in clinical practice in con-
Non‐colorectal hepatic metastases
junction with chemotherapy to expand the num-
(Box 20.5)
ber of patients who might undergo a potentially
curative liver resection. These include portal vein
Improvements in the perioperative mortality and
embolisation to cause hypertrophy of the pro-
morbidity of major hepatic resection have led to a
posed remnant liver, thermoablation combined
more liberal application of this procedure for meta-
with liver resection, two‐stage hepatectomy,
static disease other than from colorectal cancer.
extreme liver surgery including resection of the
However, most reports of resection for non‐colo-
vena cava, and the ALPPS (associating liver parti-
rectal metastases involve relatively small numbers
tion and portal vein ligation for staged hepatec-
of patients and hence firm conclusions are difficult
tomy) procedure. Although promising, this latter
to make. The biological behaviour of the primary
technique is associated with significant periopera-
tumours is usually so different that it is often not
tive risks and therefore has not been widely
appropriate to group these cases together for sur-
adopted.
vival analysis.
The timing of onset and the total burden of the
liver metastases, along with any patient comorbid-
Synchronous resection
ity, must be evaluated through multidisciplinary
The surgical approach in patients who present with discussion. Systemic chemotherapy, ablative thera-
synchronous CRLM can be challenging and often pies or locoregional chemoembolisation may be
depends on whether the primary tumour is sympto- used in selected patients, sometimes in conjunction
matic or not. Options include simultaneous resec- with liver resection.
tion of the primary and liver metastases or a staged Certain primary tumours, including ovarian, gas-
resection. The staged approach can be either the tric and pancreas, have a predilection for peritoneal
primary first (classic) or the liver first (reverse metastases and therefore laparoscopy is an impor-
approach). Systematic review of the literature tant part of the staging process before considering
shows no significant difference in outcomes liver resection.
between these approaches. An obvious advantage
of a synchronous bowel and liver operation for the
patient is the need for only one anaesthetic. A gen-
eral rule of thumb to avoid the risk of complica- Box 20.5 Non‐colorectal hepatic
tions is that a simultaneous operation should be metastases that may be suitable
avoided if both the bowel and liver procedures are for resection
major resections.
Definite
Neuroendocrine tumours
Surveillance after liver resection Melanoma
Renal cell carcinoma
Following a potentially curative liver resection Bladder carcinoma
patients usually undergo regular surveillance as Sarcoma
they may be considered for a second potentially Endometrial carcinoma
curative resection if recurrence occurs. Although
there is no universal consensus, a reasonable Possible
approach to surveillance advocated in several clini- Breast carcinoma
Thyroid carcinoma
cal guidelines includes:
Ovarian
• CEA testing every 3–6 months for 2 years, then
Gastrointestinal stromal tumours
every 6 months for 3 years
Pancreaticoduodenal carcinoma
• chest/abdomen and pelvis CT scan every 6
Oesophagogastric carcinoma
months for 2 years, then every 12 months up to a
Squamous cell carcinoma
total of 5 years
2 Primary sclerosing cholangitis is not associated

Further reading with:
a inflammatory bowel disease
Dhir M, Sasson AR. Surgical management of liver metas-
b carcinoma of the bile duct
tases from colorectal cancer. J Oncol Pract
2016;12:33–9. c gallstones
Guinney J, Dienstmann R, Wang X et al. The consensus d multifocal biliary strictures
molecular subtypes of colorectal cancer. Nat Med e hepatocellular carcinoma
2015;21:1350–6.
Kitisin K, Packlam V, Steel J et al. Presentation and out- 3 Which of the following does not cause primary
comes of hepatocellular carcinoma patients at a west- hepatocellular carcinoma?
ern centre. HPB (Oxford) 2011;13:712–22. a alcohol
Saha SK, Zhu AX, Fuchs CS, Brooks GA. Forty‐year b haemochromatosis
trends in cholangiocarcinoma incidence in the US:
c hepatitis B virus
intrahepatic disease on the rise. The Oncologist
d steroids
2016;21:594–9.
Soares KC, Kamel I, Cosgrove DP, Herman JM, Pawlik e gallstones
TM. Hilar cholangiocarcinoma: diagnosis, treatment
options, and management. Hepatobiliary Surg Nutr 4 Which of the following is not a treatment for liver
2014;3:18–34. metastases?
Van Cutsem E, Cervantes A, Adam R et al. ESMO consen- a arterial chemoembolisation
sus guidelines for the management of patients with b ablation
metastatic colorectal cancer. Ann Oncol c laparoscopic resection
2016;27:1386–422. d open resection
e portal venous chemoembolisation
MCQs 5 The most aggressive biliary tumour with the

shortest overall survival rate is:
a gallbladder cancer
b biliary cystadenoma
c hepatocellular cancer
1 Cholangiocarcinoma is most commonly found: d Caroli’s disease
a in the periphery of the liver e distal cholangiocarcinoma (dCCA)
b in the gallbladder
c at the biliary confluence (Klatskin tumour)
d in the distal bile duct
e in the duodenum
21 Liver infections
Vijayaragavan Muralidharan, Marcos V. Perini and
Christopher Christophi
Aetiology
Introduction Classically, pyogenic liver abscess may arise by
ascending infection from the biliary tract, haema-
Liver infections are broadly classified based on the
togenous spread via the portal vein and hepatic
infecting agent as viral, bacterial or parasitic infec-
artery or by direct extension from adjacent site of
tions. Viral aetiology includes targeted infection of
sepsis.
the liver by hepatitis viruses or secondary involve-
• Ascending biliary tract infections are responsible
ment of the liver during systemic viral infections
for 30–50% of patients presenting with pyogenic
such as cytomegalovirus (CMV), Epstein–Barr
abscess. The resultant cholangitis leads to liver
virus (EBV), herpes simplex virus (HSV) and human
abscesses, which are frequently multiple. This is
immunodeficiency virus (HIV). Bacterial infections
usually associated with biliary obstruction due
manifest as pyogenic abscesses. Parasitic infesta-
to choledocholithiasis and benign and malignant
tions include invasive amoebiasis, hydatid disease
strictures. Biliary reflux secondary to biliary bypass
and liver fluke disease. Surgical intervention forms
or endoscopic sphincterotomy and iatrogenic
part of the management strategy (Box 21.1) for
instrumentation by endoscopic retrograde cholan-
bacterial and parasitic infections, which will be the
giopancreatography (ERCP) or percutaneous
focus of this chapter.
transhepatic procedures (percutaneous transhe-
Bacterial and parasitic infections of the liver uni-
patic cholangiography/percutaneous transhepatic
versally originate at a distal site, spread to the liver
biliary drainage) are less common causes of liver
by blood, biliary tree or direct extension and may
abscess.
manifest local as well as systemic signs and symp-
• Portal vein bacteraemia/pyaemia is also a com-
toms. Diagnosis is based on a combination of clinical
mon cause for pyogenic abscess. Complicated
presentation and microbiology, heavily supported by
diverticular disease, appendicitis, peritonitis and
imaging.
pancreatitis may cause portal vein pyaemia.
Occult colorectal neoplasia should be suspected
in patients diagnosed with pyogenic liver abscess,
Bacterial infections
particularly due to Klebsiella pneumoniae and in
the absence of any obvious underlying hepatobil-
Pyogenic abscess
iary disease.
The introduction of modern antibiotic therapy • Hepatic artery seeding may occur in septicaemia
has progressively reduced the mortality from pyo- from any cause and account for 5–15% of pyo-
genic liver abscess to 5–10%. The epidemiology genic liver abscesses. Common causes include
has also shifted from the young male (20–30 bacterial endocarditis, pneumonia and intrave-
years) with a liver abscess complicating an intra‐ nous drug abuse.
abdominal infection to the elderly (60–70 years) • Other causes of liver abscess include complicated
diabetic male with previous history of biliopancre- blunt or penetrating liver trauma by direct exten-
atic pathology, biliary instrumentation or colonic sion from adjacent septic conditions such as
disease. empyema of the gallbladder.
191
liver abscesses. It will also delineate the presence

Box 21.1 Management strategy
of gas, level of parenchymal necrosis, hepatic and
Source control portal vein distortion or thrombosis and establish
Identifying the point of origin of the infection and a baseline for future reassessments. Contrast‐
treating it to prevent recurrent or persistent infections enhanced magnetic resonance imaging (MRI) has
the distinct advantage of imaging the biliary tree
Local control
using magnetic resonance cholangiopancreatogra-
Managing the local effects within the liver by a
phy (MRCP) sequence for an underlying aetiology
combination of pharmacology, interventional
while also being superior in differentiating liver
radiology and surgery
tumours and cysts. It also allows assessment of
Systemic control liver parenchymal disease and may help differenti-
Treatment of the systemic effects of the disease and ate amoebic from pyogenic abscesses.
control of the disease elsewhere in the body Determining the underlying aetiology may
require biliary imaging by MRCP, CT intravenous
cholangiogram, echocardiogram or colonoscopy
• Cryptogenic liver abscess describes the situation based on clinical suspicion.
where no cause is identified, which comprise up
to 25% of the cases. Treatment
The infecting organism varies according to the site Therapeutic principles based on systemic, local and
of entry. In biliary or portal vein sepsis, the organ- source control include resuscitation, analgesia,
isms are enteric and usually polymicrobial. appropriate antibiotic therapy, abscess drainage
Staphylococcus aureus is evident in 20% of cases and eradication of the underlying cause.
and is confirmed predominantly from haematoge- General measures include resuscitation according
nous spread. to the Surviving Sepsis Campaign guidelines in order
to maintain blood pressure and tissue perfusion.
Clinical presentation and diagnosis Symptomatic measures include a regimen of analge-
The most common presenting symptoms include sics, temperature control and nutritional support.
pyrexia and rigours associated with right upper Antimicrobial therapy is dependent on the under-
quadrant pain, general malaise, anorexia and weight lying cause. Biliary or enteric causes involve micro-
loss. In the elderly the systemic manifestations may bial cover against Gram‐negative and anaerobic
be blunted. Examination may reveal tender hepato- organisms. Haematogenous causes require antibi-
megaly. Occasionally, hypotension and cardiovascu- otic cover against staphylococcal organisms.
lar collapse may be the presenting symptoms. Administration of antibiotics is usually prolonged
Abscess rupture is a rare complication (around over several weeks to eradicate infection and avoid
3% in some series) and is associated with diameter recurrence. This usually includes 2–3 weeks of
of more than 6 cm and a background of cirrhosis. intravenous antibiotics that may be changed to oral
Pyogenic liver abscesses most commonly involve administration for another 3–4 weeks to complete
the right lobe of the liver, possibly due to its larger a total of 4–6 weeks of antibiotics. Broad‐spectrum
mass and greater blood supply than the left. antibiotics (piperacillin/tazobactam, carbapenems
or second‐generation cephalosporin with metroni-
Investigation dazole) should be started as soon as blood cultures
Liver function tests may show hyperbilirubinaemia are taken and later on tailored in accordance with
and raised alkaline phosphatase and transaminase clinical progress and microbiology results.
levels. Blood cultures are frequently positive. A leu- Local control of the liver abscess is achieved by a
cocytosis is usually evident. A reactive pleural effu- step‐up program commencing with antibiotic ther-
sion may be present in about 50% of cases and the apy for small abscesses, especially if widespread
chest X‐ray may show an elevated hemidiaphragm. and multiple. Ultrasound‐ or CT‐guided aspiration
Blood cultures are positive in up to 50% of cases is useful in unilocular abscesses of less than 5 cm
and serology for Entamoeba histolytica and hydatid diameter. In 50% of such cases a repeat aspirate
disease tested where appropriate. will be required.
The initial diagnosis is usually made with a diag- Abscesses lager than 5 cm and those failing aspira-
nostic abdominal ultrasound searching for biliary tion may be treated by percutaneous catheter drain-
pathology. Cross‐sectional imaging with contrast‐ age. Large, complex, multilocular abscesses may
enhanced computed tomography (CT) will define require a multidisciplinary approach between radiol-
the size, number and anatomical location of the ogists, infectious disease experts, endoscopists and
21: Liver infections 193
surgeons. Open or laparoscopic surgical d rainage or usually positive. Approximately 99% of patients
resection of the affected liver lobe is a last resort to with amoebic liver abscess develop detectable anti-
remove dead material not amenable to retrieval with bodies, but serologic testing may be negative in the
catheter drainage and is rarely indicated. first 7 days. In endemic areas, up to 35% of unin-
fected individuals have anti‐amoebic antibodies due
to previous infection with E. histolytica. Therefore,
Parasitic infections negative serology is helpful for exclusion of disease,
but positive serology cannot distinguish between
Amoebic liver abscess acute and previous infection. Ultrasound with nee-
Aetiology dle aspiration and culture confirm the diagnosis.
Amoebic infestation is caused by the organism
Entamoeba histolytica. It is rare in Australia but Treatment
endemic in many areas of the tropics such as India Symptomatic measures include analgesics and
and other parts of Asia. Faeco‐oral transmission attention to nutrition and hydration. Antimicrobial
occurs by passage of cysts in the stool, the cysts therapy is the mainstay of treatment, with metroni-
contaminating food or water sources due to poor dazole being the antibiotic of choice (500–750 mg
hygienic practices and being ingested. The organism orally three times daily for 10 days). The cure rate
penetrates the mucosa of the gastrointestinal tract with this therapy is over 90%. Shorter duration of
to gain access to the liver via the portal venous sys- metronidazole is not generally recommended.
tem. The resultant abscess has an ‘anchovy paste’ Metronidazole is well absorbed from the gastroin-
appearance and may be secondarily infected, usu- testinal tract. Intravenous therapy offers no signifi-
ally by enteric organisms. Amoebic liver abscess is cant advantage as long as the patient can take oral
the most common extra‐intestinal manifestation of medications and has no major defect in small bowel
amoebiasis. Risk factors include malnutrition, absorption. Needle aspiration under ultrasound or
depressed immunity and low socioeconomic status. CT guidance or insertion of a pigtail catheter are
Complications of amoebic abscess include rupture not routinely required but may be warranted if the
into the peritoneal cavity or hollow viscus such as cyst appears to be at imminent risk of rupture espe-
colon or stomach. Rarely there may be pleuro‐pul- cially if present in the left lobe, if there is clinical
monary involvement. deterioration or lack of response to empirical ther-
apy, or if exclusion of alternative diagnoses is
Clinical features needed. Mortality rate from uncomplicated amoe-
The onset of the disease may be sudden or gradual. bic abscess is less than 1%.
For individuals returning from an endemic area, the
clinical presentation typically occurs within 8–20
weeks (median 12 weeks). Right upper quadrant Hydatid disease
pain sometimes radiating to the right shoulder, Hydatid disease is caused by infection with the
associated with general malaise and weight loss, are metacestode stage of the tapeworm Echinococcus,
the most common symptoms on presentation. which belongs to the family Taeniidae. Six species
Pyrexia and sweating occurs in about 60% of of Echinococcus produce infection in humans; E.
patients. Concurrent diarrhoea is present in less granulosus and E. multilocularis are the most com-
than one‐third of patients, although some patients mon, causing cystic echinococcosis and alveolar
report a history of dysentery within the previous echinococcosis, respectively. Echinococcus vogeli
few months. Signs may include tender hepatomeg- and E. oligarthrus cause polycystic echinococcosis
aly and, occasionally, jaundice. Intra‐abdominal and are rarely seen. Two new species, E. felidis and
rupture may occur in up to 5% of cases. Other rare E. shiquicus, have been identified recently though
complications include hepatic vein and inferior little is documented of their impact on humans.
vena cava thrombosis; these have been attributed to
mechanical compression and inflammation associ- Echinococcus granulosus
ated with a large abscess.
Pathology
Investigation Dogs and other canids are definitive hosts while
Full blood examination may show leucocytosis and ungulates are intermediate hosts. The human is an
eosinophilia. Liver biochemistry is frequently aberrant intermediate host in this disease. The ova
deranged and shows a hepatocellular pattern of are ingested by humans from the faeces of tape-
injury. Amoebic serology and stool cultures are worm‐infected dogs. Dogs are usually infected by
feeding of offal of infected sheep. The ova reach the Investigations

stomach of the human, where they hatch, penetrate Liver function tests may show either an obstructive
the wall of the intestine and pass to the liver by the or hepatocellular pattern. Full blood examination
portal vein. Others may pass from the liver into the may reveal a leucocytosis or eosinophilia. There are
lung, brain or other organs. The liver is affected in numerous serological tests available. Hydatid cyst
approximately two‐thirds of patients, the lungs in fluid antigen B (AgB) and antigen 5 (Ag5) from
approximately 25%, and other organs including E. granulosus are the most specific antigens for
the brain, muscle, kidneys, bone, heart and pan- the immunodiagnosis of cystic echinococcosis. The
creas in a small proportion of patients. Single‐organ most sensitive and specific test is immunoelectro-
involvement occurs in around 80% of patients with phoresis, which is not only diagnostic but an
E. granulosus infection, and only one cyst is indicator of response to treatment. The current

observed in more than 70% of cases. When reach- enzyme‐linked immunosorbent assay (ELISA) for
ing the liver parenchyma, development of the cyst antigen has a sensitivity of 85–89%, with some
occurs. These cysts exhibit a slow growth pattern, degree of cross‐reactivity for other cestode or
typically increasing in diameter at a rate of 1–5 cm helminthic infections.
per year. Infection usually occurs in childhood but Ultrasound is an excellent cost‐effective modality
only becomes apparent in adulthood. for examining cystic lesions of the liver and the
The cyst has a characteristic appearance. The World Health Organization (WHO) has classified
capsule or exocyst is composed of compressed host them according to number, size and the presence
tissue. The endocyst includes the laminated mem- of daughter cysts, endocysts and calcification
brane from the parasite, which contains the germi- (Box 21.2). CT provides better anatomical charac-
nal layer and scolices. The cyst is fluid‐filled and terisation of cystic lesions and their relation to the
contains brood capsules. The natural history of hepatic vasculature and biliary anatomy and is use-
hydatid cysts is that of slow progressive growth. ful for preoperative evaluation and planning. It also
Apart from local compressive effects, rupture may shows extrahepatic disease (lung) and has accuracy
occur into the biliary tree causing pain, obstructive in visualising the cystic matrix. MRI/MRCP can be
jaundice, cholangitis or even pancreatitis. Rupture helpful in assessing the presence of biliary commu-
into the peritoneal or thoracic cavity may also nication or bronchobiliary fistulas.
occur in addition to haematogenous spread to other ERCP or MRCP may be specifically indicated
organs such as lung, bone, brain and spleen. The where biliary involvement is suspected. The pres-
cysts may become secondarily infected. ence of heavy calcification in the wall of the cyst is
an indicator of a dead/inactive cyst.
Clinical presentation
Hydatids are often asymptomatic and are detected Treatment
as incidental findings on radiological investigations Medical treatment is mandatory to mitigate symp-
for other conditions. Common symptoms include toms and prevent progression of the disease and
right upper quadrant pain, jaundice, pruritus and the development of secondary infections. Parasite
pyrexia. A persistent cough may indicate pulmonary
involvement. Mass effect by the cyst may cause bil-
iary obstruction, compression of the portal vein or
Box 21.2 WHO classification of cystic
inferior vena cava and rarely result in Budd–Chiari
echinococcosis
syndrome, cholestasis or portal hypertension.
Rupture into the abdominal cavity leads to pain
CE1 Unilocular simple cysts with liquid content
with peritonitis. It may result in acute hypersensi-
often with the CE1‐specific ‘double line’ sign
tivity reactions, including anaphylaxis, due to the
CE2 Multivesicular multiseptated cysts
antigenic material present in the fluid, which trig-
CE3a Cysts with liquid content and CE3a‐specific
gers an immunological reaction.
detached endocyst
Rupture into the pleural cavity results in pulmo-
CE3b Unilocular cyst with daughter cysts inside a
nary hydatidosis or bronchial fistula. Lung involve- mucinous solid cyst matrix
ment in hydatidosis may manifest with cough CE4 Heterogeneous solid cysts with degenerative
(50–60%), chest pain (50–90%), dyspnoea and CE4‐specific canalicular structure of cyst
haemoptysis (10–20%). When the lungs are content
involved by direct extension, 60% involve the right CE5 Cysts with degenerative content and heavily
lung, especially the lower lobes. Lung involvement calcified wall
occurs more commonly in children.
eradication is a long‐term achievement. Treatment

may be medical, percutaneous or surgical and is
dependent on the stage of the cyst based on the
WHO classification.
Conservative
Asymptomatic CE4 and CE5 cysts, which are
deep in the parenchyma, require no treatment.
Complications are rare but patients need regular
follow‐up.
Medical
Medical therapy alone may be used in small CE1–
CE3a (<5 cm) cysts and is successful in 30–50% of
Fig. 21.1 Hydatid liver lesion arising from the left lobe
cases. Drug therapy may be used alone or in con-
of liver.
junction with surgical procedures. Mebendazole or
albendazole may be used in patients with hydatid
disease who are regarded as poor risk for surgery or
with widely disseminated disease. Albendazole
Liver resection is rarely indicated and is suitable for
gives excellent bioavailability and concentration in
peripheral or pedunculated cysts.
the cyst at a dose of 10–15 mg/kg daily. It may also
More commonly used is the conservative option
be delivered by percutaneous injection under ultra-
of de‐roofing of the cyst (endocystectomy).
sound localisation directly into the cyst. These
Scolicidal agents are frequently injected into the
drugs may be administered either before or after
cyst prior to manipulation to destroy active
definitive surgery to minimise the risk of recur-
components and prevent recurrence if spillage

rence. Prolonged courses over 3–6 months are rec-
occurs. Commonly used agents include cetrimide or
ommended. These drugs may be toxic to the liver
hypertonic saline. The contents of the cyst are then
and bone marrow and require careful monitoring.
evacuated. The residual cavity may be filled with
saline and closed (capittonage) or obliterated by
Percutaneous treatments
an omental pedicle, especially in infected cysts.
This involves drainage of the cysts and destruction
Biliary communications may need to be closed
of the germinal layer under ultrasound guidance. It
and bile duct explored to remove hydatids causing
involves puncture of the cyst, aspiration of the con-
biliary obstruction.
tent, injection of a protoscolicidal agent (95% etha-
nol, 20% saline) and re‐aspiration of fluid (or
Alveolar echinococcosis
PAIR). This is used in larger CE1 and CE3a cysts
(>5 cm), in patients unable to undergo surgery or Pathology
where recurrence occurs after surgery. When This is a rare condition caused by E. multilocularis,
applied for CE2 and CE3b cysts there is a high whose life cycle is different from that of E. granu-
recurrence rate. It is contraindicated in superficial losus. Natural hosts include foxes, rodents, dogs
cysts, those that are inactive or heavily calcified and and cats. It is endemic in the northern hemisphere,
in the presence of biliary communication. especially Japan, China and central Europe.
Humans are an unusual and intermediate host. It is
Surgery a progressive, destructive disease. Death results
The principles of surgical management include (i) from liver parenchymal destruction and liver fail-
complete neutralisation and removal of the parasite ure. The disease may extend to the brain and lung
components, including the germinal membrane, and may be associated with severe myositis.
scolices and brood capsules; (ii) prevention of con- Vesicles invade the host liver tissue by extension of
tamination or spillage to prevent anaphylaxis or the germinal layer, which remains in an active pro-
recurrence; and (iii) management of the residual liferative state.
cavity. Surgery is the first choice for large CE2–
CE3b cysts or those that are superficial with a risk Clinical features
of rupture (Figure 21.1). Early symptoms are usually non‐specific and vague.
Procedures may be radical, including liver resec- The most common initial presentation is mild right
tion with total excision of the cyst or pericystectomy. upper quadrant pain. Tender hepatomegaly or a
mass may be present. As the disease progresses, pyrexia or cholangitis and symptoms of allergic
jaundice, ascites and hepatic insufficiency occur. In reactions. Hepatosplenomegaly may be present.
the early stages, a high index of suspicion in Chronic symptoms include intermittent biliary
endemic areas is required. Differential diagnosis colic, cholecystitis, jaundice, anaemia and
includes hepatoma, tuberculosis, haemangioma or hypoproteinaemia.
focal nodular hyperplasia.
Investigation
Investigation
Full blood examination may show eosinophilia.
Radiological investigations such as ultrasound, CT
Liver function tests show features consistent with
and MRI may provide additional information.
cholestasis. Stools are examined for the presence of
Serology may be inconclusive in the early stages of
ova. Specific serological testing usually confirms
the disease but may subsequently confirm the
the diagnosis.
underlying process. Occasionally, laparoscopy and
biopsy may be required. Even at operation, the
accuracy of diagnosis is only 50%. Treatment
The condition is treated with albendazole, praziqu-
Treatment antel or bithional. Cholecystectomy and explora-
The only known definitive cure for E. multilocula- tion of the common bile duct by ERCP may be
ris is liver resection. Transplantation has been per- necessary.
formed in selected patients but long‐term outcome
is uncertain. Albendazole, although unable to elimi- Clonorchis sinensis
nate the parasite, may slow progression of the dis-
ease and should be administered on an indefinite Pathology
basis in conjunction with surgery. Clonorchis sinensis is a flatworm that inhabits the
biliary tree. Cysts from infected fish are ingested
and migrate from the duodenum into the bile
Liver fluke disease ducts. Ova are excreted from the stools. The inter-
mediate host is a snail, which completes the life
Infestations of clinical importance include those by cycle by infecting fish. Humans are infected by
Fasciola hepatica and Clonorchis sinensis. These eating raw fish.
parasites are trematodes and undergo both sexual The biliary epithelium becomes inflamed from
(definitive host) and asexual (intermediate host) constant irritation, leading to cholangitis, ductal
reproduction. fibrosis, biliary strictures and stone formation.
There is a high incidence of cholangiocarcinoma.
Fasciola hepatica
Pathology Clinical features
This is prevalent all over the world and commonly The classic symptom associated with Clonorchis
seen in Europe, South America, Africa and the infestation is recurrent pyogenic cholangitis. There
Caribbean. It is known as the common sheep fluke are recurrent attacks of right upper quadrant pain,
and is found in sheep‐ and cattle‐rearing countries. jaundice and pyrexia. Examination may reveal
The parasite inhabits the gallbladder and bile ducts tender hepatomegaly and splenomegaly if portal

and passes ova in the stool. Humans are incidental hypertension exists.
hosts, especially those eating raw vegetables. Cysts
are ingested from vegetables and subsequently pen-
etrate the intestinal wall. They then migrate by the Investigation
transperitoneal route and invade the liver capsule Imaging of the biliary tree by MRI or ERCP is
and enter the biliary system, where they may be essential for delineating the distribution of stones
mistaken for gallstones. and strictures. Ova are demonstrated in faeces or
duodenal aspirate.
Clinical features
Patients may be asymptomatic or present with Treatment
acute or chronic symptoms. Acute symptoms The drug of choice is praziquantel. Surgery is indi-
include sudden onset of right upper quadrant pain, cated if stones or strictures are present.
Biliary ascariasis b Staphylococcus aureus is the most common

pathogen
Pathology
c they are usually incidental findings in patients
The roundworm Ascaris lumbricoides is endemic in
with abdominal pain
tropical and subtropical areas. The worms inhabit
d drainage of the abscess and appropriate antibiotic
the small intestine and enter the common bile duct
therapy are the mainstay of management
by the duodenal ampulla of Vater.
e laparoscopy is the less invasive approach for the
treatment of liver abscess
Clinical features
They induce mechanical obstruction of the biliary
2 Regarding amoebic liver abscesses, which one of
tree. Cholangitis, empyema of the gallbladder and
the following is false?
multiple liver abscesses may occur as a result of sec-
a poor sanitary hygiene is the most determinant factor
ondary infection.
b mainstay of treatment is intralesional
Investigation antimicrobial therapy
Stool examination commonly demonstrates the c for asymptomatic small abscesses, oral antibiotics
presence of worms. Ultrasound is highly accurate in can achieve high rates of cure
delineating the worms in the biliary tree. d presence of positive serology and a cystic liver
lesion are the two main diagnostic criteria in the
Treatment diagnosis of amoebic liver abscess
Non‐operative management is successful. e amoebic liver abscess can be drained by
Mebendazole and pyrantel palmoate are used over percutaneous technique
3 days. ERCP may be required for patients with
cholangitis and biliary stones. 3 Regarding hydatid disease, which one of the
following is incorrect?
a the human is an end host, which breaks the
Further reading development cycle of the parasite
b initial infection occurs through the alimentary
Mezhir JJ, Fong Y, Jacks LM et al. Current management tract and is asymptomatic
of pyogenic liver abscess: surgery is now second‐line c the natural history of a hydatid cyst in the
treatment. J Am Coll Surg 2010;210:975–83. human is one of slow progressive growth
Nunnari G, Pinzone MR, Gruttadauria S et al. Hepatic d rupture of a hydatid cyst is a common event
echinococcosis: clinical and therapeutic aspects. World e most symptoms are related to pressure effects on
J Gastroenterol 2012;18:1448–58.
the liver and surrounding organs
Pang TC, Fung T, Samra J, Hugh TJ, Smith RC. Pyogenic
liver abscess: an audit of 10 years’ experience. World J
Gastroenterol 2011;17:1622–30. 4 Which one of the following statements regarding
Stojkovic M, Rosenberger K, Kauczor HU, Junghanss T, the management of hydatid cysts is false?
Hosch W. Diagnosing and staging of cystic echinococ- a extremely small cysts may be managed
cosis: how do CT and MRI perform in comparison to conservatively provided they are followed up to
ultrasound? PLoS Negl Trop Dis 2012;6(10):e1880. monitor growth
Xia J, Jiang SC, Peng HJ. Association between liver fluke b medical management is successful in the vast
infection and hepatobiliary pathological changes: a majority of cases
systematic review and meta‐analysis. PLoS One
c medical therapy is usually used to supplement
2015;10(7):e0132673.
surgical intervention
d the most common surgical technique is that of
evacuation of the contents and de‐roofing of the
MCQs cyst and the placement of an omental patch in
the cavity
e prevention of spillage of the contents into the
peritoneal cavity is of critical importance
1 Regarding pyogenic liver abscesses, which one of 5 You are at the emergency department and have
the following is true? been called to give a second opinion in a young
a mortality rate is high even with drainage patient with right upper abdominal pain, fever and
a history of recent travel to India. He presented

with fever, chills and rigors. On examination his
heart rate is 110 and blood pressure 90/60 mmHg.
His white cells are elevated and liver function tests
are slight deranged. Ultraound was done and a
cystic liver lesion in the right lobe measuring 10 cm
was seen. What is your initial management?
a call a surgeon to evaluate the patient
b ask for a CT scan to better assess the liver lesion
c request blood culture and wait for the results to
start antibiotics
d treat the pain, resuscitate the patient and start
broad‐spectrum antibiotics
e transfer the patient to the intensive care unit to
be better assessed
a liver haemangioma
6 In outpatient clinic, you are called by a colleague to b liver cancer
give an opinion on a liver MRCP scan requested for c cholecystitis
a middle‐aged man presenting with vague d hydatid liver lesion
abdominal pain for months. The MRCP scan is e normal liver
shown below. What is the main diagnosis?
22 Pancreatitis
Peter S. Russell1 and John A. Windsor1,2
1
Department of Surgery, University of Auckland
2
Auckland City Hospital, Auckland, New Zealand
and impairment of exocrine and endocrine pancre-

Introduction atic function.
There are two recognised phases in the course of
Until recently pancreatitis has been considered two
this dynamic disease. In the early phase, lasting
distinct diseases, acute pancreatitis and chronic
around a week, systemic disturbances to the patient
pancreatitis. Now they are considered part of a
are a result of the host response to pancreatic
continuum, which also includes recurrent acute
inflammation. This inflammation triggers cytokine
pancreatitis. Acute pancreatitis is one of the most
cascades that drive the systemic inflammatory
common acute gastrointestinal presentations. It
response syndrome (SIRS) and can result in early
usually resolves but when severe is associated with
organ failure. The later phase occurs only in patients
a significant risk of mortality. Chronic pancreatitis
with more severe pancreatitis and is characterised
is progressive and one of the most painful diseases.
by persistent organ failure, usually secondary to
When severe it is associated with malnutrition and
infected necrosis.
diabetes. Although there is no specific treatment for
The incidence of acute pancreatitis is estimated
either disease, important advances in management
to be 13–45 per 100 000 and is increasing in most
have resulted in improved outcomes.
developed nations. The incidence and aetiology
vary with country, age and gender. Gallstone‐
induced pancreatitis is more common in females
Acute pancreatitis
and patients presenting in the sixth decade, while
alcohol‐induced pancreatitis is more common in
Acute pancreatitis is an acute inflammatory disor-
males and patients in the third or fourth decades.
der characterised by oedema and, when severe,
necrosis of the pancreas. It is a protean disease with
Aetiology and pathogenesis
a wide range of severity and a highly variable
course, ranging from mild self‐limiting disease to There are many recognised causes of acute pancrea-
critical illness involving infected pancreatic necro- titis with the two most common being gallstones
sis, multiple organ failure and mortality. Acute pan- and alcohol, which combined account for approxi-
creatitis is divided into two types; interstitial mately 80% of presentations. Other causes include
oedematous pancreatitis and necrotising pancreati- hyperlipidaemia, iatrogenic, trauma, gene muta-
tis. The former involves acute inflammation of the tions, tumours and hypercalcaemia. Drugs can also
pancreatic parenchyma and peripancreatic tissues cause acute pancreatitis, including thiazide diuret-
without recognisable necrosis and usually resolves ics, frusemide, oestrogen replacement therapy, ster-
within a week or two. The latter is characterised by oids, chemotherapy and immunosuppression. If a
inflammation associated with pancreatic and/or cause cannot be determined after a systematic
peripancreatic necrosis. Necrotising pancreatitis is search, it is considered to be idiopathic acute
seen in about 5–10% of cases, is more variable in pancreatitis.
its course and is almost always more severe. The The pancreas produces digestive enzymes (e.g.
traditional view is that acute pancreatitis com- amylase, lipase) that break down the complex
pletely resolves with no morphological, functional structure of carbohydrates, lipids, proteins and
or symptomatic sequelae. However, necrotising nucleic acids into simple molecules such as amino
pancreatitis can leave significant scarring, strictures acids and glucose for absorption in the small
199
intestine. These enzymes are stored in membrane‐ activation of trypsinogen to its active form trypsin.
lined zymogen granules in acinar cells. Several This in turn activates other proenzymes such as
mechanisms have evolved to prevent their prema- prophospholipase, proelastase and prekallikrein,
ture activation, including synthesis as inactive pre- the latter activating the clotting and complement
cursors (zymogens), secretion into an alkaline fluid systems. The resultant inflammation and small‐
that dilutes the inactivated enzymes, activation in vessel thromboses further damage the acinar cells
the duodenum separate from the site of production, and amplify the autodigestion caused by the diges-
and presence of trypsin inhibitors within the pan- tive enzymes.
creas. Acute pancreatitis occurs when these physio- The severity of acute pancreatitis is generally
logical protective mechanisms break down, causing determined by the events that occur after trypsin
acinar cell injury and local inflammation. activation and initial acinar cell injury. Activated
The exact means by which gallstones cause acute macrophages release cytokines that mediate both
pancreatitis has not yet been proven. Previous sug- local and systemic inflammation. On a local level,
gestions include gallstones impacting at the sphinc- these mediators can lead to haemorrhage, oedema
ter of Oddi causing reflux of bile into the pancreatic and microthrombi. Fluid can collect in and around
duct, or the passage of a gallstone causing transient the pancreas, which may compress the bile duct
incompetence of the sphincter allowing reflux of causing obstructive jaundice, or the duodenum
duodenal fluid. A third possibility, perhaps the causing vomiting.
most likely, is that a gallstone obstructing the pan- When failure of the pancreatic microcirculation
creatic duct, leading to ductal hypertension, causes is severe, it will result in pancreatic and peripancre-
disruption of the minor ducts and extravasation of atic hypoperfusion and necrosis. If this becomes
pancreatic juice back into the less alkaline inter- infected, which usually occurs at least 2 weeks fol-
stitium of the pancreas, thus promoting intra‐ lowing the onset of illness, disease severity will
pancreatic enzyme activation. Other causes of duct increase and can lead to organ failure. In roughly
obstruction such as pancreatic neoplasm may half of cases the infection is enteric in origin (e.g.
cause pancreatitis via the same mechanism. Alcohol bacterial translocation from the adjacent colon, or
can also lead to ductal hypertension due to deposi- lymphogenous spread via mesenteric lymph), with
tion of protein plugs that can obstruct small pan- extrapancreatic infections (e.g. pneumonia, bacte-
creatic ducts. raemia) being another major source. Calcium can
Other causes of acute pancreatitis are due to also be deposited in these areas of necrosis and
direct injury to the acinar, ductal or stellate cells. result in a fall in serum calcium.
Alcohol is metabolised by acinar cells via oxidative On a systemic level, pancreatic inflammation has
and non‐oxidative pathways. It, and its metabo- the potential to lead to systemic inflammation and
lites, can damage all three cell types by a variety of multiorgan failure, which is the major determinant
mechanisms, such as increasing intracellular levels of severity and mortality. The mechanism leading
of digestive enzymes and decreasing zymogen gran- to systemic inflammation is still to be fully eluci-
ule stability. Pancreatic cells can also be damaged dated but involves the recruitment and activation
by surgical procedures including biopsy, bile duct of neutrophils and macrophages releasing multiple
exploration, distal gastrectomy and splenectomy. cytokines and chemokines. It appears these proin-
Endoscopic retrograde cholangiopancreatography flammatory mediators, travelling via mesenteric
(ERCP) is by far the most frequent iatrogenic cause, lymph, bypass the liver and directly contribute to
where acute pancreatitis occurs after about 5–10% dysfunction of the lungs (acute respiratory distress
of procedures. syndrome), heart (ventricular dysfunction) and
The most common mutation leading to heredi- kidney (acute tubular necrosis). In the acute set-
tary pancreatitis is in the cationic trypsinogen ting, local and systemic inflammation, along with
gene (PRSS1). This leads to premature activation oedema and fluid collections, lead to hypovolae-
of trypsinogen to trypsin as well as abnormalities mia and hypotension.
of ductal secretion, leading to acute pancreatitis.
This mutation has an autosomal dominant mode
Surgical pathology and complications
of inheritance but other mutations leading to
hereditary pancreatitis may have an autosomal The pancreas in acute pancreatitis can vary from
recessive mode. swollen and inflamed through to necrotic, infected
Despite the diverse aetiologies, evidence suggests or haemorrhagic. Complications of acute pancrea-
that each causative mechanism results in a single titis are divided into local and systemic. The local
precipitating event common to all – the premature complications have been redefined by the Revised
22: Pancreatitis 201
Table 22.1 Definitions of local complications of acute pancreatitis based on CT morphology.
Acute (<4 weeks, no defined wall) Chronic (<4 weeks, defined wall)
Content No infection Infection No infection Infection
Fluid APFC Infected APFC Pseudocyst Infected pseudocyst

Solid ± fluid ANC Infected ANC WON Infected WON
APFC, acute peripancreatic fluid collection; ANC, acute necrotic collection; WON, walled‐off necrosis.
Source: modified from Escott ABJ, Phillips AJ, Windsor JA. Part B: Locoregional pathophysiology in acute
pancreatitis: pancreas and intestine. In: Adams DB, Cotton PB, Zyromski N, Windsor JA (eds) Pancreatitis: Medical
and Surgical Management. Oxford: Wiley Blackwell, 2017. Reproduced with permission of John Wiley & Sons.
Atlanta Classification in 2012, and are classified Determinant‐based Classification that defines
according to chronicity, content and infection severity as mild (no (peri)pancreatic necrosis or
(Table 22.1 and Figure 22.1). They include acute organ failure), moderate (sterile necrosis and/or
peripancreatic fluid collection (APFC), pancreatic transient organ failure), severe (infected necrosis or
pseudocyst, acute necrotic collection (ANC) and persistent organ failure) and critical (infected necro-
walled‐off necrosis (WON), all of which can be sis and persistent organ failure). Both these interna-
either infected or sterile. An APFC is peripancreatic tional multidisciplinary classification systems are
fluid associated with interstitial oedematous pan- validated, though differences indicate that further
creatitis with no necrosis. It is differentiated from a refinement will be necessary.
pseudocyst because it occurs within 4 weeks of
onset of symptoms and has no defined wall. A pseu- Clinical presentation
docyst is an encapsulated fluid collection with a
Acute pancreatitis most often presents with the sud-
defined inflammatory wall that develops after 4
den onset of severe and persistent epigastric pain
weeks. It is not a true cyst because the wall is not
that radiates to the middle of the back. Nausea and
lined by epithelial cells. An ANC occurs within 4
vomiting may also be present. It is important to
weeks and contains variable amounts of both fluid
determine the presence of any known aetiological
and necrosis with no definable wall. This is differ-
risk factors, including gallstones, alcohol consump-
entiated from WON that occurs after 4 weeks and
tion or recent procedures such as ERCP.
does have a defined inflammatory wall. Other pos-
Examination will vary depending on the severity
sible local complications include gastric outlet dys-
of the attack, but may reveal a patient distressed
function, splenic and portal vein thrombosis,
from severe pain. In some cases the patient may
paralytic ileus and colonic necrosis.
present with hypotension, tachycardia and tachyp-
Systemic complications include new‐onset organ
noea. The abdomen will be tender in the epigas-
failure, as well as exacerbation of a pre‐existing
trium, possibly with guarding but usually without
comorbidity, such as coronary artery disease or
peritonism. Other findings will be based on the
chronic lung disease. Organ failure is defined as
later development of complications such as a palpa-
either transient (resolves within 48 hours) or persis-
ble mass from a fluid collection or distension due to
tent (persists beyond 48 hours) and requires a score
a developing ileus. Rarely, flank ecchymosis (Grey
of 2 or more for at least one of the three major
Turner’s sign) or periumbilical ecchymosis (Cullen’s
organ systems (respiratory, cardiovascular and
sign) will be present, which results from haemor-
renal) using the modified Marshall scoring system
rhagic fluid tracking from the retroperitoneum.
(Table 22.2).
The presence of local and systemic complications
Investigation
determines the severity of pancreatitis and subse-
quently guides the management. The Revised The diagnosis of acute pancreatitis requires two of the
Atlanta Classification defines severity as mild following three features: (i) abdominal pain consistent
(absence of local and systemic complications), with acute pancreatitis; (ii) serum lipase or amylase at
moderately severe (transient organ failure or local least three times greater than the upper limit of nor-
or systemic complications in the absence of persis- mal; and (iii) characteristic findings of acute pancrea-
tent organ failure) and severe (characterised by per- titis on contrast‐enhanced computed tomography
sistent organ failure). An alternative is the (CT) or magnetic resonance imaging (MRI).
(a) (b)
(c) (d)
(e)
Fig. 22.1 CT scans of various complications of acute pancreatitis. (a) A 38‐year‐old woman with acute interstitial
oedematous pancreatitis and acute peripancreatic fluid collection (APFC) in the left anterior pararenal space (white
arrows showing the borders of the APFC). The pancreas enhances completely, is thickened and has a heterogeneous
appearance due to oedema. APFC has fluid density without an encapsulating wall. (b) Patient with acute necrotising
pancreatitis and acute necrotic collection (ANC): there is extensive parenchymal necrosis (white stars) of the body and
tail of the pancreas. Heterogeneous collections are seen in the pancreatic and peripancreatic tissues (white arrows
pointing at the borders of the ANC) of the left anterior pararenal space. (c) A 47‐year‐old man with acute necrotising
pancreatitis complicated by infected pancreatic necrosis. There is a heterogeneous ANC in the pancreatic and
peripancreatic area (white arrows pointing at the borders of the ANC) with presence of gas bubbles (white
arrowheads), usually a pathognomonic sign of infection of the necrosis (infected necrosis). (d) A 40‐year‐old man with
two pseudocysts in the lesser sac 6 weeks after an episode of acute interstitial pancreatitis on CT. Note the round to
oval, low‐attenuated, homogeneous fluid collections with a well defined enhancing rim (white arrows pointing at the
borders of the pseudocysts), but absence of areas of greater attenuation indicative of non‐liquid components. White
stars denote normal enhancing pancreas. (e) Patient with walled‐off necrosis (WON). A heterogeneous, fully
encapsulated collection is noted in the pancreatic and peripancreatic area. Non‐liquid components of high attenuation
(black arrowheads) in the collection are noted. The collection has a thin, well‐defined and enhancing wall (thick white
arrows). Source: modified from Banks PA, Bollen TL, Dervenis C et al. Classification of acute pancreatitis – 2012:
revision of the Atlanta classification and definitions by international consensus. Gut 2013;62:102–11. Reproduced
with permission of SAGE Publications.
Table 22.2 Modified Marshall scoring system for organ dysfunction: a score of 2 or more in any system defines
the presence of organ failure.
Score
Organ system 0 1 2 3 4
Respiratory (Pao2/Fio2) >400 301–400 201–300 101–200 ≤101

Renal*
Serum creatinine (μmol/L) ≤134 134–169 170–310 311–439 >439
Serum creatinine (mg/dL) <1.4 1.4–1.8 1.9–3.6 3.6–4.9 >4.9
Cardiovascular: systolic blood
pressure (mmHg)† >90 <90, fluid <90, not fluid <90, pH <7.3 <90, pH <7.2
responsive responsive
For non‐ventilated patients, the Fio2 can be estimated from:
Supplemental oxygen (L/min) Fio2 (%)
Room air 21
2 25
4 30
6–8 40
9–10 50
*
A score for patients with pre‐existing chronic renal failure depends on the extent of further deterioration of baseline
renal function. No formal correction exists for a baseline serum creatinine ≥134 μmol/L or ≥1.4 mg/dL.
†
Off inotropic support.
Source: modified from Banks PA, Bollen TL, Dervenis C et al. Classification of acute pancreatitis – 2012: revision of
the Atlanta classification and definitions by international consensus. Gut 2013;62:102–11. Reproduced with
permission of SAGE Publications.
The diagnosis is most often confirmed by ele- their accuracy is often only 70–80% for actual
vated serum levels of the enzymes lipase or amylase, severity (as per the Revised Atlanta Classification).
which are released into the bloodstream from the Current guidelines recommend that the prediction
damaged pancreas. However, hyperamylasaemia of severe acute pancreatitis is best with the presence
cannot be relied on alone as it can also occur from of two or more SIRS criteria (temperature >38 or
other conditions including parotitis, renal failure, <36°C; heart rate >90 beats/min; respiratory rate
small bowel obstruction and perforated duodenal >20 breaths/min or Paco2 <32 mmHg; white cell
ulcer. At times serum amylase may be completely count >12 × 109/L, <4 × 109/L or >10% bands).
normal, as in the presence of extensive necrosis. Other prognostic markers in common use include
Usually serum amylase increases almost immedi- blood urea nitrogen (BUN), the Bedside Index for
ately with symptom onset and peaks within several Severity in Acute Pancreatitis (BISAP) score and C‐
hours. Both amylase and lipase are rapidly cleared reactive protein (CRP). Despite the limitations of
from the serum by the kidneys and so the peak is accuracy in applying predictors to individual
often short‐lived and serum amylase returns to nor- patients, prognostication on admission is important
mal after 3–7 days. Serum lipase is now preferred as it allows early identification of those with more
because of a slower return to normal. Urinary levels severe disease who might require transfer to an
of amylase or lipase, which peak and fall later, can intensive care unit (ICU) or tertiary hospital.
also be measured and may be more sensitive than Contrast‐enhanced CT may be important in the
serum levels. diagnosis, but there is no routine role within the
Elevations of pancreatic enzymes, while useful in first 5–7 days of admission. It is not better at pre-
diagnosing pancreatitis, are not useful in predicting dicting severe disease than other approaches, but is
or determining the severity of acute pancreatitis. very important for the diagnosis of local complica-
There have been numerous prognostic systems vali- tions, including the extent of necrosis when sus-
dated in trials, such as the commonly used modified pected. If using CT to determine the extent of
Glasgow criteria and Ranson’s criteria, which rely necrosis, it is best to wait at least 5 days from the
on clinical and biochemical parameters scored over onset of illness to determine the full extent. MRI is
the first 48 hours of admission. Although prognos- superior to contrast‐enhanced CT in detecting any
tic scoring systems attempt to predict the severity, solid content within collections. Ultrasonography is
used to determine any evidence of gallstones. If ad libitum. If the acute pancreatitis is more severe,
choledocholithiasis is suspected, it is usually con- it has been shown that enteral nutrition (via
firmed by magnetic resonance cholangiopancrea- nasogastric or nasojejunal tube) is superior to par-
tography (MRCP) before ERCP, unless the patient enteral nutrition or no nutrition. This is because
has overt cholangitis, cholestasis and a dilated duct gut rest is associated with villous atrophy, gut bar-
on ultrasonography. rier failure, bacterial overgrowth and subsequent
bacterial translocation, which can drive systemic
Treatment inflammation and multiple organ dysfunction. On
rare occasions it is necessary to give parenteral
All patients with suspected acute pancreatitis
nutrition if the nutrition goals are not being met
should be admitted to hospital. Management then
due to feeding intolerance (e.g. ileus). This may be
varies depending on the severity of the attack.
combined with trophic enteral feeding at a reduced
Patients with mild pancreatitis have a less than 1%
rate to maintain enterocyte health and mucosal
risk of mortality and usually stay in hospital for less
barrier function.
than a week. At the other end of the spectrum,
Prophylactic antibiotics, aiming to prevent the
patients with critical disease have a mortality rate
development of infected necrosis, should be
above 40% and may require many weeks or months
avoided, as it has been shown they are ineffective
of intensive multidisciplinary treatment. The essen-
and can lead to antibiotic resistance and fungal
tial aspects of management are accurate diagnosis,
infection. However, patients with suspected or con-
appropriate triage based on predicted severity,
firmed infected complications should be started on
high‐quality supportive care, detection and treat-
intravenous antibiotics. A carbapenem (e.g. imipe-
ment of local complications, and treatment of the
nem) or a quinolone and metronidazole can be
underlying cause.
used empirically until bacterial sensitivities are
known.
Supportive care
As there is currently no specific treatment for
Managing local complications
inflammation of the pancreas, management focuses
on good supportive care. For patients with evidence Local complications are suspected if there is no
of organ dysfunction or failure it is important for clinical improvement or deterioration on serial
them to be managed in an ICU setting. Supportive clinical examinations and elevated inflammatory
care in acute pancreatitis centres on pain manage- markers. Contrast‐enhanced CT is performed to
ment, fluid resuscitation and nutritional support. diagnose any local complication, such as necrosis
Pain is the cardinal symptom of acute pancreati- or a fluid collection. The decision to intervene is
tis and rapid and effective analgesia (non‐steroidal based on the patient’s clinical status and response
anti‐inflammatory or opioid, administered intrave- to supportive care, not on the CT findings per se.
nously) should be given early. Fluid resuscitation is In the acute setting, intervention is usually reserved
the most important intervention in the early man- for an infected fluid collection or infected necrosis
agement, especially if the patient presents with in a patient not responding to antibiotics. Infection
haemodynamic instability or hypotension. Fluid is diagnosed on contrast‐enhanced CT with the
should be given as a balanced crystalloid solution presence of extraluminal air within the suspected
(lactated Ringer’s being preferred) aiming to area, or rarely by positive microbial culture from a
restore normal blood volume, blood pressure and fine‐needle aspirate. If possible, any treatment of a
urine output. Evidence suggests that aggressive local complication, including infected necrosis, is
fluid resuscitation is associated with increased risk delayed to allow the lesion to become walled off
and that the aim should be normalising haemato- (encapsulated) and therefore safer to treat. If inter-
crit over 48 hours. Historically, the patient was vention becomes necessary, a ‘step‐up’ approach is
made ‘nil by mouth’ on admission to hospital, but used, with percutaneous or endoscopic drainage
this is no longer required. Acute pancreatitis is a first, followed by percutaneous or endoscopic
highly catabolic state associated with rapid nutri- debridement (depending on location and topogra-
ent depletion and there is good evidence that nutri- phy of the collection) if required. Open surgery to
tional support, implemented from early in the drain and debride the area is rarely required, but
disease (after volume repletion), is important in may be indicated for abdominal compartment syn-
determining a favourable outcome. In mild pan- drome or if non‐occlusive mesenteric ischaemia is
creatitis the patient can be allowed to drink and eat suspected.
Treatment of the cause (tropical pancreatitis) and distal pancreatitis result-

ing from trauma. As with acute pancreatitis, a rela-
Patients with predicted severe gallstone‐associated
tively significant number of patients have no
pancreatitis may benefit from early ERCP (within
discernible cause found after extensive investiga-
24–48 hours of admission) but only if there is clear
tion and are deemed to have idiopathic chronic
evidence of cholangitis. This is because ERCP may
pancreatitis. This patient group is now smaller as
exacerbate pancreatitis in the acute setting and this
more genetic mutations are found and implicated in
risk needs to be weighed against any potential ben-
the aetiology.
efit. Patients with cholestasis without cholangitis
All forms of chronic pancreatitis are associated
may need delayed ERCP for this reason. Cholestasis
with the development of fibrosis, caused by the
may resolve spontaneously after the passage of a
activation of pancreatic stellate cells. These cells are
stone into the duodenum. All patients with gall-
activated by proinflammatory cytokines and other
stone‐associated pancreatitis should have a chole-
proliferative factors, which are released in response
cystectomy following recovery from an attack of
to pancreatic injury. Once activated, stellate cells
acute pancreatitis in order to prevent repeated
transform into myofibroblast‐like cells, proliferate,
attacks. Those with mild to moderate acute pan-
secrete collagen and transform the extracellular
creatitis should have the cholecystectomy before
matrix, resulting in fibrosis and eventually acinar
discharge. Timing of cholecystectomy is more chal-
cell loss.
lenging for severe disease, and is usually delayed
The pathogenesis of chronic pancreatitis varies
unless surgery is required for other reasons. Patients
depending on the cause. One common mechanism,
with alcohol‐associated pancreatitis should
especially prevalent in alcohol abuse, is the devel-
embrace abstinence to avoid further episodes, and
opment of calcific pancreatic stones or concretions.
often require extensive community support to
It has been shown that alcohol reduces the secre-
achieve this. Hyperlipidaemia usually requires
tion of a potent inhibitor of calcium carbonate
treatment with a statin and dietary advice. In the
crystal formation. These concretions can cause
rare instances of sphincter of Oddi dysfunction,
mechanical damage to the ductal epithelium or
division of the sphincter is sometimes associated
cause obstruction of the distal ductal network.
with a good response, but this is controversial.
Another mechanism leading to chronic pancreatitis
is compression or occlusion of the proximal ductal
system (for example, by tumour, gallstone, post‐
Chronic pancreatitis
traumatic scar or pancreas divisum). This can result
in diffuse fibrosis, dilated main and secondary pan-
Chronic pancreatitis is an incurable, irreversible
creatic ducts, and acinar atrophy.
condition characterised by fibrosis and chronic
inflammation. It is variable in presentation and
aetiology, and very difficult to treat successfully. Surgical pathology and complications
The prevalence ranges from 5 to 40 per 100 000
In chronic pancreatitis the pancreas is characterised
population, with considerable geographic varia-
by fibrosis and atrophy, often with parenchymal
tion, and the incidence has been increasing over the
and ductal calcifications. There is a variable amount
past 50 years.
of duct dilation, strictures and ductal epithelial dys-
plasia. In severe advanced chronic pancreatitis,
Aetiology and pathogenesis
broad coalescing areas of fibrosis replace acinar tis-
Chronic pancreatitis most often follows recurrent sue and there is a reduction in the size of islet
acute pancreatitis, and therefore has a similar range tissue.
of aetiologies. The most common cause in devel- Atrophy and destruction of pancreatic paren-
oped countries is alcohol abuse, as these patients chyma can eventually result in exocrine and endo-
are more likely to have repeated acute attacks, as crine dysfunction, leading to both malabsorption
opposed to patients with gallstone‐related acute and diabetes respectively. Because of chronic
pancreatitis where cholecystectomy offers complete inflammation and epithelial dysplasia there is an
cure. Recent evidence shows that smoking is a very increased risk of developing pancreatic adenocarci-
important risk factor, often combined with excess noma, which is progressive and cumulative relative
alcohol. Other causes include genetic mutations, to the duration of the disease. Pseudocyst develop-
which account for up to 25% of patients, long‐ ment is more common compared with acute pan-
standing obstruction of the duct by a neoplasm or creatitis and is caused by a pancreatic duct leak and
calculi, autoimmune pancreatitis, nutritional causes subsequent extravasation of pancreatic juice and
encapsulation. If the extravasation of pancreatic and, importantly, is highly reliable in ruling out
juice does not form a pseudocyst it can drain feely pancreatic carcinoma through EUS‐guided fine‐
into the peritoneal cavity, causing pancreatic ascites, needle aspiration for cytology.
or rarely into the thoracic cavity, causing a pancre-
atic pleural effusion.
Treatment
Clinical presentation There is no specific proven treatment for chronic
pancreatitis, with care focusing on symptom man-
Epigastric pain that radiates through to the back is
agement and treatment of complications. The long‐
the most common symptom of chronic pancreatitis.
term outlook is generally poor, with 10‐ and 20‐year
It is usually steady and lasts for hours or days.
survival rates approximately 70% and 45%,
Patients will often be unable to find a position of
respectively, compared with 93% and 65% for
comfort and sit or lie with their hips flexed. Pain is
patients without pancreatitis. Survival declines even
usually recurring, and exacerbations may be
further for patients with alcoholic chronic pancrea-
brought on by eating or alcohol or may occur with-
titis who continue to abuse alcohol. It is therefore
out any precipitating cause. Anorexia, nausea and
essential that these patients abstain from alcohol in
vomiting are all common associated symptoms.
order to improve both their symptoms and survival
Generally, as the disease progresses pain may
rate.
become less of a feature and symptoms of malab-
Autoimmune pancreatitis is a rare subset of
sorption (e.g. steatorrhoea, weight loss) and diabe-
chronic pancreatitis that responds to steroid ther-
tes become more prominent. Frank malabsorption,
apy. Plasma IgG4 may be elevated and other organs
evidenced by steatorrhoea, is indicative of advanced
affected. This diagnosis should always be consid-
disease and pancreatic exocrine function that has
ered, particularly before embarking on invasive
fallen below 10% of normal. Because untreated
interventions.
malabsorption is associated with long‐term adverse
Effective analgesia is required for the pain, which
effects such as malnutrition and osteoporosis, there
often requires oral opioids. Care should be taken,
is a trend towards early enzyme supplementation
as it is common for these patients to become opioid
before overt symptoms develop.
dependent, and all alternative strategies should be
explored, including cognitive behavioural therapy.
Investigation
Attempts to alleviate pain with anti‐secretory ther-
Diagnosis is based on clinical presentation, labora- apy (e.g. octreotide, a somatostatin analogue) has
tory investigation of pancreatic function and imag- had mixed success. The development of central sen-
ing. Unlike acute pancreatitis, serum levels of lipase sitisation in patients with chronic pancreatitis is
and amylase are seldom helpful in the diagnosis. associated with a worse response to endoscopic or
Pancreatic function can be assessed in a variety of surgical intervention and these patients should be
ways. Exocrine function can be measured directly under the care of a pain specialist. Those with pan-
via aspiration of pancreatic juice but is more often creatic exocrine insufficiency will need pancreatic
measured indirectly. Common methods include the enzyme replacement therapy, which not only
measurement of faecal fat content, or of faecal lev- reverses the malabsorption but also prevents sec-
els of chymotrypsin and elastase. As well as stand- ondary complications such as metabolic bone dis-
ard tests for diabetes (e.g. HbA1c), endocrine ease from inadequate absorption of fat‐soluble
function can be assessed by the pancreatic polypep- vitamins. Patients with diabetes will likely require
tide response to a test meal. When severe, chronic treatment with insulin.
pancreatitis is associated with a blunted or absent Endoscopic therapies can also be utilised to man-
pancreatic polypeptide response to feeding. age symptoms and complications when indicated,
A plain abdominal X‐ray may reveal a calcified especially in those not fit for surgery. Pancreatic
pancreas and CT may show calcification, duct dila- duct decompression (via surgical or endoscopic
tation and cystic disease. MRCP is a sensitive radio- approach) is the only therapy shown to delay or
logical test for the diagnosis of chronic pancreatitis prevent the progression of chronic obstructive pan-
and may show duct dilatation, stricture formations creatitis (a subset of patients with chronic pancrea-
and calculi. ERCP is also valuable, but invasive. titis). Endoscopic therapies (via ERCP) include
Overall, however, endoscopic ultrasound (EUS) is pancreatic duct stenting, which is used to treat
the preferred imaging for diagnosis as it offers high‐ proximal pancreatic duct stenosis, endoscopic stone
resolution images of the pancreatic parenchyma, removal, and sphincterotomy for conditions such
ductal systems, cystic lesions and calcific changes as pancreas divisum.
Operative management b gene mutations

c smoking
Surgery is the most effective treatment for pain,
d alcohol
although it is common practice to offer endoscopic
e gallstones and alcohol equally
treatment first. It has been shown that surgery is
much less effective if there is a delay of more than
2 Which of the following findings would classify the
3 years, opioid dependence has occurred and if five
patient as having actual severe acute pancreatitis?
or more endoscopic treatments have been given.
a Glasgow score of 4 after 48 hours in hospital
Patients who require a drainage procedure to relieve
b creatinine of 175 μmol/L that has risen from a
an obstructed duct are best treated with a Frey pro-
normal value and persists at that level for 3 days
cedure, which involves a Roux‐en‐Y pancreatico‐
c presence of pancreatic necrosis on contrast‐
jejunostomy and ‘coring out’ of the head of the
enhanced CT scan
pancreas. If there is an inflammatory mass, and
d heart rate of 112 and temperature of 38.5°C on
when pancreatic cancer is suspected, then pancreatic
admission to hospital
resection is indicated. Patients with multiple stric-
e all of the above
tures might also require pancreatic resection. Other
pancreatic resections are more extensive and include
3 Alcohol can cause pancreatitis by:
a pancreaticoduodenectomy (Whipple procedure) or
a increasing the rate of conversion of inactive
duodenum‐preserving pancreatic head resection
trypsinogen to the active form trypsin
(Beger procedure). Recurrence of pain does occur,
b obstruction of small pancreatic ducts leading to
but overall there is significant benefit with an
ductal hypertension
improvement in the quality of life following surgery.
c increasing formation of calcium concretions in
Total pancreatectomy is also possible, and is now
the pancreatic duct
being offered with islet autotransplantation to
d increasing instability of zymogen granules
reduce the severity of diabetes. This is now being
e all of the above
considered for patients with a genetic basis for the
chronic pancreatitis and before advanced disease
4 Which of the following is the most important initial
occurs.
step in management of an unwell patient with
acute pancreatitis?
a administer strong analgesia via an intravenous line
Further reading b ensure the patient is given intravenous crystalloid
fluid
Adams DB, Cotton PB, Zyromski N, Windsor JA (eds)
c determine the predicted severity by calculating
Pancreatitis: Medical and Surgical Management.
the Glasgow score
Oxford: Wiley Blackwell, 2017.
Banks PA, Bollen TL, Dervenis C et al. Classification of d commence broad‐spectrum antibiotics
acute pancreatitis – 2012: revision of the Atlanta clas- intravenously
sification and definitions by international consensus. e arrange an urgent ERCP if the patient has a fever
Gut 2013;62:102–11. with rigours, cholestatic liver function tests and
Beger HG, Warshaw A, Hruban R et al. (eds) The Pancreas: tenderness in the right upper quadrant
an Integrated Textbook of Basic Science, Medicine, and
Surgery, 3rd edn. Oxford: Wiley Blackwell, 2018. 5 Chronic pancreatitis most often presents with:
Crockett SD, Wani S, Gardner TB, Falck‐Ytter Y, Barkun a weight loss
AN. American Gastroenterological Association Institute
b steatorrhoea
guideline on initial management of acute pancreatitis.
c diabetes mellitus
Gastroenterology 2018;154:1096–101.
d fractures
e recurrent epigastric pain
MCQs 6 Regarding surgery in acute pancreatitis, which of

the following statements is true?
a a patient with mild uncomplicated gallstone
pancreatitis should have a cholecystectomy
booked as an outpatient to occur within 3
1 There are many recognised causes of chronic months from discharge
pancreatitis but the most common is: b a patient with infected necrosis found on
a gallstones contrast‐enhanced CT, which was performed for
a temperature, should have minimally invasive renal impairment and shortness of breath should
surgery to debride the area within the next 24 have radiologically guided drainage within the
hours next 24 hours
c a patient with an infected fluid collection found d all of the above
on contrast‐enhanced CT who has been on e none of the above
antibiotics for 48 hours and is developing new
23 Pancreatic tumours
David Burnett1 and Mehrdad Nikfarjam2
1
John Hunter Hospital, Newcastle, New South Wales, Australia
2
While moderate alcohol intake does not appear

Introduction to be directly associated with pancreatic cancer,
heavy alcohol intake (eight or more standard
In 2017, pancreatic cancer was the 10th most
drinks per day for 6–8 years) can lead to chronic
common cancer in Australia, but the fifth leading
pancreatitis. Chronic pancreatitis has a cumulative
cause of cancer death. The estimated individual
association with malignant transformation of
Australian’s risk of being diagnosed with pancreatic
about 1.7% at 10 years in the best study to date.
cancer is 1 in 57 (male) and 1 in 73 (female), at
Less than one in twenty cases of pancreatic cancer
a median age of 70 years. The 5‐year survival of
are preceded by chronic pancreatitis.
patients after diagnosis is only 9.8%. Based on
Approximately 10–15% with pancreatic cancers
large US registry data (Surveillance, Epidemiology,
are thought to be familial in origin. Most of these
and End Results Program or SEER), 52% of pan
patients have two or more close relatives affected by
creatic cancer patients have metastatic disease at
pancreatic cancer, but without a known specific
presentation (Figure 23.1). More than 85% of
genetic defect. However, there are certain inherited
pancreatic tumours are adenocarcinoma (exocrine)
cancer syndromes associated with pancreatic cancer,
tumours, with the remainder made up of neu
including BRCA1, BRCA2, Lynch syndrome, familial
roendocrine, lymphoma and premalignant/benign
atypical multiple mole melanoma (FAMMM) syn
lesions. Unfortunately, despite radical surgery and
drome and Peutz–Jeghers syndrome.
dramatic progress in the survival of other solid
organ tumours around the world, there has been
little improvement in pancreatic adenocarcinoma Molecular pathogenesis
survival for more than 40 years.
There are three main morphological pathways to
pancreatic adenocarcinoma: pancreatic ductal
Aetiology/risk factors intraepithelial neoplasia (PanIN) (Figure 23.2), con
version of intraductal papillary mucinous neoplasm
The incidence of pancreatic cancer increases with (IPMN), and malignant mucinous cystic neoplasm
age and is most frequently diagnosed in the 65–74 (MCN). On a cellular level, there are multiple step
age bracket. Tobacco smoking is the oldest and wise epigenetic pathways to carcinogenesis. It is felt
strongest known risk factor which, proportional to that loss of heterozygosity (i.e. loss of a normal gene
exposure, doubles an individual’s risk. It is felt that on one chromosome, leaving a faulty chromosome
smoking alone contributes to around one‐quarter on the other to act homozygously) leads to the loss
of cases. There is a slight preponderance for males, of pathways associated with normal cell division.
although it is possible that differential smoking The most common genetic mutations in pancreatic
rates between genders may account for this differ cancer include the proto‐oncogene KRAS (which
ence. Diabetes mellitus increases the risk of pancre prescribes a component of a growth factor receptor),
atic cancer by approximately twofold. Abdominal occurring in over 90% of cases, and loss of the
obesity also increases the risk of pancreatic cancer tumour suppressor genes p16, CDKN2A and p53
by approximately one‐fifth. There may also be ele (inactivated in 50–75% of pancreatic cancer).
vated risk from occupational exposure to benzene The precise cell of origin is unknown. The
or organochlorines. expression of acinar, ductal and islet cell markers
209
9% 10%
Localized (10%)
Confined to primary site
Regional (29%)
Spread to regional lymph nodes
Distant (52%)
29% Cancer has metastasised
Unknown (9%)
Unstaged
SEER 18 2007–2013
52%
Fig. 23.1 Surveillance, Epidemiology and End Result Program (SEER) database: percentage of cases by stage. Source:
https://seer.cancer.gov/. Reproduced with permission of National Institutes of Health (NIH).
PanIN-1A PanIN-1B
PanIN-2 PanIN-3
Fig. 23.2 Pancreatic intraepithelial neoplasia progression from early changes (PanIN‐1) to carcinoma in situ (PanIN‐3):
PanIN‐1A (flat), PanIN‐1B (papillary), PanIN‐2 (papillary with nuclear changes), and PanIN‐3 (severely atypical with
mitoses, luminal necrosis and budding structures). Source: images from Johns Hopkins website, http://pds17.pathology.
jhmi.edu/N/n.web?EP=N&URL=/MCGI/SEND^WEBUTLTY(12774)/982334336minal necrosis. Reproduced with
permission of Johns Hopkins University.
has been described in pancreatic ductal adenocarci adenocarcinoma, invasive IPMN, particularly the
noma. KRAS mutation activation is an early change colloidal histological subtype, has a better overall
that controls cell division, accumulation and apop 5‐year survival, up to 70% in some series. This
tosis. The accumulation of genetic changes over compares to an overall 20–25% postoperative
time within the duct epithelium leads to intraepi 5‐year survival reported for pancreatic ductal
thelial dysplasia, which subsequently transitions adenocarcinoma.
into invasive cancer. The third pathway to cancer is MCNs. The pre
Primary pancreatic adenocarcinoma can also cursor lesions do not communicate with the main
arise from an IPMN, which are premalignant cystic pancreatic duct, are characterised by an ovarian‐like
tumours involving either the side‐branch, main stroma and have a variable benign/premalignant
pancreatic duct or both. In contrast to sporadic period prior to transition to cancer.
23: Pancreatic tumours 211
compared with the normal enhancing parenchyma.

Clinical presentation Indirect signs such as dilation of the common bile
duct and/or pancreatic duct can help in cases
Three‐quarters of pancreatic cancers occur in the
where the tumour is iso‐attenuating within the
pancreatic head. The classical presentation of jaun
parenchyma (10%). Multiple sequences through
dice and weight loss is present in only about half of
arterial, portal venous and delayed imaging define
patients at diagnosis. Importantly, one in four
the relationship between the tumour and the major
patients with pancreatic cancer have symptoms
vessels (superior mesenteric vein/portal vein,
associated with another upper gastrointestinal
superior mesenteric artery and hepatic artery).
pathology for up to 6 months prior to diagnosis,
It provides excellent specificity and sensitivity for
and 15% of patients present to medical services
both diagnosis and the presence of vascular inva
early for symptoms later attributed to pancreatic
sion, though it can overstate resectability in up to
cancer. Up to 80% of cancer patients have hyper
one‐quarter of cases. CT may not detect small
glycaemia or diabetes at the time of presentation.
peritoneal nodules or small liver metastases which
A diagnosis of pancreatic cancer should be enter
preclude cure.
tained in patients with new‐onset diabetes without
Magnetic resonance imaging (MRI) combined
clear risk factors for diabetes. It is thought that
with magnetic resonance cholangiopancreatogra
some cancers may produce factors such as islet
phy (MRCP) is rarely required for staging of pan
amyloid polypeptide that can lead to impaired glu
creatic adenocarcinoma. It can be utilised in cases
cose tolerance. Vague abdominal or back pain is
of MDCT contrast allergy, for further delineation
often present many months before diagnosis and
of isodense lesions on CT and to differentiate
may be a symptom of perineural invasion. Because
between tumour and focal fatty infiltration of
of the lack of jaundice, body and tail lesions often
the pancreas. MRI combined with liver‐specific
present at a more advanced stage.
contrast is useful for characterisation of indeter
minate liver lesions detected by other imaging
modalities. MRI/MRCP is commonly used for
Investigations
assessment of cystic pancreatic lesions and follow‐
up of IPMN and can delineate the relationship
Laboratory tests
between cyst and pancreatic duct, as well as identify
Routine measurement of liver function, full blood solid components.
count, electrolytes, urea and creatinine are per 18
F‐Fluorodeoxyglucose positron emission tomo
formed. Carbohydrate antigen (CA)19‐9, a Lewis graphy (FDG‐PET) has an emerging role in the
(a) blood group antigen secreted by pancreatic assessment of pancreatic cancer. FDG‐PET has a
cancer cells, is elevated in 90% of patients. A small sensitivity of up to 71% in adenocarcinoma. The
percentage of the population are lacking the presence of acute pancreatitis can lead to intense
enzyme fucosyltransferase, which prevents secre uptake of FDG in benign parenchyma, and thus
tion and elevation of CA19‐9. These people are false‐negatives should be considered. FDG‐PET
said to be Lewis antigen negative. High levels can change management in up to one‐quarter of
(>1000 U/mL) are more likely to be associated cases, but currently lacks the special resolution of
with metastatic disease. Benign conditions (particu MDCT and is an adjunct to other imaging modal
larly jaundice, cirrhosis, cholangitis) can also elevate ities. The ability to monitor treatment effect
serum CA19‐9 so it is important that the baseline (including in the neoadjuvant setting) has increased
measure is taken without cholangitis/biliary its utility.
obstruction. The greatest utilisation of CA19‐9 Endoscopic ultrasound (EUS), although inva
levels are in serial observation over time, such as sive, boasts the highest sensitivity for the diagno
monitoring for recurrence following surgery or sis of small pancreatic adenocarcinoma (99% vs.
assessing response to chemotherapy. 55% for MDCT). A high negative predictive value
means that it is useful for confirming tumour
diagnosis of iso‐attenuating lesions noted on
Imaging MDCT and for identifying tumours in the setting
Multidetector computed tomography (MDCT), of concurrent pancreatitis. The ability to biopsy
with fine (1‐mm slice) resolution, is the standard tumours with a fine‐needle aspirate can confirm
of care for pancreatic imaging in patients being the diagnosis, and is essential prior to the initia
assessed for surgical resection. Pancreatic adeno tion of chemotherapy, particularly in the neoadju
carcinoma is usually (90%) hypo‐attenuating vant setting.
Disease staging Surgical management
Where disease is localised and the patient is being Curative intent

considered for surgery, involvement of major blood
Approximately 20% of patients are resectable in
vessels on imaging defines resectability, according
the first instance, and a further 30% are locally
to the National Comprehensive Cancer Network
advanced. With advances in neoadjuvant chemo
(NCCN) guidelines. In general, localised tumours
therapy with or without radiotherapy the number
which may abut (≤180°) but do not encase (>180°)
of resectable patients may increase. Even with
the superior mesenteric vein/portal vein (SMV/PV)
radical surgery, there is only a 20–25% chance of
or cause vein contour irregularity are considered
cure, with an overall median survival of 22–24
resectable. Tumours which encase the SMV/PV
months. Small tumours (<25 mm) with one or
(>180° or impingement) or cause vein contour
fewer lymph nodes may do better, with a median
irregularity or abut (≤180°) the surrounding arteries
survival of 70 months in one series. This compares
are borderline resectable, and neoadjuvant therapy
with an average survival of 9–14.8 months in non‐
may be considered. Reconstruction of the SMV/PV
operative patients receiving palliative chemother
must be technically feasible to proceed. Encasement
apy with gemcitabine/nanoparticle albumin bound
(>180°) of the superior mesenteric artery (SMA),
(nab)‐paclitaxel.
coeliac axis or hepatic artery designates a tumour as
The type of surgery performed to remove a pan
locally advanced (unresectable) and palliative treat
creatic cancer is guided by its location. In cases of
ment options should be considered.
cancers within the head of the pancreas, a pancrea
Tumours that are resected are assessed patho
ticoduodenctomy is most commonly performed.
logically using the American Joint Committee on
Also known as a Whipple procedure (Figure 23.3),
Cancer (AJCC) TNM system (Box 23.1), which
the head of the pancreas is transected at the level of
accounts for tumour size, lymph nodes involved
the SMV/PV confluence. It is removed en bloc with
and the presence of metastatic disease. Stage I/II
the duodenum, common bile duct, gallbladder and
disease includes potentially resectable tumours,
peripancreatic lymphatics. The SMA is skeletonised
while stage III disease is locally advanced and is any
and detached from the uncinate process of the pan
T4 tumour with or without nodal involvement.
creas. Clear surgical margins (R0 resection) are
Stage IV disease is defined by distant metastases.
critical for maximising chance of cure and increas
ing length of disease‐free postoperative survival.
Hence en‐bloc venous resection of the SMV/PV
Box 23.1 TNM staging system
branches should be performed where necessary to
Tumour obtain clear margins. Arterial resection is rarely
indicated and should generally be limited to clinical
Tx Unable to assess primary tumour
trials. The involvement of perineural infiltration
T0 No evidence of primary tumour
around SMA, hepatic artery or coeliac axis often
Tis Carcinoma in situ
T1 Tumour ≤2 cm in greatest dimension, limited to
represents aggressive systemic disease. Arterial
pancreas resection and/or reconstruction of a short length of
T2 Tumour >2 cm in greatest dimension, limited to hepatic artery or accessory hepatic vessels has been
pancreas performed in extraordinary or rare circumstances,
T3 Tumour extending beyond pancreas but without particularly if neoadjuvant therapy results in a very
involvement of coeliac or superior mesenteric favourable response. The decision whether to per
artery form classical pancreaticoduodenectomy (Whipple
T4 Tumour involving coeliac or superior mesenteric procedure) or pylorus‐preserving pancreaticoduo
artery (unresectable primary) denectomy is controversial. A 2016 Cochrane
review failed to demonstrate any difference between
Nodes
the two approaches.
NX Unable to assess regional lymph nodes The most feared complication after Whipple
N0 No regional lymph node involvement
pancreaticoduodenectomy is clinically relevant
N1 Regional lymph node involvement
postoperative pancreatic fistula (CR‐POPF). Risk
Metastasis factors include a soft pancreas, narrow pancreatic
duct (without chronic obstruction) and significant
M0 No distant metastasis
blood loss during the resection. With these factors
M1 Distant metastasis
present, the risk of CR‐POPF can be as high as
(a) (b)
Oesophagus
Liver Spleen
Stomach
Liver
Joint between
Common pancreatic body
hepatic duct and small intestine Joint between
stomach and
Stomach small intestine
Joint between
bile duct and
small intestine Small intestine
Body and tail
of pancreas
Drain tube
Hand of
pancreas Small intestine Drain tube
Duodenum
Cancer
Colon
Small bowel
Fig. 23.3 (a) Pancreaticoduodenectomy consists of partial gastrectomy, partial pancreatectomy, and excision of the distal bile duct and all of the duodenum.
(b) Reconstruction after pancreaticoduodenectomy.
Chemotherapy for pancreatic
adenocarcinoma
The use of chemotherapy in a neoadjuvant setting
A for pancreatic cancer remains controversial but is
increasing around the world. Because of the current
lack of level 1 evidence, there is significant varia
tion in practice regionally, and it is uncertain which
group of patients will benefit most. Proponents of
B
this approach argue for an increased likelihood
of completing a full course of treatment and an
increased complete resection (R0) rate. R0 resec
tion gives the best chance of long‐term survival for
patients with pancreatic cancer. Undertaking neo
adjuvant therapy does necessitate a tissue diagnosis
C (usually via EUS) and decompressive biliary stenting.
Initial reports suggest approximately one‐third of
borderline‐resectable patients can be down‐staged
to become resectable after neoadjuvant chemother
apy, while 3–5% of patients can expect a complete
Fig. 23.4 Palliative bypass of the bile duct and stomach pathological response (no viable tumour left).
in a patient with a non‐resectable pancreatic cancer. FOLFIRINOX (combination therapy comprising
(A) Choledochojejunostomy, (B) gastroenterostomy, oxaliplatin, leucovorin, fluorouracil and irinotecan)
(C) entero‐enterosotomy. has been utilised successfully in the neoadjuvant
setting even for locally advanced tumours. A 61%
R0 resection rate was achieved as opposed to 46%
25%. Other complications include exocrine pan for gemcitabine and radiation. An average decrease
creatic failure, worsening diabetes, impaired gastric in size from 3.6 to 2.2 cm was noted, with a median
emptying or ‘dumping syndrome’. decrease in CA19‐9 from 169 to 16 U/mL. In the
Pancreatic cancer in the body and tail is more largest dataset to date, equivalent outcomes were
likely to present late due to the absence of jaun noted between a FOLFIRINOX locally advanced/
dice, and are thus less likely to be resectable. borderline‐resectable group and the comparison
Where cure is possible, resection of the body and group containing upfront resectable tumours.
tail of the pancreas, including the spleen and its Additionally, a 3‐year survival of 28% in the
associated vessels, using a technique referred to as FOLFIRINOX group compares favourably with
radical anterior modular pancreatosplenectomy 23% in those receiving neoadjuvant gemcitabine/
(RAMPS procedure) is the standard of care for radiotherapy. Nab‐paclitaxel and gemcitabine have
malignant tumours, and offers the best lymph also been used in this setting and about one‐third of
node yield. Laparoscopic distal pancreatectomy patients have shown some tumour regression on
(often with preservation of the splenic vessels) is pathological analysis.
appropriate for benign pathology. Regardless of the regimen chosen, the degree of
tumour response achieved when considering resec
tion can be difficult to assess. Desmoplasia from
Palliative intent
tumour regression can appear similar on cross‐
Priorities of palliative management are to resolve sectional imaging to residual tumour. Reduction in
symptomatic jaundice and prevent gastric outlet tumour marker (CA19‐9) levels and decrease in
obstruction. Depending on the presence/burden of avidity on FDG‐PET imaging further aids in predic
metastatic disease, endoscopic options can allow tion of tumour response to therapy. Some authors
stenting of the bile duct or the duodenum or both. recommend surgical exploration with intraopera
If a reasonable life expectancy is predicted, surgical tive pathological examination of periarteriolar
bypass (hepaticojejunostomy and gastrojejunos tissues using frozen section histology if the serum
tomy) provides the most reliable relief of symptoms CA19‐9 halves during the course of neoadjuvant
(Figure 23.4). therapy.
Preoperative chemotherapy does not seem to

increase complication rates; indeed the CR‐POPF
Pancreatic neuroendocrine tumours
rate may be decreased due to a firmer pancreas
Pancreatic neuroendocrine tumours (PNETs) are
with decreased enzymatic secretions. The combi
most easily divided into functional and non‐func
nation of radiotherapy with chemotherapy may
tional tumours, based on syndromes of hormone
add up to 10% to the rate of resectability, but at
secretion. Overall, 60–90% of tumours are non‐
the cost of a more technically difficult operation.
functional. PNETs are not infrequently seen in a
With data available to date, postoperative compli
number of hereditary conditions, including multi
cation rates appear similar to those who have not
ple endocrine neoplasia type 1 (MEN‐1) syndrome,
had radiotherapy.
von Hippel–Lindau syndrome, neurofibromatosis
type 1 and tuberous sclerosis.
Adjuvant chemotherapy In terms of the functional tumours, the consensus
is to divide them into three groups: insulinomas,
Patients who have undergone upfront resection for
gastrinomas and rare functional tumours. Functional
pancreatic adenocarcinoma will be considered for
and well‐differentiated neuroendocrine tumours are
adjuvant chemotherapy. However, not all patients
best visualised on gallium‐68 DOTA‐TATE PET.
are suitable and serious complications (e.g. pancre
The radioisotope has an affinity for somatostatin
atic fistula) reduce the likelihood of completing
receptors. In contrast, high‐grade neuroendocrine
chemotherapy. In fact, only around half of patients
carcinomas may lose some of their neuroendocrine
actually complete the full course of chemotherapy
differentiation but may be visible on FDG‐PET
treatment following resection.
imaging. The tumour marker chromogranin A is
Currently, combination adjuvant chemotherapy
positive in approximately 70% of cases. Low and
with gemcitabine and capecitabine is standard care,
moderately differentiated tumours tend to have an
achieving a 5‐year survival of 29% in the ESPAC‐4
indolent course, with long median survival intervals.
trial. Median postoperative survival is 28 months
following resection with such a regimen, but in
patients with R0 resection the median survival Functional tumours
approaches 40 months. The addition of radiotherapy
Insulinoma
may reduce local recurrence rates, particularly in
microscopically incomplete (R1) resection, though Insulinomas are commonly described with the ‘rule
data on overall survival is less convincing. More of 10’, as they are less than 10% malignant, 10%
recently, the use of FOLFIRINOX chemotherapy in associated with MEN‐1 and 10% extrapancreatic.
the adjuvant setting has shown further survival They represent 1–2% of pancreatic tumours and
improvements. can be found anywhere in the pancreas. They pre
For those patients unable to tolerate combination sent classically with Whipple’s triad of fasting
therapy due to frailty, surgical complication or hypoglycaemia, symptoms of hypoglycaemia
comorbidities, single‐agent gemcitabine still offers (diaphoresis, tremors and decreased level of con
significant benefit and is (for the most part) well sciousness) and immediate relief with glucose.
tolerated. However, 18% can present with postprandial
hypoglycaemia alone. Diagnosis is based on a
supervised fast, with measurement of fasting insulin,
Palliative chemotherapy
C‐peptide and proinsulin. Around two‐thirds can
More than half of patients have metastatic disease be seen on CT, with a higher sensitivity with the
at presentation. In the 2011 ACCORD study, addition of MRI. They are hypervascular, with arte
FOLFIRINOX chemotherapy showed the most rial‐phase contrast enhancement when compared
promise for metastatic pancreatic cancer, increasing with normal pancreatic parenchyma. EUS is often
survival from 6.8 to 11 months. Unfortunately, this required, with sensitivities approaching 100% in
comes at the cost of significant treatment‐related some series. Invasive testing, such as arterial calcium
side effects, and not all patients with metastatic dis stimulation with hepatic venous sampling, can be
ease are suitable for such an aggressive approach. helpful to confirm the location of isodense tumours
Nab‐paclitaxel has also been combined with or identify the active lesion in the case of multiple
gemcitabine for a modest increase in survival com tumours such as MEN‐1. Primary lesions are often
pared with gemcitabine alone (9 vs. 6.6 months). very symptomatic and should almost always be
Overall, less than one‐third of patients have signifi excised. Enucleation for tumours of less than 2 cm,
cant response to palliative chemotherapy. located away from the main pancreatic duct, is a
valid treatment option in selected cases, given the fitness for surgery and nuclear imaging findings.
low rate of malignancy and metastatic lymph node When a major pancreatic resection is required,
spread. early data suggest that initial observation is a safe
strategy for PNETs under 2 cm.
Gastrinoma The management of metastatic disease should be
within a multidisciplinary setting and depends on
Zollinger–Ellison syndrome is the presence of
the function and proliferation rate (grade) of the
multiple peptic ulcers driven by hypersecretion of
tumour. Low‐grade, non‐functional, widespread
gastrin leading to over‐production of gastric acid.
metastatic disease has excellent long‐term survival
Gastrinomas are usually located within a triangle
characteristics with somatostatin analogues. The
marked by the junction between the cystic duct and
aim for any surgical approach should be R0 resec
common duct, the junction between the second
tion. Resectable liver‐only metastases should have
and third part of duodenum, and the neck of the
surgery, with a 5‐year survival of 60–70% com
pancreas. Gastrinomas can be hard to visualise on
pared with 30% for medical therapy alone. Liver‐
conventional imaging, are often within the duode
directed therapy, such as selective internal radiation
nal wall and at least half of them are malignant.
therapy (SIRT) and drug‐eluting beads, has a role in
Gastrinomas can be very difficult to image preop
unresectable disease. For metastatic insulinoma and
eratively on conventional imaging or endoscopy.
in cases of carcinoid syndrome, improvement in
Current recommendations support surgical explo
symptomatology has been reported with debulking
ration up to and including pancreaticoduodenec
procedures. Carcinoid syndrome comprises the
tomy for patients with Zollinger–Ellison syndrome
symptoms of flushing and diarrhoea and, less fre
without MEN‐1 syndrome. In contrast, gastrino
quently, heart failure and bronchoconstriction. It is
mas are present in up to half of patients with
the result of vasoactive substances, including sero
MEN‐1, are often multiple and tumours under 2
tonin, released from neuroendocrine tumours into
cm rarely metastasise. Metastatic gastrinoma is a
the systemic circulation. Usually these substances
cause of premature death in up to 40% of patients
undergo hepatic degradation, but in cases of high‐
with MEN‐1 syndrome.
volume liver metastases, the liver’s ability to metab
Rare functional tumour syndromes have been
olise these substances is overcome and they escape
described as per their hormonal products, including
into the systemic circulation.
VIPoma, glucagonoma and somatostatinoma.
The role of liver transplant for metastatic neu
Localised functional tumours should be resected
roendocrine tumours is very controversial, given
where technically feasible in a fit patient.
that excellent long‐term survival is achievable with
liver‐directed therapy and hormonal control.
Peptide receptor radionuclide therapy targeting the
Non‐functional somatostatin receptor is an experimental second‐
Non‐functional tumours are described pathologi line treatment with promising early results for well‐
cally in terms of size, histological grade and degree differentiated tumours.
of proliferation (marked by the Ki‐67 index). It is Neuroendocrine carcinoma (high proliferative
uncommon for tumours smaller than 1 cm to index, Ki67 >20%) tends to be more aggressive and
metastasise and non‐functional tumours of this size visible on standard FDG‐PET imaging. Metastatic
are often best observed with serial imaging follow‐ high‐grade neuroendocrine carcinomas are unlikely
up. At a diameter of 2 cm, up to 48% may have to benefit from resection or hormonal treatment
nodal metastases. However, despite the common and often require systemic cytotoxic chemotherapy.
presence of lymph node metastases, patients with
an isolated PNET of less than 2 cm may have an
excellent chance, with 15‐year survival of up to Rare malignant disease
100%. In metastatic disease, the extent of liver
metastases correlates with survival, with an overall Primary pancreatic lymphoma is rare, comprising
10‐year survival of 30% in patients with liver 0.5% of pancreatic tumours. Management is sys
metastases. temic chemotherapy rather than resection. Metastases
In a fit patient, primary neuroendocrine tumours to the pancreas are rare, though a small number of
greater than 2 cm should be resected in the first cancers like melanoma, renal cell carcinoma and
instance. The management of non‐functional small cell lung cancer do occasionally metastasise in
tumours measuring between 1 and 2 cm is more isolation to pancreas. There is a role for resection of
controversial and is guided by the patient’s age, isolated renal cell carcinoma metastasis, though
improvements in chemotherapy have diminished the Serous cystadenoma

role in the other two.
A truly benign cystic neoplasm is the serous cystad
Solid pseudopapillary neoplasms are rare indolent
enoma, usually found in women. These microcystic
tumours affecting predominantly young women,
tumours classically demonstrate a ‘starburst’ appear
with a preponderance to local invasion but infre
ance on cross‐sectional imaging and are found most
quent metastasis. Resection offers a 95% 5‐year sur
commonly in the pancreatic head. This lesion is
vival for localised disease. High survival rates have
usually incidental and requires no further investiga
also been described in cases of liver‐only metastases
tion or management.
treated by surgery or liver‐directed chemotherapy.
Diagnosis
Cystic lesions of the pancreas The diagnosis of IPMN over other cystic neoplasms
is based on communication with the pancreatic
Intraductal papillary mucinous neoplasm duct, best seen initially on MRCP or invasively at
ERCP. With regard to the diagnosis of MCN com
The incidence of premalignant pancreatic tumours
pared with other cystic lesions, EUS gives superior
such as IPMN has increased by more than 14 times
spatial resolution for microcystic changes, internal
over the last 20 years. This is partly due to the
septations and nodularity. Fine‐needle aspiration
increasing use of cross‐sectional imaging for other
allows cyst fluid analysis. A cyst fluid carcinoem
indications, particularly CT. Benign cystic lesions
bryonic antigen (CEA) level above 800 ng/mL
have been found in up to 25% of autopsy specimens
strongly suggests mucinous pathology. In contrast,
in a Japanese study, which raises the question of
high levels of cyst fluid amylase suggest communi
whether the increasing incidence truly represents
cation with the pancreatic duct, seen commonly in
the discovery of clinically significant disease.
pancreatic pseudocyst and IPMN.
The cystic appearance of IPMN is related to
ductal obstruction and subsequent dilatation.
There are two classifications: main duct (MD)‐
IPMN (50–90% risk of malignant transformation) Further reading
and side‐branch (SB)‐IPMN (best retrospective
data suggest 3–5% risk of malignancy at 5 years Brugge WR, Lauwers GY, Sahani D, Fernandez‐del
from diagnosis). A main pancreatic duct of 1 cm or Castillo C, Warshaw AL. Cystic neoplasms of the
more strongly suggests MD‐IPMN, whereas the pancreas. N Engl J Med 2004;351:1218–26.
Crippa S, Capurso G, Cammà C, Fave GD, Castillo CF,
presence of a mucinous cyst communicating with
Falconi M. Risk of pancreatic malignancy and mor
the pancreatic duct without main duct dilatation
tality in branch‐duct IPMNs undergoing surveillance:
suggests SB‐IPMN. Most cases are asymptomatic, a systematic review and meta‐analysis. Dig Liver Dis
but acute pancreatitis is occasionally the present 2016;48:473–9.
ing symptom, caused by partial mucous obstruc Kamisawa T, Wood LD, Itoi T, Takaori K. Pancreatic can
tion of the pancreatic duct. cer. Lancet 2016;388:73–85.
The current recommendations are for resection of Lewis A, Li D, Williams J, Singh G. Pancreatic neuroendo
all MD‐IPMNs and resection of SB‐IPMNs greater crine tumors: state‐of‐the‐art diagnosis and management.
than 3 cm, or with main duct dilatation above 7 mm Oncology 2017;31:e1–e12.
with or without nodular components. Recommended
surveillance (consensus guidelines) is for annual
MRI/MRCP to identify early changes in small lesions. MCQs
Mucinous cystic neoplasms Select the single correct answer to each question. The
In contrast, MCNs are macrocystic and have a sig
nificant risk of malignant transformation. They
occur (almost) exclusively in females and are more 1 The most specific symptom associated with
common in the body and tail of the pancreas. pancreatic adenocarcinoma is:
Features of malignancy include size over 3 cm, wall a weight loss
thickening, or solid components. Histological exam b painless jaundice
ination of MCNs reveals an ovarian‐type stroma, c epigastric pain
and the lesions may even represent ectopic ovarian d right upper quadrant pain, jaundice and fever
tissue. MCNs should be resected in fit patients. e back pain relieved by leaning forwards
2 Which of the following cystic neoplasms are found c gallbladder carcinoma

almost exclusively in women? d pancreatic adenocarcinoma
a serous cystadenoma e chronic pancreatitis
b mucinous cystadenoma
c intraductal papillary mucinous neoplasm 5 Which of the following statements is false
d pancreatic pseudocyst regarding intraductal papillary mucinous neoplasms
e pancreatic gastrinoma (IPMNs)?
a very commonly seen in autopsy series
3 Which factor is most important in deciding whether b main duct IPMN has a higher risk of malignancy
a pancreatic adenocarcinoma is resectable? than side‐branch IPMN
a tumour size c most patients present with symptoms of acute
b tumour invasion of the portal vein pancreatitis
c metastatic disease d small side‐branch IPMN without nodules is
d enlarged peripancreatic lymph nodes usually followed up by serial cross‐sectional
e serum CA19‐9 levels imaging
e usually have high CEA and amylase levels in cyst
4 Palpable gallbladder in the absence of pain is most fluid aspirate
likely associated with:
a gallstones
b hilar cholangiocarcinoma
24 Portal hypertension and surgery
on the patient with cirrhosis
Michael A. Fink
Introduction Pathophysiology
Portal hypertension is associated with many of the The aetiology of portal hypertension can be classi-
most severe complications of cirrhosis and conse- fied as prehepatic, intrahepatic and posthepatic.
quently with a high risk of morbidity and Prehepatic portal hypertension is usually due to
mortality. thrombosis involving the portal venous system.
Examples of prehepatic causes of portal hyperten-
sion include pancreatitis, prothrombotic states and
Anatomy umbilical sepsis in neonates. The commonest cate-
gory of portal hypertension in developed countries
The portal venous system refers to the splanchnic is intrahepatic and is caused by cirrhosis. Cirrhosis
circulation, through which blood from the intestine causes increased resistance to portal venous flow,
and associated structures (pancreas, spleen) passes resulting in increased portal venous pressure.
into the liver. The superior mesenteric vein, which Activation of stellate cells and myofibroblasts also
drains the small intestine and colon as far as the occurs, with resulting increase in secretion of vaso-
splenic flexure, joins the splenic vein behind the active agents that can increase portal venous flow.
neck of the pancreas and continues as the portal Posthepatic portal hypertension is caused by Budd–
vein into the hilum of the liver, where it divides into Chiari syndrome, in which a prothrombotic state
the right portal vein, which has a short extrahepatic results in thrombosis of the hepatic veins, or right
course, and the left portal vein, which has a longer heart failure.
extrahepatic course. The left and right portal veins
subsequently ramify within the liver to supply the
liver segments. The inferior mesenteric vein, which Presentation
drains the left colon and rectum, most commonly
enters the splenic vein behind the body of the pan- Patients with portal hypertension can remain
creas, but can enter the confluence of the superior asymptomatic or present with ascites, bleeding or
mesenteric vein and splenic vein. The right gastroe- hepatic encephalopathy. Ascites can lead to abdom-
piploic vein drains into the superior mesenteric inal discomfort, the development of hernias, par-
vein. The left gastroepiploic vein and short gastric ticularly umbilical, and spontaneous bacterial
veins drain into the splenic vein. The left gastric peritonitis. The latter results from the translocation
vein (sometimes called the coronary vein) and right of gut bacteria into ascites and has a significant risk
gastric vein drain into the portal vein. Anastomoses of mortality. Portal hypertensive bleeding results
between the portal and systemic venous systems are from the formation of portosystemic anastomoses.
found around the lower oesophagus, the rectum Increased resistance within the portal venous sys-
and anal canal, the umbilicus, the bare area of the tem results in preferential flow through these anas-
liver and the retroperitoneum. These are of impor- tomoses as a path of least resistance. The umbilical
tance in the presentations of portal hypertension. vein can dilate significantly in portal hypertension
219
large (particularly in cases of cholestatic liver dis-

ease, such as primary sclerosing cholangitis), nor-
mal in size or small. The liver edge is likely to be
firm and nodular in cases of cirrhosis. Splenomegaly,
if present, strongly supports the diagnosis of portal
hypertension, but the absence of a palpable spleen
does not exclude the diagnosis. Shifting dullness
will be present if there is a significant quantity of
ascites. Testicular atrophy may be present.
Significant portal hypertension is usually accompa-
nied by thrombocytopenia. The aetiology was thought
to be sequestration of platelets in the enlarged spleen.
However, it is likely that reduced production of
Fig. 24.1 Large recanalised umbilical vein due to thrombopoietin by the liver and increased destruction
cirrhosis. of platelets are also of importance.
Imaging may reveal evidence of cirrhosis, spleno-
(Figure 24.1), with decompression through the megaly, varices, which are often most evident in the
periumbilical veins, leading to the clinical sign of left upper quadrant and around the oesophagus,
caput medusae. Anastomoses between the coronary thrombosis involving the portal venous system,
vein and oesophageal veins leads to the develop- hepatic vein thrombosis or ascites. Oesophageal
ment of oesophageal varices. Erosion of the mucosa varices may be evident on upper gastrointestinal
overlying oesophageal varices can lead to torrential endoscopy.
life‐threatening haemorrhage. Bleeding can also The diagnosis is confirmed by demonstrating
occur due to gastric varices, portal hypertensive elevation of the hepatic venous pressure gradient,
gastropathy, rectal varices and, rarely, retroperito- calculated as the hepatic venous wedge pressure
neal varices. minus the hepatic venous pressure. Hepatic venous
wedge pressure is measured by using a balloon
catheter to occlude the hepatic vein and the result-
Diagnosis ing pressure measurement indicates the pressure
within the hepatic sinusoids, which in cirrhosis is
The patient with portal hypertension may have a equivalent to portal venous pressure. A hepatic
known diagnosis of cirrhosis or other causes of venous pressure gradient of 5 mmHg or more indi-
portal hypertension, such as pancreatitis or a pro- cates portal hypertension and is clinically relevant
thrombotic state. Symptoms due to cirrhosis such when it is 10 mmHg or more.
as jaundice and lethargy may be present. The
patient may present with symptoms of portal
hypertension itself, such as abdominal distension, Ascites
gastrointestinal bleeding or encephalopathy.
Examination should be focused on detecting the The mainstay of treatment of ascites is medical
signs of chronic liver disease, liver failure and por- therapy. Ascites can often be controlled with diu-
tal hypertension. The general appearance of the retic therapy, usually a combination of spironolac-
patient may give clues to the diagnosis. In particu- tone and frusemide. Fluid and salt restriction are
lar, there may be drowsiness or confusion due to also appropriate. Symptomatic ascites that is resist-
hepatic encephalopathy, jaundice or muscle wast- ant to diuretic therapy may require paracentesis,
ing, which is often particularly evident around the whereby a cannula is inserted percutaneously into
shoulders. The hands should be examined for the peritoneal cavity to drain ascites. Care should
clubbing, leuconychia and palmar erythema.
be taken during insertion to avoid injury to the
Dupuytren’s contracture may be present in a patient bowel, liver and spleen and this is aided by using an
with a history of alcoholism. A hepatic flap or fetor ultrasound‐guided technique. Ascites should be
hepaticus may be evident in cases of liver failure. drained slowly and intravenous concentrated albu-
Parotidomegaly may occur in cases of alcoholic cir- min given during paracentesis to avoid haemody-
rhosis. Sparsity of chest hair and gynaecomastia namic instability. For patients requiring frequent
may be present in males with cirrhosis. On inspec- paracentesis, transjugular intrahepatic portosys-
tion of the abdomen, caput medusae and abdomi- temic shunt (TIPS) may be required (Figure 24.2).
nal distension may be evident. The liver may be TIPS is a percutaneous radiological procedure that
24: Portal hypertension and surgery on the patient with cirrhosis 221
(a) (b)
(c) (d)
Fig. 24.2 Transjugular intrahepatic portosystemic shunt procedure. (a) Puncture of the right portal vein via the hepatic
vein (the middle hepatic vein in this case) with portal venogram. (b) Deployment of metal stent between the middle
hepatic vein and left portal vein. (c) Balloon dilatation of the stent. (d) Final position of the stent. The catheter was
passed into the oesophageal varices, which are displayed in the venogram (variceal sclerotherapy and embolisation were
subsequently performed in this case).
creates a low resistance channel between the portal stent can be attained with revision percutaneous
and systemic venous systems, most commonly procedures as required.
between the right portal vein and right hepatic vein, Surgery, including portosystemic shunt surgery
resulting in decompression of the portal venous sys- and peritoneo‐venous shunt surgery, has been per-
tem and thus amelioration or resolution of the formed, but has limited success and has largely
complications of portal hypertension. been replaced by TIPS procedures.
The potential complications of TIPS include tech-
nical failure, encephalopathy, bleeding, cardiac
arrhythmias, haemolytic anaemia and stent steno- Bleeding
sis. Encephalopathy in this situation is due to
metabolites from the portal venous system bypass- Multiple interventions have been developed for the
ing the liver, which would normally remove toxins prevention and management of variceal bleeding
before they can enter the systemic circulation. The complicating portal hypertension and the manage-
risk factors for encephalopathy complicating TIPS ment of this problem has evolved over time. The
procedures include a high degree of shunting, recommended approach to primary prophylaxis,
advanced age, increased severity of liver failure and management of bleeding varices and secondary
the presence of encephalopathy before TIPS was prophylaxis is shown in Figure 24.3. Patients with
performed. Bleeding can occur at the puncture site cirrhosis should undergo endoscopic surveillance to
in the neck or can occasionally occur as a perihe- detect oesophageal varices. Primary prophylaxis
patic haematoma. Recurrent portal hypertension (prevention of bleeding from varices) is undertaken
following TIPS can occur as a result of thrombosis with a non‐selective beta‐blocker or endoscopic
of the TIPS stent, kinking or retraction of the stent, variceal banding.
pseudointimal hyperplasia or the development of The patient with bleeding varices should be
right heart failure. Long‐term patency of the TIPS resuscitated immediately. In addition to the
Varices
Primary prophylaxis:
Beta-blocker or endoscopic variceal ligation
Bleeding varices
Resuscitation
octreotide or terlipressin infusion
antibiotics
Oesophageal varices Gastric varices
Endoscopic variceal ligation Large Small
Controlled Uncontrolled Yes Balloon retrograde Histoacryl

transvenous obliteration injection
Oesophago-gastric Portal vein

balloon tamponade thrombosis Uncontrolled OR Uncontrolled Controlled
Secondary prophylaxis: No TIPS Secondary prophylaxis:

Beta-blocker and Beta-blocker
endoscopic variceal ligation
Fig. 24.3 Recommended approach to primary prophylaxis, management of bleeding varices and secondary prophylaxis.
insertion of two large‐bore intravenous cannulas banding for oesophageal varices and a beta‐blocker
and commencement of blood transfusion, reversal for gastric varices.
of coagulopathy, including the use of Prothrombinex Surgical procedures for portal hypertension are
and fresh frozen plasma, may be required. A vaso- now very rarely required. The procedures that were
active agent (terlipressin or octreotide infusion) and developed included shunt procedures and devascu-
broad‐spectrum prophylactic antibiotics should be larisation procedures. Shunt surgery includes the
commenced. Emergency endoscopy is performed creation of non‐selective, selective and partial
and bleeding oesophageal varices are banded. If shunts. Non‐selective shunts divert all the portal
oesophageal varices are not controlled by endo- flow away from the liver and are effective in reduc-
scopic variceal ligation, balloon tamponade may be ing the portocaval pressure gradient, but have a sig-
required. If the portal vein is patent, TIPS should be nificant risk of hepatic encephalopathy, since there
performed. If portal vein thrombosis is present in is no first‐pass detoxification of the portal blood by
the patient with bleeding oesophageal varices the liver, and can also accelerate the progression of
refractory to endoscopic therapy, balloon‐occluded liver failure, since the liver will now lack the trophic
retrograde transvenous obliteration (BRTO) is indi- influence of portal venous inflow. Non‐selective
cated. This procedure is performed by accessing the shunts were used for active portal hypertensive
varices via a spontaneous portosystemic shunt, bleeding, medically intractable ascites, anatomical
such as a gastrorenal shunt, occluding the outflow incompatibility with a distal spleno‐renal shunt and
of the varix and injecting a sclerosing agent. bleeding stomal varices. Examples of non‐selective
Small bleeding gastric varices are managed by shunts are end‐to‐side portocaval shunt, side‐to‐
endoscopic injection of histoacryl glue. If this is side portocaval shunt, large diameter interposition
unsuccessful, TIPS is required. Large bleeding gas- portocaval shunt, interposition mesocaval shunt
tric varices can be managed by either BRTO or and side‐to‐side spleno‐renal shunt.
TIPS. Failure to control bleeding with BRTO neces- Selective shunts preserve portal perfusion to the
sitates TIPS and vice versa. liver, resulting in a lower risk of encephalopathy
Secondary prophylaxis (prevention of rebleed- and liver failure but a higher risk of portal vein
ing) is undertaken with a combination of a non‐ thrombosis. Non‐selective shunts require a splenic
selective beta‐blocker and endoscopic variceal vein of at least 6 mm diameter and proximity of the
splenic and renal veins and portal flow towards the encephalopathy, and reversal of the sarcopenic
liver (hepatopedal). The usual indication was portal effects of liver failure. In potential liver transplant
hypertension with absent or medically controlled candidates, the management of portal hypertension
ascites. Active variceal bleeding is a contraindica- should take account of technical factors that might
tion. The commonest selective shunt was the distal impact on transplantation surgery. For example,
spleno‐renal (Warren shunt), which was performed the placement of the stent in performing a TIPS
by mobilising and transecting the splenic vein close procedure has to be carefully planned to ensure the
to its insertion into the superior mesenteric/portal safe removal of the stent at the time of
vein junction and anastomosing the splenic vein transplantation.
end‐to‐side to the left renal vein and dividing the
coronary vein. This diverts the portal venous blood
in the left upper quadrant through the shunt into Hepatic encephalopathy
the systemic circulation. Another example of a
selective shunt is the left gastric‐caval (Inokuchi) Hepatic encephalopathy is a neuropsychiatric com-
shunt. plication of portal hypertension that can result in
Partial shunts were designed to incompletely symptoms ranging from subtle disturbance of mood
decompress the entire portal venous system, whilst to confusion to coma. This condition occurs as a
maintaining portal perfusion of the liver. This was result of resistance to portal venous flow in the liver
achieved by using a small‐diameter (8–10 mm) and portosystemic shunts that divert neuroactive
shunt. They were associated with a lower rate of peptides into the systemic circulation rather than
postoperative encephalopathy and liver failure through the liver, where they would normally be
compared with non‐selective shunts. Requirements detoxified. Ammonia accumulates in the circulation
for a partial shunt include compensated (Child– and can cause cerebral oedema and alterations in
Pugh A or B) cirrhosis, a patent portal vein and astrocyte mitochondrial function, although it is
preferably no previous surgery in the right upper likely that cytokines and other agents contribute.
quadrant. Examples of partial shunts are small‐ Strategies that reduce production and absorption
diameter portocaval, mesocaval and mesorenal of ammonia in the intestine, such as lactulose and
interposition shunts and the small‐diameter side‐to‐ antibiotics including rifaximin, are used to reduce
side portocaval shunt. the severity of hepatic encephalopathy.
Devascularisation procedures involve devascu-
larisation of the lower oesophagus over a variable
extent (generally 5 cm) and stomach (usually spar- Surgery on the patient with cirrhosis
ing the stomach distal to the incisura), usually
accompanied by splenectomy and sometimes by There are several principles in considering surgical
oesophageal transection. These operations are to intervention in the patient with cirrhosis. Firstly,
some extent simpler than shunt procedures and one should determine whether the operation is
were therefore suited to less specialised centres and really indicated. The balance of risks and benefits in
in developing countries. They have a lower rate of the presence of cirrhosis is skewed because of the
encephalopathy than shunt procedures, but a higher increased risks of surgery, including increased risks
rate of rebleeding. When accompanied by oesopha- of bleeding and decompensation of liver function
geal transection, there is a risk of stricture and leak. and therefore an increased perioperative mortality
The indications include an unshuntable patient, risk. Liver function should be assessed. The Child–
such as one with diffuse splanchnic venous throm- Pugh score is a measure of liver function that helps
bosis, recurrent bleeding after shunt surgery and to predict the risk of morbidity and mortality in
massive splenomegaly with pressure symptoms or patients with cirrhosis who require surgery
hypersplenism. Examples of devascularisation (Table 24.1). Liver function can also be quantified
include the Sigura procedure (which is performed by the model for end‐stage liver disease (MELD)
via the chest and abdomen) and the modified Sigura score. The MELD score is calculated as:
procedure (which is performed via the abdomen
only and includes excision of the fundus). 9.57 log e creatinine,mg / dL 3.78 log e
Liver transplantation results in surgical correc- bilirubin,mg / dL 11.2 log e INR 6.43
tion of portal hypertension and is the treatment of
choice for appropriately selected patients with end‐ rounded to the nearest integer. Online calculators
stage liver disease (see Chapter 10). It results in are available to calculate these scores. Both Child–
decompression of varices, resolution of ascites and Pugh and MELD scores have been shown to be
Table 24.1 Calculation of Child–Pugh score.
Score 1 2 3
Bilirubin (μmol/L) <34 34–51 >51

Albumin (g/L) >35 28–35 <28
INR <1.7 1.7–2.2 >2.2
Ascites Absent Slight Moderate
Encephalopathy None Grade 1 or 2 Grade 3 or 4
Patients with a Child–Pugh score of 5 or 6 are class A, those with a Child–Pugh score of 7–9 are class B and those
with a Child–Pugh score ≥10 are class C.
Table 24.2 The 90‐day mortality following abdominal coagulation factors, such as fresh frozen plasma and
surgery in patients with cirrhosis. cryoprecipitate, may be required intraoperatively.
Thromboelastography, which enables point‐of‐care
Variable 90‐day mortality (%)
assessment of clot formation and thrombolysis, can
Child–Pugh class be used in addition to standard coagulation tests to
A 12 guide management of coagulation. The intraoperative
B 24 management of the patient with cirrhosis requires
C 70 experienced anaesthetic and surgical teams.
MELD score
6–9 12 Cholecystectomy
10–19 29
20–29 75 For the patient with cirrhosis requiring cholecystec-
30–40 91 tomy, the basic approach is similar to that in the
patient without cirrhosis, although there are some
Source: modified from Neeff HP, Streule GC, Drognitz details which require attention. The Hasson port
O et al. Early mortality and long‐term survival after should be placed in an infraumbilical position to
abdominal surgery in patients with liver cirrhosis. minimise the risk of bleeding from the umbilical
Surgery 2014;155:623–32. Reproduced with vein and adjacent veins. Care should be taken when
permission of Elsevier.
retracting the gallbladder, since a tear at the edge of
the gallbladder fossa can cause bleeding that is
predictive of perioperative mortality for a variety extremely difficult to control. If there are varices in
of surgical procedures (see Table 24.2). Secondly, non‐ Calot’s triangle, subtotal cholecystectomy, dividing
surgical alternatives should be contemplated for man- the neck of the gallbladder, can be performed
agement of the problem. For example, endoscopic (Figure 24.4). In addition, the gallbladder wall can
stenting should be considered as an alternative to be left on the liver to prevent bleeding from the
resection or bypass and conservative management of gallbladder fossa. Placement of a subhepatic drain
gallstones should be considered as an alternative to is recommended in such cases.
cholecystectomy. Thirdly, consideration should be
given to transferring the patient to a hepato‐pancre- Umbilical hernia
ato‐biliary or transplant unit. However, conditions Umbilical hernia commonly occurs in patients with
requiring emergency surgical management should be cirrhosis, particularly in the presence of ascites.
dealt with locally, as delay in arranging transfer could Umbilical hernia repair can be performed safely, even
result in deterioration in the patient’s condition. in patients with decompensated cirrhosis. The mortal-
Fourthly, if surgery is to be performed, attention to ity rate (1%) and recurrence rate (3%) are acceptable,
appropriate preoperative preparation is required. although the morbidity (26%) is higher than in
Consultation with a hepatologist is recommended. patients without cirrhosis. The morbidity is higher for
Preoperative management may include hydration and emergency than elective surgery and therefore it is
possibly commencement of a terlipression infusion to preferable to manage umbilical hernia electively if pos-
reverse the impact of hepatorenal syndrome, reversal sible. The sac should be left intact if possible or closed
of coagulopathy as well as the standard preparation in watertight fashion if this is not possible. Mesh repair
normally required for the patient’s surgical condition. is recommended. Meticulous haemostasis is required.
Blood should be cross‐matched. Platelets and The subcutaneous space should be drained.
(a) (b)
(c) (d)
Fig. 24.4 Subtotal cholecystectomy in a patient with frequent biliary colic and compensated cirrhosis. (a) Gallbladder
and cirrhotic liver. (b) The cystic duct has been clipped and divided. Varices can be seen around the cystic artery.
(c) Subtotal cholecystectomy, starting with transection through the neck of the gallbladder, performed with Ligasure,
leaving gallbladder wall on liver. (d) Mucosa of residual gallbladder ablated with argon beam coagulator.
Bowel resection liver resection. Small (<3 cm) tumours that are not
subcapsular or close to portal structures can be
Bowel resection is generally performed in similar
treated with percutaneous radiofrequency or micro-
fashion to that in the non‐cirrhotic patient. As with
wave ablation with similar results to resection.
any operation in a patient with cirrhosis, care is
Laparoscopic resection can be performed with
required to ensure adequate haemostasis during
reduced perioperative morbidity and length of hos-
entry into the abdomen and during mobilisation.
pital stay in comparison with open resection. The
The use of the Ligasure and argon beam coagulator
minimum future liver remnant required for safe
can assist with this. If the procedure is being per-
liver resection in the presence of cirrhosis is gener-
formed for an indication other than cancer, the
ally considered to be 40% of the preoperative non‐
mesentery should be divided close to the bowel.
tumour liver volume.
Care should be taken to ensure haemostasis when
dividing the mesentery, such as by performing
suture ligation. Proctectomy should be avoided in
Further reading
the patient with cirrhosis. For example, a patient
with ulcerative colitis and primary sclerosing chol- Bloom S, Kemp W, Lubel J. Portal hypertension: patho-
angitis can be managed with total colectomy, if physiology, diagnosis and management. Intern Med J
required, with proctectomy deferred until after liver 2015;45:16–26.
transplantation. Hew S, Yu W, Robson S et al. Safety and effectiveness of
umbilical hernia repair in patients with cirrhosis.
Liver resection Hernia 2018;22:759–65.
Neeff HP, Streule GC, Drognitz O et al. Early mortality
Liver resection may be required in the patient with and long‐term survival after abdominal surgery in
hepatocellular carcinoma complicating cirrhosis. patients with liver cirrhosis. Surgery
Decompensated cirrhosis is a contraindication to 2014;155:623–32.
3 A patient with hepatitis C virus cirrhosis has a

MCQs bilirubin of 30 μmol/L, albumin of 33 g/L, INR of 1.4,
slight ascites and no encephalopathy. Which of the
following describes the patient’s Child–Pugh status?
a class A
b class B
1 Clinically significant portal hypertension: c class C
a occurs with a hepatic venous pressure gradient d cannot be calculated without knowing the
of 5–9 mmHg creatinine
b occurs as a result of decompression of the e cannot be calculated without knowing the
systemic venous system through the portal platelet count
venous system
c frequently results in bleeding from the caput 4 A 67‐year‐old woman presents with a large painful
medusae umbilical hernia that is not reducible. She has a history
d requires endoscopic evaluation of the oesophagus of alcoholic cirrhosis complicated by ascites and has a
e is a contraindication to diuretic therapy for Child–Pugh score of 12. Repair of the hernia:
ascites a should be performed
b should be deferred until she is abstinent from
2 Large bleeding gastric varices in the presence of alcohol
portal vein thrombosis should be managed with: c should not be performed because of the high risk
a endoscopic variceal ligation of perioperative mortality
b endoscopic histoacryl glue injection d should be performed without mesh because of
c balloon retrograde transvenous obliteration the risk of infection
d transjugular intrahepatic portosystemic shunt e should be deferred until the time of liver
e distal spleno‐renal shunt transplantation
Section 4
Lower Gastrointestinal Surgery
25 Principles of colorectal
and small bowel surgery
Ian Hayes
University of Melbourne and Colorectal Surgery Unit, Royal Melbourne Hospital, Melbourne, Victoria,
Australia
and hypertension stabilised. Cigarette smoking

Introduction should cease, alcohol use decrease, the obese should
lose weight, and nutritional supplements should be
Surgical procedures for small and large bowel
considered for the undernourished.
pathology involve major operations, often in acutely
Anticoagulant use and antiplatelet agents need to
ill patients with pre‐existing medical problems. The
be carefully considered. Good haemostasis is very
physiological impact of abdominal surgery is signifi
important in bowel surgery. A haematoma in the
cant, even in previously healthy patients. Postoperative
mesentery can contribute to anastomotic leak, and
complications develop out of sight, in the closed
bleeding into the peritoneal cavity can be very
cavity of the abdomen and it can be difficult to
significant as there is nothing to tamponade it.

determine if the patient’s physiological alterations are
Anticoagulants and antiplatelet agents should be
just the expected changes of the recovery process or
ceased if this is medically safe. If it is not medically
the first manifestations of a major complication. An
safe to cease these agents, then irreversible agents
understanding of the preoperative preparation, of the
need to be converted to reversible agents and/or
principles underlying the operative procedures and of
long‐acting agents converted to short‐acting. For
the issues specific to postoperative care is relevant to
example, anticoagulants for low‐risk atrial fibrilla
any doctor involved with these patients.
tion can often be ceased for several weeks, whilst
anticoagulants used with a mechanical mitral valve
repair may need to be converted to short‐acting
Preoperative preparation
agents and only withheld for the immediate periop
erative period.
As for any major surgical procedure, the patient’s
Patients receiving chemotherapy for cancer or
general medical fitness is important. The majority
immunosuppressants for inflammatory bowel
of patients having major abdominal surgery are
disease may be able to have surgery scheduled

older and will have medical comorbidity. The sur
during a medication‐free interval. Alternatively, the
geon must be familiar with the patient’s pre‐existing
surgical plan may need to change in anticipation of
medical conditions. The decision as to which, if
poor wound healing, creating a stoma for instance
indeed any, operation is appropriate for the patient
rather than a higher‐risk anastomosis.
is based on an understanding of his or her ability to
In emergency cases or cancer procedures, there
withstand the operation and anaesthetic; to heal
may not be enough time available to optimise all
the tissues that have been operated on; and, impor
the medical conditions of the patient; nevertheless,
tantly in abdominal surgery, to withstand the
the surgical plan should still be based on the
physiological challenges of the recovery process.
patient’s underlying fitness.
A separate consideration is the issue of optimising,
rather than just assessing, medical fitness. Condi
Who will require a stoma?
tions such as aortic stenosis and reversible myocardial
ischaemia may require intervention prior to abdomi A stoma may be created proximally to protect
nal surgery. Tachyarrhythmias may require rate an anastomosis or it may be created instead of
control, diabetic control may need to be improved an anastomosis (e.g. Hartmann’s procedure).
229
230 Lower Gastrointestinal Surgery
The following conditions make stoma creation Bowel preparations can be divided into two
more likely. types, hyperosmolar and iso‐osmolar.
• Bowel quality factors: chronic radiation change, • Hyperosmolar preparations are usually phosphate
acute colitis, faecal peritonitis, ischaemia or or sulphate salt solutions taken orally as a rela
obstruction may create poor local conditions for tively small‐volume drink. The bowel is cleaned by
the formation of an anastomosis and mean that a their powerful osmotic effect. Although patients
stoma is a safer option. often prefer these small‐volume formulations, they
• Patient factors: malnutrition, immunosuppres can cause fluid and electrolyte disturbances in
sion, haemodynamic instability or multiorgan medically frail patients.
failure could mean that an anastomosis is likely • Iso‐osmolar preparations are usually polyeth
to have poor healing and make a stoma a safer ylene glycol‐based. These involve drinking
choice. several litres of fluid but with minimal risk of
• Deep pelvic anastomosis: most patients with systemic fluid and electrolyte shifts because the
ileo‐anal pouch or ultra‐low anterior resection solution remains in the bowel lumen without
will receive a temporary defunctioning loop ile exerting an osmotic effect. Paradoxically, these
ostomy to divert the faecal flow away from the high‐volume solutions are safe for patients with
anastomosis during the first 3 months to facili renal and cardiac failure who may be on oral
tate healing. fluid restriction.
• Low rectal cancer: if an adequate distal clearance Bowel preparation will require the patient to be
margin cannot be obtained, the patient is likely restricted to just clear fluids by mouth on the day
to receive an abdomino‐perineal excision with before the procedure. This generally decreases
permanent colostomy. Patients with rectal cancer caloric intake and will have implications for diabe
less than 5 cm from the anal verge have a high tes management.
likelihood of permanent colostomy.
• Anticipated faecal incontinence: a restorative
Preoperative investigations
resection will generally not be performed in
patients who have pre‐existing poor sphincter Operative planning is highly dependent on preop
function, as the loss of colonic length with resec erative imaging. Colonoscopy is the principal
tion is likely to worsen incontinence. means of viewing the colorectal and distal ileal
• Irresectable disease (e.g. advanced cancer): a mucosa, but to view the surrounding extraluminal
proximal defunctioning stoma may be required tissues requires a three‐dimensional imaging tech
due to obstruction or perforation. In this case the nique such as CT or MRI.
area of disease has not been resected and the Colonoscopy is performed for most patients
stoma is used as a temporising manoeuvre or for having colorectal or ileal resection. In addition to
palliation. allowing biopsy and visualisation of the mucosal
Preoperative planning of stoma site is very disease being considered for resection, a complete
important and stoma therapy nurses play a crucial preoperative colonoscopy excludes other unex
role in education, planning and management. The pected tumours or major polyps. It can also be used
stoma must be sited away from incisions, bony to insert submucosal marker dye at the site of a
prominences, skin creases and give due attention to lesion to allow the area to be found from the sero
position of clothing. Stomas are also discussed in sal surface at operation. It can be very helpful to
Chapter 26). have repeated confirmation of the exact position of
a lesion, especially the distance from the anal verge
and the amount of normal bowel distal to the lesion
Mechanical bowel preparation
that will remain after resection. If conditions pre
Mechanical cleansing of the bowel prior to colorec vent complete colonoscopy, CT colonography is a
tal surgery is not an absolute prerequisite but many useful method of imaging the mucosa.
surgeons prefer to operate with the bowel prepared. CT is an important part of cancer staging but
There is good evidence that it is safe to perform also gives information about the relationship of the
colonic anastomosis without bowel preparation. area of interest to surrounding structures such as
Full preparation of the colon remains a requirement ureter, iliac vessels and duodenum. Magnetic reso
for colonoscopy. For rectal resections, at the very nance enterography is used in the assessment of
least a preoperative enema is required to remove stool small bowel Crohn’s disease.
mass from the rectum to facilitate use of a circular Routine blood tests will be required for patients
stapler that will be inserted through the anus. having major surgery.
25: Principles of colorectal and small bowel surgery 231
the IM pedicle is ligated. This creates an ischaemic

Conceptualising the anastomosis segment of sigmoid, possibly extending as far as the
as a ‘graft’ descending colon. In this operation, the sigmoid
and most of the rectum are resected. This means
It seems obvious to state that surgery on small and
that the remaining viable, proximal end of descend
large bowel usually involves removal of a segment
ing colon will need to be mobilised from its normal
of bowel and anastomosis of the two ends. However,
position in the mid abdomen down to the deepest
to achieve this the two ends of bowel, especially if
part of the pelvis to create an anastomosis near the
colon is involved, will need to be mobilised quite a
anorectal junction. An important technical point is
long distance from their previous anatomical sites,
that the blood supply will need to travel a consid
whilst preserving an intact blood supply. In many
erable distance from its origin at the middle colic
ways, such an anastomosis is similar to a vascular
artery, along a small‐calibre marginal vessel. It is
ised pedicle graft in plastic and reconstructive sur
vital that the marginal vessel is not damaged during
gery, except that the graft is no longer visible to the
dissection.
surgeon once the abdomen is closed and any
Occasionally, colonic vascular pedicles are
leakage from the suture line is potentially life‐

divided, not for oncological reasons but to
threatening. Continuing with this analogy, main
increase mobility of a segment of bowel. Dividing
taining a well‐perfused graft requires that the
the IM vessels close to their origin near the aorta
patient has a good cardiac output, adequate blood
creates much more mobility of the left colon than
pressure and haemoglobin, and be well oxygenated
dividing distal branches of these vessels close to
and nourished. Thus, for patients having major
the bowel wall. In a non‐cancer operation, such
surgery of the lower gastrointestinal tract, it is

as resection of sigmoid diverticular disease, this
important that their general physiological state be
may allow creation of an anastomosis with less
kept as normal as possible, during and after the
tension.
operation, to optimise perfusion of the pedicle
graft that forms their bowel anastomosis.
Rectal anatomy: mesorectum

Colon: significance of blood supply
The surgical anatomy of the rectum has some dif
The colon has three main vascular pedicles: the ferences to the rest of the large bowel. The colon
ileocolic vessels supplying right colon; middle can be regarded as a tube‐like hollow organ, with a
colic vessels supplying transverse colon; and veil of mesentery and blood supply suspended from
inferior mesenteric (IM) vessels supplying left
its posterior aspect. In early fetal development, the
colon. Connecting these pedicles are the marginal rectum starts as a similar tube with a posterior
vessels which run in the mesentery, parallel and mesentery and blood supply derived from the IM
close to the colonic wall. The multiple vascular vessels. With growth, the rectum is elongated down
arcades of the small bowel mesentery, which into the pelvis but its main vascular pedicle remains
ensure a rich blood supply, are not present in the in position proximally. The usual configuration of
colonic mesentery. a posteriorly situated mesentery now changes to
Most colon cancer operations involve resecting wrap around the posterolateral aspects of both
the tumour‐containing segment of large bowel, its sides of the rectum, forming the mesorectum. The
mesentery and associated vascular pedicle. The vas mesorectum attenuates at the distal rectum and ter
cular pedicle contains the lymph nodes to which the minates near the anorectal junction (Figure 25.1).
tumour is likely to metastasise and its resection The significance of the mesorectum is that it con
achieves lymphatic clearance. However, this inter tains the lymphatic drainage of the rectum and thus
rupts the blood flow to the bowel and creates an needs to be removed as an intact package in rectal
ischaemic segment of colon. Exactly how much cancer surgery. Furthermore, the dissection plane
colon is made ischaemic will depend on the collat just outside the fascia encompassing the mesorec
eral flow along the marginal vessels coming from tum is relatively bloodless. Total mesorectal exci
adjacent vascular pedicles. This is the reason why sion refers to a surgical technique that carefully
resection of a relatively small cancer involves follows this plane to allow oncologically complete
removal of a much larger segment of large bowel resection of rectal cancer while minimising damage
than might have been expected. For instance, in to the autonomic nerves of the pelvis and limiting
ultra‐low anterior resection to treat a rectal cancer, blood loss.
Anal canal and sphincters
Serosa of anterior
wall of upper rectum
Lateral
surface
Mesorectum
Pedicle of inferior
mesenteric artery
Fig. 25.1 Abdomino‐perineal excision specimen showing rectum and anal canal. The blood supply is from the inferior
mesenteric artery pedicle which curves downwards into the mesorectum. The mesorectal ‘package’ can be seen to wrap
around the lower rectum, contour to fill the hollow of the sacrum and attenuate at the anorectal junction.
Achieving colon mobility: embryological Anastomoses

basis
Anastomoses can be classified by their configuration
To reconstruct the colon and rectum after resection (end‐to‐end, end‐to‐side, side‐to‐side) or technique
requires mobilisation of the remaining proximal (hand‐sewn or stapled). Usually, anastomoses of the
and distal segments. The length of bowel resected lower rectum are stapled due to the access difficul
with some operations can be greater than 60 cm, ties of hand‐sewing deep in the pelvis. For all other
which leaves a significant distance to bridge anastomoses, technique is largely based on surgeon
between the ends. Although much of the colon is preference and there is little difference in outcome
tethered to the retroperitoneum, it is possible to among the various types.
restore the colon to its mobile, early embryologi
cal, midline position by appropriate division of
Configuration
adhesions while preserving vascular supply.
The whole gastrointestinal tract starts as a • End‐to‐end is the most intuitive way to approx
midline organ in utero with its mesentery and imate two segments of bowel. Difficulties may
blood supply coming from the aorta posteriorly. arise, however, if there is discrepancy between
From the 10th week of life onwards, the gut the luminal diameter of the two ends (e.g. end
undergoes an anticlockwise 270° rotation to of ileum to rectum). Furthermore, because the
occupy its final position. This leaves the colon blood supply is derived from vessels which run
overlying the duodenum, with lateral adhesions at 90° to the direction of the bowel lumen, the
on the right and left side keeping it in a fixed, end of the bowel segment may be the least
mostly retroperitoneal, position. Dividing these vascularised.
embryological adhesions (zygoses) and straight • End‐to‐side or side‐to‐side generally ensures a
ening out the acute angles of the splenic and well‐vascularised anastomosis but each requires
hepatic flexures creates considerable length of plenty of mobility to align the bowel in this
mobile bowel. fashion.
Method sigmoid can be treated using shorter transverse or

oblique muscle‐splitting incisions.
Suturing
Laparoscopic surgery is now the preferred approach
This can be done by multiple methods, with mul when possible. It is important to understand that the
tiple different suture materials. What is required intra‐abdominal component of laparoscopic surgery
of any method of securing an anastomosis is that is very similar to what is done during open surgery.
the two ends of bowel are approximated and held In general, the bowel mobilisation and division of
together until reasonably strong wound healing vascular pedicles are performed laparoscopically; the
with native tissue is achieved. Most commonly, a mobilised bowel is brought up to the surface using
single layer of interrupted sutures is used. The a short umbilical or suprapubic incision; and the
sutures must exert sufficient tension to create an diseased area is resected and the anastomosis formed
airtight seal but not be so tight as to cause tissue at the surface.
ischaemia. Dense adhesions from previous surgery, complex
tumours and complex Crohn’s disease may favour
Staplers open laparotomy over a laparoscopic approach.
There are three types: linear staplers, linear cutting
staplers and circular staplers. Stapling devices are
loaded with multiple small titanium staples that are Operative issues relevant
deployed in rows. to postoperative care
• Linear staplers simply fire a linear double row of
staples to close off one end of a bowel segment The detail of the conditions encountered during
(e.g. proximal end of rectal stump in Hartmann’s the procedure informs the postoperative care. For
procedure). example, extensive division of intraperitoneal
• Linear cutting staplers fire two parallel double adhesions, with associated tissue trauma and
rows of staples and automatically cut between prolonged bowel handling, is likely to result in a
them. These are the typical staplers used to join prolonged postoperative ileus. It also has a risk of
the two lumens of a side‐to‐side anastomosis. unseen injury to the bowel wall and subsequent
The term ‘functional end‐to‐end anastomosis’ leakage. Extensive intraoperative bleeding can
usually refers to a type of side‐to‐side configura result in ongoing bleeding. Intraoperative spillage
tion performed with two separate firings of a lin of enteric contents can cause postoperative infec
ear cutting stapler. The two ends are joined like tion, collections and ileus.
the legs of a pair of trousers. The anatomical site of the bowel resection also
• Circular staplers are inserted into the bowel alerts the surgical team to potential complications
lumen and fire a circular double row of staples to resulting from damage to other organs. The caecum
join two ends of bowel. These instruments con is close to the right ureter and the s igmoid is close
sist of two parts: a circular anvil which is secured to the left. Mobilisation of the right colon can
to the open end of the proximal bowel and the injure the duodenum; the spleen and the pancreatic
main part introduced though the anus. Docking tail are at risk of injury during splenic flexure mobi
of these components brings the two ends of lisation. Nerve damage from pelvic dissection can
bowel together, after which the staple line is fired produce urinary retention or incontinence.
and two ‘doughnuts’ of redundant tissue from
each end are produced. Most commonly, this
type of anastomosis is performed though a rectal
Postoperative care
stump previously stapled off with a linear stapler;
the resulting join is referred to as a double‐stapled
Operations on the large and small bowel cause
anastomosis.
significant changes to the patient’s physiological
state. It is important to become familiar with the
usual patterns of these physiological changes and
to note that all physiological parameters improve
Surgical approach quite quickly during a routine recovery process
(Box 25.1). What is important to recognise is devi
Traditionally, surgery of the small and large bowel ation from the expected pattern and to distinguish
has been performed through a vertical midline between the normal recovery process and the
laparotomy. In appropriate cases, the right colon or warning signs of complications.
postoperative outcomes. The regimens used vary

Box 25.1 Expected postoperative
between hospitals and continue to evolve over time.
changes
Protocols are instituted preoperatively, intraop
Abdominal pain eratively and postoperatively.
Abdominal tenderness near the wound • Preoperative interventions include decreased
Decreased mobility fasting and careful preoperative counselling.
Ileus (anorexia, nausea, abdominal distension, • Intraoperative interventions include the use of
constipation) minimally invasive surgical techniques, restricted
Atelectasis use of intravenous fluids, use of short‐acting
Low urine output anaesthetic agents and decreased opioid use.
Mild fever • Postoperative interventions include early mobili
Mild tachycardia sation and early feeding, minimisation of opioid
Blood tests: increased C‐reactive protein; decreased and intravenous fluid use, avoiding routine
potassium, haemoglobin, albumin nasogastric tubes and drains, and early removal
of urinary catheters.
Even in hospitals which do not formally use these pro
grams, there has been a general acceptance that bowel
With any deviation in the patient’s course from
preparation is not mandatory, that the period of preop
the expected pattern, the treating doctors must ask
erative fasting can be shortened, that restricting intrave
themselves whether this could be a manifestation of
nous fluid use is safe and that low urine output, of
an intra‐abdominal complication. The most serious
itself, does not need to be aggressively corrected. Early
of these will be gut ischaemia or anastomotic leak.
mobilisation after gastrointestinal surgery and early
These catastrophic complications are uncommon
feeding are safe. Setting expectations for early discharge
but may start insidiously and escalate to sepsis,
is beneficial for the patient and the health system.
peritonitis and multiorgan failure. Thus, a single
abnormality in a patient who is progressing well
should be examined but is unlikely to represent a
Further reading
major complication. An example of this is a raised
temperature of 38.1°C in a patient who is otherwise Heald RJ. The ‘Holy Plane’ of rectal surgery. J R Soc Med
progressing well. However, the finding of a fever in 1988;81:503–8.
a patient with prolonged ileus, escalating abdominal Kiran RP, Murray AC, Chiuzan C, Estrada D, Forde K.
pain and tachycardia is much more concerning. Combined preoperative mechanical bowel preparation
A further important issue is that all postoperative with oral antibiotics significantly reduces surgical site
complications must be treated proactively. A chest infection, anastomotic leak and ileus after colorectal
infection arising from postoperative atelectasis may surgery. Ann Surg 2015;262:416–25.
not seem to have implications for the bowel recov Ljungqvist O, Scott M, Fearon KC. Enhanced recovery
after surgery: a review. JAMA Surg 2017;152:292–8.
ery but if the patient becomes systemically unwell
from this, perfusion of the anastomosis may be
compromised and could result in anastomotic leak. MCQs
In simplistic terms, the patient must be kept well
to maximise the likelihood of the anastomosis heal Select the single correct answer to each question. The
ing. If the patient becomes unwell postoperatively, correct answers can be found in the Answers section
the clinician must also be alert to the possibility at the end of the book.
that this could be the first sign of an intra‐abdominal
1 Which of the following statements regarding right
complication.
hemicolectomy for cancer is incorrect?
a a defunctioning loop ileostomy is usually required
b the ileocolic vessels are ligated and divided close to
Enhanced recovery after surgery their origin to maximise the number of draining
lymph nodes removed
Enhanced recovery after surgery (ERAS) programs c the junction of the second and third parts of the
usual consist of a series of 15–20 interventions duodenum could be injured during mobilisation
designed to accelerate recovery after lower gastro of the right colon
intestinal surgery and decrease the rate of complica d it is safe to perform an anastomosis for right
tions. Individually, the treatments do not always hemicolectomy without mechanical bowel
have a strong evidence base to support their use, preparation
but used together they have been shown to improve e the anastomosis can be stapled or sutured
2 Which of the following statements regarding a c most patients are not hungry
defunctioning loop ileostomy is incorrect? d the pain from the abdominal wound can lead to
a it is likely to be required if an ultra‐low anterior splinting of the diaphragm and atelectasis
resection has been performed e new‐onset rapid atrial fibrillation at day 4 could
b it diverts the faecal flow away from a distal be precipitated by an intra‐abdominal problem
anastomosis to enhance healing
c it is used to protect the anastomosis in an 4 Which of the following statements regarding
abdomino‐perineal resection enhanced recovery after surgery (ERAS) programs
d it may be created proximal to a right hemicolec- is incorrect? ERAS programs
tomy anastomosis if the surgeon felt the anasto- a encourage the use of longer‐acting anaesthetic
mosis to be at higher risk of leak than usual agents for convenience and better pain control
e it has two openings b do not require the patient to have passed flatus
postoperatively before starting oral intake
3 Following a laparotomy for colon resection, which c encourage early mobilisation postoperatively
of the following statements is incorrect? d encourage the avoidance of routine use of
a the patient is likely to experience pain when surgical drains and nasogastric tubes
attempting to sit out of bed e have been shown to result in earlier patient
b a urine output of less than 1 mL/kg per hour discharge
should be treated with diuretics
26 Physiology of small and large
bowel: alterations
due to surgery and disease
Jacob McCormick1,2 and Ian Hayes1,3
1
Colorectal Surgery Unit, Royal Melbourne Hospital
2
Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia
3
Department of Surgery, University of Melbourne, Parkville, Victoria, Australia
duodenojejunal junction daily but due to the sig-

Introduction nificant reabsorptive capacity of the small bowel,
only 1 L of fluid arrives in the caecum. Thus, as
The small and large bowel are responsible for
described in Chapter 27 on small bowel obstruc-
absorption of fluid and nutrients. Obstruction of
tion, if reabsorption is impaired very large volumes
the bowel or loss of functional absorptive capacity
of fluid can be sequestered in the lumen of the small
through surgical resection, injury or disease may
bowel (Box 26.1).
cause severe derangements in circulating volume,
electrolytes and nutrition. An understanding of the
Electrolytes
normal physiology of bowel function and an ability
to anticipate the likely results of resection and dis- Sodium and nutrients are absorbed actively through
ease are important for the care of gastrointestinal the bowel mucosa, whereas absorption of water is a
surgery patients. Patients with established intestinal passive process. Gastric juice contains about half
failure or short bowel syndrome are uncommon the sodium concentration of extracellular fluid
but have prolonged and repeated hospital stays. (ECF) but bile, pancreatic juice and small bowel
Much more common are patients with prolonged fluid have a sodium concentration similar to that of
ileus after abdominal surgery who require manage- ECF. Gastric juice has a high acid content, pancre-
ment of their short‐term issues of fluid and nutri- atic juice is rich in bicarbonate and small bowel
tional support. fluid has a high potassium concentration. In gen-
eral, if intravenous fluid is required to compensate
for loss of small bowel content, it will need to have
Fluid volume a sodium concentration similar to that of ECF (e.g.
0.9% normal saline or Hartmann’s solution).
The length of the small bowel can vary between 3 Vomiting, or loss via nasogastric tube, of pure gas-
and 8 m. Over 8 L of fluid per day circulates tric secretions (as in cases of gastric outlet obstruc-
through the lumen of the gastrointestinal tract but tion) can produce hypochloraemic alkalosis, while
only about 200 mL is excreted in faeces. The most excessive loss of pancreatic juice (from proximal
rapid small bowel transit occurs in the jejunum (the small bowel obstruction) can produce acidosis.
name means ‘empty’).
Approximately 3 L/day are ingested as fluid and
food but this does not represent the largest compo- Nutrients
nent of gut fluid. The gastrointestinal tract pro-
duces an additional 0.5 L of saliva, 2 L of gastric The three classes of macronutrients – protein, car-
secretions, 1.5 L of pancreatico‐biliary secretions bohydrate and fat – are absorbed through the
and approximately 3 L of small bowel fluid each bowel. Most protein absorption occurs in the first
day. A total of 7 L of fluid passes through the 100 cm of the jejunum. Lipids and carbohydrates
237
the skin. To minimise skin damage, the inner lining

Box 26.1 Gut fluid volumes produced
of the end of the ileostomy is everted back over
per day
itself for 2–4 cm to create a raised spout (Brook
Ingested: 3 L ileostomy) (Figure 26.1). An ileostomy is usually
Saliva: 0.5 L sited in the right iliac fossa. The output should be
Gastric secretion: 2 L less than 1 L/day of fluid with porridge‐like consist-
Pancreatico‐biliary secretion: 1.5 L ency. In the first few weeks following construction,
Small bowel secretion: 3 L the luminal diameter of an ileostomy can be quite
narrow and thus at risk of obstruction due to a
bolus of undigested food. For this reason, patients
with ileostomy are advised to avoid foods which
are absorbed in the jejunum and ileum. The ileum may be poorly digested, including sweet corn, peas,
has some very specific additional functions, includ- dried fruits and nuts. Generally, patients with an
ing absorption of bile salts and vitamin B12. The ileostomy created from terminal ileum have no
colon has some nutritional function with absorp- nutritional problems.
tion of medium‐chain triglycerides and complex When a stoma is created from more‐proximal
carbohydrates. small bowel, the volume of output can be much
Overall, the proximal jejunum is probably the higher, thus creating a potential need for supple-
most important area for nutrition. Some patients mental fluid administration.
can manage with as little as 35 cm of jejunum if it
is anastomosed to an intact ileum or 60 cm if the Colostomy
residual jejunum is anastomosed to intact colon,
Stomas created from colon have a lower‐volume
but at least 150 cm of jejunum is required if there is
output than small bowel stomas and the faecal
an end‐jejunostomy. The gut has a great capacity
material is less irritant to skin, and thus they are
for adaptation and for increasing its absorption but
sutured without an elevated spout. Most end‐
this can take up to 2 years to achieve.
colostomies utilise descending or sigmoid colon
and are sited in the left iliac fossa. The output is
very similar to normal faeces. Colostomies
Stomas
involving transverse or right colon are avoided
because they produce high volumes of thick fluid
Stoma is the Greek word for ‘mouth’ and refers to
which smells more offensive than ileostomy fluid
creating an opening of the bowel to the external
(Box 26.2).
environment through the abdominal wall. The out-
put is collected in an appliance (stoma bag) that is
Loop stomas
attached to the skin with specially formulated glue
(stomahesive). Depending on the type of output, the Loop stomas are easier to construct and do not
appliance can either be emptied or changed. require a laparotomy to close. However, they are
Whilst modern management of stomas is quite often bulkier and less easy to fit an appliance to.
straightforward and patients can lead a normal life-
style with few restrictions, having a stoma is an End stomas
alteration of body image. Colorectal surgeons try to End stomas are usually the best construction.
avoid creating stomas unless there is no safe or
practical alternative. The reasons for creating a
stoma are covered in Chapter 25.
In the presence of distal obstruction, there needs
Short‐gut syndrome
to be a means of escape for mucus created by the
segment of bowel between the stoma and the
Definition
obstruction. This requires either a loop stoma or a
separate mucous fistula. Short‐gut syndrome is loss of bowel mass due to
resection, congenital defects or disease and is usu-
Principles of stoma construction ally defined as a residual length of small bowel of
less than 200 cm. Short‐gut syndrome may occur
Ileostomy
due to disease, surgical resection or enterocutane-
This type of stoma produces a high‐volume output ous fistulas. It may be transient, with the ability to
of liquid small bowel fluid that is very corrosive to reconstruct intestinal continuity at a later date, or
26: Physiology of small and large bowel: alterations due to surgery and disease 239
(a) (b)
Fig. 26.1 (a) Construction of an end‐ileostomy. (b) Eversion and maturation of an end‐ileostomy.
available for absorption. Transit time is lengthened,

Box 26.2 Complications of stomas
and the activity of brush‐border enzymes and the
High‐volume output (requiring fluid and electrolyte bowel’s absorptive capacity are increased. These
support) adaptive changes occur as a result of enteral feeding
Stenosis and are not seen in patients solely fed parenterally.
Food bolus obstruction (ileostomies) Thus, it is important to re‐establish enteral feeding
Hernia as early as is practical. The 5‐year survival data for
Prolapse short‐gut syndrome is difficult to interpret as it is
Skin excoriation clouded by the cause of the short gut (often neopla-
sia or thromboembolic events) but appears to be in
the region of 70–80%.
permanent. The exact amount of bowel required to
survive, independent of supports, varies between
Management
patients, with younger patients able to adapt more
easily. Many patients with short‐gut syndrome Initially in the perioperative period after exten-
achieve adequate nutrition with the aid of oral sup- sive bowel resection, the major issues relate to
plements or intermittent injections (such as vitamin electrolyte and fluid replacement due to ileus,
B12 with the loss of terminal ileum). A subset of sequestration of fluid, diarrhoea or high‐output
short‐gut patients develop intestinal failure. This is stoma. Clinical examination, chart assessment
defined as inability to meet nutritional needs with and biochemical analysis of serum electrolytes
oral intake alone and requiring parenteral nutri- will guide fluid replacement and maintenance.
tion. As already discussed, the relationship between Enteral intake should be commenced early if
remaining gut length and function is determined by possible.
the region of bowel remaining and the presence or In the longer term, patients are encouraged to
not of a stoma. The remaining bowel adapts over a increase their oral intake to 1.5–2 times their previ-
period of 6–24 months, so the need for parenteral ous intake, as this greater intake will somewhat
nutrition may not be lifelong. Adaptive changes counteract their relative malabsorption. Feeding
include cellular hyperplasia, increase in villous should be continuous throughout the day and not
height and crypt depth, intestinal lengthening limited to three meals a day. Often high‐calorie
(slightly) and dilatation to increase the surface area enteral nutrition drinks supplement the diet.
Diarrhoea and high‐output stomas cause electro- seen in up to 84% of patients on parenteral nutri-
lyte imbalance and are some of the major impedi- tion, thought largely to be due to a reduction in the
ments to quality of life in patients with short‐gut absorption of vitamins, particularly vitamin D.
syndrome. Opiates are the mainstay of treatment Normally, reabsorption of bile salts occurs in the
for the control of diarrhoea. Loperamide is com- terminal ileum. Short‐gut patients have frequently
monly used and may require very high dosage. had their terminal ileum resected or their bowel
Codeine may be added, but it has the possible side diverted proximally with a stoma. As a result, bile
effects of nausea (which in turn reduces oral intake) salt depletion is a common occurrence. This, along
and sedation. Octreotide (a somatostatin analogue) with reduced gallbladder emptying and the use of
should be limited to patients with high‐volume octreotide, serve to promote gallstone formation.
diarrhoea refractory to other treatment modalities, Some studies have shown the prevalence of gall-
as it may increase the risk of biliary disease (to stones in this population to approach 100%. Bile
which these patients are already predisposed) and salt depletion reduces the body’s ability to absorb
decrease gut adaptation. Water (without added fats, which in turn leads to deficiency of the fat‐
electrolytes), particularly in large volumes, may soluble vitamins A, D, E and K. Kidney stones are
paradoxically result in greater net loss of liquid as common in patients with short‐gut syndrome.
the body attempts to equilibrate sodium concentra- These may be calcium oxalate (in patients with an
tions between plasma and the bowel lumen. This intact colon) or uric acid (in patients with a high‐
dehydration stimulates more thirst and leads to a output stoma). Hepatic steatosis and cholestasis
vicious cycle of further water intake, further enteric may be seen in up to 50% of patients with short gut
fluid secretion and worsening of dehydration. Oral fed parenterally.
rehydration solution, a balanced salt and glucose
solution, helps to overcome this.
The role of the colon
A functioning colon is an important factor in the
Nutritional requirements
management of short‐gut syndrome. The pres-
The baseline adult energy requirement is 20 kcal/kg ence of a colon allows water and electrolytes to
per day of non‐protein energy, 30% of which should be absorbed against a concentration gradient.
be fat and 70% carbohydrate. The adult protein Bacteria in the colon ferment polysaccharides to
requirement is 1.5 g/kg per day. These requirements short‐chain fatty acids which may then be
are modified by sex, height, weight and disease pro- absorbed. Excess monosaccharides or oligosac-
cess. For instance, in severe sepsis requirements charides may cause d‐lactic acidosis via abnor-
increase 45%. Protein losses and requirement can mal bacterial colonisation of the colon (humans
be very high with enterocutaneous fistula. create the l‐isomer). d‐lactic acidosis may cause
ataxia, blurred vision, ophthalmoplegia and
nystagmus. Humans do not metabolise the d‐iso-
Total parenteral nutrition
mer. Treatment is with broad‐spectrum antibiot-
In cases of gut failure, nutrition may be adminis- ics and changing the diet to one that is high in
tered parenterally as total parenteral nutrition polysaccharides. Patients who do not have a
(TPN). The fluid is hyperosmolar and must be colon require a diet that is iso‐osmolar (300 mos-
administered via a central venous cannula to a mol/kg) and has a sodium concentration of about
high‐flow central vein. The contents of a typical 100 mmol/L.
daily 2‐L bag of TPN are carbohydrate, 800 mL as
a 50% dextrose solution; lipid, 500 mL as a 10%
solution; and amino acids, 700 mL as a 10% solu-
tion. Carbohydrate and protein each provide 4 Enteric fistula
kcal/g of energy, while lipid provides 9 kcal/g. Thus,
the major macronutrient requirements are delivered An enteric fistula is an abnormal communication
with nearly 3000 kcal of energy. between a loop of bowel and another epithelial‐
lined surface. The anatomical classification of this
condition names the fistula according to the
Long‐term complications of short‐gut syndrome
organs involved. The high‐pressure organ from
Long‐term complications in short‐gut syndrome which the fistula arises is named first, followed by
pertain to absorption problems. Osteomalacia and the organ to which it travels (e.g. colovesical,
osteoporosis (with overall decrease in bone mass) is enterocutaneous).
26: Physiology of small and large bowel: alterations due to surgery and disease 241
of morbidity. Patients with enterocutaneous fistulas

require diligent care, as they are at risk of recurrent
bouts of sepsis (both local and systemic). Line sep-
sis is not uncommon.
Malnutrition is potentially a major issue due to
losses from the fistula tract and loss of absorptive
capacity of bypassed segments. High‐volume fistu-
las, defined as more than 200 mL per 24 hours, may
require supplementation with parenteral nutrition
or intravenous fluids (particularly if proximally
located in the small bowel).
The acronym SNAP is a useful mnemonic for the
Fig. 26.2 Entero‐atmospheric fistula showing large skin management of patients with intestinal fistulas.
defect and multiple fistulating loops of small bowel. • S is for control of sepsis and appropriate skin
care. Fistulas are unlikely to heal in the presence
of sepsis and the patient may deteriorate clini-
• An enterocutaneous fistula is an abnormal com- cally if sepsis is left untreated. This may require
munication between a loop of bowel and the antibiotics and/or a drainage procedure. Skin
skin. Large‐diameter fistulas, where bowel care is crucial. Leaking small bowel fluid from an
mucosa is visible, are generally referred to as enterocutaneous fistula severely damages skin.
entero‐atmospheric fistulas and these are unlikely Uncontrolled output is very unpleasant for the
to heal spontaneously (Figure 26.2). patient and socially isolating. All the skills of
• An entero‐enteric fistula is a communication experienced stoma therapy nurses will be
between two loops of bowel that results in enteric required to help with these patients. Usually the
contents bypassing a segment of bowel. They best way to control the fluid is to use individually
may be created surgically (e.g. to bypass a stric- tailored stoma‐type appliances.
tured or obstructed segment of bowel) or occur • N is for nutrition. This often requires a combina-
as a result of inflammatory bowel disease. There tion of enteral and parenteral nutrition.
is loss of absorptive capacity as enteric contents • A is for anatomy. It is important to define the
do not pass through the bypassed segment. anatomy as clearly as possible prior to re‐opera-
Enterocutaneous fistulas are typically accompa- tive surgery.
nied by intra‐abdominal sepsis; 75–85% are iatro- • P is for planning definitive repair.
genic in origin and most occur after surgery for Re‐operative surgery is difficult within 100 days
inflammatory bowel disease, cancer or adhesioly- of the primary procedure due to inflammation and
sis. The original operation is likely to have dam- dense adhesions. There is a definite risk of creating
aged a segment of bowel which has then leaked. more fistulas. Early re‐operation should be avoided
Rather than leading to generalised peritonitis, the unless the patient is clinically deteriorating and
leak has partially walled off and eventually fistu- there is no alternative option (e.g. worsening sep-
lated to the surface. Other causes include percuta- sis, bowel ischaemia). There is some evidence that
neous drainage of an abscess (e.g. appendicitis, suggests better outcomes are achieved by waiting
diverticulitis) or foreign‐body erosion (e.g. mesh at least 6 months before attempting further surgery
hernia repair). and by resecting the fistula rather than attempting
A small number of enterocutaneous fistulas may to repair it. Surgery should ideally be performed in
close with conservative management, especially if a major centre that has expertise in hostile abdomi-
there is low‐volume output with a long narrow nal surgery and the support of a nutrition service.
tract. If spontaneous closure is to occur, it will be
within the first 6 weeks. Fistulas associated with
Crohn’s disease, previous radiation, downstream Further reading
obstruction, complete anastomotic dehiscence,
Bleier JIS, Hedrick T. Metabolic support of the enterocu-
ongoing intra‐abdominal sepsis, malnutrition, for-
taneous fistula patient. Clin Colon Rectal Surg
eign body or diseased bowel are unlikely to heal 2010;23:142–8.
spontaneously. Carroll RE, Benedetti E, Schowalter JP, Buchman AL.
The mortality rate for enterocutaneous fistula is Management and complications of short bowel syn-
up to 10%. In addition to this high rate of mortal- drome: an updated review. Curr Gastroenterol Rep
ity, enterocutaneous fistulas are a significant source 2016;18:40.
Nightingale JD. The medical management of intestinal b Crohn’s disease

failure: methods to reduce the severity. Proc Nutr Soc c distal obstruction of the alimentary canal
2003;63:703–10. d foreign body
Polk TM, Schwab CW. Metabolic and nutritional support e low output
of the enterocutaneous fistula patient: a three‐phase
approach. World J Surg 2012;36:524–33.
3 Which of the following statements is not correct
with regard to intestinal fistulas?
a require careful planning prior to operation
MCQs
b have a mortality rate up to 10%
Select the single correct answer to each question. The c may heal spontaneously
correct answers can be found in the Answers section d should be repaired not resected
at the end of the book. e are often iatrogenic in origin
1 Which of the following is not an adaptation that 4 Which of the following is not a long‐term compli-
occurs in the small bowel in the setting of short‐gut cation of short‐gut syndrome?
syndrome? a decrease in bone mass
a cellular hyperplasia b bile salt depletion
b increase in villous height and crypt depth c kidney stones
c intestinal lengthening and dilatation d obesity
d reduction in transit time e malnutrition
e increased activity of brush‐border enzymes
2 Which of the following is not a factor associated

with non‐healing of an enterocutaneous fistula?
a sepsis
27 Small bowel obstruction
and ischaemia
Ian Hayes and the late Joe J. Tjandra
Colorectal Surgery Unit, Royal Melbourne Hospital and Department of Surgery,
University of Melbourne, Parkville, Victoria, Australia
increase in compressive force may compromise the

Introduction blood supply to that segment of bowel. Venous
return may be impaired at a relatively low compres-
There is significant overlap between the clinical
sive force; this increases oedema, further limiting
manifestations of small bowel obstruction (SBO)
blood flow. Tissue perfusion of the bowel is coun-
and acute ischaemia of the small intestine. It is the
teracted by increased wall tension due to disten-
danger of developing secondary ischaemia in an
sion, and thus cellular ischaemia is produced.
obstructed segment of small bowel that makes
Hypovolaemia may further impair tissue perfusion.
SBO a serious condition, which sometimes requires
These factors can combine to create a vicious cycle
emergency surgery. On the other hand, many cases
of ischaemia, necrosis, perforation and ultimately
of SBO due to adhesions can be managed non‐
multiorgan failure (Figure 27.1).
operatively. It is crucial that clinicians can confi-
dently diagnose SBO and recognise features
suggestive of ischaemia. Symptoms
The characteristic symptoms of SBO are listed in
Small bowel obstruction Box 27.2. The order of appearance and the promi-
nence of these symptoms are affected by how d istal
Aetiology the obstruction is. The pain is characteristically
periumbilical, reflecting the embryological inner-
The most common causes of SBO in western society vation of the small bowel. The colicky quality is
are adhesions and hernia (Box 27.1). In consider- due to stimulation of stretch receptors with waves
ing the possible causes of this condition, a helpful of opposed peristalsis. Pain becoming constant
framework can be to divide the causes into the and more localised suggests that the patient may
following groups: be developing inflammation of the parietal perito-
• extramural (e.g. adhesions) neum due to ischaemia of the underlying small
• mural (e.g. stricture, malignancy) bowel.
• intraluminal (e.g. food bolus obstruction at new Vomiting due to SBO is usually bile‐stained (green)
ileostomy). because the obstruction is distal to the second part of
the duodenum where bile flows into the gut.
Pathophysiology
Prolonged obstruction or distal obstruction leads to
Several litres of enteric fluid circulate through thick brown feculent vomitus due to bacterial over-
the small bowel each day. Obstruction leads to growth in a static column of enteric fluid.
decreased absorption of this fluid, distension of the The degree of distension is related to how distal
bowel and vomiting. This in turn leads to hypo- the obstruction point is. Proximal SBO may be asso-
volaemia and electrolyte depletion. Whilst a certain ciated with relatively little abdominal distension.
degree of extrinsic compression from a narrow‐ Constipation may be a late feature. Strong per-
necked hernia or a dense adhesion band will cause istalsis may cause the colon to empty for some
obstruction by occluding the lumen, any further hours after the onset of SBO.
243
Clinical examination findings more than five air–fluid levels in distended small
bowel on an erect X‐ray is diagnostic of SBO but a
The patient is often in moderate abdominal dis-
supine X‐ray showing distended small bowel is also
comfort, nauseated and dehydrated. The abdomen
useful. CT scan of abdomen and pelvis showing
is distended, tympanitic and bowel sounds are high‐
dilated small bowel with a transition point at the
pitched. Note should be made of previous abdomi-
site of obstruction is a diagnostic feature of mechan-
nal incisions and a careful examination performed
ical SBO. CT may give additional information
to exclude hernias. A key concept is that the pres-
about the cause of the obstruction and suggest fea-
ence of peritonism suggests ischaemia. In the case
tures of ischaemia. The radiological diagnosis is
of a strangulated hernia, the hernial mass is likely
strengthened if it can be demonstrated that there is
to be tender and irreducible. There may be redness
failure of transit of contrast administered orally or
in the overlying skin if the bowel is ischaemic.
via nasogastric tube. However, in the setting of very
When the necrotic tissue is confined to the hernial
dilated bowel or distal obstruction, the contrast may
sac, examination of the rest of the abdomen may be
become too dilute in the static column of fluid to be
normal despite a strangulated hernia.
of diagnostic value. Furthermore, if the CT scan is
performed too soon after administration of lumi-
Investigations
nal contrast, the contrast will not have progressed
Plain abdominal X‐ray is a useful screening test to the site of obstruction.
for SBO. Typical findings are dilated small bowel Gastrografin follow‐through, involving repeat
(>2 cm diameter), centrally located and with char- plain X‐rays over a time sequence to monitor the
acteristic spiral valvulae conniventes. The finding of progress of luminal Gastrografin contrast, has an
important diagnostic role in helping to distinguish
ileus from mechanical obstruction. This test can
Box 27.1 Causes of small bowel obstruc- also confirm ongoing complete obstruction
tion (in order of frequency)
after an attempt at conservative treatment of
• Adhesions
• Hernia Box 27.2 Characteristic symptoms
• Neoplasm: primary or secondary of small bowel obstruction
• Strictures: Crohn’s disease, fibrosis following
ischaemia, chronic radiation changes • Crampy abdominal pain
• Volvulus • Nausea and vomiting
• Bezoar/food bolus • Abdominal distension
• Gallstone ileus • Constipation
Fig. 27.1 Laparotomy displaying a single band adhesion causing closed‐loop obstruction of small bowel with ischaemia.
27: Small bowel obstruction and ischaemia 245
adhesion‐related SBO. The finding of complete

Box 27.3 Primary tumours of the small
obstruction contributes to the decision to operate.
bowel
Blood tests may show impaired renal function
and hypokalaemia if the patient is dehydrated and • Adenocarcinoma
vomiting. Raised white cell count and metabolic • Lymphoma
acidosis suggest ischaemia. • Neuroendocrine tumours (carcinoid)
• Gastrointestinal stromal tumours (GIST)
Treatment
Patients with SBO are usually dehydrated and need (Box 27.3). These tumours can present with non‐
intravenous fluid resuscitation and electrolyte specific symptoms and are occasionally incidental
replacement. Insertion of a nasogastric tube diagnoses on imaging. They can also present
decompresses the stomach and upper small bowel, urgently with complications of bleeding, obstruc-
improving patient comfort and relieving vomiting. tion or perforation. However, it should be noted
When patients have adhesion‐related obstruction, that the most common cause of malignant SBO is
this decompression may be enough to release the intraperitoneal metastatic spread of other tumours
obstructed segment. Adhesional SBO usually such as ovarian or colorectal cancer.
resolves within several days. Failure to resolve Metastases from malignant melanoma and breast
means that nutritional support with total paren- cancer can form deposits within the wall of the
teral nutrition will need to be considered and surgi- small bowel mimicking a primary small bowel
cal intervention may now be required. tumour.
Surgery for SBO is challenging. Entry to the
abdomen carries the risk of damaging oedematous
dilated loops of bowel. Surgery to divide adhesions
Adenocarcinoma of the small bowel
may, of course, create further adhesions in the The risk of developing adenocarcinoma of the
future. Laparoscopic surgery for SBO is sometimes jejunum and ileum is increased in patients with
possible but open laparotomy is usually safer. Crohn’s disease, coeliac disease and Peutz–Jeghers
Patients who have not had previous major syndrome. Patients with familial adenomatous
abdominal surgery (virgin abdomen) are less likely polyposis, Lynch syndrome and sporadic colorectal
to have adhesions causing their obstruction and cancer also have an elevated risk of small bowel
will generally require operative treatment. Patients cancer. Treatment is similar to that of colorectal
with SBO due to a hernia or who have peritonitis cancer except that extensive lymphadenectomy is
require urgent surgery. more difficult to achieve than in the colon.
Differential diagnosis Small bowel lymphoma

Often the diagnosis of SBO rests on the basis of a Small bowel lymphoma is associated with coeliac
plain abdominal X‐ray in the setting of abdominal disease and HIV. Most are B‐cell non‐Hodgkin’s
pain and vomiting. Gastroenteritis can be associ- lymphomas. Surgical resection is frequently required
ated with multiple air–fluid levels on a plain X‐ray for definitive diagnosis; in early‐stage, localised,
but in non‐dilated small bowel. The presence of low‐grade disease this may be definitive treatment.
diarrhoea in this setting makes obstruction less More advanced disease will require chemotherapy
likely. Ileus, either postoperative or secondary to postoperatively.
other acute intra‐abdominal pathology, may dis-
play dilated small bowel on a plain X‐ray but the
characteristic transition point of mechanical
Neuroendocrine tumours of the small bowel
obstruction will be absent on CT. Acute ischaemia Neuroendocrine tumours (previous called carcinoid
of the small bowel may also be associated with tumours) arise in the enterochromaffin cells in the
dilation of the bowel on imaging. wall of the bowel. Most originate in the appendix
and about one‐third are multifocal. These tumours
are slow‐growing and the primary tumour usually
Small bowel malignancy remains small. Nodal metastases in the mesentery
can produce large masses and a dense desmoplastic
Primary cancers of the small bowel are much reaction which can even lead to ischaemia of the
rarer than colorectal malignancy, accounting for small bowel. The tumours release vasoactive
less than 2% of gastrointestinal malignancies amines, including serotonin, which are metabolised
by the liver. However, once the tumour has metasta-

Box 27.4 Warning signs for the possibility
sised to the liver, carcinoid syndrome may occur.
of acute ischaemia
This syndrome is characterised by diarrhoea, facial
flushing, tachycardia and bronchospasm, and can • Pain out of proportion to signs (early)
lead to right heart failure. Carcinoid crisis can be • Peritonism in the setting of dilated bowel on X‐ray
precipitated by general anaesthesia and this is an (late)
important consideration when operating on these • New history of atrial fibrillation
patients. Carcinoid syndrome is treated with • High white cell count
somatostatin analogues. • High lactate
Diagnosis of neuroendocrine tumours may • Metabolic acidosis
often be an incidental finding after appendicec- • Thickened, non‐perfused bowel on CT
tomy. Biochemical tests include chromogranin A
level and urinary levels of 5‐hydroxyindoleacetic
acid (5‐HIAA). CT may reveal the characteristic non‐occluded main vessels in patients in the inten-
desmoplastic reaction in the mesentery and liver sive care unit (ICU) or after major trauma.
metastases. Gallium‐68 DODA‐TATE positron
emission tomography (PET)/CT is the most specific Clinical features
imaging modality. The diagnosis of acute small bowel ischaemia is
Surgical treatment involves resection of the pri- notoriously difficult in the early phase and it may
mary tumour and involved mesentery. Appropriately be too late once the condition becomes clinically
sited liver metastases are resectable. obvious (Box 27.4). Patients are usually elderly,
with significant comorbidities. The new onset of
Gastrointestinal stromal tumours atrial fibrillation preceding abdominal pain is
These tumours arise from the interstitial cells of important to note, as is a history of peripheral vas-
the muscularis propria. The majority have been cular disease. In an anaesthetised ICU patient, the
found to have mutation in the KIT oncogene, thus only diagnostic feature may be the new onset of
allowing successful treatment with tyrosine‐kinase unexplained metabolic acidosis.
inhibitor drugs such as imatinib. Tumours less The pain with ischaemic gut is constant, central
than 2 cm in diameter are very low risk and can and characteristically described as being out of pro-
simply be monitored. Larger tumours require sur- portion to signs. Initial abdominal examination
gical excision but not extensive lymphadenectomy. may be normal. As bowel ischaemia and necrosis
The decision about adjuvant therapy with imatinib progress, acute inflammatory changes will lead to
is based on tumour size, mitotic index and history peritonitis. Ischaemia leads to breakdown of nor-
of tumour perforation. mal mucosal defences and bacterial translocation
to the portal venous system. The patient may be
tachypnoeic as a result of respiratory compensation
for metabolic acidosis. Systemic sepsis and multior-
Acute small bowel ischaemia gan dysfunction soon follow. An elderly patient
with severe abdominal pain, who ‘looks sick’ but
Secondary ischaemia in the presence of obstruction initially has few abdominal signs, should alert the
has been discussed. Primary acute ischaemia of the clinician to the possibility of acute small bowel
small bowel can be due to: ischaemia or ‘dead gut’.
• embolism
• arterial thrombosis
Investigations
• venous thrombosis
• severe hypoperfusion. Blood tests may reveal a high white cell count
Embolism to the superior mesenteric arterial tree with a neutrophilia often greater than 20 × 109/L.
is usually of cardiac origin, due to atrial fibrillation Elevated serum lactate is a frequent but non‐spe-
or post‐infarct cardiac mural thrombus and is the cific finding. Arterial blood gas measurement can
most common cause of primary acute ischaemia. be used to confirm metabolic acidosis. Plain X‐ray
Arterial thrombosis occurs in patients with pre‐ may show dilated small bowel, mucosal thickening
existing atherosclerotic stenosis at the origin of the with ‘thumb‐printing’ or gas in the bowel wall
superior mesenteric artery. Venous thrombosis can (pneumatosis intestinalis) as a late sign. Catheter
occur in patients with hypercoagulable states. angiography is highly sensitive and specific but
Ischaemia due to hypoperfusion can occur with is usually a secondary investigation in the rare
27: Small bowel obstruction and ischaemia 247
subgroup of patients suitable for revascularisation. splenic flexure. This position is a watershed of blood
CT with arterial phase contrast can reveal an arte- supply between the middle colic and inferior mes-
rial occlusion with an associated non‐perfused enteric arteries. Because the muscle of the bowel wall
segment of bowel. However, CT does not always remains viable, the cascade of necrosis and subse-
confirm the diagnosis and exploratory laparotomy quent multiorgan failure associated with full‐
may be required on the basis of clinical suspicion in thickness ischaemia does not occur. As the ischaemic
a patient who lacks definitive imaging but is dete- mucosa sheds, bleeding occurs from the underlying
riorating physiologically. submucosa. Patients are generally older and present
with left‐sided abdominal pain, rectal bleeding, local-
ised peritonism and a high white cell count. The com-
Treatment
bination of left‐sided abdominal pain and rectal
Acute ischaemia of the small bowel carries a very bleeding strongly suggests the diagnosis. The bleeding
high mortality. Treatment may require several lapa- is rarely heavy and the symptoms usually settle within
rotomies and ICU support and the patient may be several days. Occasionally the area can develop a
left with a permanent stoma or long‐term bowel fibrous stricture in the following months and this can
dysfunction. In patients who are elderly and frail or lead to obstructive symptoms. There is rarely evi-
who have dementia, it is appropriate to discuss dence of underlying arterial stenosis as a cause.
with the patient and family the issue of setting lim-
its to treatment and possibly just focusing on good
palliation, before embarking on what may be a Further reading
complex surgical course with a poor outcome.
Chen SC, Lin FY, Lee PH, Yu SC, Wang SM, Chang KJ.
Initial resuscitation will require intravenous flu-
Water‐soluble contrast study predicts the need for early
ids and broad‐spectrum antibiotics. In most cases, surgery in adhesive small bowel obstruction. Br J Surg
bowel ischaemia will have reached an irreversible 1998;85:1692–5.
level before surgery. Usually the ischaemic segment Ellis H, Moran BJ, Thompson JN et al. Adhesion‐
is not salvageable. Thus the purpose of the opera- related hospital readmission after abdominal and
tion is to resect the non‐viable bowel before sys- pelvic surgery: a retrospective cohort study. Lancet
temic sepsis and multiorgan failure occur, and to 1999;353:1476–8.
hopefully reverse the processes of sepsis and multi- Harpreets S. Radiological evaluation of bowel ischaemia.
organ failure if they have already commenced. Radiol Clin North Am 2015;53:1241–54.
Reynolds I, Healy P, McNamara DA. Malignant tumours
In those uncommon cases where bowel viability
of the small intestine. The Surgeon 2014;12:263–70.
has not reached an irreversible level, it may be pos-
sible to perform revascularisation of the mesentery
and salvage the bowel. Revascularisation can be MCQs
performed by interventional radiology, open sur-
gery or by combined techniques. Embolectomy, Select the single correct answer to each question. The
thrombectomy, bypass or stenting may be required. correct answers can be found in the Answers section
When bowel is resected for ischaemia, primary at the end of the book.
re‐anastomosis is sometimes appropriate when
there is only a short ischaemic segment and the 1 Three days after a myocardial infarction with
patient is physiologically stable. Frequently, a sec- cardiogenic shock, a 75‐year‐old man develops
ond‐look laparotomy is planned to assess that there abdominal pain and distension. The abdomen is
has been no further ischaemia prior to re‐anasto- slightly tender with reduced bowel sounds. A plain
mosis. In some cases, too much bowel is necrotic to abdominal X‐ray shows distended small bowel
be compatible with survival. Unfortunately, all that without fluid levels. Blood tests reveal a metabolic
can be done in such cases is to close the laparotomy acidosis. The most likely diagnosis is:
incision without resection and palliate the patient. a perforated peptic ulcer
b mesenteric ischaemia
c pseudo‐obstruction of the colon
Ischaemic colitis d acute pancreatitis
e diverticulitis
This is a very different condition to full‐thickness
ischaemia of the bowel or ‘dead gut’. In the condition 2 Investigations in a patient with acute small bowel
of ischaemic colitis, there is acute mucosal ischaemia, obstruction may include the following except:
usually involving a segment of the colon near the a supine and erect abdominal radiographs
b blood urea and electrolyte estimation 4 Which of the following features of small bowel
c Gastrografin small bowel follow‐through obstruction is incorrect?
d technetium‐labelled iminodiacetic acid (HIDA) scan a colicky periumbilical pain due to stimulation of
e computed tomography of the abdomen stretch receptors relating to the midgut
b vomiting of clear, yellow, bile‐stained fluid
3 Which of the following statements regarding c minimal abdominal distension if the obstruction
neuroendocrine tumours of the small and large is proximal
bowel is incorrect? d possible bowel action some hours after the onset
a generally slow‐growing of pain
b most often found in the appendix e vomiting of brown feculent fluid if obstruction is
c responsive to treatment with tyrosine‐kinase distal
inhibitors
d not at risk of carcinoid syndrome without liver
metastases
e characterised by intense mesenteric desmoplastic
changes on CT
28 The appendix and Meckel’s
diverticulum
Rose Shakerian1 and the late Joe J. Tjandra1,2
1
2
12–24 hours. The usual sequence is anorexia,

Acute appendicitis followed by central abdominal pain, then vomiting
and finally pain in the right iliac fossa.
Acute appendicitis is the most common intra‐ The initial periumbilical pain is due to obstruc-
abdominal surgical condition that requires operation and inflammation of the appendix and is medi-
tive intervention. It has an incidence of 7–12% in ated through the visceral pain fibres as a midgut
the adult population, occurring most frequently in pain. When appendicitis becomes transmural, the
the second and third decades of life. serosa of the appendix and the parietal peritoneum
are involved, causing a localised pain mediated
through the somatic pain fibres in the right iliac
Surgical pathology fossa.
Atypical presentations may be due to the location
With acute appendicitis, organisms invade the of the inflamed appendix. These include pain in the
wall of the appendix and are lodged in the submu- right upper quadrant from a long appendix or a
cosa. Eventually, the full thickness of the wall is right loin pain from a retrocaecal appendix. Patients
involved by acute inflammation and becomes presenting with peritonitis from perforated appen-
swollen and reddened. With delay in diagnosis, dicitis have generalised abdominal pain.
the appendix becomes distended, especially if
there is obstruction of the lumen. Venous stasis Diarrhoea
and then arterial occlusion result in gangrene at
the tip of the appendix where the blood supply is This is an atypical or non‐specific feature in acute
precarious, or at the site of obstruction in the appendicitis. Diarrhoea and tenesmus are most
appendix because of pressure necrosis. Perforation likely in the presence of an inflamed pelvic appen-
may follow and can be localised by the greater dix irritating the rectal wall or a retroileal appendix
omentum and loops of small bowel or may irritating the terminal ileum. Severe and persistent
become generalised with diffuse contamination of diarrhoea is more likely to be due to gastroenteritis
the peritoneal cavity. or inflammatory bowel disease.
Signs
Clinical features
General
Symptoms With more advanced inflammation, the patient may
Abdominal pain look unwell. Moderate fever and tachycardia may be
present and reflect the underlying infective process.
The nature of the pain may be highly variable. The
most common initial presentation is a periumbili-
Local
cal gnawing pain that migrates within a few hours
to the right iliac fossa. There may be a preceding Tenderness over the site of the appendix is the
period of anorexia, nausea and vomiting that lasts most important sign of appendicitis. The tenderness
249
Box 28.1 Investigations in suspected

appendicitis
• Leucocytosis is usual in the range of 11–17 × 109/L

with a neutrophilia.
• Elevated serum C‐reactive protein (CRP) >10 mg/L
Retrocaecal combined with leucocytosis is indicative of an
Retroileal inflammatory/infective process.
• Urinalysis by ward test and microscopy is useful in
order to rule out urinary tract infection, in addition
Pelvic
to exclusion of pregnancy. However, pyuria may
occur due to irritation of the bladder or ureter by
an inflamed appendix.
Fig. 28.1 The various positions of the appendix.
• Plain abdominal X‐ray is not recommended in the
diagnostic work‐up of appendicitis.
• Ultrasound may show a thick‐walled appendix with
a dilated lumen. The sensitivity and specificity for
is localised and persistent and is classically at
appendicitis using ultrasound are 85 and 90%,
McBurney’s point (one‐third of the way from the
respectively. However, its greatest value is to rule
anterior superior iliac spine to the umbilicus),
out gynaecological pathology.
although it may vary depending on the location
• Computed tomography (CT) has a higher
of the appendix (Figure 28.1). Tenderness may be
diagnostic accuracy than ultrasound, with a
minimal early in the course of the illness and sensitivity of 95% and specificity of 96%.
hard to elicit in the obese or if the appendix is Intravenous and oral contrast administration is
retrocaecal. recommended for diagnosis of appendicitis. It
Local muscular rigidity in the right iliac fossa is allows percutaneous drainage of a localised
produced by inflammation of the parietal perito- peri‐appendiceal abscess and is useful in the
neum overlying the appendix. Subtle rigidity can evaluation of older patients as well as those with
be detected by gently moving the palpating hand atypical pain.
toward the area of maximal pain in the right iliac
fossa while talking with the patient. This helps to
differentiate true rigidity or guarding from volun-
tary spasm associated with nervousness. It is also Investigations
helpful to ask the patient to cough or to sit up
while watching the patient’s facial expression; a Investigations that are useful in the diagnosis of
grimace further suggests the presence of local suspected appendicitis are given in Box 28.1.
peritonitis.
With local peritonitis, palpation in the left lower
quadrant may cause pain in the right lower quad- Differential diagnosis
rant (Rovsing’s sign). Signs of local peritonitis may
be minimal in patients with retrocaecal or pelvic Diagnosis of appendicitis is particularly difficult
appendicitis. The psoas sign – pain caused by the with a retrocaecal appendix. The pain is not as
extension of the right hip to stretch the psoas severe as that associated with abdominal or pelvic
muscle – is generally present in retrocaecal appen- appendicitis and it does not always localise to the
dicitis. Pelvic appendicitis is often difficult to dif- right iliac fossa. The pain vaguely localises to the
ferentiate from pelvic inflammatory disease but is right side of the abdomen and rarely to the right
usually associated with a right‐sided tenderness on flank or right upper quadrant. In neglected cases, a
rectal examination. retrocaecal abscess develops as a result of perfora-
Patients who present late with appendicitis tion of the appendix.
may have generalised tenderness and rigidity, Diagnosis in the elderly is often delayed because
indicating perforation and peritonitis. Rebound of late and less typical presentation. The incidence
tenderness indicates peritoneal inflammation and of perforation is therefore higher. In patients aged
is best elicited by percussion. The delayed presen- over 40 years, underlying malignancy needs to be
tation of a tender, inflammatory appendiceal considered and excluded.
mass may occur in the right iliac fossa after three During pregnancy, the appendix may be displaced
or more days. cephalad by the gravid uterus. In the second
28: The appendix and Meckel’s diverticulum 251
trimester of pregnancy, the appendix is displaced Other conditions

upwards to the right upper flank. Appendicitis may
Bacterial or viral gastroenteritis causes vomiting,
be confused with pyelonephritis, as pyuria is com-
profuse diarrhoea and diffuse abdominal pain
mon during pregnancy. Owing to abdominal laxity,
without localised tenderness. Diarrhoea associated
the abdominal findings are also less acute. Mild leu-
with appendicitis is rarely prolonged or severe.
cocytosis is also a normal physiological response in
Non‐specific ileitis may be secondary to Yersinia or
pregnancy.
Campylobacter infection.
Perforated caecal carcinoma with a pericolic
Mesenteric adenitis
abscess may mimic appendicitis, but the patients
About 5% of patients undergoing an appendicec- are usually elderly.
tomy for ‘acute appendicitis’ are found to have Acute cholecystitis may be confused with a high
mesenteric adenitis. The patient has clinical features retrocaecal appendicitis.
similar to those of appendicitis, but the appendix is Diverticulitis of a long redundant sigmoid colon
normal and there are several enlarged lymph nodes lying on the right of midline may cause confusion.
in the mesentery of the terminal ileum. Rarely, a solitary caecal diverticulum becomes
The condition is most common in children. Some inflamed; this is usually seen in Asian patients.
have a history of a recent sore throat together with Meckel’s diverticulitis is rare and the diagnosis is
a high fever. There is no muscle rigidity on presenta- usually made at surgery.
tion. The cause of the illness is obscure but is self‐
limiting, with spontaneous improvement over
24–36 hours. Ultrasound is recommended to make
the diagnosis and exclude appendicitis in this
Management
patient population.
If the diagnosis is clear, an appendicectomy is
Gynaecological conditions performed. If the diagnosis is suspected but not
definite, a period of observation (usually in hospi-
Mittelschmerz pain occurs at mid‐menstrual cycle tal) is appropriate. Over the following 12–24 hours,
from the rupture of a follicle at ovulation. Fever is the nature of the illness should clarify itself.
uncommon and most patients have had previous Acute appendicitis is routinely managed with
painful ovulation. combination of intravenous antibiotics and surgery.
In pelvic inflammatory disease, including salpin- Clinically stable patients with computed tomogra-
gitis and tubo‐ovarian abscess, there is a longer phy (CT) diagnosis of uncomplicated appendicitis
duration of symptoms, higher fever, greater leucocy- (absence of faecalith and perforation) can be
tosis and more pelvic pain. Gonococcal and managed conservatively with intravenous antibiotics
chlamydial infection are the most common causes. only. Approximately 20% of these patients fail con-
Careful gynaecological history and examination are servative management and can re‐present with ongo-
helpful. ing abdominal pain, requiring surgical intervention.
Torsion of a fallopian tube and torsion or haem- Laparoscopic appendicectomy has replaced open
orrhage of an ovarian cyst tend to present with pain surgery as the operative approach of choice. The
of sudden onset. Pelvic examination and ultrasound benefits of laparoscopic surgery include smaller
will help with the diagnosis. skin incisions, reduced postoperative pain, earlier
Ectopic pregnancy needs to be excluded early in discharge and resumption of normal activities.
any patient presenting with abdominal or pelvic Additionally, where the diagnosis is unclear despite
pain, with or without abnormal vaginal bleeding. A a period of observation, a laparoscopic approach
positive pregnancy test (urine or serum) in the enables assessment of the intra‐abdominal organs
absence of an intrauterine pregnancy on ultrasound and exclusion of gynaecological conditions such as
is highly suggestive of an ectopic pregnancy. pelvic inflammatory disease.
Alternatively, an appendicectomy can be per-
Urological conditions
formed as an open procedure. A skin crease incision
Urinary tract infection presents with urinary symp- is made over the point of maximal tenderness in the
toms and rigors. Lack of abdominal rigidity and right iliac fossa. Under anaesthesia, a mass may be
presence of pus and organisms in the urine indicate palpable. The external and internal oblique muscles
the diagnosis. Right ureteric colic may cause confu- are split. The caecum is identified and the appendix
sion but the radiation of pain and haematuria is traced at its base on the posteromedial aspect.
should give the diagnosis. The mesoappendix is ligated and divided. The base
of the appendix is ligated and transected. The

appendix stump may be inverted using a purses-
Clinical syndromes
tring in the caecum, although there is no firm evi-
Bleeding peptic ulceration adjacent to ectopic
dence to suggest that this is necessary. All patients
gastric epithelium is found. This usually occurs in
should receive prophylactic antibiotics adminis-
young patients.
tered preoperatively, usually in the form of a
Small bowel obstruction due to intussusception
second‐ or third‐generation cephalosporin and met-
may occur. The apex of intussusception is usually
ronidazole. When there is severe sepsis, a full course
the inflamed heterotopic tissue at the mouth of the
of 5 days of therapy is recommended.
diverticulum. Obstruction of the small bowel may
Patients presenting late may have a right iliac fossa
also be caused by the presence of a band between
mass. A CT scan is performed to determine whether
the apex of the diverticulum and the umbilicus,
it is an abscess or a phlegmon. If an abscess is present,
causing kinking or volvulus.
it is drained percutaneously under CT guidance. This
Meckel’s diverticulitis is usually due to lodge-
obviates the need for surgery in most cases in patients
ment of enteroliths or a sharp foreign body in the
with active sepsis. An appendiceal phlegmon is
diverticulum or narrowing of the mouth of the
treated with bowel rest and intravenous antibiotics.
diverticulum. The clinical features are similar to
Non‐operative therapy is successful in 85% of cases
those of appendicitis. Perforation may occur, caus-
and most patients are sent home after 7–10 days.
ing generalised peritonitis.
Interval appendicectomy is no longer advocated
Gastric heterotopia may cause peptic ulcer‐like
as routine treatment for appendiceal phlegmon. In
symptoms, with meal‐related pain around the
patients older than 40 years, a follow‐up colonos-
umbilicus because of its midgut location.
copy is recommended to exclude underlying malig-
nancy. Otherwise in the absence of clinically
significant symptoms, no further investigations or Diagnosis
follow‐up is required.
Meckel’s diverticulum is more likely to be discovered
incidentally during abdominal surgery for another
Meckel’s diverticulum condition. Where it is believed to be the cause of
gastrointestinal bleeding, particularly in younger
Meckel’s diverticulum is a congenital condition that patients, a Meckel’s scan should be performed. This
arises from failure of embryonic obliteration of the is a nuclear medicine study in which technetium‐
omphalo‐mesenteric duct connecting the fetal gut to 99m pertechnetate is used intravenously to localise
the yolk sac. As distinct from other small bowel heterotopic gastric mucosa in Meckel’s diverticulum.
diverticula, Meckel’s diverticulum is antimesenteric, Another useful investigation tool is CT angiography
contains all coats of the bowel and has its own which can detect active signs of bleeding that may be
blood supply (Figure 28.2). It is present in 2% of the difficult to detect with other techniques.
population and is commonly within 1 m of the ile- When the clinical presentation is due to obstruc-
ocaecal valve. In 20% of cases, the mucosa contains tive or inflammatory complications of Meckel’s
heterotopic epithelium of gastric, colonic or pancre- diverticulum, CT of the abdomen with oral and
atic origin. Symptomatic cases are usually males. intravenous contrast can be helpful in making the
diagnosis.
Treatment
Complicated or symptomatic Meckel’s diverticu-

lum should be treated with resection of the segment
of the small bowel containing the diverticulum.
Incidental Meckel’s diverticulum found at lapa-
rotomy is usually left alone because most remain
asymptomatic. Any band to the umbilicus or other
viscus is divided. Resection is considered in children
younger than 2 years; with the presence of palpable
heterotopia (especially in males); and with evidence
Fig. 28.2 Meckel’s diverticulum. of prior Meckel’s diverticulitis, such as adhesions.
28: The appendix and Meckel’s diverticulum 253
b may present as a wound infection

Further reading c is reduced by prophylactic perioperative
antibiotics
Kotha VK, Khandelwal A, Saboo SS et al. Radiologist’s
perspective for the Meckel’s diverticulum and its com-
d is increased by laparoscopic rather than open
plications. Br J Radiol 2014;87(1037):20130743. appendicectomy
Lamb P. Acute conditions of the small bowel and appen- e is most often associated with anaerobic
dix. In: Paterson‐Brown S (ed.) Core Topics in General bacteria
and Emergency Surgery, 5th edn. Edinburgh: Saunders
Elsevier, 2014. 3 Which of the following statements about Meckel’s
Poon SHT, Lee JWY, Ng KM et al. The current manage- diverticulum is incorrect?
ment of acute uncomplicated appendicitis: should there a may cause small bowel obstruction due to
be a change in paradigm? A systematic review of the intussusception
literatures and analysis of treatment performance.
b may be located in the mesenteric border of the
World J Emerg Surg 2017;12:46.
small bowel
Sauerland S, Jaschinski T, Neugebauer EA. Laparoscopic
versus open surgery for suspected appendicitis. Cochrane c may present with meal‐related central abdominal
Database Syst Rev 2010;(10):CD001546. pain
d may present with melaena and a normal upper
gastrointestinal endoscopy
MCQs e may be diagnosed with technetium‐99m
pertechnetate scan in some cases
correct answers can be found in the Answers section 4 Which of the following statements concerning
at the end of the book. acute appendicitis is incorrect?
a the diagnosis can be made based on history and
1 Right iliac fossa pain and nausea in a 62‐year‐old clinical examination alone, in the appropriate
woman may be due to the following except: patient
a acute appendicitis b elevated CRP and white cell count can be
b caecal cancer indicative of the condition
c urinary tract infection c plain abdominal X‐ray is a standard investigation
d Mittelschmerz pain tool
e sigmoid diverticulitis d in patients aged over 40, CT scan is recommended
to exclude underlying malignancy
2 Which of the following statements about sepsis e urinalysis should be routinely performed
associated with appendicectomy for acute
appendicitis is incorrect?
a may present with a pelvic abscess
29 Inflammatory bowel disease
Susan Shedda1, Britt Christensen2 and the late
Joe J. Tjandra1,3
1
Department of Surgery, Royal Melbourne Hospital, Melbourne, Victoria, Australia
2
Inflammatory Bowel Disease Unit, Department of Gastroenterology, Royal Melbourne Hospital,
3
mucosa. The glandular structure is distorted, with

Introduction goblet cell depletion and crypt abscesses. In chronic
quiescent phases, the glands may be shortened and
Inflammatory bowel disease comprises a group of
atrophic, although the endoscopic appearances
inflammatory diseases of unknown aetiology which
may be relatively normal.
vary in distribution from the colon and rectum
In severe disease the differentiation between ulcera-
alone in ulcerative colitis to any part of the gastro-
tive colitis and Crohn’s disease is difficult. In fulminant
intestinal tract in the case of Crohn’s disease. These
cases, the colitis is transmural, with deep ulceration
conditions can have a wide spectrum of disease
and fissures. The histopathology can be confusingly
activity. Their treatment requires a multidiscipli-
similar to that of Crohn’s disease. In some cases, diag-
nary approach where both medical treatment and
nosis is made only after the rectum is removed or
surgery interplay to maximise the outcome for
when Crohn’s disease appears in the small bowel or
patients.
the perianal region. Sometimes, the diagnosis remains
uncertain and is labelled as ‘indeterminate colitis’.
Ulcerative colitis Colitis and dysplasia
Ulcerative colitis occurs most commonly in temper- Long‐standing colitis (whether Crohn’s or ulcera-
ate climates and in Caucasians. It is rare in Africa tive colitis) may be associated with dysplasia of the
and the East. Ulcerative colitis is about two to three epithelium. The incidence of dysplasia in long‐
times more common than Crohn’s disease, although standing total colitis is probably around 5–10%.
the incidence of Crohn’s disease is increasing. The The risk for cancer in colitis increases with the
disease is usually diagnosed between 15 and 45 years extent and duration of the disease. For pancolitis,
of age. The aetiology of ulcerative colitis is uncertain, the risk for cancer is 3% at 10 years, rising by
although familial clusters occur and some, as yet 1–2% per year thereafter. Colonoscopic surveil-
unknown, environmental factors may be relevant. lance with multiple biopsies is generally com-
menced after 7 years of disease in patients with
disease beyond the sigmoid, at 2‐year intervals.
Pathology The risk of cancer rises significantly with the
presence of a dysplasia‐associated mass lesion (a
Ulcerative colitis is a mucosal disease that almost plaque or large polyp) or stricture. The tumours are
invariably affects the rectum and spreads proxi- more likely to be multiple and more likely to occur
mally in a continuous manner. Inflammation is lim- in the right or transverse colon. Carcinoma in ulcer-
ited to the mucosa except in fulminant cases, where ative colitis may occur in flat mucosa and may not
transmural changes may occur. The mucosa is con- be easily visible on colonoscopy. This fact provides
gested and friable, with varying degrees of ulcera- a strong argument for routine use of biopsy.
tion. Microscopy shows diffuse infiltration of acute Biopsy specimens are taken from specific lesions
and chronic inflammatory cells limited to the and from random sites of the colon. The risk of
255
cancer in patients with left‐sided colitis is much exacerbation of pre‐existing ulcerative colitis, it can
lower but rises sharply after 25–30 years of disease. present as the first manifestation of colitis.
Acute toxic colitis is characterised by the abrupt
onset of bloody diarrhoea, urgency, anorexia and
Clinical features abdominal cramps. Patients are often ill with severe
anaemia and dehydration. A patient is regarded as
The clinical features depend on the severity and ‘toxic’ when, in addition to severe colitis, there is
extent of colitis and have a natural history of periods evidence of at least two of the following:
of exacerbation and remission (Box 29.1). Extra‐ • tachycardia above 100 beats/min
intestinal manifestations are listed in Box 29.2. • temperature above 38.6°C
The most common presentation is bloody diar- • leucocytosis more than 10.5 × 109/L
rhoea in an otherwise fit patient. Patients with • hypoalbuminaemia below 3.0 g/dL.
proctosigmoiditis may complain of tenesmus as Other features commonly present include stool
well. More severe disease with extensive colonic frequency of more than nine per day, abdominal
involvement may cause severe diarrhoea with distension, tenderness, mental changes, electrolyte
abdominal cramps and urgency at stool. Endoscopy disturbances (hyponatraemia, hypokalaemia) and
shows a confluent proctitis with mucosal friability, alkalosis.
contact bleeding, ulceration and granularity. Abdominal distension often indicates colonic dil-
atation, and tenderness suggests impending perfora-
Acute toxic colitis tion or ischaemia. Toxic dilatation or megacolon is
usually defined as a diameter exceeding 6 cm in the
Toxic colitis and toxic megacolon are part of the
transverse colon on plain abdominal X‐ray. Signs of
spectrum of severe ulcerative colitis and are more
septicaemia may be masked by using steroids.
common in patients with pancolitis. While acute
fulminating colitis usually occurs as an acute
Investigations
Box 29.1 Spectrum of ulcerative colitis Colonoscopy

• Proctitis Characteristic appearances include an erythema-
• Proctosigmoiditis tous mucosa with contact bleeding. The normal
• Acute ulcerative colitis vascular pattern is lost and there may be blood and
• Chronic ulcerative colitis pus in the lumen. Biopsies are taken to establish the
• Relapsing chronic ulcerative colitis extent of the disease and the presence of dysplasia.
• Complicated ulcerative colitis A full colonoscopy may not be performed in acute
⚬⚬ Toxic colitis/toxic megacolon colitis because of the risk of perforation.
⚬⚬ Perforation
⚬⚬ Haemorrhage General investigations
⚬⚬ Dysplasia/carcinoma
• Extra‐intestinal manifestations General investigations include full blood examina-
tion, C‐reactive protein (CRP) and liver function test.
Box 29.2 Extra‐intestinal manifestations Therapy for chronic ulcerative colitis

of ulcerative colitis
Before initiating therapy for ulcerative colitis,
Present with active disease
• Skin: erythema nodosum, pyoderma gangrenosum
assessment of disease extent by colonoscopy is
• Mucous membranes: aphthous ulcers of mouth required. Disease extent is usually defined by the
and vagina Montreal System as:
• Eyes: iritis • proctitis (E1, limited to rectum)
• Joints: flitting arthralgia/arthritis of large joints • left‐sided disease (E2, extending up to the splenic
flexure)
Present independent of disease activity
• pancolitis (E3, disease beyond the splenic
• Joints: sacroiliitis, ankylosing spondylitis
flexure).
• Hepatobiliary: chronic active hepatitis, cirrhosis,
There are many therapies available for ulcerative
sclerosing cholangitis
colitis. These can generally be broken down into
29: Inflammatory bowel disease 257
three major categories: aminosalicylates, immu- Side effects from sulfasalazine are more com-
nomodulators and biological agents. mon than with other aminosalicylates but sul-
fasalazine is cheaper and may be more effective for
joint pains. One‐fifth of patients will have side
Sulfasalazine and aminosalicylates
effects to sulfasalazine, which can include dyspep-
Sulfasalazine and the aminosalicylates are com- sia, nausea, anorexia and headache. In addition,
monly used to treat ulcerative colitis and have anti‐ due to the sulfa component, allergic reactions
inflammatory activity by inhibiting the formation (rash or fever), haematological side effects (hae-
of prostaglandins. They are available in both oral molysis or neutropenia) and sperm abnormalities
and topical forms. can occur. Sulfasalazine also affects folate absorp-
Sulfasalazine is composed of sulfapyridine and tion, so for females it is important to educate
5‐aminosalicylate (5‐ASA) joined by an azo‐bond. about folate supplementation in regard to preg-
5‐ASA is the active therapeutic moiety and acts by nancy planning.
inhibiting prostaglandin synthesis. The sulfapyri- If patients are intolerant of sulfasalazine, the
dine alone has no therapeutic effect and is responsi- aminosalicylate medications can be used. Side
ble for most of the side effects. A small amount effects are rarer and consist usually of headache,
(approximately 20%) is absorbed by the small diarrhoea and nausea. Aminosalicylates can also
bowel and most of the sulfasalazine enters the rarely exacerbate colitis.
colon, where the azo‐bond is cleaved by colonic
bacteria. 5‐ASA is poorly absorbed from the colon
Corticosteroids
and remains intraluminal, where it exerts the thera-
peutic effects. Sulfapyridine is absorbed and metab- If patients remain symptomatic despite maximal
olised by the liver. The 5‐aminosalicylates are better doses of aminosalicylates, escalation of therapy
tolerated than sulfasalazine and are prescribed with oral corticosteroids can be used to induce
when patients demonstrate intolerance to sulfasala- remission. This is usually achieved with oral predni-
zine or allergy to sulfa drugs. There are several for- solone at a dose of 40 mg daily for several weeks
mulations of 5‐ASA available which have specific and slowly weaned over a month or two.
formulations and dosage schedules. Intravenous corticosteroids can be used in more
For patients with proctitis or proctosigmoiditis, severe disease. Corticosteroids are effective at
topical therapy is possible and is more effective inducing remission but are not used to maintain
than treatment with oral aminosalicylates alone. 5‐ remission due to lack of efficacy and significant
ASA suppositories and/or enemas are given rectally side effects. Side effects include moon facies, weight
and induce remission in more than 90% of patients gain, mood swings, sleep disturbance, diabetes and
with mild to moderate proctitis or proctosigmoidi- increased infection risk with short‐term use; and
tis. In mild disease confined to the rectum, topical osteoporosis, aseptic necrosis, adrenal suppression
mesalazine given by suppository is the preferred and cataracts with long‐term use.
therapy. Suppositories only act in the distal 5–8 cm Budesonide is a potent corticosteroid that under-
of the rectum. Enemas and foams are less effective goes first‐pass metabolism by the liver and there-
for proctitis because their concentration in the rec- fore is associated with minimal systemic side effects
tum rapidly diminishes. when used enterally. It has been found to be safe,
In patients with more extensive disease, however, efficacious and well tolerated for inducing remis-
foam enemas can treat the mid‐sigmoid colon and sion in patients with mild‐to‐moderate disease.
liquid enemas reach the splenic flexure. In these
patients, a combination of a mesalazine supposi-
Immunomodulators
tory and an enema may be more effective. Treatment
is required for at least 4–6 weeks intensely, fol- If patients require more than one course of oral cor-
lowed by a gradual taper as tolerated. For patients ticosteroids in a year despite optimisation of their
who are more symptomatic, who have disease oral and topical 5‐aminosalicylate therapy or if
extending more proximally or who fail to respond patients are steroid‐dependent, a steroid‐sparing
to topical therapy, a combination of oral and topi- agent is necessary.
cal therapy has been found to be more effective The thiopurines azathioprine (dose 2–2.5 mg/day)
than either one alone. Higher doses are used to and 6‐mercaptopurine (1–1.5 mg/day) are the most
induce remission and once remission is achieved commonly used immunomodulators in ulcerative
doses are decreased. After remission, long‐term colitis. Before commencing therapy, a genetic test
maintenance therapy is encouraged. for thiopurine S‐methyltransferase (TPMT) activity
Table 29.1 Pre‐immune suppression screen.
Testing before immunomodulator Testing before biologics
Thiopurine S‐methyltransferase (TPMT) As for immunomodulator

phenotype or genotype Interferon‐γ assay for tuberculosis (e.g. QFN‐gold)
Hepatitis B sAg/cAb Chest X‐ray
Hepatitis C Ab
HIV serology
Varicella serology
should be undertaken, as patients with no activity injection every 2 weeks, golimumab by injection
are at risk of severe myelosuppression, which can every 4 weeks and infliximab is an intravenous
result in sepsis and even death. In addition, prior to infusion. Both have similar efficacy with response
commencing therapy with an immunomodulator, rates of approximately 80%. Combination therapy
patients should have a pre‐immune suppression with a thiopurine results in the highest response
screen (Table 29.1) and have their vaccination status rates and decreases the risk of anti‐drug antibody
assessed and updated. Patients cannot receive live formation, which can result in loss of response.
vaccines while on these medications. These medications are well tolerated but patients
Immunomodulators are slow‐acting and require require close monitoring. Adverse events include
at least 3 months of therapy to assess efficacy. They skin injection site reactions or infusion reactions,
are therefore not ideal agents for inducing remission increased risk of infection, demyelinating disease,
but are routinely used to maintain remission after heart failure, psoriasis, malignancy or a lupus‐like
induction with corticosteroids. 6‐Mercaptopurine is reaction.
the prodrug of azathioprine and may be better toler-
ated in patients who suffer from side effects with
azathioprine. Both drugs can be optimised with test- Anti‐integrin agent: vedolizumab
ing of thiopurine metabolite levels.
Vedolizumab acts by blocking the α4β7 integrin, pre-
Although these agents have potentially serious
venting the migration of leucocytes into the gut. It is
side effects, adverse events associated with lower
administered intravenously. It appears to be slower‐
doses used in treating inflammatory bowel disease
acting than anti‐TNF therapy but still works more
are infrequent. Patients can initially experience
quickly than the thiopurines. Its advantage is that it
nausea, vomiting or headaches which often subside.
is very safe and is a good option in patients with a
Pancreatitis (3% of patients), leucopenia (2%) and
previous cancer or any infection risk. Side effects are
abnormal liver function tests (5%) are the most
minimal but include flu‐like symptoms, joint pains,
common more serious side effects that can warrant
headaches and increased sinus infections.
treatment cessation. These agents increase the risk
of non‐Hodgkin’s lymphoma and non‐melanoma
skin cancer.
Janus kinase inhibitors: tofacitinib
Biological agents Tofacitinib is an oral selective janus kinase (JAK)
inhibitor. JAKs are enzymes that are involved in
In patients who are steroid‐refractory or steroid‐
activating the body’s immune response, and by
dependent despite thiopurines, up‐titration to a
blocking this tofacitinib may stop the inflammatory
biological agent is required. There are two major
process in ulcerative colitis. It is fast‐acting and
groups currently available, the anti‐tumour necro-
effective at inducing and maintaining remission in
sis factor (TNF) agents (adalimumab and inflixi-
patients with moderate to severe ulcerative colitis
mab) and the anti‐integrin agent vedolizumab.
who have failed other biological therapies or are
biological therapy‐naive. The most common side
effects include diarrhoea, headache, nasopharyngi-
Anti‐TNF agents: adalimumab, golimumab
tis and upper respiratory tract infections. It can also
and infliximab
increase the risk of infections and malignancy, and
Anti‐TNF agents are fast‐acting and effective at because of an increased risk of shingles patients
inducing remission in patients with moderate to should be vaccinated with the shingles vaccine if
severe ulcerative colitis. Adalimumab is given by possible before initiation.
used for elective surgery but are contraindicated

Surgical management in emergency surgery. Prophylaxis for deep vein
thrombosis is prescribed.
Indications for surgery
Acute illness Surgical options
Evidence of free perforation, generalised peritonitis Restorative proctocolectomy
and massive colonic haemorrhage indicates the
Restorative proctocolectomy entails removal of the
need for emergency surgery. Surgery is indicated
entire colon and rectum. A J‐pouch is constructed
with deterioration of acute colitis (increasing toxic-
using loops of the terminal 40–50 cm of ileum to
ity or colonic dilatation) at any time after initiation
replace the rectum and is anastomosed to the upper
of adequate medical management. If the improve-
anal canal (Figure 29.1).
ment has been minor after 5–7 days of adequate
The double stapled J‐pouch leaves approximately
medical management, a long‐term remission is
2 cm of distal rectal mucosa in the anal canal. In
unlikely. In these cases, surgery is also recom-
certain circumstances, this small amount of mucosa
mended in conjunction with management by the
needs to be removed and therefore a mucosectomy
gastroenterologist. With adoption of more aggres-
and hand‐sewn anastomosis between the J‐pouch
sive resuscitation, a coordinated plan of manage-
and the proximal anal canal is fashioned.
ment and early operative intervention, mortality is
After consideration of the comorbidities, includ-
less than 3%. In contrast, colonic dilatation compli-
ing degree of immunosuppression and operative
cated by perforation has a mortality of 33%. About
half the patients with acute fulminating colitis
respond to medical therapy, thereby avoiding emer-
gency surgery.
Chronic illness
The main indication for elective surgery is chronic ill-
ness that responds poorly to medical treatment or
recurrent acute colitis. The threshold for surgery by
gastroenterologists and patients is variable. Sphincter‐
preserving restorative proctocolectomy may now
avoid the presence of a permanent stoma and there-
fore increase its acceptance. Severe extra‐intestinal
manifestations are rare indications for surgery.
Cancer risk
Dysplasia is currently the most sensitive marker of
premalignancy. The presence of dysplasia from a vil-
lous or polypoidal lesion or from a stricture is an indi-
cation for prophylactic proctocolectomy. The presence
of severe dysplasia from an area of flat mucosa at two
separate sites in the colon is also an indication for sur-
gery. The presence of low‐grade dysplasia in flat
mucosa may require surgery due to concerns regard-
ing the underlying malignancy risk of 1–2%.
Preoperative preparation
The patient and the family are counselled jointly by
the gastroenterologist and colorectal surgeon. The
need for a stoma is discussed and the stoma site is
marked preoperatively. Immunosuppression is min-
imised and broad‐spectrum antibiotic prophylaxis
is used. Mechanical bowel preparations may be Fig. 29.1 A stapled ileal pouch–anal anastomosis.
conditions, a temporary diverting loop ileostomy is adolescence without a stoma or until conversion to
generally performed. The loop ileostomy is then a pouch.
reversed through a small parastomal incision about
3 months later. In selected ‘healthier’ patients, a Emergency surgery for severe acute colitis
diverting stoma may safely be omitted if the surgery
The optimal operation is subtotal colectomy and
proceeds smoothly.
end‐ileostomy (Figure 29.2) because it avoids a pel-
Specific postoperative complications include pel-
vic dissection in an unwell patient and because it
vic sepsis, with or without anastomotic breakdown,
allows the later possibility of restorative surgery.
adhesive small bowel obstruction and ileostomy‐
Restorative proctocolectomy in the emergency set-
related problems. Overall, 80% recover unevent-
ting is associated with a higher operative morbidity,
fully and 20% experience some morbidity.
especially in patients on high‐dose steroids, and
Functional results following restorative procto-
should be avoided. It would seem perverse to not
colectomy continue to improve within the first 18
remove what is often the most diseased segment of
months after surgery. Most patients defecate five to
bowel, but the aim of surgery in these circumstances
six times daily and will be able to defer defecation
is to reduce the inflammatory load or remove the
without urgency. Few patients suffer severe faecal
bowel which is perforated. In the acute situation, it
incontinence, although minor faecal spotting occurs
is often unclear as to whether the final diagnosis
in up to 25% during the day and 40% at night.
will be ulcerative colitis or Crohn’s disease.
Some 50% of patients use antidiarrhoeal or bulk-
ing agents at least intermittently.
Major failure requiring excision of the pouch
occurs in only 2% of patients. The usual causes are
persistent pelvic sepsis, unsuspected Crohn’s dis-
ease or faecal incontinence.
Long‐term sequelae of the ileal pouch include
‘pouchitis’, a syndrome associated with pouch dys-
function. This may manifest as an increase in the
number of bowel actions per day or poor emptying
of the pouch. It may be associated with endoscopic
and histologic evidence of inflammation of the ileal
pouch. Treatment of pouchitis is empirical. Most
cases respond to ciprofloxacin or metronidazole.
Some require long‐term low‐dose antibiotics to
control symptoms. Enemas containing steroid or
5‐ASA can be used. In very severe cases, Crohn’s
disease must be excluded.
Complete proctocolectomy and permanent

end‐ileostomy
With the advent of restorative surgery, complete
proctocolectomy and permanent end‐ileostomy is
currently indicated only in elderly patients with
incontinence, in patients with advanced‐stage rectal
cancer and in those unwilling to undergo the more
complicated restorative proctocolectomy.
Colectomy with ileorectal anastomosis

Fig. 29.2 Abdominal colectomy for toxic megacolon.
Colectomy with ileorectal anastomosis is rarely
Lateral view showing the end‐ileostomy and the
performed because it leaves the rectum with a con-
implanted rectosigmoid stump. Source: Tjandra JJ. Toxic
tinuing risk for inflammation and cancer. It might colitis and perforation. In: Michelassi F, Milsom JW (eds)
be considered in patients with coexisting severe Operative Strategies in Inflammatory Bowel Disease.
portal hypertension where rectal dissection is haz- New York: Springer‐Verlag, 1999:239. Reproduced with
ardous or in children to allow them to pass through permission of Springer Nature.
The best method to manage the distal stump is to formation of pseudopolyps. Fistulas and abscesses
staple‐transect the distal sigmoid colon at a level result from full‐thickness penetration of the ulcers.
where it will lie without tension in the subcutane- The bowel wall may become thickened with fibrosis,
ous plane, at the lower end of the midline incision. leading to stricture formation.
This technique avoids a troublesome discharging Perianal Crohn’s disease includes large oedema-
mucous fistula but allows for discharge of blood tous skin tags, deep fissures, perianal fistulas and
and pus through the wound should the distal stump abscesses.
break down. It also allows the rectum to be easily The histological appearance varies depending on
identified at a future laparotomy. the severity of the disease, but a lymphocytic infil-
trate is usually seen in all layers of the bowel. Non‐
caseating granulomas are noted in about 50% of
Crohn’s disease surgical specimens.
In 1932, Crohn and his colleagues described an

inflammatory disease of the terminal ileum character- Crohn’s disease and cancer
ised by ulceration and fibrosis with frequent stenosis
and fistula formation. They called it ‘regional ileitis’. It The risk of gastrointestinal malignancy in Crohn’s
was later recognised that a similar inflammatory pro- disease is increased. The small bowel cancers are
cess could also affect the colon and perianal region. predominantly adenocarcinomas in the distal small
The cause of Crohn’s disease remains unknown, bowel and the tumours have a poor prognosis.
although immunological mechanisms play a role in Long‐standing Crohn’s colitis has a similar risk of
the pathogenesis of mucosal inflammation. dysplasia and malignancy as ulcerative colitis.
Crohn’s disease is a disease of young adults. The Clinical manifestations
age at which Crohn’s disease is first diagnosed Patterns of intestinal involvement in Crohn’s disease
peaks between 20 and 29 years, with a second are often separated into three main categories: colonic
smaller peak between the ages of 60 and 80 years. (25%), ileocolic (40%) and small intestine alone
(30%). Duodenal involvement occurs in only about
2%. The symptoms depend on the location of disease.
Pathology Extra‐intestinal manifestations are similar to
those described for ulcerative colitis (see Box 29.2).
Crohn’s disease can affect any part of the gastroin-
testinal tract. Multiple areas may be involved with
intervening areas of normal bowel, referred to as Small intestinal Crohn’s disease
skip areas (Figure 29.3). The mesentery is thickened
and the mesenteric fat creeps along the sides of the Clinical features
bowel wall toward the antimesenteric border. This is The most common symptoms of small intestinal
termed ‘fat wrapping’. The disease involves all layers Crohn’s disease are diarrhoea (90%), abdominal
of the bowel wall. Ulcerations range from small shal- pain (55%), anorexia, nausea and weight loss.
low aphthous ulcers to deep fissuring ulcers. The fis- Malaise, lassitude and anaemia are frequently pre-
suring of the mucosa and submucosal oedema can sent. Most patients present with long‐standing
give the bowel a cobblestone appearance with the symptoms. Some patients present acutely with a
complicated episode such as obstruction, inflamma-
tory phlegmon, intra‐abdominal abscess or fistula.
Occasionally, the initial presentation is with a more
acute history of right iliac fossa pain and fever, and a
misdiagnosis of acute appendicitis is made. The true
diagnosis is revealed only at operation. Careful ques-
tioning often reveals a more chronic history that sug-
gests Crohn’s disease. Complications of small
intestinal Crohn’s disease are given in Box 29.3.
Investigations
Fig. 29.3 Short strictures of the small bowel separated Computed tomography (CT) or magnetic resonance
by normal skip areas. imaging (MRI) enteroclysis defines the mucosal
Medical management
Box 29.3 Complications of Crohn’s
disease There is no cure for Crohn’s disease and ongoing
disease activity can lead to multiple complications
• Obstruction from fibrous stricture or inflammatory including strictures and fistulating disease. It is
oedema therefore important to treat inflammation in
• Fistulas to neighbouring loops of small or large
patients with Crohn’s disease.
bowel, or to bladder or vagina
• Perforation and intra‐abdominal abscesses
• Massive haemorrhage Aminosalicylates
• Gallstones, especially if the terminal ileum has been
Aminosalicylate medications have, if any, only
resected for the disease. This is due to interruption
minimal efficacy in Crohn’s disease. These agents
of the enterohepatic circulation and eventual
should only be used in patients with very mild dis-
depletion of bile salts
ease with no risk of complications. Most expert
• Right ureteric involvement from ileocolic phlegmon
may lead to a recurrent pyelonephritis or a right
guidelines do not recommend using these agents.
hydronephrosis. Renal stones, especially oxalate
stones, are common, especially in the presence of Corticosteroids
steatorrhoea
As in ulcerative colitis, corticosteroids are the main-
• Adenocarcinoma of the small bowel, usually in the
terminal ileum
stay of treatment in Crohn’s disease for inducing
• Colonic dysplasia and malignancy remission. Prednisolone is usually commenced at
40 mg daily and slowly weaned; however, in
patients with less severe disease restricted to the ter-
minal ileum and ascending colon, controlled ileal‐
release budesonide can also be used. Corticosteroids
should not be used for maintenance of remission in
Crohn’s disease due to side effects (see ulcerative
colitis section) and lack of efficacy.
Immunomodulators: azathioprine, 6‐
mercaptopurine and methotrexate
Most patients who have Crohn’s disease, unless it is
very mild, will require an immunomodulator. As in
ulcerative colitis, azathioprine and 6‐mercaptopu-
Fig. 29.4 Computed tomography scan showing thick‐ rine are the most commonly prescribed agents and
walled bowel loops in a patient with recurrent Crohn’s are used in a similar fashion, with the same dosing
disease after a prior ileocolic resection.
and monitoring. These agents are slow‐acting and
response usually takes more than 3 months.
pattern in detail and therefore demonstrates aph- Methotrexate is also an option for patients with
thous ulcers, fissures and mucosal oedema. Crohn’s disease who are intolerant of, or do not
Colonoscopy enables a full assessment of the colon. respond to, thiopurines. Methotrexate is an antime-
Focal inflammation and granulomas can be seen his- tabolite medication that is given once weekly. It can
tologically even when the mucosa is macroscopically take up to 3 months to see a response. To guarantee
normal. Colonoscopy may also allow biopsy of the bioavailability, the recommended dose is 25 mg
terminal ileal orifice when the radiological appear- intramuscularly each week and patients require
ances of the terminal ileum are not conclusive. folic acid supplementation to reduce side effects,
CT may demonstrate internal fistulas, intra‐ which commonly include nausea, vomiting and
abdominal abscesses and thickening of the bowel fatigue. These can be dose‐dependent and often
wall (Figure 29.4). improve with time. Methotrexate can also cause
Symptoms in Crohn’s disease may be due to bone marrow suppression, opportunistic infections,
active inflammation or obstruction or result interstitial pneumonitis and hepatotoxicity. Patients
from previous surgery or bacterial overgrowth. need to avoid excessive alcohol intake, as this can
Laboratory tests including full blood examination, result in cirrhosis. Importantly, methotrexate is ter-
CRP, albumin and faecal calprotectin frequently atogenic and results in birth defects so appropriate
help to determine disease activity. contraception is required in females, and ideally the
medication should be ceased 3 months before con- require repeated resections with time. Thus, there is
ception. It is not safe during breastfeeding. a tendency towards more conservative or minimal
surgery to minimise the risk of short‐bowel syn-
Biological agents: adalimumab, infliximab, drome from excessive resections of the small bowel.
vedolizumab and ustekinumab Surgery is mainly indicated for:
• stricture‐causing obstructive symptoms
In a similar fashion to ulcerative colitis, when patients • phlegmonous disease not responding to medical
continue to have symptoms on immunomodulators therapy
or if they are steroid‐dependent or steroid‐refractory, • enterocutaneous or enterovesical fistulas
escalation to biological therapy is required. Anti‐TNF • intra‐abdominal abscesses (most are now drained
agents were the first biological agents that became by percutaneous radiological techniques)
available for Crohn’s disease. They are effective at • acute or chronic blood loss (this is a rare
treating moderate‐to‐severe Crohn’s disease. indication).
Treatment with an anti‐TNF improves quality of life,
reduces hospital admissions and surgery. Anti‐TNF
therapy is also very effective at treating extra‐intesti- Surgical options
nal manifestations of Crohn’s disease including joint Conservative resection
pains, fistulating disease, erythema nodosum and The severely diseased segment is resected with a 2‐
pyoderma gangrenosum. As in ulcerative colitis, the cm margin of macroscopically normal bowel on
combination of an immunomodulator and anti‐TNF either side. With extensive disease, minor evidence
therapy appears to be more efficacious than either of Crohn’s disease at the anastomotic site does not
therapy alone, although it is associated with increased matter. The emphasis should be on preserving
risk of infection and lymphoma. bowel length.
Vedolizumab is also an effective therapy for The cumulative re‐operation rate after the first
Crohn’s disease and is not associated with the resection for distal ileal disease is 25% at 5 years
malignancy risk or immunosuppression of anti‐ after the first operation. Aphthous ulceration on the
TNF therapy. However, it is slower‐acting than the ileal side of the ileocolic anastomosis is present in
anti‐TNF therapies and requires up to 6 months of almost all patients within 12 months of ileocolic
therapy for its full effect to be felt. It also appears to resection. Although recurrent disease after surgery is
be less effective at treating the extra‐intestinal man- common, surgery rapidly restores patients with inca-
ifestations of Crohn’s disease. pacitating obstructing symptoms to good health.
Ustekinumab is the newest agent recently
approved for Crohn’s disease. Ustekinumab is a Strictureplasty
human IgG monoclonal antibody that blocks the In selective cases, strictures of the small bowel may
activity of interleukin (IL)‐12 and IL‐23. Clinical be overcome by strictureplasty without resection.
trials have demonstrated that ustekinumab is effec- The stricture is incised longitudinally along the
tive at treating moderate‐to‐severe Crohn’s disease. antimesenteric border and then sutured transversely
It is a well‐tolerated medication that appears to as in Heineke–Mikulicz strictureplasty (Figure 29.5)
have minimal side effects. or in a side‐to‐side bypass as in Finney strictureplasty
(Figure 29.6). Strictureplasty can be accomplished
Symptomatic treatment with a surgical morbidity similar to that of resec-
tion. It relieves obstruction, modifies progression of
Treatment of diarrhoea depends on its causation;
the disease and allows preservation of functional
treatment of active disease has been discussed and
small bowel.
bacterial overgrowth is treated with metronidazole.
Bile salt‐induced diarrhoea following ileal resection
is treated with colestyramine. Finally, antidiarrhoeal Enteric fistula and intra‐abdominal abscess
agents such as codeine phosphate, loperamide and
Fistula and abscess often coexist. Magnetic
diphenoxylate hydrochloride may have a small role.
resonance enterography is used to evaluate the

extent of Crohn’s disease in the small bowel and the
Surgical management
presence of fistulas. Colonoscopy is performed to
Crohn’s disease is a diffuse intestinal problem and rule out severe disease in the colon, and especially
there is a high incidence of disease recrudescence at the rectum. A CT scan will demonstrate any
various sites. Crohn’s disease cannot be cured by abscesses that may be appropriately treated by CT‐
surgical excision and a group of patients will guided percutaneous drainage.
(a)
(b)
Fig. 29.5 Heineke–Mikulicz strictureplasty. The stricture is (a) incised longitudinally along the antimesenteric border
and (b) then sutured transversely.
Fig. 29.6 Finney strictureplasty for a longer stricture using a side‐to‐side bypass. Source: Tjandra JJ, Fazio VW.
Strictureplasty in Crohn’s disease. In: Cameron JL (ed.) Current Surgical Therapy, 4th edn. Philadelphia: Mosby Year
Book, 1992:108–13. Reproduced with permission of Springer.
Internal fistulas are often asymptomatic and are surgery. Subtotal colectomy and ileorectal anasto-
identified incidentally at surgery. Ileosigmoid fistulas mosis is appropriate if the rectum is relatively free
are usually due to ileal disease. Enterovesical fistulas of disease and the patient is fit.
cause recurrent urinary tract infections and pneuma-
turia. At operation, the small bowel disease is resected Elective surgery
and the viscus that is secondarily involved is closed
locally. Following repair of an enterovesical fistula, a Segmental colectomy of the involved section of colon
Foley catheter is left in the bladder for at least a week. may be appropriate for localised disease. Subtotal
Enterocutaneous fistula in the early postopera- colectomy and ileorectal anastomosis is indicated in
tive period is a challenging problem. It arises from patients with severe diffuse colonic disease and rectal
anastomotic breakdown or from inadvertent dam- sparing, especially in younger patients. This opera-
age to the small bowel that is unrecognised at the tion may not be appropriate if there is severe perianal
time of surgery. Principles of management are dis- or rectal disease or if the anal sphincters are function-
cussed in Chapter 26. ally inadequate. Recurrent disease tends to occur in
the pre‐anastomotic segment of bowel and is more
frequent in patients with a limited resection. Many of
Crohn’s colitis these recurrences may be treated medically.
Total proctocolectomy and end‐ileostomy is
Clinical features indicated for extensive Crohn’s colitis involving the
rectum, with or without perianal disease. Sometimes
Colonic disease presents with bloody diarrhoea,
this is performed for severe perianal Crohn’s dis-
urgency and frequency. Fibrosis and stricture may
ease. There is a high incidence of delayed perianal
lead to subacute large bowel obstruction. Fistulation
wound healing, especially if there is severe perianal
to adjacent viscera can produce colovesical or rec-
Crohn’s disease.
tovaginal fistulas. Perianal disease commonly
accompanies Crohn’s colitis: fleshy anal skin tags,
anorectal strictures, relatively painless chronic anal
Perianal Crohn’s disease
fissures and painful anal canal ulcers with complex
perirectal fistulas. The differences between ulcera-
More than half the patients with Crohn’s disease have
tive colitis and Crohn’s colitis are given in Table 29.2.
anal lesions, especially those with rectal disease.
Surgical management Medical therapy

Emergency surgery
Patients with perianal fistulating Crohn’s disease
Acute fulminant colitis with toxic dilatation and have a severe phenotype of Crohn’s disease and
perforation may occur as in ulcerative colitis. require aggressive medical therapy.
Perforation can occur without toxic dilatation. The Treatment of perianal disease is with a multidisci-
procedure of choice is a subtotal colectomy with plinary approach between the gastroenterologist
formation of an end‐ileostomy and mucous fistula. and colorectal surgeon. Medical treatment with
Severe colonic bleeding may also necessitate urgent antibiotics, namely ciprofloxacin or metronidazole,
Table 29.2 Differentiation between ulcerative colitis and Crohn’s colitis.
Ulcerative colitis Crohn’s colitis
Distribution Continuous Segmental

Inflammation Mucosal and submucosal Transmural
Mucosa Granular, ulcerated Cobblestone, patchy inflammation
Involvement of small No Common
bowel
Complex anal lesions No Common
Internal fistula No Possible
Granulomas No Common
Fibrosis No Common
Carcinoma More common in extensive and More common in extensive and
long‐standing cases long‐standing cases
improves fistula symptoms and may contribute to Gomollón F, Dignass A, Annese V et al. Third European
healing. Therefore, antibiotics should be used as an Evidence‐based Consensus on the Diagnosis and
adjunctive treatment for active perianal fistulas. Management of Crohn’s Disease 2016: Part 1:
Anti‐TNF therapy is recommended for anyone with Diagnosis and Medical Management. J Crohns Colitis
2017;11:3–25.
active fistulating perianal disease and results in heal-
Toh JW, Stewart P, Rickard MJ, Leong R, Wang N, Young
ing in approximately 50% of patients. Infliximab
CJ. Indications and surgical options for small bowel,
has the most established evidence and is even more large bowel and perianal Crohn’s disease. World J
effective when combined with an immunomodula- Gastroenterol 2016;22:8892–904.
tor. Hence, combination therapy with infliximab
and an immunomodulator should be used in
patients with active perianal fistula where possible.
MCQs
Surgical therapy Select the single correct answer to each question. The
The most common anal lesions are fleshy anal skin correct answers can be found in the Answers section
tags or anal fissures. These anal fissures are often at at the end of the book.
atypical sites and cause little pain, unless there is a 1 Extra‐intestinal manifestations of ulcerative colitis
cavitating ulcer or an associated abscess. Perianal fis- include the following except:
tulas and abscesses are often multiple and complex. a pyoderma gangrenosum
Stricture at the anorectal ring is common as well. b iritis
Conservative medical and surgical treatment is c sacroiliitis
the key. The underlying anal sphincter is preserved d sclerosing cholangitis
as much as possible. Many anal lesions are rela- e eczema
tively asymptomatic and do not require specific
treatment. Proper assessment may demand an 2 Which of the following statements about Crohn’s
examination under anaesthesia, especially in the disease is correct?
presence of anorectal stricture and undrained pus. a adenocarcinoma of the small bowel never occurs
Endoanal ultrasound or MRI facilitates assessment as a complication of Crohn’s disease
of complex fistulous tracts and abscesses. b when operative resection is required, the sites of
Haemorrhoids are common problems but most anastomosis should be macroscopically normal
have few symptoms. Dietary and topical management c strictureplasty does not preserve length of the
alone are adequate. In troublesome cases, elastic‐band small bowel
ligation may be performed. A haemorrhoidectomy d haemorrhoidectomy should be performed as early
should be avoided because of the risk of secondary as necessary because severe symptoms are likely
sepsis and fistula formation. Anal surgery for fissure e inflammation of the colon and rectum cannot be
should be avoided whenever possible. Associated due to Crohn’s disease
abscesses are drained but the anal sphincters must be
preserved as much as possible. With more complex
3 Ulcerative colitis:
fistulous abscesses, a long‐term seton through the fis-
a is a transmural disease that affects both the large
tula functions as an effective drain. A tube drain is
and small bowel
also effective. If the disease is progressive or fails to
b has a higher risk of colorectal cancer compared
respond to adequate local drainage procedures,
to Crohn’s disease
consideration should be given to faecal diversion,

c surveillance for colon cancer is mandatory,
followed by a proctectomy in severe cases.
starting at diagnosis
d toxic megacolon exclusively occurs in this disease
e immunomodulators act within a week of
Further reading
commencement of treatment
Colonoscopic Surveillance Guidelines: Inflammatory bowel

4 Indications for restorative proctocolectomy in
disease. Available at https://wiki.cancer.org.au/australia
wiki/images/4/43/Algorithm_for_Colonoscopic_ ulcerative colitis include:
Surveillance_Intervals_‐_IBD.pdf#_ga=2.65169134.1343 a toxic megacolon
277047.1518337521‐726258687.1518337521 b a patient responding to medical therapy after 2 days
Gionchetti P, Dignass A, Danese S et al. Third European c possible Crohn’s‐related stricture in the small
Evidence‐based Consensus on Diagnosis and Management bowel
of Ulcerative Colitis 2016: Part 2: Surgical Management d severe sacroiliitis
and Special Situations. J Crohns Colitis 2017;11:135–49. e dysplasia on rectal biopsy
30 Diverticular disease of the colon
Ian Hastie and the late Joe J. Tjandra
Diverticula penetrate through the circular muscle

Introduction in four main sites, each relating to penetrating vasa
recta (Figure 30.1).
The term diverticulum (pleural, diverticula) indicates
The sigmoid colon affected by diverticulosis
an abnormal outpouching of the wall of a hollow
appears shortened and thickened. The muscular
viscus such as the colon. Colonic diverticula are
abnormality is the most important and consistent
‘false’ diverticula because they only contain mucosa
feature. There is gross thickening of both the longi-
and serosa in their wall. The term diverticulosis
tudinal and circular muscles of the colon, and pro-
refers to the presence of diverticula in the bowel
gressive elastosis of the taeniae coli. This muscular
wall but without complications or symptoms.
abnormality often precedes the development of
Diverticular disease implies that pathophysio-
diverticulosis and occurs predominantly in the sig-
logical changes and symptoms are arising due to
moid colon. The muscle of the sigmoid colon and
the diverticula. Diverticulosis of the sigmoid colon
rectosigmoid is different from that of the more
is associated with a western lifestyle, whilst right‐
proximal colon, in that it is thicker and more prone
sided diverticulosis is predominantly associated
to spasm. The colonic mucosa is pleated, with a sac-
with people of Asian backgrounds. The incidence of
cular appearance. Narrowing of the lumen is due to
diverticulosis increases with age and is identified
muscular hypertrophy, redundant mucosal folds
in over 50% of the population over the age of 60
and pericolic fibrosis.
years, with an increasing incidence in individuals
In classic situations, diverticula with associated
under 40 years. The male to female ratio varies with
muscular hypertrophy occur predominantly on the
age, being more predominant in males under 50
left side of the colon and are characterised by
years, and in females over this age.
inflammatory and perforative complications. There
appears to be another kind of diverticular disease
that is present throughout the entire colon without
Pathology associated muscle abnormality. This latter group
tends to occur in younger patients and may be due
Diverticulosis of the colon comprises acquired to a connective tissue abnormality that allows
mucosal herniations protruding through the cir- development of diverticula. Bleeding as a complica-
cular muscle at sites weakened by entry of blood tion is more common in this atypical group. Right‐
vessels. The incidence appears to be related to the sided diverticulitis with right‐sided abdominal pain
amount of fibre intake in the diet. The over‐refined occurs almost exclusively in the Asian population
and fibre‐deficient diet of western countries pro- but whether this is due to genetic or dietary factors
duces small hard stools. As the faecal stream is remains undetermined.
more viscous by the time it reaches the sigmoid Microscopically, diverticula have two coats, an
colon, hypersegmentation of the colon occurs to inner mucosal and an outer serosal layer. An artery,
generate higher pressures to propel these stools. vein or attenuated muscle may be present close to
Diverticula are thus the result of increased intralu- the neck of the diverticulum. Antimesenteric diver-
minal pressure within the colon. However, this ticula do not herniate fully through the circular
does not readily explain the cause of caecal or pan‐ muscle coat and have a thinned layer of circular
colonic diverticular disease. muscle in their wall.
267
Mesocolon
Vessel
Diverticulum Taenia coli
Fig. 30.1 Diverticulosis: diverticula protrude through the

circular muscle at the points where the blood vessels Fig. 30.2 Colonoscopic view of sigmoid diverticula.
penetrate the colonic wall.
Box 30.1 Common complications Investigations

of diverticulosis
Colonoscopy or flexible sigmoidoscopy
• Acute diverticulitis
• Inflammatory phlegmon Colonoscopy or flexible sigmoidoscopy is most use-
• Pericolic or mesenteric abscess ful in differentiating diverticular disease from carci-
• Perforation with local or generalised peritonitis noma and has the advantage of allowing tissue to be
• Fistula biopsied (Figure 30.2). Stricturing and angulation
• Diverticular stricture may limit the endoscopic evaluation of complicated
• Distal large bowel obstruction diverticular disease and necessitate contrast imaging.
• Colonic bleeding
CT colonography
CT colonography or ‘virtual colonoscopy’ allows
evaluation of the colonic mucosa as well as the colonic
The majority of patients with diverticulosis will
wall and pericolic tissues. The radiation exposure is
remain asymptomatic. Of those with symptomatic
significantly reduced compared with barium enema.
diverticular disease, about 30% will develop trouble-
In complex diverticular disease, where complete colo-
some complications that may require an operation
noscopic evaluation may not be not achievable, CT
in their management. The disease tends to pursue
colonography is a reliable alternative.
a more aggressive course in the young. The likeli-
hood of complications is unrelated to the number
of diverticula present. Common complications are
listed in Box 30.1.
Acute diverticulitis
A diagnostically difficult group involves
patients with proven diverticulosis who present
Pathology
with chronic pain but do not have objective evi-
dence of pericolonic inflammation on computed Approximately 30% of patients with known diver-
tomography (CT) or other features of compli- ticulosis will develop one or more bouts of divertic-
cated diverticular disease. Some of these patients ulitis. Among patients who require hospitalisation,
may have concurrent irritable bowel syndrome 20% require an emergency operation. The primary
or other causes of their pain. Treatment of these pathogenesis is thought to be related to obstruction
patients with antibiotics or indeed resection is at the neck of the diverticulum, giving rise to
questionable. an inflammatory reaction in the pericolic tissues.
30: Diverticular disease of the colon 269
In severe cases, an inflammatory phlegmon will Flexible endoscopy adds little useful information
form. Resolution may result in fibrosis. Progression and risks perforating an acutely inflamed bowel.
of sepsis can result in perforation, which is often It may have a role if ischaemic colitis, Crohn’s coli-
contained locally in the form of an abscess. Pericolic tis or carcinoma is strongly suspected.
abscesses are usually walled off and, with repeated CT colonography is generally contraindicated
episodes, the colon may become ensheathed in during the acute episode because instillation of
fibrous tissue and adherent to surrounding structures. the contrast may disrupt a well‐contained sepsis.
Less commonly, free perforation from the divertic- Contrast examination and flexible endoscopy are
ulum or the pericolic abscess may ensue, resulting best deferred for 6 weeks after an acute episode
in pelvic or generalised peritonitis. Fistulation to has settled.
adjacent organs such as bladder, small bowel or Plain abdominal X‐ray is rarely helpful because
vagina may occur. there are no specific features.
Clinical features
Acute diverticulitis is associated with constant and Management
protracted pain in the left iliac fossa, with systemic
Medical management
symptoms and fever, leucocytosis and sometimes an
abdominal mass. Alteration of bowel habit, with Mild diverticulitis
constipation or diarrhoea, may occur. If the inflam- Patients with mild symptoms, minimal abdominal
matory process involves the bladder, urinary symp- signs and minimal features of systemic sepsis can be
toms may be present. In more severe cases, managed with broad‐spectrum oral antibiotics
abdominal distension is also present, either second- (ciprofloxacin and metronidazole or amoxicillin/
ary to ileus or to partial colonic obstruction. Rectal lavulinic acid) for 7 days, as outpatients.
examination may reveal tenderness in the pelvis and
a mass or pelvic collection may be felt. Use of rigid Severe diverticulitis
sigmoidoscopy is usually limited because of pain. Patients with localised peritonitis need to be hospi-
Differential diagnoses are listed in Box 30.2. talised for resuscitation. The diagnosis is confirmed
with CT scanning. Intravenous fluid replacement
Investigations is provided. A nasogastric tube is only indicated if
there is evidence of significant ileus or bowel
CT scanning provides good definition of the extralu-
obstruction. Hospitalised patients are generally
minal extent of the disease and is particularly helpful
given intravenous antibiotics (e.g. cefotaxime and
in diagnosing complications such as abscesses and
metronidazole) that cover Gram‐negative organ-
colovesical fistula. The key finding is the presence of
isms and anaerobes. Adequate analgesia should be
diverticula and pericolic inflammation. Percutaneous
prescribed.
drainage of localised collections of pus can also be
Symptoms should begin to subside within 48 hours.
performed under CT guidance.
If resolution continues, further investigation with
Ultrasound can provide information similar to
colonoscopy is performed 6 weeks later. If medical
CT and can facilitate percutaneous drainage of a
therapy should fail, a repeat CT scan may be neces-
localised abscess. However, with the extent of
sary looking for the development of complications
gaseous dilatation of the bowel during acute diver-
such as abscess. Approximately one‐fifth of patients
ticulitis, images from sonography may be limited.
with severe diverticulitis will require operation
during the first hospital admission, and a further
one‐fifth radiological drainage in the setting of
Box 30.2 Differential diagnosis of acute abscess formation.
diverticulitis For patients with an initial uncomplicated attack
• Pelvic inflammatory disease
of diverticulitis who have responded to medical
• Appendicitis: when the diverticulitis occurs in the therapy, 70% will have no recurrence.
mid‐sigmoid area of a redundant colon that lies on
the right side of the abdomen Radiological options: percutaneous drainage
• Crohn’s colitis of diverticular abscesses
• Ischaemic colitis With a confined pericolic or pelvic abscess, CT‐ or
• Perforated colonic carcinoma
ultrasound‐guided percutaneous drainage is helpful
• Pyelonephritis
(Figure 30.3). The drainage catheter is kept patent
by regular irrigation with normal saline and kept in Hartmann’s procedure

place until drainage ceases and the abscess cavity Hartmann’s procedure (Figure 30.4) involves
has completely collapsed. resecting the diseased segment of colon, stapling
off the rectal stump and bringing out the proximal
Acute operative management end of colon as an end‐colostomy. It has the advan-
tage of removing the septic focus (i.e. phlegmonous
Indications for operative management during the
or perforated sigmoid colon) and avoids an anasto-
acute admission include generalised peritonitis and
mosis in the presence of gross sepsis and faecal
failure of non‐operative therapy after 3–5 days. The
contamination. However, a second‐stage operation
decision to intervene depends on the severity and
is necessary after 4–6 months to re‐establish intes-
extent of peritonism and systemic disturbance.
tinal continuity and entails a further laparotomy
and bowel mobilisation (and often further resec-
Laparoscopic lavage
tion), with all the attendant risks of colorectal
Early laparoscopic intervention with lavage of the
anastomosis.
inflamed area and drainage of collections is
Hartmann’s procedure has evolved as the treat-
favoured in some centres. Severe cases with faecal
ment of choice for patients with faecal peritonitis. It
peritonitis will still require resection but this tech-
is no longer the treatment of first choice in patients
nique has a role in purulent peritonitis.
with an abscess, which should be treated primarily
by percutaneous drainage.
Resection and primary colorectal anastomosis

Resection and primary colorectal anastomosis has
the advantage that the diseased segment is resected
and an anastomosis is established. However, in the
acute setting, it involves extensive dissection in the
presence of intraperitoneal sepsis with the atten-
dant risk of spreading the infective process. When
primary anastomosis is performed in cases of severe
acute diverticulitis, a proximal diverting ileostomy
may be used. Subsequent closure of the diverting
ileostomy is more straightforward than the second‐
Fig. 30.3 Computed tomography scan showing a stage reversal of Hartmann’s procedure. The divert-
localised abscess in the left pelvic region due to ing stoma is generally closed after 2–3 months.
complicated diverticulitis. A limited Gastrografin enema is performed prior to
Fig. 30.4 Hartmann’s procedure.

30: Diverticular disease of the colon 271
closure of the stoma to ensure healing and patency Colovesical fistula

of the colorectal anastomosis.
Most patients are male; presumably the uterus
On‐table large bowel irrigation, resection and
protects the bladder from the colon in females
primary colorectal anastomosis is also another
(women who develop colovesical or colovaginal
option to avoid a Hartmann’s procedure. On‐table
fistulas have often had a hysterectomy). Common
colonic washout is performed to remove the faecal
symptoms are those of cystitis. There is usually a
residue in the otherwise unprepared colon. This
history of recurrent urinary tract infections that
manoeuvre is cumbersome and may contaminate
fail to respond to appropriate antibiotic therapy.
the operative field. This technique should be con-
Faecaluria is diagnostic, as is passage of vegetative
sidered only in highly selected situations where the
matter. Pneumaturia that occurs at the end of
sepsis is confined, with minimal bowel distension
voiding is strongly suggestive but gas‐forming
and oedema. A proximal diverting ileostomy is
organisms in the bladder can simulate the condi-
often performed in combination with on‐table
tion. Bowel symptoms may be absent.
colonic lavage.
Flexible sigmoidoscopy will rule out inflamma-
tory bowel disease and may identify the fistula and
Transverse colostomy and drainage
the presence of diverticula. Barium enema will
This outdated three‐stage procedure involves an
show the diverticular disease but demonstrates
initial diverting transverse loop colostomy and tube
the fistulous communication in only about 50% of
drainage of the septic area, a subsequent sigmoid
cases. Cystoscopy may reveal cystitis and the fistu-
resection and, finally, closure of the colostomy. The
lous opening. Cystograms may demonstrate the
combined morbidity and mortality of the three
fistula in 30% of cases. CT scan or CT colonography
stages of operations are high and the procedure is
can define the extent and degree of pericolic inflam-
associated with long periods of hospitalisation.
mation and may detect air in the bladder that is
associated with a colovesical fistula, along with
contrast extravasation. Treatment involves separa-
Bleeding diverticular disease tion of the sigmoid colon from the bladder, and
sigmoid resection followed by a primary colorectal
Massive diverticular bleeding probably arises from
anastomosis. The opening in the bladder is often
injury to the vasa recta. The characteristic presenta-
not obvious. If an opening in the bladder is seen, it
tion is that of an otherwise well individual who
is repaired. The omentum is interposed between the
suddenly passes a large amount of maroon‐col-
colorectal anastomosis and the bladder.
oured stool. Characteristically, the bleeding is not
associated with significant pain or abdominal ten-
derness. Bleeding stops spontaneously in about Other fistulas
80% of cases.
Other rarer forms of fistula present with discharge
Management of massive rectal bleeding is dis-
of purulent fluid, flatus or faeces on the abdominal
cussed in Chapter 65. Considerable difficulty exists
wall (colocutaneous fistula), via the vagina
in identifying the source and cause of colonic bleed-
(colovaginal fistula) or with diarrhoea (coloenteric
ing, and CT angiography and labelled red cell scan
fistula).
should be considered. In patients with a minor
degree of persistent rectal bleeding, the bleeding
should not be attributed too readily to the diver-
ticular disease. In many such patients, there is a Indications for elective operative
coexistent carcinoma or polyp of the colon. If treatment
diverticular disease is identified confidently as the
source of recurrent colonic bleeding, segmental Determining factors include the patient’s age,
resection is recommended. general health, and the severity and frequency of
the symptoms. Indications for surgery include:
• chronic symptoms despite the use of a high‐fibre
Fistula diet and bulk‐forming agents
• recurrent acute diverticulitis
Fistulas develop from localised perforations to • persistent tender mass
which an adjacent viscus becomes adherent. • inability to distinguish colonic lesion from carci-
Eventually the abscess or faeces drains through that noma or inability to exclude carcinoma
viscus. • fistulas.
Elective operations for symptomatic diverticular

disease are more commonly recommended in
MCQs
younger patients (<55 years), in those who are
immunosuppressed (e.g. after renal transplanta-
tion) because of the potential morbidity of further
diverticular complications, and in patients with
significant radiological abnormalities such as 1 A 72‐year‐old woman presents with left iliac fossa
extravasation of contrast or a sigmoid stricture. pain and is found to have a fever and left iliac fossa
The timing of elective operation should ideally peritonism. The most likely diagnosis is:
be about 12 weeks after the most recent attack of a left ureteric calculus
diverticulitis. Only the segment of colon affected b tubo‐ovarian abscess
by the diverticular inflammatory reaction needs to c irritable bowel syndrome
be removed. In general, this includes the entire d acute diverticulitis
sigmoid colon and the rectosigmoid junction. The e sigmoid volvulus
distal margin of resection must extend below the
level of muscular thickening and is usually in the 2 Diverticulosis of the sigmoid colon is associated with:
upper rectum (the level at which the teniae coa- a thickening of the longitudinal but not circular
lesce). The proximal extent of transection should muscle of the colon
include all induration palpable at the junction of b narrowing of the lumen from mucosal hyperplasia
the mesocolon with the colon itself and is usually c increased intraluminal pressure within the colon
in the descending colon. It is not usually necessary d high‐fibre and high‐fat diet
to resect the entire diverticula‐bearing proximal e a high incidence of anastomotic breakdown in
colon. A primary colorectal anastomosis is gen- elective surgery
erally utilised. In most cases, a laparoscopic
approach is possible, rather than the conventional 3 Surgical management of perforated diverticular
laparotomy. disease with faecal peritonitis includes:
a preoperative mechanical bowel preparation
b Hartmann’s
procedure and sigmoid end‐colostomy
Further reading c preoperative barium enema to define the anatomy
d anterior resection and primary colorectal
Angenete E, Bock D, Rosenberg J, Haglind E. Laparoscopic
lavage is superior to colon resection for perforated anastomosis whenever possible
purulent diverticulitis: a meta‐analysis. Int J Colorectal e preoperative nasogastric feeding to optimise
Dis 2017;32:163–9. nutrition
Aydin HN, Remzi FH. Diverticulitis: when and how to
operate? Dig Liver Dis 2004;36:435–45. 4 The complications of sigmoid diverticular disease do
Boynton W, Floch M. New strategies for the management not include which of the following?
of diverticular disease: insights for the clinician. Ther a sigmoid inflammatory phlegmon
Adv Gastroenterol 2013;6:205–13. b colonic bleeding
Feingold D, Steele SR. Practice parameters for the treat-
c purulent peritonitis
ment of sigmoid diverticulitis. Dis Colon Rectum
d colovaginal fistula
2014;57:284–94.
e colon cancer
31 Colorectal cancer
Ian T. Jones and the late Joe J. Tjandra
Department of Surgery, University of Melbourne and Colorectal Surgery Unit, Royal Melbourne
Hospital, Melbourne, Victoria, Australia
a clearer understanding of the series of cellular

Introduction genetic mutations that result in the onset of malig-
nancy and these same events are also at play in spo-
Colorectal cancer (CRC) is the most common inter-
radic or non‐inherited cancers.
nal cancer in the western world. It is the second
Two major carcinogenesis sequences have been
most common cause of death from cancer and
identified.
accounts for one in eight of all new cancer diagno-
• Chromosomal instability (CIN) pathway refers
ses. However, the prognosis for patients with CRC
to the traditional adenoma–carcinoma pathway
is superior to that of many other solid tumours,
described by Vogelstein in 1990. This pathway
such as lung and pancreas, and Australian cancer
accounts for approximately 85% of all CRCs.
statistics reveal that 69% of patients diagnosed
Progression from benign adenomatous polyps
with CRC between 2009 and 2013 survived more
to more dysplastic lesions, invasive cancer and
than 5 years. Even so, CRC accounts for 8.6% of all
metastases is associated with an aggregation of
Australian cancer deaths.
genetic mutations, the most important of which
affects the adenomatous polyposis coli (APC)
Epidemiology gene. An inherited APC mutation is responsible
for FAP.
It is estimated that in 2019, 16 398 new cases of • Microsatellite instability (MSI) pathway is the
CRC will be diagnosed in Australia, 9069 in males second major pathway of carcinogenesis and is
and 7329 in females. The gender difference is largely associated with dysfunction of mismatch repair
due to the higher incidence of rectal cancer in males (MMR) genes that protect the integrity of cellu-
as the incidence of colon cancer is about equal in lar DNA. An inherited mutation of one or more
men and women. These figures are similar on a per‐ MMR genes leads to the development of Lynch
capita basis to other parts of the western world. In syndrome.
the USA, it is estimated that over 145 600 new cases Whilst inherited CRC syndromes account for
of CRC will be diagnosed in 2018. perhaps only 5% of all CRCs, family history is a
The lifetime risk for CRC is 1 in 18 for men and 1 critical factor in CRC. Individual risk for CRC is
in 24 for women. The peak age of onset is the seventh increased two‐and‐a‐half to three times for those
decade of life (mean age 64 years). CRC is less com- with a first‐degree relative with CRC but this
mon in those under 50 years of age (except in indi- increases up to six times when a relative is diag-
viduals with an inherited bowel cancer syndrome). nosed under the age of 55 years.
Epidemiological studies suggest that environ-
mental factors predominate in the causation of
Aetiology most CRCs. A diet rich in fat and meat, and low
in fibre, is commonly associated with colorectal
Whilst most cases of CRC are sporadic, the inher- cancers. Obesity and alcohol intake are increas-
ited CRC syndromes such as familial adenomatous ingly recognised as major risk factors for CRC
polyposis (FAP) and Lynch syndrome have allowed (Box 31.1).
273
Box 31.1 Risk factors for colorectal cancer Table 31.2 Prognosis in colorectal cancer: 5‐year
survival rates (%).
• Environmental factors: fat, red meat, alcohol, obesity
• Adenomatous polyps: most cancers originate Stage Colon cancer Rectal cancer
within an adenoma
Dukes’ A (stage I) 99 90
• Family history of CRC
Dukes’ B (stage II) 80 60
• Genetic syndromes (e.g. FAP)
Dukes’ C (stage III) 50 40
• Inflammatory bowel disease: ulcerative colitis and
Distant metastases <10 <10
Crohn’s disease especially when long‐standing and
(stage IV)
extensive
• Irradiation: the risk of rectal cancer is increased following
pelvic radiation therapy (e.g. for cancer of the cervix)
Histopathology
Poorly differentiated cancers (including signet ring,
Pathology mucinous and small cell cancers) have a worse
outlook than those that are well to moderately
The outcome of CRC depends on its biological differentiated. Other adverse features include lym-
behaviour. The clinicopathological stage (the phovascular or perineural invasion.
amount of spread) of the disease is a ‘snapshot’ in
the life of a cancer and provides the most accurate
prognostic index at the present time. Prognosis
Staging Tumour stage (Table 31.2) is the main determi-
The most common staging method is the Union for nant of prognosis. Most patients with Dukes’
International Cancer Control (UICC) TNM classi- A (stage I) cancers are cured after surgery. Lymph
fication (Table 31.1), which has largely superseded node metastases (Dukes’ C, stage III) are a signifi-
the traditional Dukes’ classification. cant adverse prognostic factor. Long‐term survival
can be achieved after treatment of distant metas-
tases (especially those that are solitary or confined
Table 31.1 Staging methods for colorectal cancer. to one organ) but 5‐year survival for stage IV disease
is low.
Modified Dukes’ staging
A Tumour confined to bowel wall
B Tumour invading through serosa Clinical presentation
B1 Through muscularis propria
B2 Through serosa or perirectal fat This varies depending on the primary site and
C Lymph node involvement extent of disease.
C1 Apical node not involved
C2 Apical node involved
Caecal and right‐sided carcinoma
UICC TNM staging
Tumour depth (T) These account for 20% of all large bowel cancers.
T1 Submucosa Clinical presentations include:
T2 Muscularis propria • Iron deficiency anaemia from occult intestinal
T3 Subserosa or pericolic tissues blood loss
T4 Invade adjacent organs or visceral peritoneum
• Small bowel obstruction due to occlusion of the
Nodes (N)
ileocaecal valve
N0 Nodes not involved
• Palpable mass
N1 1–3 pericolic nodes involved
N2 ≥4 pericolic nodes involved • Lethargy, weight loss and hepatomegaly, which
Metastasis (M) may be features of metastatic disease.
M0 No distant metastases
M1 Distant metastases Left‐sided and sigmoid carcinoma
Stage I T1–2 N0
Half of CRCs arise in the sigmoid colon and rec-
Stage II T3–4 N0
tum. Clinical presentations include:
Stage III T1–4 N1–2
Stage IV M1 • Alteration of bowel habit, such as constipation
alternating with diarrhoea
31: Colorectal cancer 275
• Lower abdominal colic, distension and a desire

to defecate
• Passage of altered blood and sometimes mucus in
the stool.
Rectal cancer
Unfortunately, the diagnosis is often delayed
because symptoms are attributed to haemorrhoids
or similar. Rectal examination is essential in all
patients with rectal bleeding. Clinical presentations
include:
• Rectal bleeding may be dark and mixed with Fig. 31.1 Computed tomography scan of the abdomen
stool or bright and quite separate from the showing multiple metastases in both the right and left
faeces. lobes of the liver.
• Tenesmus (an urge to use the bowels but with
unsatisfied defecation) is common Magnetic resonance imaging
• Anorectal pain usually indicates locally advanced
Magnetic resonance imaging (MRI) is a critical
disease.
investigation for assessing local spread of rectal
cancer, which guides surgeons in performing sur-
Metastatic disease
gery to remove sites of local spread in continuity
Liver metastases are asymptomatic in the early with the primary rectal cancer (total mesorectal
stages; hepatomegaly indicates substantial liver excision or TME). It also allows selection of patients
involvement. Lung metastases are also usually who might benefit from preoperative neoadjuvant
asymptomatic. Ovarian metastases arise in up to chemoradiotherapy.
5% of female CRC patients and are referred to as
Krukenberg tumours. Peritoneal spread may pro- Positron emission tomography
duce ascites and carries a poor prognosis.
Positron emission tomography (PET) is an alterna-
tive form of body imaging based on gamma rays
Clinical assessment emitted by biologically active molecules, usually the
glucose analogue fluorodeoxyglucose (FDG). Its
A careful history and physical examination particular advantage is its superior sensitivity in the
remain the most important assessments with detection of metastatic disease. Its disadvantages
regard to diagnosis, extent of spread and fitness include cost and difficulty in differentiating malig-
for surgery. For rectal cancer, digital rectal exam- nancy from other metabolically active conditions
ination and rigid sigmoidoscopy allow an assess- such as infection.
ment of tumour size and height above the anal
verge (critical in determining the appropriate sur- Carcinoembryonic antigen
gical procedure). Carcinoembryonic antigen (CEA) is a circulating
tumour‐associated antigen in CRC. It has little
diagnostic value but has a significant role in the
Investigations follow‐up after resection leading to the earlier
diagnosis of metastatic disease.
Colonoscopy
Colonoscopy is the key investigation for the diag-
Treatment of colorectal cancer
nosis of CRC and is used to examine symptomatic
patients. It has entirely replaced traditional barium
When CRC is confined to the primary site, surgery
enema.
with satisfactory resection margins provides the
best chance of cure. Quality of surgery, particularly
Computed tomography
for rectal cancer, has a major impact on cancer
Computed tomography (CT) scanning (Figure 31.1) outcome. Surgeons performing TME surgery have
is an essential tool in staging and treatment reduced the dreaded complication of pelvic cancer
planning. recurrence from about 30% in the pre‐TME era to
less than 10%. If unfavourable tumour grade, Surgery for colon cancer

extramural vascular invasion or metastatic deposits
Carcinoma of the caecum or ascending colon
in regional lymph glands are found by histological
examination of the cancer (or on preoperative MRI Right hemicolectomy is the standard operation
for rectal cancer), surgery can be supplemented by (Figure 31.2). The ileocolic vessels are divided at
postoperative adjuvant chemotherapy for colon their origins while maintaining the blood supply to
cancer or neoadjuvant (preoperative) chemoradia- the residual terminal ileum. The right colic vessels
tion for rectal cancer. and the right branch of the middle colic vessels are
The principles of surgery are to remove the seg- also removed. The amount of bowel removed is
ment of bowel containing the cancer, along with a influenced by the extent of lymphovascular clear-
margin of healthy uninvolved bowel in continuity ance, which in turn is dependent on the site of the
with regional lymph nodes adjacent to the bowel primary colon cancer.
and alongside mesenteric blood vessels. Bowel con-
tinuity is restored by constructing an anastomosis Carcinoma of the transverse colon
between the bowel ends.
The blood supply to this area is derived from the
Traditional CRC surgery is undertaken through
middle colic vessels as well as from the right colic
an abdominal wall incision as an open procedure
vessels. If the cancer is at the hepatic flexure end of
(laparotomy). Increasingly, minimally invasive
the transverse colon, a right hemicolectomy is per-
approaches using laparoscopic‐assisted tech-
formed. Lesions of the mid‐transverse colon are
niques are being used. For colon cancer, onco-
treated by extended right hemicolectomy, which
logic results have been shown to be equivalent to
entails an anastomosis between the terminal ileum
those achieved at open surgery and have the
and the descending colon. The omentum is removed
advantage of smaller incisions, less postoperative
en bloc with the tumour. A carcinoma at the splenic
pain and shorter length of hospital stay. The use
of laparoscopic or minimally invasive techniques
in rectal cancer is more controversial as large
clinical trials have been unable to confirm an
equivalent outcome compared with traditional
open surgery, possibly due to the adequacy of the
TME that can be achieved by minimally invasive
techniques.
Preparation for surgery
MCA
Bowel preparation RCA
Mechanical bowel preparation with dietary restric-

tion and laxatives similar to those used for colonos-
ICA
copy are frequently employed.
Antibiotic prophylaxis
Prophylactic antibiotics against aerobic and
anaerobic bowel pathogens (usually a cephalo-
sporin and metronidazole) are given on induction
of anaesthesia. Such regimens have been shown to
substantially reduce the risk of postoperative
wound infection.
Prophylaxis for venous thromboembolism

Patients undergoing surgery for CRC carry a sig- Fig. 31.2 Right hemicolectomy for ascending colon
nificant risk for venous thromboembolism. cancer. Dashed line indicates resected material. RCA,
Mechanical and chemical prophylaxis are given right colic artery; MCA, middle colic artery; ICA,
unless contraindications exist. ileocolic artery.
flexure can spread to regional lymphatics along the Surgery for obstructing colon cancer
middle colic and left colic arteries. Adequate lym-
This is discussed in Chapter 32.
phatic clearance may require subtotal colectomy
with an ileosigmoid anastomosis.
Surgery for perforated colon cancer
Carcinoma of the descending colon Perforation is less common than obstruction and
usually occurs as a result of tumour necrosis. It car-
Left hemicolectomy is the operation of choice
ries a poor prognosis as the risk of local recurrence
(Figure 31.3). The inferior mesenteric artery is
is high. Right colon perforations are managed by
divided at its origin and the left colic and sigmoid
right hemicolectomy. For left colon perforations,
vessels are included in the resection. An anastomo-
Hartmann’s procedure (see Figure 31.7) is generally
sis is performed between the transverse colon and
performed with excision of the perforated bowel.
the upper rectum.
The proximal colon is brought out as an end‐colos-
tomy and the distal bowel end oversewn. A primary
Carcinoma of the sigmoid colon
anastomosis is generally not performed because of
A high anterior resection is favoured, anastomosing the higher leak rate in the presence of sepsis.
the descending colon to the upper rectum. The infe-
rior mesenteric artery is ligated close to the aorta. It
is preferable to resect the entire sigmoid colon Surgery for rectal cancer
(which can be affected by diverticular disease) and
Management of rectal cancer is challenging because
to anastomose the descending colon to the upper
of the anatomical location of the tumour (particu-
rectum. Most surgeons believe this has a lower inci-
larly in the narrow male pelvis), the greater diffi-
dence of anastomotic leak.
culty in performing low colorectal anastomoses
and the potential for pelvic recurrence with inade-
quate surgery. Rectal cancer surgery is best per-
formed by specialist colorectal surgeons who
receive training in TME surgery. Apart from the
superior oncologic outcomes with TME, colorectal
surgeons have been able to reduce the need for per-
manent colostomy from around 80% 40 years ago
to around 10% in the current era. There is also evi-
dence that TME has a lower incidence of pelvic
autonomic nerve injury leading to a lower rate of
sexual and bladder dysfunction in men.
Factors influencing choice of operation for rectal

cancer
IMA
Location of tumour
LCA
LCA The height of the lower edge of the cancer above
the anal verge is the most important factor in the
choice of operation. In general, a tumour less than
5 cm from the anus requires abdominoperineal
excision (APE) of the rectum with permanent colos-
tomy, as a restorative anastomosis is usually not
possible.
Nature of tumour
A high‐grade, poorly differentiated tumour tends to
be widely infiltrative and requires wide excision to
achieve clear margins. Tethered or fixed tumours
are locally advanced and require neoadjuvant
Fig. 31.3 Left hemicolectomy for descending colon chemoradiation with subsequent en bloc excision
cancer. Dashed line indicates resected material. IMA, of any invaded adjacent organs (e.g. prostate or
inferior mesenteric artery; LCA, left colic artery. vagina).
Patient factors resection as high (anastomosis >10 cm above anal

The age and medical fitness of the patient and the verge), low (6–10 cm) and ultra‐low (<6 cm).
presence of metastases are important factors in The anastomosis is a critical part of the proce-
determining the magnitude of the operation. dure, second only to performance of TME.
Obesity, male gender and previous pelvic surgery Traditionally, anastomoses have been constructed
significantly add to the difficulty of rectal cancer by hand suturing techniques but this is technically
surgery. difficult deep in the pelvis and, in most cases, dis-
posable stapling devices have replaced hand
suturing (Figure 31.5). Even in expert hands there
Anterior resection
is a risk of anastomotic leak (about 2–4%) which is
Anterior resection (Figure 31.4) is the standard greater for low‐lying anastomoses. A proximal loop
operation for cancers of the rectum. This entails ileostomy is often used to divert the faecal stream
excision of the sigmoid colon and a variable por- away from the anastomosis to reduce the incidence
tion of the rectum. The inferior mesenteric artery of leak. When healing is confirmed, the ileostomy
and vein are divided at the highest possible level to can be reversed, usually after 3 months. Bowel
achieve maximal lymph node clearance and to function after anterior resection is altered due to
allow mobilisation of the splenic flexure and loss of the rectal ‘reservoir’ and low‐lying anasto-
descending colon so that they reach into the pelvis moses may be associated with urgency, increased
to enable a tension‐free anastomosis between colon frequency and clustering of bowel movements.
and rectum. For mid‐to‐low rectal cancers, TME
removes all the rectal mesentery so that the anasto-
Abdominoperineal excision of the rectum
mosis typically lies at the level of the pelvic floor.
The level of the anastomosis above the anal verge APE is required for low‐lying rectal cancers
(determined by the site of the cancer in the rectum) (Figure 31.6). The rectum is mobilised down to the
is frequently used to further define anterior pelvic floor through an abdominal incision. The
descending colon is divided and brought out as a
colostomy. A separate perineal incision is then made
IMA to excise the sigmoid colon, distal rectum and anus.
Transanal local excision

Transanal excision of small, early‐stage (T1), low‐
lying rectal cancers may be considered in highly
selected cases where cure can be anticipated and
where radical rectal excision would otherwise
require a permanent colostomy. It can also be con-
sidered when age or infirmity of the patient or pres-
ence of metastases precludes major resection.
Neoadjuvant chemoradiotherapy
Based on evidence from large clinical trials which
have shown reduced local recurrence when neoad-
juvant chemoradiation is combined with TME sur-
gery, combined modality treatment is recommended
for T3/4 or N1/2 rectal cancers (as demonstrated
on MRI). For patients who receive neoadjuvant
chemoradiation, as many as 15% will be found to
have no viable malignant cells in the surgically
removed rectum. This raises the question as to
whether surgery can be avoided in these patients.
The major problem is that predicting which patients
Fig. 31.4 Anterior resection for rectal cancer. Dashed have a complete remission is difficult and poten-
line indicates resected material. IMA, inferior mesenteric tially puts patients who forgo surgery (so called
artery. ‘watch and wait’) at risk of recurrence.
(a) (b)
(c)
Anastomosis
Circular
stapler
Fig. 31.5 (a) Hand‐sewn anastomosis. (b) Double‐stapled anastomosis where the rectal stump has been occluded with a
linear stapler followed by construction of a colorectal anastomosis with a circular stapler. (c) Single‐stapled anastomosis
using a circular stapler.
Palliative procedures Adjuvant therapy

Palliative procedures include a low Hartmann’s In combination with high‐quality cancer surgery,
procedure (Figure 31.7) or a diverting stoma only. postoperative chemotherapy for node‐positive colon
cancer (stage III) has been shown in multiple studies
IMA to improve overall survival by 10–15%. The usual
postoperative regimen consists of 5‐fluorouracil,
folinic acid and oxaliplatin (FOLFOX) given for a
6‐month period.
As already discussed, neoadjuvant chemoradio-
therapy has a major role in locally advanced rectal
cancer. Perhaps the most influential study was the
Dutch trial published in 2001 that evaluated preop-
erative radiotherapy combined with TME surgery
and demonstrated a further significant reduction in
pelvic recurrence rates already achieved by TME
alone. A subsequent UK study (CR07) confirmed
the results of the Dutch trial and also showed a
small improvement in disease‐free survival.
Treatment of metastatic disease

Treatment for incurable disease should be consid-
ered in terms of the possible benefit to be gained
from symptom relief against the risk of treatment‐
associated morbidity in a patient who may have a
limited remaining lifespan. In some cases, radical
therapy of isolated metastases can achieve long‐
term survival. The treatment options for metastatic
disease are listed in Box 31.2.
Follow‐up after treatment for colorectal cancer

Fig. 31.6 Abdominoperineal excision of the rectum.
Dashed line indicates resected material. IMA, inferior The need for follow‐up is a source of debate.
mesenteric artery. Follow‐up provides reassurance for patients and
Fig. 31.7 Hartmann’s procedure for perforated colon cancer (which can be modified to a lower resection for palliation
of rectal cancer).
For individuals at higher risk of CRC (e.g. those

Box 31.2 Treatment of metastases
with a family history), colonoscopy is preferred
Liver over FOBT because of its greater accuracy.
• Resection for single or closely grouped multiple
tumours
• Selective internal radiation therapy (SIRT) by Colorectal polyps
targeted hepatic artery injection of radioactive
yttrium microspheres A polyp is the term used to describe a tissue growth
• Chemotherapy projecting into the bowel lumen. Certain polyps are
• Radiofrequency ablation entirely benign and have limited clinical signifi-
Lung cance (e.g. inflammatory, lymphoid and lipomatous
• Resection by video‐assisted thoracoscopic surgical polyps). Most interest is centred on precancerous
techniques (VATS) adenomas.
Peritoneum
• Peritonectomy in association with heated intraperi-
toneal chemotherapy (HIPEC) in selected cases Adenoma
Small bowel An adenoma is a benign neoplasm of the large
• Resection
bowel that is associated with CRC. The most com-
• Bypass
mon variety is a tubular adenoma that is usually
Pelvic/local recurrence
well‐differentiated and pedunculated (Figure 31.8).
• Pelvic exenteration procedures when distant
By contrast, a villous adenoma is less differentiated
metastases have been excluded
and usually sessile.
• Radiotherapy
• Chemotherapy
At least 85% of CRCs arise from pre‐existing
adenomas. The risk of malignancy increases with
the size and the histology of the adenoma. Large
villous adenomas have the greatest risk (Table 31.3).
allows surgical audit of outcomes but is costly and
Carcinoma in polyps smaller than 1 cm in diameter
may have a low yield in terms of improved survival.
is uncommon. The malignant potential of adeno-
A structured and targeted protocol (by CEA and
mas is dramatically demonstrated in the inherited
CT) may detect early onset of recurrent disease,
polyposis syndrome FAP, where hundreds or thou-
enabling treatment and in some cases long‐term
sands of adenomas arise in the colon resulting in
cure. Follow‐up facilitates colonoscopy, which is
early‐onset CRC. More recently, the importance of
recommended every 3–5 years for the detection of
sessile serrated adenomas has been recognised.
metachronous CRC.
These are usually sessile polyps found mostly in the
right colon.
Most adenomas are asymptomatic and only
Screening for colorectal cancer diagnosed during the investigation of bowel symp-
toms or by FOBT screening and colonoscopy.
Screening is appropriate for cancers that are com- Colonoscopy allows therapeutic removal of polyps
mon and curable, where early detection is accom- and a variety of techniques are available, using
panied by improved outcome and when it is endoscopic instruments with diathermy to achieve
cost‐effective. CRC unquestionably meets these polyp removal (polypectomy) and retrieval
requirements. It is recommended that CRC screen- (Figure 31.9).
ing commence at age 50 and continue to an age Large polyps may require surgery. Accessible rec-
beyond the peak onset of CRC (e.g. to age 75). The tal villous adenomas may be treated by transanal
two most common screening modalities are faecal excision, which can be improved by the superior
occult blood testing (FOBT) and colonoscopy. visualisation and instrumentation of transanal
FOBT is recommended screening for most indi- endoscopic microsurgery (TEMS). For large proxi-
viduals of average risk. In Australia, national CRC mal adenomas, conventional bowel resection is
screening commenced in 2006 as the National recommended.
Bowel Cancer Screening Programme (NBCSP). This For patients who have had multiple or advanced
has been progressively expanded and the aspiration adenomas removed, surveillance by colonoscopy
is for all Australians between the ages of 50 and 74 is required because of the high incidence of new
to be offered 2‐yearly FOBT by 2020. When FOBT adenomas subsequently arising elsewhere in the
is positive, colonoscopy is required. bowel.
(b)
Superficial carcinoma Invasive carcinoma

(into head)
(a)
Invasive carcinoma
Invasive carcinoma
(into stalk)
Mucosa
Muscularis mucosa
Submucosa
Muscularis propria
Serosa
Fig. 31.8 Sessile (a) and pedunculated (b) polyp.
Table 31.3 Relationship of adenoma to invasive

carcinoma.
Incidence of malignancy (%)
Size Tubular Tubulo‐villous Villous
<1 cm 0.3 1.5 2.5

1–2 cm 4 6 6
2–3 cm 7 12 17
>3 cm 11 15 20
Inherited cancer and polyposis Fig. 31.9 Endoscopic snare polypectomy during

syndromes colonoscopy.
Familial adenomatous polyposis

FAP is a disorder characterised by autosomal dominant
inheritance of a mutation in the tumour‐suppressor
gene APC located on chromosome 5 (5q21) which,
when inactivated, results in loss of control over cell
proliferation, thus promoting neoplasia. FAP is
associated with the formation of multiple colorectal
adenomas (Figure 31.10). If left untreated, all FAP
patients will develop CRC. Although uncommon,
FAP accounts for 0.5% of all CRCs.
Most affected individuals develop polyps by the
age of 15 years. Effective management of FAP
requires a carefully researched family history and
construction of family pedigrees. This and patient
education is often best done by dedicated familial Fig. 31.10 Colonoscopic view of familial adenomatous
cancer clinics. polyposis.
Bowel symptoms associated with FAP usually indi- • Restorative proctocolectomy and ileal pouch–
cate the development of cancer. Therefore, it is crucial anal anastomosis removes the entire colon and
to diagnose the condition at a pre‐symptomatic stage. rectum, thus having the major advantage of
Endoscopic surveillance is giving way to genetic eliminating CRC risk. Bowel function is pre-
testing to allow recognition of affected offspring of served by construction of an ileal reservoir joined
FAP patients. Those family members who test nega- to the upper anal canal. Surgical complications
tive on genetic testing are not at risk for FAP. are higher than for IRA and bowel function is
Almost all FAP patients have gastroduodenal polyps, marginally worse.
and around 5% go on to develop duodenal cancer. • Total proctocolectomy and permanent ileostomy
Duodenal adenomas at the ampulla of Vater are is reserved for FAP patients presenting with
particularly prone to malignancy. Many duodenal rectal cancer.
adenomatous polyps can be treated endoscopically
but radical surgery including pancreaticoduodenec- MUTYH‐associated polyposis
tomy (Whipple procedure) may be necessary in
Mutations in the MUTYH gene (chromosome 1)
patients with severe duodenal polyposis or cancer.
cause defects in base‐excision DNA repair that
Several extracolonic manifestations of FAP can
results in a polyposis syndrome with an autosomal
arise, including abdominal desmoid tumours that
recessive pattern of inheritance. Polyps are typically
occur in about 10% of patients (Figure 31.11).
fewer in number and arise later than in FAP. The
These are fibroblastic tumours commonly affecting
lifetime risk of CRC is 80% (mostly right‐sided)
the abdominal wall or small bowel mesentery. They
with an average age of onset of 45 years. Treatment
are considered benign because they do not metasta-
is by colectomy and IRA.
sise but can be lethal because of aggressive local
growth causing small bowel obstruction and ure-
Lynch syndrome
teric compression. Treatment of desmoids is diffi-
cult, as complete resection is rarely achieved and Lynch syndrome (LS, previously called hereditary
response to medical therapy is variable. They are non‐polyposis colon cancer) is an inherited autoso-
not radiosensitive. Brain tumours are also seen in mal dominant disease arising due to mutations of
FAP (Turcot’s syndrome). MMR genes (MLH1, MSH2, MSH6 and PMS2). It
The principal treatment of FAP is prophylactic carries a lifetime risk of colon cancer of around
colectomy timed to occur before the onset of CRC, 80%. Cancer development is substantially faster
usually before the age of 20. The surgical options than for sporadic CRC. The cardinal features are
include the following. early age of cancer onset (approximately 44 years),
• Total colectomy and ileorectal anastomosis right‐sided cancers in 70%, an excess of synchro-
(IRA) eliminates colonic polyps. This opera- nous and metachronous CRCs and an association
tion has a low complication rate and good with certain extracolonic cancers (endometrial car-
postoperative bowel function and avoids pelvic cinoma, transitional cell carcinoma of the urinary
nerve dysfunction. The retained rectum requires tract, adenocarcinomas of the stomach and small
regular surveillance as the risk of rectal cancer bowel, and other cancers including those of ovaries,
is about 15% at 15 years. pancreas and biliary tract). Polyposis is not a fea-
ture of LS, and the incidence of adenomas in LS
approximates that of the general population. The
colon cancers of LS are more likely to be poorly
differentiated and mucinous.
The clinical diagnosis of LS once depended only
on family history (Bethesda criteria) but this is
imprecise. Suspicion for LS is now guided by
immunohistochemistry testing of tumour speci-
mens. Genetic testing can then be initiated to
identify a specific MMR gene mutation. As the
penetrance of CRC is not 100% (as it is in FAP),
prophylactic colectomy is not usually offered.
However, annual colonoscopic surveillance is
Fig. 31.11 Computed tomography scan of an abdomen recommended because of the rapid onset of CRC
showing a large desmoid tumour occupying almost the in LS. Total colectomy and IRA is undertaken
entire peritoneal cavity. when colon cancer occurs.
Juvenile polyposis syndrome Quirke P, Dudley P, Dixon MF, Williams NS. Local recur-
rence of rectal adenocarcinoma due to inadequate surgical
Juvenile polyposis syndrome may arise in an auto- resection. Histopathologic study of lateral tumour spread
somal dominant fashion due to mutations in the and surgical excision. Lancet 1986;ii(8514):996–9.
tumour suppressor gene SMAD4 (MADH4). It is Taylor FG, Quirke P, Heald RJ et al. Preoperative mag-
characterised by hamartomatous (juvenile) polyps netic resonance imaging assessment of circumferential
in the colon, rectum and small bowel and stomach. resection margin predicts disease free survival and local
The number of polyps is less than seen in FAP and recurrence: 5 year follow up results of the MERCURY
the lifetime risk of colon cancer is 40%. Surveillance study. J Clin Oncol 2014;32:34–43.
by gastroscopy and colonoscopy is commenced at
the age of 15 years.
MCQs
Peutz–Jeghers syndrome Select the single correct answer to each question. The
Peutz–Jeghers syndrome (PJS) is due to an autosomal
dominant inherited mutation in the tumour‐
suppressor gene STK11. Hamartomatous polyps 1 Which of the following is not a symptom of caecal
can occur anywhere in the gastrointestinal tract. cancer?
Symptoms occur from early teenage years. As the a iron deficiency anaemia
polyps are particularly common in the small bowel, b a palpable mass in the right lower quadrant
bowel obstruction due to intussusception and gas- c large bowel obstruction
trointestinal bleeding are common presentations. d small bowel obstruction
Family history, oral mucocutaneous pigmentation e liver metastases
and genetic testing aid the diagnosis of PJS. There
is a lifetime risk of cancer approaching 85% (over 2 Which of the following statements regarding FAP is
50% in the gastrointestinal tract). Patients with incorrect?
PJS require surveillance colonoscopy and gastro‐ a inheritance is autosomal dominant
duodenoscopy from an early age. b the condition accounts for 20% of all colorectal
cancers
Serrated polyposis syndrome c most affected individuals develop polyps by the
age of 15 years
Serrated polyposis syndrome (formerly called d desmoid tumours are an association
hyperplastic polyposis) is an uncommon polyposis e without colectomy, affected individuals will
syndrome with the finding of multiple or large develop CRC
serrated polyps in the colon. The inheritance pattern
is unknown. There is a definite increase in risk for 3 Which of the following proven factors associated
CRC (especially right‐sided cancers) but the actual with the development of CRC is incorrect?
lifetime risk is uncertain. Individuals with serrated a long‐standing colitis
polyposis syndrome require regular colonoscopic b family history of CRC in a parent or sibling
surveillance. Colectomy and IRA is recommended c recurrent diverticulitis
for patients with uncontrolled polyposis or colon d adenomatous polyps
cancer. e pelvic irradiation
4 Which of the following oncologic outcomes for

Further reading rectal cancer is incorrect?
a improved by preoperative staging by MRI
Heald RJ, Moran BJ, Ryall RD, Sexton R. Rectal cancer:
b improved by neoadjuvant chemoradiotherapy
the Basingstoke experience of total mesorectal excision,
c influenced by surgical technique
1978–1997. Arch Surg 1998;8:894–9.
Kapiteijn E, Marijnen CA, Nagtegaal ID et al. Preoperative d always improved by early detection of metastases
radiotherapy combined with total mesorectal excision e improved by extensive en‐bloc resection of
for resectable rectal cancer. N Engl J Med 2001;345: surrounding structures adherent to locally
638–46. advanced tumours
32 Large bowel obstruction
Raaj Chandra
LBO and require surgical treatment. Diverticular

Introduction disease is discussed in Chapter 30. Strictures from
inflammatory bowel disease, including Crohn’s dis-
Large bowel obstruction (LBO) needs to be man-
ease and ulcerative colitis, as well as strictures
aged as a surgical emergency, although not all cases
caused by radiation and bowel ischaemia are
will need an operation. It can occur anywhere in the
known causes of LBO but are less common. Other
colon and rectum due to various causes and has a
uncommon causes include extrinsic tumours, for-
100% mortality if left untreated. This is why LBO
eign bodies and faecal impaction.
must be diagnosed and treated promptly with early
An obstruction in the colon or rectum leads to
surgical team referral. Traditionally, LBO has been
significant dilatation of the bowel proximal to the
defined as the absence of flatus or bowel move-
obstruction. This leads to a cascade of events
ments for greater than 24 hours associated with
including mucosal oedema, venous congestion and
abdominal distension, and the visualisation of
reduced arterial flow to the bowel. This increases
dilated colon on plain abdominal X‐ray. More
the mucosal permeability of the colon which pro-
recently, with modern CT techniques and the use of
gresses to bacterial translocation, the systemic
oral, intravenous and rectal contrast, the diagnosis
inflammatory response syndrome (SIRS), dehydra-
of LBO has become much easier and more accurate.
tion and electrolyte abnormalities. Eventually
This chapter discusses the aetiology, clinical fea-
ischaemia progresses to infarction, perforation and
tures, investigations and treatment of LBO.
soiling of the peritoneal cavity, resulting in general-
ised peritonitis, multiorgan failure and potentially
death.
Aetiology and pathophysiology
The majority of LBO cases are caused by primary Clinical features

or secondary neoplasms. Just over 50% are caused
by colorectal cancers (discussed in Chapter 31). Patients with LBO commonly present with abdomi-
Approximately 10–17% are caused by sigmoid or nal pain, distension and absolute constipation or
caecal volvulus. This occurs when the colon twists the inability to pass flatus or bowel movements.
on its mesentery causing bowel obstruction and is Nausea and vomiting are less common and usually
discussed later. Sigmoid volvulus occurs much more a late sign, depending on the competency of the ile-
commonly than caecal volvulus. A further 10% are ocaecal valve. For example, if the obstruction is in
attributed to diverticular strictures which result as the rectum, then it may take several days for the
a complication of diverticular disease. Diverticular proximal colon to distend to a point where perfora-
strictures may be classified as inflammatory or non‐ tion is imminent. If the ileocaecal valve is incompe-
inflammatory. Inflammatory strictures result from tent, then nausea and vomiting may be further
an episode of acute diverticulitis, in which the delayed since the small intestine will also take time
inflammatory process results in transient LBO that to become distended. Colonic perforation is more
resolves as the inflammatory process is treated, usu- likely if the ileocaecal valve is competent since the
ally with antibiotics. Non‐inflammatory strictures colon is unable to decompress into the small intes-
are more chronic and result after recurrent episodes tine. The presentation of LBO depends on the
of diverticulitis. These are more likely to result in underlying aetiology. For example, it is acute in the
285
case of sigmoid volvulus but can be more chronic in Tachycardia, hypotension and fever may also be
the case of bowel cancer. present. A distended abdomen is an important sign
in LBO, although the presence of ascites can also
paint the same picture and must be excluded. The
History presence of shifting dullness on percussion will con-
firm ascites while percussion over distended colon
When LBO is suspected, the following focused will remain tympanitic, producing a low‐pitched,
questions will help confirm the diagnosis. drum‐like sound.
• Is the presentation acute or chronic? • Is there local or generalised tenderness with signs
• Is there abdominal pain? If so, is the pain colicky of peritonism? This includes percussion and
or constant? Obstructive pain is colicky but can rebound tenderness.
progressively become constant if generalised • Is there a mass present? This is a sign of advanced
peritonitis develops. disease.
• What is its severity? Pain from LBO is usually • The absence of bowel sounds raises the suspicion
severe. of colonic pseudo‐obstruction and can be high‐
• Are there any aggravating or relieving factors? pitched with a mechanical obstruction, although
Any form of bowel obstruction is aggravated by this is an unreliable sign.
eating food. In the advanced stages of LBO where • A per rectal examination is mandatory to exclude
generalised peritonitis has developed, any form a rectal tumour or the presence of blood.
of movement or even coughing will cause severe
pain and the patient will much prefer to lie still.
• Vomiting may provide some temporary relief. Investigations
The contents of the vomitus will be useful.
Vomiting from an LBO is commonly described as These patients are often elderly with significantly
feculent. It will be foul‐smelling and look like deranged biochemical markers suggestive of malnu-
faeces, while vomitus from a proximal small trition, renal failure and multiorgan failure.
bowel obstruction will be bile‐stained and green- Classically, patients with bowel ischaemia will have
ish in keeping with small intestinal contents. an elevated white cell count and serum lactate and
Other associated symptoms include recent weight have a metabolic acidosis.
loss (a non‐specific indicator of malignancy),
change in bowel habit, rectal bleeding and pas-
sage of mucus. These symptoms should raise the
Blood tests
possibility of an underlying colorectal cancer. The following blood tests should be performed.
• Is there a family history of bowel cancer or • Full blood count looking for anaemia or an ele-
inflammatory bowel disease? vated white cell count.
• Has the patient had a previous colonoscopy or • Electrolytes, urea and creatinine will confirm
undertaken the National Bower Cancer Screening dehydration and/or renal failure as well as elec-
Test? It is unlikely that a malignancy is the cause trolyte disturbances. Renal function should be
if a colonoscopy has been performed successfully checked prior to CT with intravenous contrast
in the preceding 2 years. due to the potential for nephrotoxicity from con-
• Has the patient had previous abdominal surgery trast media.
and for what reason? A past history of colorectal • Deranged liver function tests can be a sign of
cancer would raise the possibility of recurrent or multiorgan failure and a low albumin level is a
metastatic disease. If a bowel resection has been marker of malnutrition. A preoperative level
performed, there could be a stricture at the site of below 30 g/L is a marker of increased periopera-
the old anastomosis. tive morbidity.
• C‐reactive protein is an acute‐phase reactant pro-
duced in the liver and is raised in the setting of an
Examination acute inflammatory process. It is a useful test
since it may be markedly elevated despite a nor-
A detailed examination is very important. On gen- mal white cell count.
eral inspection, signs such as cachexia and pallor • A coagulation profile should be performed in all
may suggest malignancy. Other signs of altered patients who are unwell and potentially requir-
physiology include dry mucous membranes and ing surgery. Severely unwell patients regularly
low urine output, suggestive of dehydration. become coagulopathic, which needs urgent
32: Large bowel obstruction 287
correction and control, often concurrent with the introduction of multidetector CT technology with
operation. intravenous contrast medium has made it possible
• Serum lactate is a useful test, particularly if bowel to gather critical information regarding the site of
ischaemia is a concern. A raised lactate level is a obstruction, aetiology and extent of the lesion as
sign of tissue hypoxia. well as associated bowel ischaemia. Multidetector
• An arterial blood gas (if available) is also impor- CT is a well‐tolerated rapid imaging mode that pro-
tant. This will give important information on the duces images in one breath‐hold. The addition of
acid–base status of the patient. rectal contrast is very helpful in distinguishing
• In the subacute setting, iron studies should be between mechanical distal LBO and pseudo‐
included since preoperative iron infusion (time obstruction. However, in cases where there is a
permitting) has been shown to significantly reduce clear transition point separating severely dilated
red blood cell transfusion requirements and length proximal colon and collapsed distal colon, rectal
of hospital stay, with higher percentages of nor- contrast may not be required. If CT is not available
malised haemoglobin levels both at time of dis- or if the results are equivocal, fluoroscopy with
charge as well as at 30 days after surgery. contrast enema remains a helpful investigation. The
main advantage is that it allows easy distinction
Imaging between LBO and colonic pseudo‐obstruction. It
may also be used to confirm a colonic volvulus.
If the patient is unwell with signs of generalised peri-
Water‐soluble iodinated contrast material such as
tonitis, then an erect chest X‐ray and plain abdomi-
Gastrografin should be used as it is easily absorbed
nal films are quick and inexpensive while sufficient
in the peritoneum should there be a perforation.
to make the diagnosis and exclude perforated viscus
requiring immediate laparotomy. The presence of
free gas under the diaphragm will confirm the diag-
nosis of a perforated viscus, while dilated colonic Treatment
segments proximal to an obstruction with no rectal
gas on an abdominal plain film will be suspicious for This will depend on the aetiology, site of obstruc-
LBO after correlation with the clinical picture. tion and the expertise available at the hospital. It is
In most cases, high‐definition CT scanning is the recommended that, where possible, treatment is
imaging modality of choice (Figure 32.1). The under the care of a specialist colorectal surgery unit
or, at the very least, a general surgical team. If this
service is unavailable, then the patient should be
transferred to another centre after initial manage-
ment is commenced. Figure 32.2 provides an algo-
rithm to help guide surgical management.
Initial management
All patients with suspected LBO should receive
appropriate volume resuscitation with intravenous
fluids and be offered adequate pain relief.
Communication with the anaesthetic team is essen-
tial and they should be notified as early as possible
after the diagnosis is made so that resuscitation can
begin with the correction of biochemical abnormal-
ities well before any planned surgical intervention.
A urinary catheter should be inserted so that strict
fluid balance information can be obtained.
Intravenous broad‐spectrum antibiotics may be
commenced in the setting of sepsis.
A nasogastric tube should be inserted, particu-
larly in patients who are vomiting with significant
abdominal distension. This will help relieve the
Fig. 32.1 CT scan with intravenous contrast patient’s discomfort and enable decompression of
demonstrating an obstructing neoplasm at the hepatic the distended proximal bowel. It is expected that
flexure (arrow). the patient will develop a paralytic ileus after
Large bowel obstruction
Sigmoid
volvulus Malignant
Left Right Metastatic
Colonoscopic decompression
Trained
colorectal General surgeon
Unsuccessful surgeon
Right
hemicolectomy
Surgery Risk factors for

anastomotic
Resection +
leak
primary
anastomosis Hartmann’s
OR procedure
Resection; OR
anastomosis + Resection +
diverting stoma primary
OR
Anastomosis +
Hartmann’s loop ileostomy Right
procedure hemicolectomy Palliative
+ loop colonic stent
ileostomy OR
right hemi +
end ileostomy
Fig. 32.2 Algorithm for the management of LBO.

surgery, and so the nasogastric tube should remain colorectal teams are available, include resection of
in situ postoperatively until bowel function has the affected segment of colon with primary anasto-
returned and nasogastric output reduces to an mosis, or primary resection with anastomosis and a
acceptable level. diverting stoma. Both procedures may include
intraoperative colonic lavage with saline. This
Malignant LBO reduces the amount of faecal matter in the colon,
thereby theoretically reducing the risk of anasto-
Right‐sided obstruction (proximal to splenic motic leak. However, debate continues over whether
flexure) intraoperative lavage is necessary, or even helps. In
A right hemicolectomy with primary anastomosis is all cases, the major arterial supply and draining
the operation of choice, where the distal ileum is lymph nodes should be removed for oncological
anastomosed to the proximal transverse colon after reasons.
high ligation of the ileocolic vessels close to their In less common circumstances a diverting loop
origin at the superior mesenteric artery for onco- colostomy proximal to the site of obstruction or,
logical clearance of the draining lymph nodes. This rarely, a caecostomy can be formed as a temporis-
is known as an oncological resection. If the tumour ing measure to decompress the colon. Proximal
is closer to the splenic flexure, then an extended diversion is a good option if the obstructing lesion
right hemicolectomy should be performed with is in the rectum since the management of rectal can-
anastomosis of the distal ileum to either the distal cer is different from that of colon cancer in some
transverse colon or the proximal descending colon. circumstances (see Chapter 31). In cases of locally
In this case both the ileocolic and middle colic ves- advanced rectal cancer, it is better to treat these
sels should be ligated, divided and all draining patients with preoperative chemoradiotherapy
lymph nodes removed. If there are significant risk since this has been shown to reduce local recur-
factors for anastomotic leak, then a diverting loop rence rates and helps to down‐stage the tumour
ileostomy may be considered to protect the anasto- prior to a curative resection. Therefore, a loop
mosis. High‐risk patients include those who are colostomy allows the patient to recover from the
malnourished (albumin <30 g/L), have chronic or effects of the obstruction and provides the opportu-
preoperative renal failure, are immunosuppressed, nity to stage the disease. The patient then undergoes
or have an American Society of Anesthesiologists a period of chemoradiation therapy before a defini-
(ASA) score of III/IV. tive resection is performed.
Occasionally, a right hemicolectomy with an end‐ A final option in the management of LBO is the
ileostomy and stapling of the colonic stump may be use of colonic stents (Figure 32.3). These can be
necessary if the patient is very unwell. In this situa- used for both left‐ and right‐sided obstructions.
tion, the colonic stump may be brought out and Their use is beneficial particularly in the setting of
sutured superficial to the rectus sheath as a buried metastatic disease when a major operation may be
mucous fistula. Thus, if the colonic end leaks, the high risk and will not improve the patient’s overall
contamination can be controlled as a wound prob- survival. As mentioned in the introduction, if left
lem without the more serious complication of intra‐ untreated LBO has a 100% mortality. However,
abdominal sepsis. with emergency surgery the mortality is still high at
Recommendation: In most cases of right‐sided 15–20%.
LBO, a right hemicolectomy is the procedure of Insertion of a stent provides immediate relief
choice. from the obstruction and gives good palliation. It
can be performed in an endoscopy suite under light
sedation if the patient is too unwell to undergo a
general anaesthetic. However, the use of colonic
Left‐sided obstruction (distal to splenic flexure)
stents is controversial when used as a bridge to sur-
There are a number of options when managing left‐ gery if there is no metastatic disease. This is because
sided obstruction. Hartmann’s procedure is the stents are not without complications, of which the
most commonly performed. This is a surgical resec- most serious is perforation of the colon. If perfora-
tion of the sigmoid colon and part of the upper rection occurs, this in theory converts a curable cancer
tum. The proximal colon is then brought out into a potentially incurable one due to the spillage
through the abdominal wall as an end‐colostomy. of cancer cells into the peritoneal cavity. Colonic
The rectal stump is closed with a stapler and left in stenting should only be performed by experienced
situ. Other options, particularly when specialist endoscopists who have expertise in stenting.
(a) Sigmoid volvulus

Endoscopic reduction is the treatment of choice in
the acute setting, with an 80% success rate. A colo-
noscope is passed via the rectum and the insuffla-
tion of gas is able to untwist the colon. The
endoscope also allows for decompression of the
dilated colon proximal to the obstruction. There is
evidence that after a single episode, the rate of
recurrence is as high as 50%. Recurrent volvulus is
more likely to lead to ischaemic complications and
therefore a semi‐elective sigmoid resection with pri-
mary anastomosis is the treatment of choice once
the patient has recovered from the acute episode.
This can be performed using a limited left iliac
fossa incision due to the length and redundancy of
the sigmoid colon, which can be delivered through
a small incision. This avoids the need for a midline
laparotomy.
(b)
Caecal volvulus
Unlike sigmoid volvulus, colonoscopy for caecal
volvulus is not recommended. The operation of
choice is a right hemicolectomy with primary anas-
tomosis. The right colon is usually very mobile and
therefore minimal mobilisation is required. In the
past, caecopexy used to be performed, and involved
suturing of the untwisted colon to the abdominal
wall at multiple points to prevent it from twisting
again. This is now not recommended due to its high
recurrence rates. Similarly, pexy procedures should
not be performed for sigmoid volvulus.
Diverticular and other benign strictures

Stenting or dilatation of ‘benign’ strictures in the
colon is generally discouraged due to the risk of
malignancy, (i.e. not resecting a lesion that later
Fig. 32.3 (a) CT scan with intravenous contrast proves to be malignant). In the acute setting, these
demonstrating an obstructing neoplasm in the sigmoid should be treated in a similar fashion to malignant
colon. (b) The obstruction has been relieved with a LBO.
colonic stent which can be seen on this plain X‐ray.
Acute colonic pseudo‐obstruction

(Ogilvie’s syndrome)
Recommendation: In a patient with significant
comorbidities and risk factors, Hartmann’s proce- Acute colonic pseudo‐obstruction (ACPO) is a
dure is the operation of choice. Primary resection syndrome characterised by a clinical picture sug-
with anastomosis may be performed but only in gestive of mechanical obstruction in the absence
expert hands. The use of stenting as a bridge to sur- of any demonstrable evidence of such an obstruc-
gery is not recommended due to the risk of perforation in the intestine. Therefore, it is important
tion and converting a potentially curable cancer that this differential diagnosis is considered in any
into an incurable one. Stenting as a palliative meas- case of suspected LBO. The colon may become
ure is recommended but only if the expertise is massively dilated. If it is not decompressed, the
available. patient risks perforation, peritonitis and death.
The mortality rate can be as high as 40% when • Insert a nasogastric tube if the patient is vomiting.
perforation occurs. • Insert a rectal tube which can be therapeutic in
ACPO generally develops in hospitalised patients. some cases.
Studies have documented that as many as 95% of • Consider the use of neostigmine, an acetylcho-
cases of colonic pseudo‐obstruction are associated linesterase inhibitor. Neostigmine inhibits
with medical or surgical conditions, the rest being destruction of acetylcholine by acetylcholinester-
classified as idiopathic. The most commonly associ- ase, thereby facilitating transmission of impulses
ated conditions include trauma, pregnancy, caesar- across the myoneural junction and enhancing
ean section, severe infections, and cardiothoracic, colonic motility. Neostigmine has a significant
pelvic or orthopaedic surgery. These patients are side‐effect profile, particularly cardiovascular
commonly bed bound, have serum electrolyte and respiratory effects. Cardiovascular complica-
imbalances and are taking high doses of opiates, all tions include arrhythmias and non‐specific ECG
of which have negative effects on colonic motility. changes as well as cardiac arrest, syncope and
The exact pathophysiology of ACPO is unclear. hypotension, particularly when given intrave-
Current theories continue to suggest the idea of an nously. Respiratory complications include
imbalance in the autonomic nervous system. These increased oral, pharyngeal and bronchial secre-
theories focus on the increased sympathetic tone tions, dyspnoea, respiratory depression/arrest
(which results in inhibition of colonic motility) and and bronchospasm. Therefore, it is important
decreased parasympathetic tone (which then also that neostigmine is administered in an intensive
reduces colonic motility), or a combination of both care setting with the availability of cardiac
as the cause. monitoring.
If colonic pseudo‐obstruction is suspected, then • Colonoscopic decompression can be used as an
some form of dynamic contrast imaging study is alternative to neostigmine or if neostigmine fails.
recommended to exclude a mechanical bowel It has been shown to be effective in 85% of cases
obstruction. This is essential since the management but must be performed by an experienced
is different from that of LBO. The mode of imaging endoscopist. It is a technically difficult procedure
study will depend on availability of services and since the bowel is unprepared. Therefore, colonic
will include either a CT scan of the abdomen and perforation is a significant possibility.
pelvis with rectal contrast, or a contrast enema Colonoscopic decompression may need to be
study using fluoroscopy. repeated several times to achieve full resolution.
The principles of management for ACPO include In the case of bowel perforation, laparotomy and
the following. bowel resection with end‐ileostomy is usually
• Correct any underlying biochemical abnormalities. required. An algorithm for the management of
• Reduce opiate intake. ACPO is shown in Figure 32.4.
Acute colonic
pseudo-obstruction
Rigid sigmoidoscopy
Correct biochemical
Reduce opiates + rectal tube
abnormalities
decompression
Unsuccessful
Consider
neostigmine or Repeat if recurs
colonoscopic
decompression
Unsuccessful
Surgery
Fig. 32.4 Algorithm for the management of ACPO.

Conclusions MCQs
LBO needs to be considered a surgical emergency Select the single correct answer to each question.The
since it leads to significant morbidity and mortality correct answers can be found in the Answers section
if not treated promptly. Early surgical team referral at the end of the book.
is essential. There are many causes of LBO, although 1 Which of the following symptoms and signs does
colorectal cancer is the commonest. It is imperative not commonly present in complete LBO?
that LBO is not mistaken for a colonic pseudo‐ a abdominal pain
obstruction since the treatment is different. The b abdominal distension
treatment of LBO will depend on the location of c absolute constipation
the obstruction and whether metastatic disease is d inability to pass flatus
present. Surgical resection is required in most cases. e diarrhoea
However, colonic stenting may be used particularly
in the setting of metastatic disease. If left untreated, 2 Which of the following is the imaging modality of
the mortality rate is 100%. choice for the diagnosis of LBO?
a plain abdominal X‐ray
b abdominal ultrasound
c Gastrografin enema
d multidetector CT scan of the abdomen and pelvis
Further reading e MRI of the abdomen and pelvis
Cancer Council Australia. Colorectal Cancer Guidelines

3 Which of the following is not an accepted treat-
Working Party. Clinical practice guidelines for the
prevention, early detection and management of colo- ment option in left‐sided LBO?
rectal cancer. Available at https://wiki.cancer.org.au/ a Hartmann’s procedure
australiawiki/index.php?oldid=173168 (accessed 28 b chemoradiation therapy
January 2018). c colon resection with primary anastomosis
Frago R, Ramirez E, Millan M, Kreisler E, del Valle E, d colon resection, anastomosis and diverting stoma
Biondo S. Current management of acute malignant e colonic stenting
large bowel obstruction: a systematic review. Am J Surg
2014;207:127–38. 4 Which of the following is not an acceptable measure
Saunders MD. Acute colonic pseudo‐obstruction. In:
to take in the initial management of ACPO?
Talley NJ, DeVault KR, Wallace MB, Aqel BA, Lindor
a correction of underlying biochemical
KD (eds) Practical Gastroenterology and Hepatology
Board Review Toolkit. Hoboken, NJ: Wiley Blackwell, abnormalities
2016:343–8. b reduce opiate intake
Yassaie O, Thompson‐Fawcett M, Rossaak J. Management c administer neostigmine
of sigmoid volvulus: is early surgery justifiable? ANZ J d perform colonoscopic decompression
Surg 2013;83:74–8. e perform a laparotomy
33 Perianal disorders I: excluding
sepsis
Ian Hayes1,2 and Susan Shedda1,3
1
Colorectal Surgery Unit, Royal Melbourne Hospital, Melbourne, Victoria, Australia
2
3
Royal Women’s Hospital, Melbourne, Victoria, Australia
luminal contents. This rectoanal inhibitory reflex

Anatomy and physiology allows for sampling of the contents. If defacation
then occurs, there is voluntary relaxation of the
The anal canal extends from the puborectalis mus-
external anal sphincter and straightening of the
cle to the anal verge and has a variable length
anal canal with relaxation of the puborectalis.
depending on gender. In the male it can be up to
6 cm long, whilst in the female the average length is
closer to 2 cm. The anal verge can be identified as History
the point of transition from hair‐bearing to non‐
hair‐bearing skin, visible on inspection of the peri- Four cardinal symptoms, their details and how they
neum. The major structures of the anal canal are the combine, form the basis of diagnosing most peria-
sphincter complex, anal glands, columnar and squa- nal conditions:
mous epithelium and the dentate line (Figure 33.1). • pain
The sphincter complex consists of the external • bleeding
and internal sphincter muscles. The external sphinc- • presence of a ‘lump’
ter is the continuation of the puborectalis and is • discharge.
skeletal muscle under voluntary control. It is often
divided into three parts but functionally acts as a Pain
single unit to provide additional strong contraction
when defecation is deferred voluntarily. The inter- The nature of perianal pain can help differentiate
nal sphincter is a continuation of the circular mus- perianal conditions. Pain worse with defecation is
cle layer of the rectum (involuntary, smooth muscle) characteristic of anal fissure. A short history of
and is the main muscular component of resting constantly increasing, severe pain suggests sepsis.
tone (Figure 33.2). The lower part of the anal canal Localised pain and a discrete lump suggest peria-
consists of non‐hair‐bearing squamous epithelium, nal haematoma.
with the line of transition called the dentate line
Bleeding
(Figure 33.3). At this point, the anal glands dis-
charge into the lumen of the anal canal to provide Blood from the perianal region is generally bright
lubricant for the passage of the stool. The proximal red, of small volume and not mixed with stools.
part of the anal canal merges with the columnar Bleeding is generally with defecation but blood which
epithelium of the rectum and is often referred to as stains underclothes strongly suggests a cause that is
the ‘transition zone’. In the non‐diseased state, the located external to the sphincter muscles. Blood from
haemorrhoidal complex of blood vessels lies deep haemorrhoids can squirt onto the toilet bowl.
to the mucosa at this level. Bleeding and anal pain suggest fissure. Any rectal
When stool passes into the distal rectum, it causes bleeding should be regarded as an abnormal symp-
reflex relaxation and distension of the internal anal tom. It can sometimes be difficult to differentiate
sphincter, allowing the mucosa of the transition bleeding due to an insignificant anal cause from
zone in the upper anal canal to be exposed to the bleeding due to colorectal malignancy. Bleeding
293
from colonic lesions may appear bright red even if and position are relevant, as is the question of
their location is as far proximal as the descending whether the lump prolapses (large haemorrhoids
or sigmoid colon. Colonoscopy to exclude neopla- and rectal prolapse) and if it needs to be manually
sia should be considered in patients over 40 years reduced back into the anal canal. How long the lump
of age, those who have a significant family history has been present (years for skin tags and warts) and
of bowel cancer, those with other colorectal symp- if it is increasing in size should be ascertained.
toms such as change in bowel habit, and in all cases
where a clear anal cause of the bleeding cannot be Discharge
identified.
It is important to confirm if the discharge is from
the anus itself or from the surrounding perianal
Lump
skin. Purulent discharge suggests a fistula. Mucous
Patients’ description of a perianal lump is often leakage may represent prolapse of haemorrhoids or
vague because the area is not directly visible. The size full‐thickness prolapse of the rectum or it may be a
manifestation of incontinence due to mild sphincter
weakness. Any leakage of mucus or pus onto the
perineal skin is very irritating and is an important
cause of pruritus ani.
Levator
ani
Anorectal
ring
External
sphincter
Internal
sphincter
Dentate line
Fig. 33.1 Anatomy of the rectum and anal canal. Fig. 33.3 Anal canal. DL, dentate line.
400 110
410 100
90
420
80
430
70
440
60
450 50
460 40
470 30
480 20
10
490 2
500 –6
510 –1.5
Fig. 33.2 Anal manometry pressure tracing using continuous perfusion catheter. The horizontal axis shows time, the
right vertical axis pressure (mmHg). The end of the catheter is in the rectum at the top of the trace. The anal canal is
represented by the pink/black horizontal pressure zone and atmospheric pressure is at the bottom of the trace. The three
black zones represent three episodes of voluntary contraction of the external sphincter. The baseline pink/orange trace
represents resting internal sphincter tone.
33: Perianal disorders I: excluding sepsis 295
Box 33.1 Conditions visible in the

perianal region
Perianal skin
• Psoriasis
• Changes of chronic itching
• Fistula
• Abscess
• Hidradenitis
• Warts
Anal verge
• Skin tags
• Perianal haematoma
• Prolapsing haemorrhoids
• Rectal prolapse
• Thrombosed haemorrhoids
• Anal intraepithelial neoplasia (AIN)
• Anal cancer
• Anal fissure Fig. 33.4 Endoanal ultrasound of the mid‐anal canal.
The probe is in the lumen, represented by the centre
black solid circle. The next grey zone is mucosa with a
Examination dense black circle of internal sphincter surrounding this.
The broad grey/black striped zone peripheral to this is
the external sphincter.
Many perianal diagnoses are visible without per-
forming an internal examination (Box 33.1). The
patient is examined in the left lateral position with
good lighting. Patients with chronic anal fissure, important test if inflammatory bowel disease is
intersphincteric abscess or thrombosed haemor- suspected.
rhoids may be too tender to allow digital internal MRI is used selectively and is helpful in cases of
examination without anaesthesia. However, the complex fistula or sepsis. MRI is the main imaging
distal edge of a fissure may be visible externally mode for perianal neoplasia. CT has limited appli-
without causing the patient undue discomfort. cation for most perianal conditions.
If possible, rigid sigmoidoscopy should be part of Endoanal ultrasound (Figure 33.4) involves plac-
routine examination for patients with perianal con- ing an ultrasound probe (the diameter of a finger)
ditions. It should be noted that, in clinical practice, into the anal canal. Anaesthesia is not required.
examination with a rigid sigmoidoscope is an This technique provides very good visualisation of
examination of the anal canal and rectum, rather the anal sphincters and anal fistulas.
than of the sigmoid. Defecating proctography involves using video‐
fluoroscopy and a rectal contrast medium to
observe dynamic movement of the rectum and pel-
Investigations vic floor during defecation. This test is useful in
diagnosing occult rectal prolapse and rectocele in
Clinical examination alone is sufficient to make a patients with symptoms of obstructed defecation.
confident diagnosis in most perianal conditions. Blood tests have minimal diagnostic use in most
However, examination under anaesthesia is fre- perianal conditions. Information about blood glu-
quently used as a further investigation when: cose and white cell count (WCC) is relevant in peri-
• a lesion requires biopsy for histological anal sepsis. C‐reactive protein and WCC are useful
confirmation markers of activity if inflammatory bowel disease
• when the area is too tender to allow clinical (IBD) is suspected. Faecal calprotectin can be used
examination as a screening test for IBD.
• when fistula or sinus tracks need to be probed. In the investigation of faecal incontinence, the
Colonoscopy is a common ancillary investigation function of the internal and external sphincters is
in patients with perianal conditions. It can be used tested by measuring resting and squeeze pressure in
to exclude causes of bleeding situated more proxi- the anal canal using a manometry catheter. Pudendal
mally in the bowel (such as neoplasia) and it is an nerve function is tested by measuring pudendal
nerve terminal motor latency using an electrode fissure symptoms against the possible risk of
placed in the anal canal which stimulates the sphincter weakness from surgery
pudendal nerve and records sphincter contraction. In most cases, initial outpatient treatment with 6
Endoanal ultrasound is used to examine the integ- weeks of topical 0.2% glyceryl trinitrate (GTN)
rity of the sphincter muscles. cream is trialled. GTN acts as a nitric oxide donor
causing relaxation of the smooth muscle of the
internal sphincter. Its main side effect is headaches
and it is effective in approximately 50% of cases.
Conditions presenting with pain The calcium channel blocking agents diltiazem and
nifedipine can be formulated as creams and used
Anal fissure topically in a similar manner to GTN but with
lower risk of headache.
Anal fissure refers to a split in the mucosa of the
If topical treatment fails, the next level of inter-
anal verge causing pain and minor bright‐red bleed-
vention often involves botulinum toxin injection
ing. Acute fissure refers to a simple split in the
into the sphincters, performed under anaesthesia.
mucosa that heals quickly and rarely requires
This is slightly more effective than the topical treat-
treatment.
ments and has a much lower risk of permanent
Chronic fissure is the main condition of impor-
sphincter impairment than sphincterotomy.
tance. It is defined by the fissure symptoms persist-
Surgical lateral internal sphincterotomy involves
ing for some weeks. The most distressing symptom
dividing the most distal portion of the internal
is severe pain on defecation localised to the site of
sphincter. If surgery is performed, the associated
the fissure. In addition, a less well‐defined pelvic
sentinel tag and hypertrophic anal papilla can be
pain can persist for hours after defecation, possibly
excised. Any associated fissure/fistula can be
due to spasm in the pelvic floor muscles.
de‐roofed. Sphincterotomy carries a low risk of
The characteristic clinical findings with a chronic
long‐term incontinence but is by far the most effec-
fissure include a sentinel tag at the most distal part,
tive treatment for fissure. In general, women have
a hypertrophic anal papilla at the proximal extent,
less reserve of sphincter muscle than men and are at
and visible white transverse fibres of the underlying
risk of previous, or subsequent, obstetric trauma to
internal sphincter muscle at the base. Usually, a
the pelvic floor. Because of this, sphincterotomy is
chronic fissure is located in the posterior midline of
rarely used as a first treatment in women.
the anal verge but can be located in the anterior
Occasionally, if pain is very severe, the most
midline. Multiple fissures or fissures in lateral posi-
effective treatment may be to proceed to urgent sur-
tions raise the possibility of underlying IBD.
gery and perform lateral sphincterotomy or inject
The initiating cause of anal fissure is uncertain.
botulinum toxin, as appropriate. In this circum-
Relative ischaemia of the base may play a role and
stance, the patient may be too tender to allow con-
there is often a history of passing a hard stool and
firmation of the presence of a fissure preoperatively.
traumatising the mucosa prior to the onset of symp-
Under anaesthesia, the fissure can be confirmed and
toms. However, persistence of the fissure is associ-
treated, and other important differential diagnoses,
ated with spasm of the smooth muscle of the
such as intersphincteric abscess, excluded.
internal sphincter which, in turn, limits blood sup-
ply to the base of the fissure and impairs healing
(the bleeding is from the mucosal edges). Perianal haematoma
Clinical examination is difficult because the area
Patients with this condition present with fairly sud-
is tender and the anus is tightly closed with sphinc-
den onset of a painful hard lump at the anal verge.
ter spasm. Usually the lower edge of the fissure can
It is important to note that the lesion is subcutane-
be visualised with gentle separation of the buttocks.
ous in the perianal skin rather than prolapsing from
Digital rectal examination is not usually possible.
the anal canal. The lump is dark blue in colour and
about the size of a pea. Patients often give a history
Treatment
of straining prior to the onset of the lump. The
Most modes of treatment of chronic fissure are lesion is due to rupture of a small blood vessel.
directed towards decreasing the spasm in the inter- Because of the dense subcutaneous fibrous bands in
nal sphincter muscle. Treatment of constipation, the perianal skin, a contained haematoma is formed
fibre supplements and analgesia are important rather than a spreading bruise.
additions to any regimen. Treatment decisions for The natural history is that the lump can be quite
this condition involve balancing the severity of the painful for several days but gradually resolves.
Occasionally the overlying skin necroses, releasing difficulty with anal hygiene. Clinical examination
a small dark haematoma. If the patient is seen in the may reveal externally prolapsed haemorrhoids but
first day or two, relief of symptoms can be quickly often proctoscopy/sigmoidoscopy is required to
obtained by incising the lesion to release the hae- visualise smaller haemorrhoids. It is important to
matoma. After this period, the haematoma is organ- note that non‐prolapsed haemorrhoids are gener-
ising and is less easily released. Most patients can ally too soft to palpate on digital rectal examina-
be managed with reassurance about the diagnosis, tion. It should also be noted that small haemorrhoids
warm baths and analgesia. are common and may not always be the source of
the bleeding.
Thrombosed haemorrhoids The cause of haemorrhoids remains unclear and
previously was thought to be due to repeated strain-
Patients with thrombosed haemorrhoids often
ing, resulting in engorgement of the haemorrhoidal
describe a past history of prolapsing haemorrhoids
complex and progressively larger vessels. A more
which have become painful and irreducible follow-
recent hypothesis suggests that haemorrhoids are in
ing an episode of severe straining (childbirth or
fact a prolapse of the anal canal tissue.
severe constipation). The pathological process is
Haemorrhoids are graded I–IV depending on
that the previously moderately large haemorrhoids
whether they are externally visible or not, and if
become further engorged with blood and oedema,
they are manually reducible (Box 33.2). The initial
and their increased size results in them becoming
treatment consists of improving the quality of the
partially trapped external to the sphincters. The
stool with increasing fibre and water intake. This is
pain results in sphincter spasm, worsening the situ-
usually successful for the lesser grades of haemor-
ation. The static blood within the haemorrhoids
rhoid. If this is unsuccessful, then more invasive
thromboses making them irreducible. On examina-
treatments will be required. The further treatment
tion, the patient will be in discomfort and have
of haemorrhoids depends on the grade of the haem-
circumferential, large, dark purple‐coloured, irre-
orrhoid. Rubber‐band ligation is reserved for
ducible haemorrhoids.
grades I and II, whereas grades III and IV usually
The natural history of the condition is that the
require excisional haemorrhoidectomy.
swelling usually settles over several days. Most
Rubber band ligation is done transanally through
patients can be managed conservatively with rest,
a proctoscope and can be performed on a non‐
analgesia and topical application of ice to help
anaesthetised patient in an outpatient setting. The
reduce the swelling. Urgent haemorrhoidectomy is
mucosa proximal to the area of haemorrhoid is
required if the prolapsed tissue becomes necrotic or
grasped and a narrow‐diameter rubber ring placed
infected, or when patients are not improving with
over it. It is important to note that the band does
conservative treatment. Surgery in this situation is
not encircle the haemorrhoid itself. Generally, the
problematic because excising all the haemorrhoidal
band falls off 2 weeks following the procedure leav-
tissue would remove most of the anal verge skin
ing a small ulcerated area that gradually heals by
and mucosa, resulting in long‐term stenosis. The
fibrosis. This process draws the haemorrhoidal
solution is to remove the worst of the prolapsed
tissue proximally and may also interfere with the
tissue but leave adequate bridges of skin and
blood supply of the haemorrhoid. The zone where
mucosa, albeit quite swollen, to avoid fibrosis.
the band is placed should be insensate but it is not
Generally, patients feel much more comfortable
uncommon for patients to experience discomfort
postoperatively.
after the procedure. This is also a risk of secondary
haemorrhage when the band sloughs 2 weeks fol-
Perianal sepsis lowing the procedure.
This is described in Chapter 34.
Box 33.2 Haemorrhoid grades
Conditions presenting with bleeding • Grade I: enlarged internal haemorrhoids that do

not prolapse
Haemorrhoids • Grade II: prolapsing haemorrhoids that spontane-
ously reduce
Haemorrhoids are a very common condition and
• Grade III: prolapsing haemorrhoids that require
usually present with painless, bright red, per rectal
manual reduction
bleeding. Patients may also complain of a pro-
• Grade IV: irreducible prolapsed haemorrhoids
lapsing lump, itching (due to mucous leakage) and
Haemorrhoidectomy involves surgically excising Anal cancer/anal intraepithelial neoplasia

the redundant haemorrhoidal tissue. This proce-
Anal intraepithelial neoplasia (AIN) is the precur-
dure is performed under general or spinal anaesthe-
sor to squamous cell carcinoma of the anus. It is
sia using a variety of surgical techniques but all
caused by neoplastic transformation as a result of
with similar end results. Patients need to expect dis-
HPV infection (usually subtypes 16 and 18). There
comfort for approximately 2 weeks postoperatively
are three grades of AIN: progression from grade I
and, because of this, the procedure is reserved for
to III relates to increasing depth of penetration of
patients with large haemorrhoids causing signifi-
dysplastic cells into the epithelium. The natural his-
cant symptoms
tory of AIN in non‐immunosuppressed patients
remains unclear. Treatment is generally non‐opera-
Luminal causes of bleeding tive with close observation, although visible lesions
This topic has been discussed in the section History. should be excised.
The most important diagnoses which need to be Squamous cell carcinoma (SCC) of the perianal
excluded are large polyps, cancer and IBD. skin most commonly presents with a lump which
may cause bleeding, itch and pain. SCC located
intra‐anally more commonly presents with bleed-
Conditions presenting with lump ing. Although most SCCs of the anal canal are
located distal to the dentate line, they can be located
Skin tags higher in the anal canal or even in the lower rectum
because metaplastic squamous cells can be found in
These are redundant areas of skin at the anal verge the transitional zone between lower anal squamous
which may have resulted from previously throm- and rectal columnar mucosa. On clinical examina-
bosed haemorrhoids or previous anal fissure. They tion, the lesion feels hard, with raised rolled edges
are more common in patients who have been preg- and central ulceration (Figure 33.5). Disease exter-
nant and usually increase slowly in size with age. nal to the anal verge may potentially be excised.
They are usually asymptomatic, although they may
cause concern due to cosmesis or difficulty with
anal hygiene. Often reassurance is adequate treat-
ment. Surgical excision may be cautiously offered
on the understanding that there may be subsequent
development of further skin tags and that complete
excision may not be possible due to the risk of anal
stenosis.
Anal warts
Anal warts are a sexually transmitted infection due
to human papillomavirus (HPV), most commonly
subtypes 6 and 11. Anal warts may present as non‐
tender lumps that may be itchy or may bleed if
larger. They are often multiple, have a distinctive
appearance with a ‘warty’ surface, and can be
found in perianal skin and the distal anal canal.
The normal skin around a wart may also be
infected with HPV which may have spread from
other areas of the perineum. Anal intercourse is not
required for infection of the anal canal. Importantly,
warts may be distributed up to the dentate line
inside the anal canal but do not usually progress
proximal to this. The macroscopic lumps can be
surgically removed but infection remains in the
surrounding skin leading to recurrence. Imiquimod
is an immune‐modifying agent used topically and
will act to eradicate HPV but has limited action on
large lesions. Fig. 33.5 Squamous cell carcinoma of the anal verge.
Levator Faecal incontinence

ani
Faecal incontinence is a common condition that
mainly affects women over the age of 50. The
External majority of patients will have a history of obstetric
sphincter
Internal
difficulties resulting in either direct injury to the
sphincter sphincter complex or neuronal injury. Other causes
include surgical trauma and prolonged straining.
The treatment of incontinence is determined by the
impact on quality of life rather than the aetiology. It
may be classified by the consistency of the faecal
loss: flatus, liquid or solid stool. Conservative treat-
ment consists of lifestyle and dietary modification
Full-thickness
prolapse with pelvic floor physiotherapy. These simple meas-
ures are often successful in allowing the patient to
Fig. 33.6 Anatomical features of rectal prolapse. maintain an acceptable quality of life. Further inter-
vention such as sphincter repair can correct a defi-
cit in the external sphincter. Sacral nerve stimulation
SCC limited to the anal canal usually requires more
is successful (through an unknown mechanism) in
aggressive treatment with the modified Nigro pro-
approximately 70% of patients who suffer several
tocol consisting of chemoradiation. SCC is sensitive
episodes of solid incontinence a week. This topic is
to this regimen and salvage abdominoperineal
further discussed in Chapter 64.
resection is infrequently required to ensure adequate
treatment.
Rectal prolapse Further reading

Overt rectal prolapse refers to the full thickness of the Guerra GR, Kong JC, Bernardi MP et al. Salvage surgery
rectal wall prolapsing externally through the anal for loco‐regional failure in anal squamous cell carci-
canal (Figure 33.6). Most commonly this is a condi- noma. Dis Colon Rectum 2018;61:179–86.
tion of postmemopausal females and often reflects a MacRae HM, McLeod RS. Comparison of hemorrhoidal
generalised weakness of the pelvic floor. The prolapse treatment modalities. A meta‐analysis. Dis Colon
Rectum 1995;38:687–94.
usually comes out several centimetres during defeca-
Mentes BB, Tezcaner T, Yilmaz U, Leventoglu S, Oguz M.
tion and is manually reduced by the patient. Rectal
Results of lateral internal sphincterotomy for chronic
prolapse interferes with normal sphincter closing anal fissure with particular reference to quality of life.
and leads to incontinence. The prolapsed mucosa Dis Colon Rectum 2006;49:1045–51.
produces leakage of mucus and blood. Senapati A, Gray RG, Middleton LJ et al. PROSPER: a
Treatment requires surgery. Short‐length pro- randomised comparison of surgical treatments for rectal
lapses in frailer patients usually undergo transanal prolapse. Colorectal Dis 2013;15:858–68.
repair. The Altemeier procedure excises the whole
prolapse. The Delorme procedure excises the mucosa
and plicates the underlying muscle. Transabdominal MCQs
procedures involve securing the rectum to the
sacrum using mesh or sutures. If constipation has Select the single correct answer to each question. The
been a major symptom preoperatively, the sigmoid correct answers can be found in the Answers section
colon may also be resected in a procedure called at the end of the book.
resection rectopexy.
1 Which of the following statements about the anal
Internal prolapse of the rectum can produce
canal is incorrect?
symptoms of obstructed defecation and solitary
a the internal sphincter is a continuation of the
rectal ulcer syndrome.
puborectalis muscle
b the external sphincter is skeletal muscle and
under voluntary control
Conditions presenting with discharge
c the dentate line separates the zone of squamous
mucosa from the more proximal transitional zone
Fistula
containing metaplastic squamous and columnar
See Chapter 34. mucosa
d the haemorrhoidal vessels are located deep to bright red rectal bleeding and often notice a
the mucosa proximal to the dentate line small lump at the anal verge
e the anal canal is approximately 4 cm long in males d lateral sphincterotomy has been shown to be the
most effective treatment for fissures and is
2 Which of the following statements about investiga- usually the operative treatment of first choice for
tions for anal disease is incorrect? females
a defecating proctography can be used to e although bleeding is a feature of chronic fissures,
diagnose occult rectal prolapse ischaemia of the base may contribute to their
b endoanal ultrasound is a useful test for visualising aetiology
the integrity of the internal and external sphincters
c examination under anaesthesia is an important 4 Which of the following statements about anal
investigation in delineating anal fistula neoplasia is incorrect?
d CT scanning has minimal utility in investigating a the anal canal is part of the lower gastrointestinal
perianal disease tract and thus the most common anal cancer is
e MRI scanning is contraindicated in the investiga- adenocarcinoma
tion of squamous cell carcinoma of the anal canal b unless the lesion is small and easily excised
locally, anal cancer is usually treated with
3 Which of the following statements about anal chemoradiotherapy
fissure is incorrect? c once dysplastic epithelial cells have penetrated
a a chronic anal fissure is usually located posteri- beyond the epithelium to the submucosa, an
orly at the anal verge and has white fibres of the area of anal intraepithelial neoplasia becomes a
internal sphincter visible at its base squamous cell carcinoma
b in the treatment of chronic fissure, glyceryl d anal intraepithelial neoplasia is associated with
trinitrate, botulinum toxin and lateral sphincter- HPV subtypes 16 and 18
otomy are all used to decrease spasm in the e anal intraepithelial neoplasia can be difficult to
internal sphincter muscle visualise in the perianal skin
c patients with chronic anal fissure characteristi-
cally complain of anal pain with defecation,
34 Perianal disorders II: sepsis
Ian Hayes1,2 and the late Joe J. Tjandra1,2
1
Colorectal Surgery Unit, Royal Melbourne Hospital, Melbourne, Victoria, Australia
2
develop a fever. Clinical examination will usually

Introduction reveal a patient in considerable discomfort, avoiding
sitting or lying on the affected area. There is often
Knowledge of the surgical treatment of infections
moderate cellulitis in the skin and a diffuse, raised,
in the perianal region is important. Abscess forma
indurated area. The area is very tender but gentle
tion in the perineum causes severe pain, requires
examination may find a fluctuant region at its centre.
urgent surgery, and inadequate treatment can result
in progression to dangerous necrotising infections.
Types of abscess (Figure 34.2)
There is a high rate of subsequent fistula formation,
a condition which has challenged surgeons since • Perianal abscess. Most commonly, the initial
the time of Hippocrates and continues to do so. abscess tracks inferiorly through the intersphinc
teric plane to develop a perianal abscess close to
the anal verge.
Aetiology: the crypto‐glandular • Ischiorectal abscess. If the abscess penetrates the
hypothesis external sphincter, it has the capacity to spread in
the large horseshoe‐shaped space of the ischio
The crypto‐glandular hypothesis links the various rectal fossa. In this situation, a large abscess,
manifestations of abscess and fistula that occur in which is more deeply sited than a perianal
the perianal region. Anal glands open into the anal abscess, can spread peripherally around both
canal at the dentate line, which is situated approxi sides of the anal canal.
mately 1.5 cm from the anal verge. The glands • Intersphicteric abscess. Occasionally, the abscess
reside in the intersphincteric space between the remains localised to the intersphincteric space. An
internal sphincter (the innermost cylinder of sphincter intersphincteric abscess may cause severe pain but
muscle) and external sphincter (the outer cylinder without externally visible signs of infection, such as
of sphincter muscle). In theory, if the opening of the a painful swelling and skin erythema. Usually, there
gland into the anal canal becomes blocked, bacteria is severe spasm in the sphincter muscles and the
will proliferate within the gland and an abscess will patient is too tender to allow digital rectal examina
develop in the intersphincteric space. How that tion. Similar features may be found with patients
abscess spreads determines how the patient may experiencing severe symptoms from anal fissure.
present clinically and also predicts the anatomy of Failure to consider the diagnosis of intersphincteric
any subsequent fistula (Figure 34.1). abscess may delay treatment and worsen sepsis.
• Suprasphincteric abscess. An intersphincteric
abscess or an ischiorectal abscess can also track
Perianal abscess in a cephalad direction to form a suprasphinc
teric abscess located above the levator muscles.
Clinical features
Investigations
The symptoms of abscess in the perianal region
develop over hours to days. A throbbing, unrelenting Perianal sepsis is a clinical diagnosis and imaging is
and increasing pain is the main feature. The patient usually not required. Blood glucose level should
may notice some fullness in the perianal skin and be checked to exclude diabetes as a precipitant.
301
(a) (b)
Longitudinal
muscle
Internal
sphincter Puborectalis
Abscess
External
sphincter
Fig. 34.1 Spread of infection from (a) the primary anal gland abscess to (b) the perianal region.
D A
C
Fig. 34.2 Types of abscess in the perianal region: (A) ischiorectal, (B) perianal, (C) intersphincteric and (D) submucosal.
MRI of the pelvis is the imaging modality most pus will be released under pressure. To allow
likely to reveal an abscess in unusual cases where adequate drainage, blunt dissection is used to
there is high suspicion but no clear clinical evidence break down all loculations within the abscess
of a collection. From a practical perspective, the cavity. Sometimes a drain will be left in place for
key investigation for patients with suspected sepsis a large or deeply situated cavity. The wound is
in the perianal region is examination under left open. Adequate drainage of the abscess usu
anaesthesia. ally results in rapid improvement in the patient’s
symptoms.
The finding of severe systemic sepsis and ischae
Treatment
mic tissue is suggestive of Fournier’s gangrene, a
In most cases, the clinical diagnosis of perianal rapidly progressing, mixed‐organism, necrotising
sepsis is straightforward and the patient is taken infection that may require extensive debridement of
to the operating theatre. Broad‐spectrum anti dead tissue to gain control of the sepsis. This rare
biotic treatment should be initiated early. Under but life‐threatening infection can spread upwards
anaesthesia, rigid sigmoidoscopy is done to along fascial planes to involve the external genitalia
exclude evidence of underlying malignancy or and lower abdominal wall.
inflammatory bowel disease. If there is an obvi Patients who have had an abscess in the perianal
ous abscess, an incision is made through the over region have about a 50% chance of developing a
lying skin down to the abscess cavity. Generally, fistula.
34: Perianal disorders II: sepsis 303
If the openings of multiple fistulas are seen, par

Anal fistula ticularly if associated with oedematous skin tags
and fissuring, Crohn’s disease should be considered
A fistula is an abnormal communication between
a possible underlying diagnosis (Figure 34.3).
two epithelial‐lined cavities. As discussed, perianal
sepsis starts with blockage of glands which enter
Goodsall’s law
the anal canal at the dentate line. If the sepsis is
surgically drained or spontaneously discharges Goodsall’s law is a rule of thumb which aids in the
to the skin, a communicating track can arise operative localisation of fistula tracks. It states that
between the anal canal and the perianal skin, fistulas opening into the anterior half of the peria
forming a fistula. The course that the fistula nal skin generally follow direct radial tracks to
track follows is determined by the position of the open internally at the dentate line. Thus, a fistula
original abscess. opening to the perianal skin at the 2 o’clock posi
tion will be expected to have its internal opening in
Clinical features the anal canal at the 2 o’clock position.
Fistulas opening into the posterior half of the
The main clinical feature of an anal fistula is a 2–3
perianal skin also open into the anal canal at the
mm skin opening lined by granulation tissue,
dentate line but follow curved tracks to the 6
discharging a small amount of pus, and located 1–3
o’clock position (posteriorly). A fistula having its
cm from the anal verge. The fistula track may be
external opening in the perianal skin at the 8
palpable as a subcutaneous chord heading towards
o’clock position will usually have an internal open
the anal verge, especially if the fistula is following a
ing at the 6 o’clock position (Figure 34.4). (More
relatively low trans‐sphincteric course. The internal
peripherally located anterior fistulas can originate
opening is not always palpable on digital examina
at the 6 o’clock position.)
tion. Internal examination and proctoscopy/rigid
sigmoidoscopy help to exclude uncommon, but
Types of fistulas
important, underlying causes such as cancer or
inflammatory bowel disease. Digital examination • Intersphincteric. The track starts at the dentate
also allows an assessment of the length of the anal line in the anal canal and runs between the inter
canal and strength of the sphincter mechanism, nal and external sphincters, exiting in the peria
which are important considerations if fistulotomy nal skin close to the anal verge. Because relatively
is planned. little sphincter muscle lies within the confines of
Fig. 34.3 Patient examined in the left‐lateral position showing features of Crohn’s perianal disease. Red and blue setons
are visible and a new fistula opening is seen at the 6 o’clock position (9 o’clock in photograph). There is extensive
excoriation of the skin due to irritation from discharge.
the track, this type of fistula is potentially suita Investigations

ble for treatment with fistulotomy without sig
MRI and endoanal ultrasound are both used to
nificant risk to continence.
delineate fistulas. MRI delineates the tracks very
• Trans‐sphincteric. When the track goes through
well, whilst endoanal ultrasound gives very good
the external sphincter, the fistula is described as
definition of the sphincters. In many cases, however,
trans‐sphincteric. These fistulas can be high or
much of the relevant information can be deduced by
low depending on how much external sphincter
probing the fistula track under anaesthesia.
muscle is involved. A low trans‐sphincteric fistula
can be treated with fistulotomy if less than
one‐third of the sphincter complex is liable to be Treatment
divided during the surgery.
The simplest and most effective treatment for fis
• Suprasphincteric. A suprasphincteric fistula
tula is fistulotomy. This involves dividing the skin
extends superior to the levator muscles. An
and any sphincter muscle included, down to and
extensive amount of sphincter muscle is involved,
along the track. This will allow the track to heal
precluding fistulotomy.
from its base by secondary intention. The problem
• Extrasphincteric. An extrasphincteric fistula is a
is that most fistulas are trans‐sphincteric and some
complex fistula starting from an origin higher in
sphincter muscle will need to be divided. Faecal
the pelvis and not from the anal canal. An exam
incontinence can result from dividing too much
ple is a malignant fistula from an advanced rectal
sphincter muscle. As a very general rule, providing
cancer. Treatment requires removal or control of
there is no pre‐existing sphincter damage, the most
the pelvic source of the sepsis (Figure 34.5).
distal one‐third of the sphincter complex can be
divided without significant impairment to conti
Anterior nence. However, females have shorter sphincters
than males and have a risk of previous, or future,
sphincter impairment related to childbirth.
If there is concern at operation that a significant
amount of sphincter muscle is at risk, then a seton
drain (a loop of silastic thread) is inserted (see
Figure 34.3). It is more common to insert a seton
than perform fistulotomy as a first procedure.
Setons are soft and generally well tolerated by
patients. This method allows ongoing drainage of
the fistula and minimises the risk of further abscess
formation. With time, the seton will allow the
‘sump’ cavity associated with the fistula to decrease
in size and become easier to treat. Once a seton has
been inserted, the track is easier to delineate with
ultrasound or MRI. These tests may reveal that
Fig. 34.4 Goodsall’s law.
A
B C D
Fig. 34.5 Types of perianal fistula: (A) intersphincteric, (B) trans‐sphincteric, (C) suprasphincteric and (D) extrasphincteric.
34: Perianal disorders II: sepsis 305
there is enough reserve of sphincter muscle remain involvement and the finding of similar disease in
ing deep to the fistula track to allow reconsidera other sites separate to the perianal region.
tion of fistulotomy. Mild disease may improve with prolonged
Alternatively, a different treatment plan may be courses of oral antibiotics. Abscesses may require
required which does not divide sphincter muscle. surgical drainage. Small areas can be surgically
The options include insertion of tissue glue or fis excised and primarily closed. The surgical treat
tula plug to seal the track. The fistula track can also ment of larger areas can involve significant skin
be occluded from its internal aspect with a rectal loss and extensive grafting or mobilisation of skin
mucosal advancement flap. A low well‐defined flaps for reconstruction. Occasionally, a diverting
track track can be approached through the perianal stoma may need to be constructed to facilitate
skin, divided and ligated using a LIFT (ligation of hygiene after such major excision and reconstruc
intersphincteric fistula track) procedure. All these tion. Anti‐tumour necrosis factor (TNF)‐α inhibi
procedures have a moderately high failure rate. tors have been trialled with varying success for
High complex fistulas pose a major surgical chal control of severe cases of hidradenitis.
lenge and may require several procedures before
resolution. In some cases, a long‐term seton may
need to remain in place. Occasionally, a defunction Pilonidal sinus
ing stoma is required to divert the flow of faeces
Pilonidal sinus refers to nests of hair located deep
away from the anus and gain control of the sepsis
to small midline skin openings in the natal cleft.
in a complex fistula.
The interdigital region of the hands and the umbili
When a fistula is proving difficult to eradicate, it
cus can also be involved in this disease. It is hypoth
is important to consider other causes such as missed
esised that the hairs originate from the patient’s
tracks, inflammatory bowel disease, malignancy,
back and are channelled between the buttocks
and atypical infections such as tuberculosis and
where they impale the skin, forming the sinuses.
actinomycosis.
The patients are usually hirsute young‐adult males.
The existence of the nest of hair may not, of itself,
produce symptoms apart from occasional minor
Other conditions causing sepsis
in the perineal region pressure effects. Problems begin when the sinus
opening blocks and infection develops in the cavity,
Hidradenitis suppurativa producing an abscess. The pus from the abscess
often tracks a short distance laterally to exit in
This condition is related to infection of apocrine the skin 1–2 cm from the midline. This may allow
sweat glands in hair‐bearing skin. Characteristically, the pain of the abscess to settle but there is likely
multiple small sinus openings are seen in affected to be ongoing discharge of pus and blood from this
areas of axillae, groin and perineum (Figure 34.6). secondary opening.
With recurrent low‐grade infections, scarring devel Some patients present with an abscess requiring
ops. Hidradenitis is distinguished from fistula dis urgent surgical drainage. However, most patients
ease by the multiple openings, lack of internal anal present with chronic discomfort and discharge
from the secondary openings of a chronically
infected pilonidal sinus.
This condition is usually diagnosed clinically by
the characteristic line of small pits in the midline of
the natal cleft, with underlying induration and lat
erally located secondary openings. Occasionally, a
pilonidal sinus located very distally in the natal
cleft can appear similar to an anal fistula.
Treatment
Non‐operative treatment
• If the patient simply has the presence of midline
pits but no surrounding induration or symptoms,
then treatment is not required.
Fig. 34.6 Hidradenitis of the perineum and perianal • Mild cases may improve by permanently remov
region. ing hair from the back and buttocks.
Operative treatment
• Patients presenting with an abscess require surgi
Further reading
cal incision and drainage. This will not fix the
Jemec G. Hidradenitis suppurativa. N Engl J Med 2102;
underlying problem and it is likely that a second 366:158–64.
procedure will need to be performed electively to Johnson EK, Gau JU, Armstrong DN. Efficacy of anal fis
remove the diseased area. Removing all the dis tula plug vs fibrin glue in closure of anorectal fistulas.
eased tissue in the setting of an abscess may result Dis Colon Rectum 2006;49:371–6.
in an excessively large wound. Karydakis GE. New approach to the problem of pilonidal
• Patients with significant ongoing symptoms, sinus. Lancet 1973;ii(7843):1414–15.
induration and secondary openings will require Parks AG, Gordon PH, Hardcastle JD. A classification of
surgical excision of the diseased area. fistula‐in‐ano. Br J Surg 1976;63:1–12.
• Bascom’s procedure involves a minimalist surgi
cal approach to this condition. The midline pits MCQs
are individually cored out and a lateral incision is
made to excise the hair‐filled cavity. This avoids Select the single correct answer to each question. The
the difficulties of a major wound in the natal cleft correct answers can be found in the Answers section
but recurrence rate is high. at the end of the book.
• Excision and leave open: to clear all the sinus
tissue requires quite a deep excision, creating a 1 The preferred treatment of an ischiorectal abscess is:
considerable defect. Leaving the wound open a a prolonged course of antibiotics to abort the infection
with planned healing by secondary intention b incision and drainage under general anaesthesia
is a safe method for dealing with these wounds c warm salt baths
but may require a prolonged period of d fistulotomy
dressings. e defunctioning colostomy
• Excision and closure: the wound may be primar 2 The aetiology of anal fistula does not include:
ily closed but this carries a high risk of wound a anal gland infection
breakdown. Presumably the wound breakdown b rectal cancer
problems are related to the fact that any leg c Crohn’s disease
movement causes strong shearing forces between d actinomycosis
the sides of the incision; the tissues are under e levator syndrome
some tension and contamination from perineal
3 Treatment options for anal fistula do not include:
flora is highly likely. Furthermore, a midline
a LIFT procedure, which involves using a silastic cord
suture line is a potential site of later hair
to gradually occlude the track
implantation.
b mucosal advancement flap used to close the
• Karydakis procedure: in an attempt to over
internal opening
come these issues, this procedure mobilises a
c blocking the fistula track with tissue glue
thick flap of skin and subcutaneous tissue from
d long‐term placement of a seton
one side of the wound and leaves a suture line
e fistulotomy if adequate sphincter muscle can be
offset from the midline, creating a skin closure
preserved
under less tension and avoiding residual mid
line scar tissue. In cases with large skin defects, 4 Pilonidal sinus disease:
rotation flaps, including rhomboid flaps, can a can occur in the natal cleft, the umbilicus and the
be used. axillae
The natal cleft is an unforgiving area for surgery b is characterised by midline pits in the natal cleft
and all surgical procedures for pilonidal sinus carry and secondary openings laterally
a risk of recurrent disease and prolonged wound c frequently results in fistulas to the dentate line of
healing. The addition of permanent hair removal the anal canal
from the back and buttocks may help prevent d usually becomes symptomatic as soon as
recurrence. secondary openings develop
e is not treated using a fibular free‐flap
Section 5
Breast Surgery
35 Breast assessment and benign
breast disease
Rajiv V. Dave1 and G. Bruce Mann2
1
Royal Melbourne Hospital, Melbourne, Victoria, Australia and The Nightingale Centre, Manchester
University NHS Foundation Trust, Manchester, UK
2
Royal Melbourne Hospital and University of Melbourne, Melbourne, Victoria, Australia
Introduction Assessment of the patient with

a breast lump
Management of breast disease has become increas-
ingly specialised. A multidisciplinary, integrated Many women attending a breast clinic have a
and targeted approach is used, involving oncologic benign breast lump. Assessment of a breast abnor-
and reconstructive surgeons, radiologists, patholo- mality relies heavily on the ‘triple test’. The triple
gists, oncologists and breast care nurses. A substan- test can be summarised as follows: if an abnormal-
tial component of the workload involves advising ity is clinically benign, radiologically benign and
patients about their personalised risk of breast can- cytologically or histologically benign, then the risk
cer, differentiating benign breast disease from breast it is malignant is extremely small, and excisional
cancer and allaying the patient’s anxiety about biopsy is not necessary. Adherence to this approach
breast cancer, and maintaining quality of life after has meant that the number of benign lesions being
diagnosis and treatment. excised has reduced dramatically. Importantly, if
any of the three elements of the triple test is not
clearly benign, then further investigation, often
with excision of the lesion, is required. The various
Anatomy of the adult breast
differential diagnoses for a benign breast lump are
discussed later.
The main blood supply is via the second perforat-
In most cases, a thorough history and examina-
ing branch of the internal mammary and lateral
tion is followed by radiological assessment with or
thoracic branches of the axillary artery. Lesser
without pathological assessment. It is important in
supply is via the thoracoacromial and subscapular
the multidisciplinary management of breast lumps/
arteries. A rich subareolar venous plexus drains
lesions that all aspects of the triple assessment are
via the intercostal, internal mammary and axil-
considered.
lary veins.
The distribution of major lymphatics follows the
History
blood supply. About 75% of the lymphatic vessels
drain to the lymph nodes in front of and below the A thorough clinical history should be taken, includ-
axillary vein. Most lymph drains initially to lymph ing menstrual, obstetric, family and medication
nodes in the lower axilla, while a small amount of history. A history of presentation of the lump is
lymph drains from the superior aspect of the breast required, and common concerning symptoms for
directly to the apical nodes. About 25% of lymph breast cancer include the following.
(mainly from the medial half of the breast) drains to • A firm or hard lump with varying degree of fix-
the internal mammary nodes in the second, third ity to surrounding tissues, overlying skin and
and fourth intercostal spaces. underlying pectoral muscles. While pain is an

309
310 Breast Surgery
uncommon symptom, the cancerous lump may • Red and inflamed skin due to lymphatic obstruc-
have increasing discomfort, especially prior to tion seen in inflammatory breast cancer, a rare
menstruation. and aggressive subtype of breast cancer.
• Changes to the breast that include distortion, • An appearance similar to eczema of the nipple asso-
puckering of skin and nipple retraction. ciated with underlying intraductal carcinoma, often
• A blood‐stained nipple discharge may arise from with an invasive component (Paget’s disease).
an intraductal cancer and is typically unifocal. • Enlarged and hard axillary and supraclavicular
• Rarely, distant metastases may be the cause of fossae nodes, in keeping with regional (nodal)
symptoms such as bone pain, abdominal pain or spread of the breast cancer. Clinical assessment
chest pain and dyspnoea. of the axilla is important but inaccurate, and
lymph node metastases can only be confirmed or
Clinical examination excluded by histological examination.
• Hepatomegaly due to liver metastases (but this is
Clinical examination is often normal in screen‐
a rare finding).
detected cancers. Clinical features of benign breast
lumps include:
• smooth and mobile (typical for a fibroadenoma, Investigations in the assessment of possible
discussed later) breast cancer
• sudden growth of a smooth lump that can be
Assessment of suspicious breast lesions usually
tense or painful (typical for a breast cyst, dis-
involves a combination of mammography, ultra-
cussed later)
sound and percutaneous needle biopsy. It should be
• non‐specific thickening of breast tissue (often
remembered that negative imaging does not com-
seen in fibrocystic change, discussed later).
pletely rule out breast cancer.
Signs of concern for a cancer include the following.
• A lump that is often around 2 cm in diameter
Mammography
when identified, and may be non‐specific on
examination. Mammography has a high level of accuracy in detect-
• A larger lump that may be firm to hard, irregular ing breast cancer and its specificity increases with
and have skin attachment or distort the breast age. It is generally carried out using digital image
shape. acquisition (Figure 35.1a). Tomosynthesis is an
• Lymphatic obstruction and ‘orange skin’ (peau advanced form of mammography that utilises lower‐
d’orange) appearance, usually seen in more dose X‐rays and computer‐generated reconstructions
advanced cancers. to create three‐dimensional images of the breasts
(a) (b)
Fig. 35.1 Craniocaudal mammogram (a) and tomosynthesis (b) showing a stellate mass with irregular margins
consistent with a breast cancer.
35: Breast assessment and benign breast disease 311
(Figure 35.1b). Suspicious mammographic features established as a screening test in those at very high
include a mass, asymmetry and microcalcification. risk of cancer, such as carriers of a BRCA1 or BRCA2
Mammography detects impalpable cancers and, in mutation, and also to screen for an occult primary
clinically palpable cancers, helps assess the extent of cancer in the unusual clinical situation where a
the disease and so helps planning of treatment. patient presents with breast cancer in axillary lymph
nodes but no apparent primary cancer in the breast.
When used in a patient with a known cancer,
Ultrasound
breast MRI identifies further unsuspected foci of
Breast ultrasound is complementary to mammogra- disease in one or other breast in up to 15% of cases,
phy in assessing breast conditions (Figure 35.2a). but it is unclear whether identification of this
Ultrasound has a high sensitivity for breast pathol- additional disease is of any benefit.
ogy and also a high negative predictive value. While
operator‐dependent, ultrasound is most useful in
Percutaneous biopsy
the following circumstances.
• Evaluation of an equivocal lump: many women Historically, many breast cancers were diagnosed
present to breast clinic after she or her GP finds a after excisional biopsy (surgery). This is now
possible lump. Ultrasound is useful for distin- uncommon, with a large majority of cancers being
guishing between a focal abnormality and promi- diagnosed on percutaneous biopsy.
nent but normal breast parenchyma.
• Further assessment of an equivocal mammo- Core biopsy
graphic abnormality. Core biopsy, guided by either ultrasound or mam-
• Determining the nature of a definite palpable mography, is the modality of choice for breast biopsy.
lump (solid vs. cystic). It results in histological proof of diagnosis and allows
• Guiding a percutaneous biopsy. most benign conditions to be diagnosed without the
Breast ultrasound is not generally used for screen- need for surgery. It can distinguish between in situ and
ing of asymptomatic women, but may have a role in invasive cancer, and determine the subtype of cancer.
adjunctive screening in certain situations such as It is performed using a 14‐ or 16‐gauge wide‐bore
those with extremely high breast density, needle under local anaesthesia, with larger‐gauge
vacuum‐assisted biopsy techniques also available.
MRI
Fine‐needle aspiration cytology
Breast MRI is a more sensitive test than either mam- Fine‐needle aspiration cytology (FNAC) yields cells
mography or ultrasound, but it is significantly less which may aid in the diagnosis or exclusion of can-
specific (Figure 35.2b). Thus false negatives are cer. It is used less frequently than in the past, as it is
less likely, but false positives are more likely. It is not possible to distinguish in situ from invasive
(a) (b)
Fig. 35.2 Ultrasound (a) and MRI (b) showing typical features of breast cancer.
312 Breast Surgery
cancer. False negatives can occur, although false Drug treatments are sometimes used. The initial
positives are most unusual. It is most often used to treatment is usually with evening primrose oil.
sample lymph nodes that are suspicious on clinical Natural or treatment‐induced remissions are com-
examination and/or ultrasound. mon, but mastalgia does recur. Second‐line treat-
ment with low‐dose tamoxifen is reserved for severe
Open surgical (excisional) biopsy refractory symptoms.
While less common that it once was, this is per-
Non‐cyclical mastalgia
formed in the following cases:
• if FNAC or core biopsy is inconclusive and there The pain has no relationship to the menstrual cycle.
is a clinical suspicion of malignancy It tends to be unilateral, more chronic and some-
• the patient is anxious and not adequately reas- times has a well localised ‘trigger spot’.
sured by standard investigations
• there is a discrete lump and the patient chooses
excision. Management
Any primary pathology of the breast and of adja-
cent structures should be excluded by a careful
BENIGN BREAST DISEASE clinical evaluation and appropriate imaging. Chest
wall pain is frequently assessed as being non‐cycli-
Many so‐called diseases of the breast are actually cal breast pain. This may respond to anti‐inflamma-
aberrations of the processes of development, cycli- tory drug treatment. Treatment involves reassurance
cal change and involution. Benign breast disease that there is no underlying pathology but drug
refers to more severe disorders. In general, there is treatment is generally unrewarding.
poor correlation between clinical, pathological and
radiological features.
Benign breast lumps
Mastalgia Fibroadenoma
Mastalgia is a common breast symptom; however, Pathology
mastalgia does not imply any specific pathological Fibroadenoma is a benign breast tumour in pre-
process and the condition is not well understood. menopausal women, often presenting between
Mastalgia can be cyclical, varying with the men- 18 and 30 years of age. It consists of fibrous con-
strual cycle, or non‐cyclical where there is no such nective tissue stroma and epithelial proliferation,
relationship. usually with low cellularity. With a benign fibroad-
enoma, the fibrous stroma has low cellularity.
Cyclical mastalgia Epithelial hyperplasia may be present but has no
prognostic importance. Coarse calcification may
Cyclical mastalgia is the most common type of
also occur later in life and be seen on screening
breast pain affecting premenopausal women. The
mammography.
median age of presentation is 35 years. The breast
discomfort lasts for a varying period prior to men-
struation and relief of the pain comes with men-
Clinical features
struation. As symptoms of cyclical mastalgia vary
with menstrual cycle, there is probably a hormonal Fibroadenoma is smooth and typically very mobile
basis in the aetiology. However, the precise patho- (hence referred to as a ‘breast mouse’). Some patients
genesis is poorly understood. have multiple fibroadenomas at presentation.
Others have multiple recurrent fibroadenomas.
Management
More than 80% of women require no treatment
Investigations and management
other than reassurance that there is no cancer. The
initial treatment is usually advice to stop smoking To satisfy the triple test, ultrasound with either
and a reduction of caffeine intake. Often, inappro- FNAC or core biopsy is usually performed
priately fitted undergarments may cause pain, and (Figure 35.3a). If this confirms a benign fibroade-
patients may be advised to amend this. noma (Figure 35.3b), no further investigation or
(a) (b)
Fig. 35.3 Ultrasound (a) and haematoxylin and eosin (H&E) section (b) of a typical fibroadenoma.
treatment is required. Some women elect to have a ultrasound and most occur in the perimenopausal
fibroadenoma excised, particularly if the lump is age group. The pathogenesis of breast cysts is not
prominent and/or tender. clear. The breast cyst may be lined by apocrine or
simple cuboidal epithelium.
Phyllodes tumour
Clinical features
Pathology
Breast cysts often appear suddenly and can be quite
Phyllodes tumour is the name given to a wide spec-
large. This is because the subclinical flaccid cyst
trum of fibroepithelial lesions that are not clearly
accumulates a small amount of fluid and becomes
benign fibroadenomas. The spectrum extends from
tense and painful. On clinical examination, the cyst
benign phyllodes with minimal clinical significance
is smooth and firm but not as mobile as a fibroad-
to a malignant soft tissue tumour. Histologically,
enoma. The diagnosis of a breast cyst is confirmed
the fibrous stoma is hypercellular with cellular
by ultrasound and sometimes cyst aspiration
atypia and mitoses.
(Figure 35.4). Cytological examination of the cyst
fluid is not done unless the fluid is evenly
Clinical features blood‐stained.
Phyllodes tumours occur in premenopausal women
Treatment
and clinically resemble fibroadenomas, but often
grow quite rapidly. Palpable breast cysts are treated by simple aspira-
tion in the consulting room. If a lump persists after
aspiration of the cyst, further investigations are
Treatment
required to define the cause of the mass.
This entails a complete local excision, avoiding tran-
section of the tumour. Depending on the nature of
the tumour, local recurrence may be common; with
malignant phyllodes, lung metastases can occur.
Nipple discharge
Breast cysts
Clinical features and investigation
Pathology and incidence
Nipple discharge is a common problem and the
Breast cysts are very common, with up to 10% of causes are outlined in Box 35.1. Investigations
women developing a clinical breast cyst during include mammography and ultrasound occasionally
their lifetime. Many women have multiple subclini- with cytology of the discharge. These investigations
cal breast cysts measuring 2–3 mm identified on are often unrevealing.
314 Breast Surgery
Fig. 35.4 Breast ultrasound showing a well‐defined breast cyst.
blood‐stained and arises from a single duct. Solitary

Box 35.1 Causes of nipple discharge
papillomas are benign and do not have malignant
• Physiological (pregnancy, lactation) potential. The clinical issue is that ductal carcinoma
• Duct ectasia in situ (DCIS), a premalignant condition described
• Galactorrhoea in Chapter 36, can present with a bloody nipple
• Duct papillomas discharge.
• Fibrocystic disease The presence of multiple papilloma is termed
• Carcinoma ‘papillomatosis’. This condition is not often associ-
ated with nipple discharge and may develop further
away from the nipple.
Management of nipple discharge

Mammary duct ectasia and periductal mastitis
Nipple discharge is managed via the usual triple
Mammary duct ectasia and periductal mastitis have assessment method. Bloody nipple discharge usu-
a diverse clinical spectrum. Nipple discharge in a ally requires surgery to exclude serious pathology.
perimenopausal woman with greenish or brown Profuse discharge from a single orifice usually
fluid arising from multiple duct orifices on one or requires surgery to make the diagnosis and treat the
both nipples is the common presentation. The aeti- problem. In most other cases surgery is not required.
ology is unclear but involves the accumulation of
secretions in the duct. Especially in smokers, there
can be inflammation of the surrounding tissues Proliferative and non‐proliferative
with infection, a thick nipple discharge and nipple conditions of the breast
retraction.
There exists a spectrum of conditions of the breast
Galactorrhoea often detected on core biopsy of an indeterminate
lesion that can be classed as either proliferative or
Galactorrhoea may be a primary physiological pro-
non‐proliferative. Commonly, a non‐proliferative
cess, occurring during menarche, menopause or sec-
condition called ‘fibrocystic change’ is seen on core
ondary to drugs that stimulate dopamine activity.
biopsy of microcalcifications following screening
Serum prolactin levels should be requested to inves-
mammography, usually in premenopausal women.
tigate for underlying prolactinoma, which may lead
It is a benign entity that does not infer an increased
to MRI of the pituitary gland.
risk of developing breast cancer. It may present as a
lump, particularly in the upper outer quadrant, and
Intraductal papilloma
may cause discomfort. The pathophysiology is
Papilloma is the commonest cause of bloody nipple poorly understood, but it is thought to be due to
discharge. The discharge may be serous but is often hormonal influences.
Proliferative conditions of the breast can be classi-

Box 35.2 Relationship between benign
fied as either without atypia or as atypical hyperpla-
and malignant breast disease
sia. Radial scars and complex sclerosing lesions are
part of the spectrum of the same condition and are Increased risk
distinguished on size criteria (<1 cm and >1 cm, • Atypical ductal hyperplasia
respectively). They appear histologically as a central • Atypical lobular hyperplasia
fibroelastic core from which ducts and lobules radi- • Lobular carcinoma in situ
ate circumferentially. Radial scars and complex scle-
No increased risk
rosing lesions therefore have a stellate appearance on
• Cysts
mammography and can mimic breast cancer. There
• Fibroadenoma
seems to be an association between radial scars and • Duct ectasia
complex sclerosing lesions, but this is controversial. • Papilloma
Atypical ductal hyperplasia (ADH) is a prolifera- • Epithelial hyperplasia without atypia
tive condition characterised by cellular prolifera- • Sclerosing adenosis
tion (hyperplasia) with atypical epithelium. It is • Apocrine change
similar histologically to low‐grade DCIS (discussed
Uncertain risk
in Chapter 36), but does not meet size criteria (<2
• Radial scar without atypia
mm) for diagnosis. Thus, excision is usually recom-
• Papillomatosis
mended, and surveillance thereafter, due to the
increased risk of breast cancer.
Lobular carcinoma in situ (LCIS) and atypical
lobular hyperplasia (ALH) are both benign entities
plaque is recommended. This is done through an
characterised by proliferation of cells within a lob-
incision at the margin of the areola to minimise the
ule, but may also involve ducts. They are both
cosmetic effect.
asymptomatic and mammographically occult, and
usually present as an incidental finding. They are a
Acknowledgement
risk factor for breast cancer (LCIS, sevenfold to 11‐
fold increased risk; ALH, fourfold to fivefold The authors wish to thank Dr Anand Murugasu,
increased risk) but are not premalignant. LCIS and Consultant Histopathologist, Royal Melbourne for
ALH do not usually require radical excision but assistance with figure 35.3b and Dr Alexandria Taylor,
careful follow‐up of the patient. Consultant Radiologist, Royal Melbourne Hospital
Some benign breast conditions are a risk for can- for assistance with figures 35.1, 35.2, 35.3a and 35.4.
cer (Box 35.2), although the literature is confusing.
The key issue is whether there is any atypical prolif-
eration in the benign breast disease; its presence Further reading
indicates a significantly increased risk, and more
frequent surveillance is appropriate. Dixon JM (ed.) ABC of Breast Diseases, 4th edn. Oxford:
Wiley Blackwell, 2012.
Dixon JM (ed.) Breast Surgery. A Companion to Surgical
Practice, 6th edn. Edinburgh: Elsevier, 2018.
Gynaecomastia in males
About one‐third of adult males and more than half

of normal pubescent boys have some degree of MCQs
gynaecomastia. Physiological gynaecomastia occurs
in the neonate because of circulating maternal sex
hormones, at puberty because of a high serum
oestradiol to testosterone ratio, and in the elderly
because of reduced testosterone production. A com- 1 A 48‐year‐old woman presents with thick greenish
mon cause of gynaecomastia in young men is due to nipple discharge from both breasts. There is no
use of anabolic steroids. Unilateral gynaecomastia, palpable breast lump, although both nipples are slightly
especially in an older man, raises the possibility of retracted. The patient does not take any medication.
breast cancer. This is investigated and managed Mammogram and ultrasound do not show any
along similar lines to female breast cancer. evidence of cancer. The most likely diagnosis is:
With significant gynaecomastia causing social a galactorrhoea
embarrassment, surgical excision of the breast b duct papilloma
316 Breast Surgery
c mammary duct ectasia b mobile

d fibroadenoma c tense or painful
e lobular carcinoma in situ d in‐drawing of the nipple
e well circumscribed on ultrasound
2 A 57‐year‐old woman presented with bloody
nipple discharge from a single duct. The most likely 4 A 36‐year‐old woman presented to the clinic with a
diagnosis is: suspicious lump, confirmed on clinical examination.
a fibrocystic change Ultrasound and mammography reveal a benign‐
b intraductal papilloma appearing mass. What would be the most appropri-
c ductal carcinoma in situ ate course of action?
d mammary duct ectasia a discharge from clinic
e lobular carcinoma in situ b repeat imaging in 3 months
c repeat imaging in 3 years
3 Which of the following is not a feature of a benign d core biopsy of the lesion
breast lump? e FNAC of the lesion
a smooth
36 Malignant breast disease
and surgery
Rajiv V. Dave1 and G. Bruce Mann2
1
Royal Melbourne Hospital, Melbourne, Victoria, Australia and The Nightingale Centre, Manchester
University NHS Foundation Trust, Manchester, UK
2
Non‐modifiable factors
Introduction
• Gender: breast cancer is about 100 times more
Breast cancer is a heterogeneous disease with a common in women than in men.
varying propensity for spread. It is now recognised • Increasing age: breast cancer is very uncommon
that breast cancer is classified not only by histological in women under 30 years of age. The mean age at
type but also by molecular type, and understanding diagnosis is 60 years.
of this tumour biology aids prognostication and • Past history of breast cancer: those having had
treatment decisions. one breast cancer are at higher risk for an entirely
Although breast cancer is generally slow growing, new one.
with pre‐invasive phases that may extend over a • Family history: most significant if there is breast
number of years, some cases are rapidly progressive. cancer in first‐degree relatives (mother, sister or
Prognosis is usually favourable with early diagnosis daughter), especially if they were under 40 years
and multidisciplinary treatment. However, breast of age when the cancer developed, or if there is a
cancer may recur many years after treatment, indi- history of bilateral disease.
cating the need for prolonged monitoring. • Previous history of benign proliferative disease
with cellular atypia, i.e. atypical ductal and
lobular hyperplasia.
Incidence • Other factors, for example nulliparity at 40 years,
previous breast irradiation (as part of treatment
The incidence of breast cancer rises with age up to for conditions such as Hodgkin’s disease), younger
age 70, and the lifetime risk by age 85 in an age at menarche.
Australian woman is 1 in 8, but is lower in Asian
countries. Over the last three decades, the 5‐year Modifiable factors
survival has increased from 72% to around 90%
due to a combination of early detection and better • Obesity is a risk factor for breast cancer, not
treatment. only in the primary setting, but also post surgery
where weight gain is associated with risk of
recurrence.
Risk factors • Alcohol. it is estimated that alcohol intake is
responsible for around 16% of breast cancer
Most breast cancer is sporadic with no specific cases in Australia.
identifiable cause. Several interrelated factors are • Sedentary lifestyle: lack of physical fitness is
associated with an increased risk of developing associated with an increased breast cancer risk.
breast cancer, which may be broadly classified into • Exogenous hormone treatment: the data on the
modifiable and non‐modifiable factors. cancer risk with hormone replacement therapy
317
318 Breast Surgery
(HRT) is conflicting. Prolonged use of combined feasible. It is often considered by carriers of genetic
oestrogen/progesterone HRT is definitely associ- mutations, and by some others at high risk.
ated with an increased incidence of breast
cancer. Short duration (<5 years) appears safe,
and oestrogen‐only HRT (used in women who Screening for breast cancer
have had hysterectomy) also appears safe. The
risks associated with the oral contraceptive pill Early detection of asymptomatic breast cancer
(OCP) are low, but recent studies have suggested by mammographic screening has been shown to
a small increase in relative risk. The fact that the improve survival. Trials of population‐based
underlying risk of breast cancer at the age of mammographic screening in many countries have
maximal OCP use is very low means this is not a confirmed the value of early detection of tumours
major concern. in reducing breast cancer mortality.
National breast screening programs have been
established in many countries. In Australia, women
Genetics aged 50–75 are invited to screen at 2‐year inter-
vals. The program has been successful in reducing
Around 5% of cases of breast cancer are due mortality from breast cancer by approximately
to identifiable genetic mutations. Most of these 21–28%, at the current participation rate of 56%.
involve the BRCA1 or BRCA2 genes, with smaller Patients have a two‐view mammogram performed
numbers due to mutations in the CDH1, ATM, and if an abnormality is identified, they are recalled
TP53 or PALB2 genes. These cases often, but not to an assessment clinic. The majority of abnormalities
always, occur in association with a family history (>90%) detected at screening are benign. The bene-
of breast and/or ovarian cancer. fits of screening are the reduction in breast cancer
Women of Ashkenazi Jewish ancestry have a mortality and a reduced intensity of treatment, as
risk of inheriting one of three ‘founder’ mutations early detection often allows treatment with less
present in this group that increases their risk of extensive surgery and less chemotherapy.
developing breast cancer. There are other founder Screening has also detected an increased number
mutations in certain communities, but it is the of cases of ductal carcinoma in situ (DCIS), many
Ashkenazi mutations that are most commonly of which may never have become clinically signifi-
seen in Australia. cant. This issue of over‐diagnosis and subsequent
The impact of common minor genetic variations – over‐treatment is a harm of screening that some
single nucleotide polymorphisms (SNPs, pronounced suggest substantially limits the overall benefit of
‘snips’) – is being studied. It has been shown that the population‐based mammographic screening
while the impact of any particular SNP on breast programs.
cancer risk is minimal, the overall pattern of SNPs
may be significant, and those with multiple higher‐
risk SNPs may be at a substantially increased risk. Spread of breast cancer
This science may be clinically useful in the near
future. Breast cancer can spread directly via local invasion,
through lymphatics or via the bloodstream. In some
patients, regional nodal and distant metastases
Prevention of breast cancer occur rapidly, even if the primary breast cancer is
small, while in others (the majority in the current
Modifiable risk factors offer a substantial opportu- age of screening) the tumour remains apparently
nity to reduce the incidence of breast cancer. localised in the breast at the time of diagnosis.
Chemoprevention with tamoxifen for ‘high‐risk’
subjects for 5 years has been shown to result in a
Local invasion
35% reduction in breast cancer development over
15 years. This is not associated with reduced breast This occurs by direct infiltration of the breast
cancer mortality, and the side effects of tamoxifen parenchyma, resulting in the characteristic stellate
limit uptake of this option. appearance of breast cancer. Direct invasion of the
Prophylactic mastectomy with or without breast overlying skin or underlying fascia and muscle can
reconstruction results in a 95% reduction in the occur but is uncommon. Local invasion of lymphatics
risk of breast cancer development, as complete and veins indicates a higher likelihood of lymph
excision of all the breast ducts is not technically node involvement and a worse prognosis.
36: Malignant breast disease and surgery 319
Regional spread disease, or when the identification of metastatic

disease would substantially alter treatment. In gen-
Lymphatic spread to axillary lymph nodes is com-
eral, tests are used if there are clinical symptoms or
mon with breast cancer. The incidence of axillary
signs suggestive of metastatic disease (bone pain,
nodal metastases is less than 20% in tumours
shortness of breath, etc.), when the lymph nodes are
smaller than 2 cm but is more than 50% in tumours
involved, or when the pathology indicates there is
larger than 5 cm. The involvement of a high number
high risk of asymptomatic metastatic disease.
of nodes (four or more) is associated with a poorer
Investigations that are commonly used for breast
prognosis. Internal mammary lymph nodes lie in
cancer include:
the anterior intercostal spaces adjacent to the internal
• full blood examination and liver function tests
mammary vessels. Spread to the internal mammary
• whole body bone scan
nodes or supraclavicular nodes is associated with a
• chest and abdominal CT scan.
poor prognosis.
Positron emission tomography is not routinely used
in breast cancer. However, studies have suggested
Distant metastases
that it may have a place in the future.
The most common sites of disease are the bone, Staging investigations are not recommended in
liver and lung. Other sites include the brain, skin situations where the chance of metastasis is very
and peritoneum. Different subtypes of breast can- low or where the outcome would not change
cer have somewhat different patterns of distant management, as they have significant false‐positive
metastasis, but bone metastasis is the most com- rates and may cause considerable anxiety and fol-
mon and the most frequent initial site of distant low‐up investigations.
relapse.
Histopathology
Staging of breast cancer
Pathological examination (Figures 36.1 and 36.2)
Staging is the process of classification of cancer
is essential in confirming the diagnosis, assessing
according to prognosis. This is complex in breast
whether the lesion has been completely excised,
cancer because of the large number of prognostic
providing prognostic information (see Box 36.1)
variables (Box 36.1) and the heterogeneity of the
and in determining the most appropriate adjuvant
disease. The most clinically relevant staging system
therapy (extra treatments used in the absence of
is the American Joint Committee on Cancer (AJCC)
known disease to reduce the risk of a subsequent
TNM classification, which provides an accurate
recurrence).
and reproducible assessment and is particularly
Breast cancer may be non‐invasive (in situ) or
useful in clinical trials. The AJCC staging system
invasive and can be divided into a number of
was originally based on T (tumour), N (node) and
molecular subtypes with prognostic and treatment
M (metastasis) criteria, constituting the TNM clas-
implications.
sification, but this has recently been expanded to
include molecular features (Box 36.2).
Ductal carcinoma in situ
Staging investigations This is a pre‐invasive breast cancer and is charac-
terised by proliferation of malignant breast epithe-
Staging investigations are used when there is a sig-
lium that is confined to the ducts and which has not
nificant chance that they would identify metastatic
invaded through the basement membrane. The
entity is often associated with microcalcification on
mammography (Figure 36.3) and is usually impal-
Box 36.1 Major prognostic determinants pable. Since the introduction of mammographic
of breast cancer screening, DCIS has risen from 2% of breast can-
cers to around 15%. This condition is premalignant
• Axillary nodal status and often multicentric in the breast.
• Tumour size While DCIS may progress to invasive cancer
• Histological grade
if untreated, not all invasive cancer has a prema-
• Hormone receptor status
lignant stage, and not all cases of DCIS will
• HER2 over‐expression
progress. This means that many cases of screen‐
• Ki67
detected DCIS are examples of over‐diagnosis – the
320 Breast Surgery
Box 36.2 AJCC staging system for breast cancer
diagnosis of conditions that would never have

Invasive ductal carcinoma
become clinically significant – and leads to over‐
treatment. The same may apply to some cases of ‘Invasive’ ductal carcinoma refers to cancer which
invasive cancer, and is the subject of ongoing has invaded the basement membrane of the ducts
debate around the potential harms of population and entered the surrounding tissue. It is classified
screening. according to differentiation as grade 1, 2 or 3
© 2009 American Joint Committee on Cancer. Reproduced with permission of AJCC.
Invasive lobular carcinoma

(low, intermediate or high grade). Most invasive
ductal carcinomas are of no special type, but sev- Invasive lobular carcinoma is a distinct type of
eral distinct types exist, including papillary, medul- breast cancer that lacks staining for the CDH
lary, tubular and mucinous, and these have distinct protein. Classical lobular carcinoma has the histo-
natural histories. logical feature of single files of malignant cells that
322 Breast Surgery
(a) (b)
(c) (d)
Fig. 36.1 Haematoxlin and eosin (H&E) sections of (a) normal duct, (b) atypical ductal hyperplasia, (c) ductal
carcinoma in situ and (d) invasive breast carcinoma.
(a) (b)
Fig. 36.2 Immunohistochemistry of (a) oestrogen‐positive and (b) HER2‐positive breast cancer.
diffusely infiltrate the breast tissue (Figure 36.4). It

may also be difficult or impossible to see on a
Molecular subtypes of breast cancer
mammogram or ultrasound, presenting as a diffuse A major change in breast cancer management has
enlargement of part or all of the breast rather than followed the recognition of a range of identifiable
as a discrete lump. molecular subtypes of cancer based on RNA
Fig. 36.3 Mammogram showing typical calcification seen in extensive ductal carcinoma in situ.
Fig. 36.4 Invasive lobular cancer showing single files of malignant cells.
expression microarrays. Studies have shown that of oestrogen and progesterone receptors, levels of
breast cancer can be largely divided into four distinct human epidermal growth factor receptor (HER2),
types based on the patterns of altered gene expres- grade and markers of cellular proliferation (Ki67).
sion. Various subdivisions of these subtypes is also
possible. The different types have different prognoses
Luminal A
and treatments. While genetic profiling is not
widely practised at present, histological findings Luminal A breast cancer is oestrogen‐receptor and
and immunohistochemistry provide a cost‐effective progesterone‐receptor positive, HER2 negative,
method of identifying subtypes for treatment pur- and has low Ki‐67. It is usually lower grade and
poses. Tumours are classified based on the expression proliferates slowly, and has the best prognosis.
324 Breast Surgery
Luminal B Breast conservation surgery

Luminal B breast cancer is oestrogen‐receptor Randomised trials from the 1980s confirmed that
positive, progesterone‐receptor low or negative,
breast‐conserving surgery, involving complete local
HER2 positive/negative with high levels of Ki‐67. excision of the primary breast tumour with a rim
It is generally higher grade. Luminal B cancers of macroscopically and microscopically normal
usually grow faster than luminal A cancers and breast tissue on all sides, followed by adjuvant
their prognosis is worse. whole‐breast radiotherapy, results in equivalent
cure rates to total mastectomy. Breast‐conserving
Triple‐negative/basal‐like surgery may be referred to as ‘wide local excision’,
‘lumpectomy’ or ‘partial mastectomy’. Surgical
This cancer is oestrogen‐receptor, progesterone‐
techniques to improve cosmesis after breast‐
receptor and HER2 negative. It is usually high
conserving surgery have allowed more patients to
grade, rapidly proliferative and with a relatively
choose breast conservation and to expect improved
poor prognosis. This type of cancer is more
cosmetic outcomes. Breast conservation surgery is
commonly seen in women with BRCA1 gene

usually followed by radiotherapy to reduce the rate
mutations.
of local recurrence.
Breast conservation surgery and radiotherapy is
HER2‐enriched
the standard procedure for patients with breast
This breast cancer is oestrogen‐receptor and pro- cancer and is performed on around 70% of all
gesterone‐receptor negative and HER2 positive. patients. In addition to equivalent survival rates,
It proliferates faster than luminal cancers and the cosmetic and psychological results are generally
though without treatment they have a poor prog- superior to those of mastectomy.
nosis, they are often successfully treated with
targeted therapies aimed at the HER2 protein, such
as trastuzumab (Herceptin). Total mastectomy
This involves complete excision of the breast and
nipple with preservation of the underlying pectoral
muscles. This is recommended for:
Treatment of breast cancer • a cancer that is large relative to the size of the
breast
The management of breast cancer involves an evi- • cancer that involves the nipple or overlying skin
dence‐based and multidisciplinary approach involv- (breast conservation surgery might still be possi-
ing surgeons, radiologists, radiation oncologists, ble in selected cases)
medical oncologists, pathologists and breast care • multifocal disease or extensive intraductal carci-
nurses. Management decisions are usually made in noma (DCIS) involving the surgical margins
a multidisciplinary team meeting, often both before • those having had prior breast irradiation
and after surgery. Patient education, counselling • women who harbour a genetic mutation such as
and informed consent play an increasing role, and BRCA1 or BRCA2 who elect to have mastec-
patients may require psychological support, often tomy to minimise the risk of further cancers
provided by psychologists specialising in treating • women who choose not to have breast
those with cancer. conservation.
It is important that the decision for either breast‐
conserving treatment or total mastectomy is an
Breast cancer surgery informed decision by the woman. A minority of
Until the 1980s, surgery for breast cancer involved fully informed women choose to have total mas-
total mastectomy and removal of the axillary lymph tectomy, and this is a legitimate decision.
nodes. A series of randomised trials demonstrated
that such radical surgery is not necessary, with
Breast reconstruction
similar results being achieved with much less exten-
sive surgery. Breast cancer surgery still involves Breast reconstruction should be offered to most
surgery on both the breast and the draining lymph women after a total mastectomy. This may be imme-
nodes, and these two components can be consid- diate (at the same time as mastectomy) or delayed
ered separately. (after treatment is complete). Reconstruction may be
implant‐based or autologous (using the patient’s Adjuvant therapy

own tissue). Autologous options include pedicled
Adjuvant therapy refers to anticancer treatments
flaps, such as the latissimus dorsi flap, and free flaps
given in the absence of known disease to reduce the
using microvascular techniques, such as the deep
chance of disease recurrence. It was first used in
inferior epigastric perforator flap that uses fat and
breast cancer in the 1980s, and has led to dramatic
skin from the lower abdomen to reconstruct the
improvements in outcomes. Adjuvant radiotherapy
breast. There is a significant psychological benefit to
is used to reduce the risk of residual disease in the
immediate reconstruction for many patients, with
breast or regional lymph nodes, while adjuvant
no evidence to suggest that it worsens oncological
systemic therapies are used to reduce the risk of
outcomes.
distant recurrence.
Lymph node surgery Adjuvant radiotherapy

For most of the twentieth century, standard s urgery Radiation therapy uses high intensity X‐rays as
for breast cancer included removal of all the cancer treatment. It takes advantage of the fact
axillary lymph nodes – an ‘axillary clearance’ or that cancer cells tend to be more sensitive to X‐rays
‘axillary dissection’ – as this is where breast cancer than normal tissue, so that if radiation is carefully
is most likely to be found beyond the breast. The delivered, it can kill cancer cells without significant
operation effectively removes the lymph nodes, but damage to normal tissue. In breast cancer, it is
is associated with substantial morbidity in the given as an adjuvant therapy after breast‐conserving
form of shoulder dysfunction, numbness and par- surgery or sometimes after mastectomy. After
aesthesia, and potential lymphoedema of the arm breast‐conserving surgery for invasive disease it is
and breast. standard treatment, although some low‐risk sub-
groups may not benefit. After breast conservation
Sentinel node biopsy for DCIS it is usually considered, but often not
given. After mastectomy for invasive disease, it is
As the size of cancers became smaller due to pop- recommended when four or more lymph nodes are
ulation screening, the incidence of nodal involve- involved, and considered in cases with less nodal
ment reduced, and techniques were developed involvement but higher‐risk disease. It also has a
to identify the key lymph node(s) that receive role in metastatic disease, especially in the bone or
primary drainage from the cancer, the so‐called brain (this is termed palliative, rather than adju-
sentinel node. The sentinel node is usually found vant, radiotherapy).
in the lower part of the axilla, just deep to the
pectoralis major muscle, and is identified via Complications of radiotherapy
injection of a radioactive colloid and a blue dye. The complications following radiotherapy vary
This node is removed in an operation called senti- with the total dose, the number of fractions and
nel node biopsy; if found to be clear of cancer, the the arrangement of the radiation fields. Recent
likelihood that any other lymph node is involved improvements in delivery techniques have signifi-
is very small and further surgery can be safely cantly reduced the complications.
omitted. Local effects occur in the first 2–6 weeks and
include redness, swelling and pain, sometimes with
blistering and ulceration of the skin. Discomfort
Axillary dissection
and swelling of the breast occur early and often
Axillary dissection is now reserved for those persist for a number of years. Rib pain and tender-
patients with proven axillary metastatic disease, ness is common and can be persistent. Lymphoedema
via either preoperative fine‐needle aspiration of of the arm occurs in a small but significant number
suspicious lymph nodes or at sentinel node of patients following surgery and radiotherapy to
biopsy. It involves removal of the fatty tissue that the axilla.
lies in the area bounded by the pectoralis major Cardiac damage particularly in patients with
and latissimus dorsi muscles, the lateral chest left breast tumours is reported, although modern
wall, and the axillary and subclavian veins. This techniques reduce this. Similarly, radiation‐
tissue contains somewhere between 10 and 25 induced cancers occur but are infrequent, and the
lymph nodes, as well as lymphatics and cutaneous benefits from radiotherapy usually outweigh the
nerves. risks.
326 Breast Surgery
Adjuvant systemic therapy Types of endocrine therapy

Systemic therapy is therapy delivered to treat the Tamoxifen
whole body. The aim of this is to eradicate micro-
Tamoxifen was the first widely used endocrine
metastases in order to ultimately improve survival.
therapy. Five years of tamoxifen reduces the risk of
Routine use of effective adjuvant systemic therapy
death by around one‐third in women with oestrogen
has been responsible for a large proportion of the
receptor‐positive tumours. It also reduces the risk
improved outcomes for breast cancer over recent
of cancer in the contralateral breast, and is also
decades. It is used primarily to reduce the risk of
used as chemoprevention. For many years, 5 years
distant metastasis and death, but has also been
of treatment was considered optimal, but recent
shown to reduce the risk of local recurrence and
evidence has shown that extending treatment to
endocrine therapy has been shown to reduce the
10 years reduces the risk of late recurrences (those
risk of new primary breast cancers.
occurring between 10 and 15 years). Decisions
In general, it is recommended that patients with
regarding duration of therapy are a matter of
oestrogen receptor‐positive cancer receive endo-
balancing likely benefits with the side effects and
crine treatment, those with receptor‐negative can-
potential risks.
cer chemotherapy, and those with HER2‐positive
Side effects of tamoxifen include hot flushes,
cancer Herceptin and chemotherapy. The most
vaginal discharge and an increased incidence of
difficult issue is which patients with oestrogen

endometrial cancer and deep vein thrombosis.
receptor‐positive, HER2‐negative cancer should
This endometrial cancer risk is increased twofold
receive chemotherapy in addition to endocrine
to threefold but still remains low, at less than 1%
therapy. Several online predictive tools are availa-
per year for a 5‐year treatment duration, and is
ble when discussing the potential benefit of chemo-
generally far outweighed by its beneficial effect.
therapy for an individual patient (e.g. PREDICT in
Abnormal vaginal bleeding should be promptly
the UK), as well as a number of commercial molec-
investigated.
ular tests.
Aromatase inhibitors
Whereas in the premenopausal woman, the majority
Traditionally, treatment of early breast cancer of oestrogen is produced from the ovaries, in the
has involved initial surgery, followed by adjuvant postmenopausal woman this occurs in peripheral
therapies of various types to reduce the risk of fat, muscle and liver. This is facilitated by the enzyme
recurrence. On the basis that adjuvant therapies aromatase, which converts androgens into oestro-
were targeting the micrometastatic disease that gens by a process called aromatisation. Aromatase
may be destined to cause recurrence, trials were inhibitors thus reduce circulating oestrogen levels in
done where chemotherapy was given prior to postmenopausal women.
surgery, so‐called neoadjuvant chemotherapy.
Several trials have demonstrated that aromatase
The hypothesis was that earlier treatment of inhibitors (anastrozole, letrozole and exemestane)
micrometastatic systemic disease would lead to are more effective at reducing the incidence of
improved survival. This has not been proven, but breast cancer recurrence compared with tamox-
it was found that many cases where primary ifen in postmenopausal women. The side‐effect
surgery would have involved mastectomy were profile of aromatase inhibitors is different to that
able to be treated successfully with breast conser- of tamoxifen, and involves hot flushes and other
vation. It was also shown that the response to menopausal symptoms (similar to tamoxifen) but
neoadjuvant chemotherapy was a powerful prog- also musculoskeletal symptoms, with arthralgia
nostic factor: those who experienced a so‐called and myalgias. Reduced oestrogen levels can cause
pathological complete response (i.e. no residual significant gynaecological and urinary side effects
cancer found at surgery after neoadjuvant chem- with vaginal dryness and urinary incontinence, as
otherapy) had a far better prognosis than those well as reduced bone mineral density.
who did not.
Neoadjuvant chemotherapy is currently consid-
Ovarian function suppression
ered for large and extensive node‐positive cancer,
especially those subtypes most likely to be sensitive Ovarian function suppression (OFS) in premeno-
to chemotherapy, such as the HER‐enriched and the pausal women is associated with improvement in
triple negative subtypes. breast cancer outcomes in higher‐risk patients. This
has been used in trials that show that in lower‐risk Detection of distant recurrence
patients, OFS can be used in place of cytotoxic
The most common sites for distant metastatic
chemotherapy, while in high‐risk patients it can be
disease are the bones, the lungs and the liver. These
used in addition to chemotherapy. OFS can be
present with new or different bone or joint pain that
followed with aromatase inhibitors, which are
does not settle spontaneously; shortness of breath,
somewhat more effective than tamoxifen, but this
chest pain or cough; loss of weight or abdominal
combination can lead to significant impacts on the
pain. Brain metastasis can occur, presenting with
quality of life of a young woman and the balance
headache or neurological symptoms.
of effectiveness and side effects can be difficult to
Follow‐up imaging with CT or bone scans in the
achieve.
absence of symptoms is not recommended, as early
diagnosis of asymptomatic metastases confers no
advantage to the patient. Thus investigations are
Supportive care reserved for those with worrying symptoms.
Breast cancer tends to be slow‐growing and may
The manner in which the diagnosis of breast cancer recur many years after apparently successful treat-
is communicated may have an important impact on ment. Metastatic spread is defined as spread
the woman’s ability to cope with the diagnosis beyond the breast and ipsilateral axillary and/or
and treatment. There are individual differences in internal mammary lymph nodes, and is deemed
women’s views about and need for information, incurable.
options and support.
Women with breast cancer and their families Screening for a new breast primary
will need further counselling to allow assimilation
of information and should be given repeated The risk of a new contralateral breast primary cancer
opportunities to ask questions. Women with good is about 0.5% per year. Annual mammography is
emotional support from family and friends tend recommended, sometimes with ultrasound as well.
to adjust better to having breast cancer. Doctors,
nurses, breast cancer support services and other Management of treatment‐associated
allied health professionals are all important toxicities
sources of support. These include problems after axillary dissection
(shoulder stiffness or lymphoedema) or adjuvant
radiotherapy (breast and chest‐wall pain and ten-
Follow‐up after treatment of early derness). Women taking tamoxifen or an aromatase
breast cancer inhibitor may have menopausal symptoms, joint
pains or gynaecological symptoms that should be
With the multidisciplinary approach in the care addressed. Women on aromatase inhibitors should
for breast cancer, it is important that follow‐up is have their bone density checked and low bone den-
coordinated so that patients are not subjected to sity should be managed.
an excessive number of visits. The rationale of
follow‐up is outlined in the following sections. Psychosocial support
The patient’s GP is a key member of the multidis-
Anxiety and depression are common following
ciplinary team, and can safely provide much of the
diagnosis and treatment. This should be acknowl-
follow‐up care in partnership with the hospital‐
edged. Sometimes referral to a psychologist is
based team.
appropriate.
Detection of local recurrence

The local recurrence rate after breast conservation Acknowledgement
surgery and radiotherapy or total mastectomy is
low. Overall the 5‐year rate is below 5%, although The authors wish to thank Dr Anand Murugasu,
late recurrences are possible many years after Consultant Histopathologist, Royal Melbourne
diagnosis. Most local recurrences are detected for assistance with figures 36.1, 36.2 and 36.4 and
on surveillance imaging, although some present Dr Alexandria Taylor, Consultant Radiologist,
as lumps after breast‐conserving treatment or Royal Melbourne Hospital for assistance with
mastectomy. figure 36.3.
328 Breast Surgery
negative, and the HER2 is negative (non‐amplified).

Further reading There is no evidence of systemic metastases on CT
and bone scan. Following a total mastectomy and
Australian Government, Department of Health.
BreastScreen Australia Evaluation Final Report. http://
axillary clearance, the most likely follow‐up
www.cancerscreening.gov.au/internet/screening/ management would be:
publishing.nsf/Content/programme‐evaluation a regular review, with reservation of chemotherapy
Australian Government, Cancer Australia. https://breast‐ for recurrent disease
cancer.canceraustralia.gov.au/treatment/surgery b adjuvant tamoxifen
Dixon JM (ed.) ABC of Breast Diseases, 4th edn. Oxford: c adjuvant chemotherapy alone
Wiley Blackwell, 2012. d adjuvant chemotherapy and post‐mastectomy
Dixon JM (ed.) Breast Surgery. A Companion to Surgical radiotherapy
Practice, 6th edn. Edinburgh: Elsevier, 2018. e oophorectomy
3 Which of the following statements concerning

MCQs ductal carcinoma in situ (DCIS) is correct?
a it is usually associated with microcalcification on
Select the single correct answer to each question. The mammography
correct answers can be found in the Answers section b DCIS is less commonly found in women
at the end of the book. undergoing routine mammographic screening
1 A 51‐year‐old woman undergoes a wide local c all DCIS will eventually progress to invasive
excision and sentinel node biopsy for a 15‐mm cancer
grade 2 invasive duct cancer, margins clear, nodes d there is a high risk for lymph node metastasis
negative, oestrogen receptor positive, HER2 positive with the papillary subtype
(amplified). What adjuvant therapy should she be e the risk for progression to invasive cancer is
offered? smaller than with lobular carcinoma in situ
a radiotherapy only
b radiotherapy and endocrine therapy 4 Which of the following statements about breast
c radiotherapy, chemotherapy, targeted anti‐HER2 cancer screening is not correct?
therapy and endocrine therapy a screening has been shown to improve survival
d chemotherapy, radiotherapy and endocrine therapy b screening detects breast cancer at an early stage
e chemotherapy only c women are invited to participate from the ages
of 50 to 75
2 A 39‐year‐old woman has a 5‐cm, grade III breast d uptake of screening in Australia is >90%
cancer. Twelve of 16 lymph nodes contain metastases. e the majority of abnormalities detected on
The oestrogen and progesterone receptor is screening mammography are benign
Section 6
Endocrine Surgery
37 Thyroid
Jonathan Serpell
Monash University and Breast, Endocrine and General Surgery Unit, Alfred Health, Melbourne,
Victoria, Australia
where it buds laterally. A contribution of neural

Introduction crest cells arising from the fourth branchial cleft
and the ultimobranchial body gives rise to the
The thyroid gland lies in the anterior triangle of the
C‐cells of the thyroid as well as to a small projec
neck. The thyroid comprises two lateral lobes, an
tion from the posterolateral surface (the tubercle of
isthmus and a pyramid, schematically represented
Zuckerkandl). As the thyroid gland descends
as a bilobed shield. The function of the follicular
during embryological development, remnants of
cells is to produce, store and release the thyroid
thyroid tissue may be left behind anywhere along
hormones thyroxine (T4) and triiodothyronine
the thyroglossal tract. Occasionally some respira
(T3). The function of the C‐cells is to produce the
tory epithelium may be included in the remnant,
calcium‐lowering hormone calcitonin.
resulting in a thyroglossal duct cyst. A non‐cystic
Diseases affecting the thyroid gland can generally
benign thyroid nodule, or even thyroid cancer,
be grouped into disorders of thyroid function
may also develop anywhere along the tract.
(including hypothyroidism and thyrotoxicosis) or
Embryological descent may also continue into the
disorders affecting thyroid structure (including
anterior mediastinum, giving rise to a thyrothymic
nodular goitre and thyroid neoplasms). Disorders
thyroid remnant. The junction of the thyroglossal
of both function and structure may coexist. A goitre
duct tract and the isthmus of the thyroid gland
refers to enlargement of the thyroid and is a term
marks the site of the pyramid, a variable‐sized
applicable regardless of the cause of the enlarge
projection superiorly of thyroid tissue.
ment. However, from the surgical point of view, a
classification of thyroid disease can be considered
as comprising the following groups: Clinical presentation
• Thyroglossal duct cyst
Thyroglossal duct cysts usually present in childhood
• Benign thyroid nodules
or adolescence but may occur at any age. However,
• Multinodular goitre
in older patients the possibility of papillary thyroid
• Thyroid cancer
cancer in a developmental remnant should be
• Thyrotoxicosis
considered as an alternative diagnosis to a de novo
• Thyroiditis.
thyroglossal duct cyst. The usual clinical presenta
tion is that of a midline swelling at or just below
the level of the hyoid bone, often slightly to one
side of the midline. Classically, the swelling elevates
Disorders of the thyroid gland with protrusion of the tongue. Inflammation may
give rise to an abscess or a fistula.
Thyroglossal duct cyst
Pathology Investigations
Thyroid follicular cells arise from the region of the The diagnosis of a thyroglossal duct cyst is usually
foramen caecum at the junction of the anterior self‐evident on clinical examination. Fine‐needle
two‐thirds and posterior one‐third of the tongue, aspiration cytology (FNAC) will confirm the nature
and during embryological development the gland of the cyst contents, although this may precipitate
descends in the midline to the level of the larynx, inflammation. Cytology will often show colloid,
331
332 Endocrine Surgery
cholesterol crystals and benign epithelial cells. nodule is that it elevates on swallowing because the
Aspiration may be therapeutic as well as diagnostic, thyroid is enveloped by the pretracheal fascia which
with resolution of the cyst. FNAC is important for attaches to the trachea. This will distinguish a thy
excluding the uncommon papillary thyroid cancer roid nodule from a lymph node swelling adjacent to
arising in a thyroglossal duct cyst. Neck ultrasound the thyroid which does not elevate on swallowing.
to confirm the presence of a normal thyroid gland Benign thyroid nodules may also present with local
and thyroid function should be undertaken. pressure symptoms. These include dysphagia from
oesophageal pressure, breathlessness or stridor
Treatment from tracheal pressure, a hoarse voice from pres
sure on the recurrent laryngeal nerve, or superior
Treatment is surgical excision through a skin‐crease
vena cava (SVC) obstruction from a large single
incision. The cyst and the thyroglossal tract must be
nodule obstructing the thoracic inlet. A toxic nod
removed, which involves excision of the mid‐
ule will present with symptoms of thyrotoxicosis.
portion of the hyoid bone and tracing of the tract
Regional lymphadenopathy should always be
to its upper limit. Failure to remove the full extent
sought.
of the tract will result in recurrence of the cyst or a
Increasingly thyroid nodules, which may or may
discharging sinus.
not be palpable, are identified incidentally on imaging
such as ultrasound, CT, MRI or positron emission
tomography undertaken for investigation of other
Benign thyroid nodules
symptoms, for example neck pain and carotid
Pathology artery studies.
Between 30 and 40% of clinically solitary thyroid
Investigations
nodules will represent a dominant nodule within an
underlying multinodular goitre. Of the remainder, Thyroid function tests, including thyroid‐stimulating
the majority will be benign nodules, comprising hormone (TSH), free T4 and free T3, should be
simple thyroid cysts, solitary colloid nodules or performed in all patients to exclude subclinical
benign follicular adenoma. Approximately 7% will thyrotoxicosis (suppressed TSH will be seen in
be a thyroid cancer and a further small group will association with normal free T4 and free T3 levels)
represent an area of nodularity within thyroiditis or to diagnose a toxic nodule or toxic adenoma.
(both Hashimoto’s and subacute). Apart from rare Ultrasound is routinely performed to establish
developmental inclusion thyroid cysts, the majority underlying multinodularity and to characterise the
of thyroid cysts form following haemorrhage into features of the nodule. Features raising an element
an underlying benign thyroid nodule, which then of suspicion as to the nature of the nodule include
matures into a thyroid mass consisting of a rim of solid as opposed to cystic, internal vascularity as
thyroid tissue and a central liquefied area. Colloid opposed to peripheral vascularity, microcalcifica
nodules and hyperplastic nodules should be consid tion, dimensions taller than wide, and irregularity
ered part of a similar pathological spectrum. of outline. Further, abnormal lymph nodes may be
identified by ultrasound.
FNAC is the definitive investigation, and the
possible cytological reports are categorised in
The most common presentation of a single thyroid Table 37.1. This Bethesda classification is widely
nodule is that of an asymptomatic swelling in the used worldwide. FNAC should only be undertaken
neck. The characteristic clinical feature of a thyroid after exclusion of thyrotoxicosis, as a toxic adenoma
Table 37.1 Bethesda system and cytology diagnostic categories for thyroid cancer.
Bethesda diagnostic criteria Risk of malignancy Recommendations
I Non‐diagnostic/unsatisfactory 1–4% Repeat fine‐needle aspiration

II Benign 0–3% Surveillance
III Atypia or follicular lesion of undetermined significance 5–15% Surveillance or surgery
IV Follicular neoplasm or suspected follicular neoplasm 15–30% Surveillance or surgery
V Suspicious for malignancy 60–75% Surgery
VI Malignant 97–99% Surgery
37: Thyroid 333
may appear concerning on cytology. Further, toxic and fibrosis occurring throughout the gland. It
adenomas are almost always benign. It is important occurs either in response to iodine deficiency or, in
to note that cytology may suggest a follicular neo iodine‐replete areas, as a result of the intrinsic het
plasm but cannot differentiate between a benign erogeneity of TSH receptors. The latter has a high
follicular adenoma and a follicular carcinoma. This familial incidence. A dominant nodule within a multi
diagnosis can only be made by the finding of either nodular goitre is most likely to be either a hyper
capsular or vascular invasion on histology, hence plastic or colloid nodule. However, the incidence of
the need for diagnostic hemithyroidectomy in these malignancy in a dominant nodule is approximately
patients. The likelihood of a follicular lesion on the same as for a single nodule (7%). Hence, multi
cytology being malignant is up to 30%. FNAC is nodular goitre has a high familial incidence, and is
best performed with ultrasound guidance in order also common in areas where iodine is deficient in
to target the most appropriate part of the nodule the diet.
and to ensure the nodule of concern is biopsied. An
inadequate or non‐diagnostic aspirate is not a
benign result and should be repeated, as up to 10% Clinical presentation
of these will be malignant. The exception here is a Most multinodular goitres present as an asympto
thyroid cyst on clinical and ultrasound features, matic mass in the neck. They may also present
where FNAC shows colloid, cyst fluid and degener with local pressure symptoms to the trachea,
ate cells only, and where overall the features are oesophagus, recurrent laryngeal nerve or SVC.
consistent with a thyroid cyst, although strictly Clinical retrosternal extension and Pemberton’s
there is no epithelial material to diagnose a benign sign should be assessed, and lymphadenopathy
thyroid nodule. FNAC may be therapeutic as well sought. Thyrotoxicosis complicating the goitre is
as diagnostic for thyroid cysts, and repeated aspira also common, especially in the elderly with large
tion will result in resolution in at least 50% of goitres. An otherwise asymptomatic retrosternal
cases. FNAC may also show features of thyroiditis, multinodular goitre may present incidentally as a
alone or in combination with other cytology. mass on a chest X‐ray or CT scan.
Hashimoto’s will show lymphocytes and suba
cute thyroiditis may show inflammatory cells and
giant cells. Investigations
The role of nuclear medicine scans is limited to
the investigation of patients with thyrotoxicosis or Thyroid function tests, as previously outlined,
thyroiditis. must be performed on all patients. Ultrasound
will document the size of the thyroid lobes and the
Treatment number and size of nodules, providing a baseline
for follow‐up, and will also indicate which nodules
Asymptomatic thyroid nodules that are benign on require FNAC. FNAC of a dominant nodule or
FNAC do not generally require treatment. nodules aims to exclude malignancy and a CT scan
However, follow‐up, at least in the short term, is (without intravenous contrast) will assess retrosternal
appropriate. Indications for surgery include the extension or tracheal compression and deviation.
presence of obstructive symptoms, thyrotoxicosis, Intravenous contrast is avoided because of its
or the finding of malignancy, suspicion of malig iodine content and the possibility it may precipitate
nancy or atypical or follicular changes on FNAC, iodine‐induced thyrotoxicosis. A thyroid nuclear
and on patient request. The minimal surgical pro medicine scan is used in a multinodular goitre to
cedure is a hemithyroidectomy, removing all thy assess for a solitary toxic nodule or multiple areas
roid tissue on the side of the lesion (including of variable activity.
isthmus and pyramidal lobe). Thyroxine suppres
sion is ineffective in decreasing the size of single
thyroid nodules. Treatment
Indications for surgical treatment of a multinod
ular goitre include the presence of obstructive
Multinodular goitre symptoms, growth of the goitre, thyrotoxicosis,
suspicious or malignant changes on FNAC, a
Pathology
strong family history of thyroid cancer, the pres
Multinodular goitre occurs as the result of repeated ence of retrosternal extension, a past history of
cycles of hyperplasia, nodule formation, degeneration head and neck irradiation (which increases the
risk of malignancy) and patient request. In a young Clinical presentation

patient with a large multinodular goitre, who is
Thyroid cancer commonly presents as either a
otherwise asymptomatic, thyroidectomy may also
single thyroid nodule or a dominant nodule in
be considered for cosmetic reasons. The only effec
a multinodular goitre. It occasionally presents as a
tive treatment is surgical excision. If surgery is
metastasis as an abnormal lateral lymph node in
undertaken, total thyroidectomy is the preferred
the neck, hence the need to undertake FNAC on all
option, because it removes all tissue likely to
abnormal lymph nodes prior to removal. Thyroid
cause symptoms and avoids the possibility of
cancer may also rarely present as distant metastatic
later recurrence (which occurs in about 30%).
disease, such as bony metastases from follicular
Lifelong thyroxine replacement is required after
cancer, or lymphangitic lung involvement from
total thyroidectomy.
papillary cancer.
Thyroid cancer
Investigation
Pathology
Thyroid function tests and neck ultrasound will
Thyroid cancer can arise from the follicular cells,
assess the nodule and possible abnormal lymph
the C‐cells, or other cells such as lymphocytes or
nodes. Depending on the presentation, the most
stromal cells, each giving rise to a different form of
useful investigation is FNAC, but CT is of value in
thyroid cancer. Papillary thyroid cancer (PTC)
determining extent of tumour and lymph node
accounts for about 85% of thyroid cancers, tends
involvement. Serum calcitonin levels may be raised
to occur in a younger age group (20–40 years), is
in medullary tumours.
often multifocal, spreads predominantly to local
lymph nodes and has a relatively good prognosis,
with 10‐year survival rates of at least 90%. Treatment
Follicular cancer occurs in an older age group
Most differentiated thyroid cancer is still treated by
(40–60 years), arises as a single tumour, metasta
total thyroidectomy, with local removal of involved
sises via the bloodstream and has a worse progno
lymph nodes. Following removal of the tumour,
sis than papillary cancer, with 10‐year survival
patients are classified into those with low‐,
rates around 75%. Together, papillary and follicu
intermediate‐ or high‐risk tumours on the basis of
lar thyroid cancers are considered differentiated
age, tumour size, lymph node involvement, extrathy
thyroid cancer, and account for the majority of
roidal extension and distant metastases (Box 37.1).
thyroid cancer resulting in the usual overall good
Subsequent treatment may involve the admin
prognosis. The incidence of PTC is increasing
istration of radioactive iodine (131I) for moderate
worldwide at an exponential rate, particularly for
or higher risk cancers, which allows for both the
tumours less than 4 cm in diameter. Further, there
detection and ablation of metastatic disease. Fol
is an increasing recognition of micropapillary thy
lowing total thyroidectomy, thyroxine replacement
roid cancer (<1 cm), which is often an incidental
is required lifelong, and for higher‐risk cancers is
pathological finding in a goitre removed for other
given in a larger dose to suppress TSH. Low‐risk
reasons, usually multinodular goitre. Anaplastic,
papillary cancer may include young patients, with
or undifferentiated, thyroid cancer occurs in the
elderly, often presents as a rapidly enlarging dif
fuse mass, spreads locally and has a very poor
prognosis, with 5‐year survival rates of less than Box 37.1 Classification of tumours
1% but is fortunately very rare. Malignancy aris
ing in C‐cells gives rise to medullary carcinoma of High risk
the thyroid. This tumour secretes calcitonin and Gross extrathyroidal extension, incomplete tumour
may be part of a familial multiple endocrine resection, distance metastases or lymph node >3 cm
neoplasia (MEN 2A) syndrome, occurring in asso Intermediate risk
ciation with phaeochromocytoma and hyperpar Aggressive histology, minor extrathyroidal extension,
athyroidism. The 10‐year survival rate is around vascular invasion, or more than five involved lymph
35%. Lymphoma of the thyroid is thought to arise in nodes (0.2–3 cm)
lymphocytes, often in association with pre‐existing
Low risk
Hashimoto’s thyroiditis. Follicular‐derived thyroid
Intrathyroidal differentiated thyroid cancer with five
cancer has an association with previous exposure
or less lymph node micrometastases (<0.2 cm)
to ionising radiation.
37: Thyroid 335
tumours less than 4 cm in diameter and with absent and/or free T3 in association with a suppressed
extrathyroidal extension or lymph node or distant TSH. Clinical examination may indicate the aetiol
metastases. In this setting, consideration for treat ogy, demonstrating a diffuse goitre, a multinodular
ment by hemithyroidectomy alone is appropriate, goitre or a single thyroid nodule. Thyroid nuclear
although total thyroidectomy is considered an scans will confirm the diagnosis (increased activity),
equally appropriate treatment option. For tumours as well as the aetiology, and exclude factitious
of less than 1 cm (micropapillary PTC) with no thyrotoxicosis and thyroiditis (absent or reduced
other risk factors, hemithyroidectomy alone is activity, respectively). Anti‐TSH receptor antibodies
considered adequate treatment. are present in Graves’ disease and are quantified as
Close follow‐up is essential, and further surgery a measure of severity and response to medical
for lymph node recurrences and use of radioiodine treatment.
usually results in a good prognosis. Newer agents
such as tyrosine kinase inhibitors are available for
Treatment
widespread disease, although rarely required.
Medullary thyroid cancer requires total thyroid Initial treatment is to render the patient euthyroid by
ectomy and a central lymph node dissection, with administration of antithyroid medications such as
lateral neck dissection and mediastinal clearance carbimazole or propylthiouracil, both of which pre
for node‐positive patients. Medullary carcinoma vent coupling of iodotyrosine. Patients with Graves’
does not respond to radioiodine ablation. disease are generally treated with medication for
Thyroid lymphoma is best diagnosed by multiple 12–18 months. Definitive treatments for Graves’
core biopsies or occasionally an open incisional disease include ablation with radioactive iodine, usu
biopsy. It is then usually treated by chemotherapy ally reserved for patients over 40 years of age because
and occasionally radiotherapy. It often responds of the theoretical teratogenic risk, or total thyroidec
well to these treatments. tomy. Graves’ disease is treated by surgery if there is
relapse following initial medical treatment (about
50% of the time) or non‐compliance with such treat
Thyrotoxicosis
ment, or if ophthalmopathy is present, in which case
Pathology radioiodine ablation is contraindicated (as radioio
dine may induce worsening ophthalmopathy). Toxic
The causes of thyrotoxicosis include Graves’ disease,
multinodular goitre and toxic adenoma are best
toxic multinodular goitre (Plummer’s disease), toxic
treated surgically once the patient is rendered euthy
follicular adenoma or in the initial stages of thyroidi
roid by antithyroid medication in order to treat the
tis (may occur in both Hashimoto’s and subacute).
thyrotoxicosis and remove the goitre.
Rare causes include a TSH‐secreting pituitary tumour
or struma ovarii. Graves’ disease is an autoimmune
condition associated with antibodies to the TSH
Thyroiditis
receptor. Toxic nodular goitre results from autono
mous activity in a neoplastic nodule. Pathology
Thyroiditis is classified as lymphocytic (Hashimoto’s),
Clinical presentation subacute (de Quervain’s), acute (bacterial) or fibro
Thyrotoxicosis presents with symptoms and signs sing (Reidel’s). Of these, the two most common are
of thyroid overactivity, including tachycardia, heat lymphocytic, which is an autoimmune condition
intolerance, sweating, fine tremor, weight loss and often forming part of a spectrum with Graves’
anxiety. In addition, Graves’ disease may be associ disease, and subacute, which is a post‐viral phe
ated with exophthalmos, ophthalmoplegia and nomenon. The other two are rare.
pretibial myxoedema. Graves’ disease typically pro
duces a smooth diffuse goitre, which because of sig Clinical presentation
nificant blood flow may exhibit a palpable thrill
and bruit. Toxic nodules may also present with Lymphocytic thyroiditis may present with hyper
local pressure or obstruction. thyroidism (early phase) or hypothyroidism (late
phase), or it may present with a nodular or diffuse
goitre. Subacute thyroiditis usually presents with
Investigation
an exquisitely tender, enlarged, firm thyroid gland,
The diagnosis of thyrotoxicosis will be confirmed with nodularity, often with systemic symptoms of
by thyroid function tests, with an elevated free T4 headache, malaise and weight loss. The history is
relatively short, usually of several weeks’ duration, urgent return to theatre and decompression and
and the nodularity may sequentially involve differ occurs in 1–2% cases. Enlarging haematoma
ent areas of the thyroid. Initial thyrotoxicosis may beneath the strap muscle layer will result in
also be present. increasing pressure, in turn causing venous and
lymphatic obstruction and submucosal oedema of
the larynx and trachea, and potential critical air
Investigation
way obstruction. Treatment is urgent release of
Thyroid function tests will determine the level of the pressure by opening the skin and deeper strap
thyroid activity. A nuclear medicine scan is often muscle layer. Usually there is time to transport the
diagnostic, showing patchy uptake in lymphocytic patient to theatre, but occasionally it is more rap
thyroiditis and no uptake at all in subacute thyroiditis. idly evolving and will need to be performed on the
The inflammatory markers erythrocyte sedimen ward. Hence the need for close observation of the
tation rate (ESR) and C‐reactive protein (CRP) neck postoperatively and a thyroid tray of instru
will be elevated in subacute thyroiditis but not ments at the patient’s bedside should they be
Hashimoto’s. Anti‐peroxidase and anti‐thyroglobulin required.
antibodies will be elevated in Hashimoto’s but not Unilateral recurrent nerve palsy leads to a hoarse
subacute thyroiditis. voice and is usually temporary, often resolving
within weeks but occasionally taking up to 6 months,
and occurs in up to 10% of cases. Recurrent laryn
Treatment
geal nerve palsy may be permanent in 1–3% of
Subacute thyroiditis usually responds to high‐dose cases. Voice quality usually improves over time, but
steroids and aspirin therapy, although it may take occasionally can be improved further by procedures
3–6 months to fully resolve. Lymphocytic thyroidi such as vocal cord medialisation. Rarely, bilateral
tis may respond to thyroxine suppression. Surgery damage may occur and require a tracheostomy
may be required for lymphocytic thyroiditis with because the vocal cords adopt a medial position,
persistent or suspicious nodules, or for pressure causing airway obstruction.
symptoms, although surgery may be more difficult If the external branch of the superior laryngeal
because of the solid non‐pliable nature of the gland. nerve is affected (estimated to occur in 10–30%),
the patient may lose the ability to sing, shout or
project their voice.
Because of postoperative changes and oedema at
Operative management: thyroidectomy the site of surgery, up to 80% of patients will expe
rience subtle alteration in their voice quality, in the
Indications absence of either recurrent or external laryngeal
nerve injury. This change often takes several months
Thyroidectomy is indicated for relief of local pres
to resolve.
sure symptoms, for the diagnosis and treatment of
Permanent damage to the parathyroid glands
thyroid cancer, for the control of thyrotoxicosis
will cause permanent hypoparathyroidism and
or for cosmetic considerations. As previously out
occurs in 1–3% following total thyroidectomy.
lined, thyroidectomy may be total or partial
Temporary hypoparathyroidism causing tempo
(hemithyroidectomy).
rary hypocalcaemia is much more common ( usually
8–12% of cases but may be even commoner) and is
Complications of thyroidectomy
due to oedema, bruising, devascularisation or inad
The complications of thyroidectomy include all the vertent removal of parathyroid glands. Treatment
general complications of any operation, such as is short‐term administration of oral calcium and/or
bleeding, wound infection and reaction to the 1,25‐dihydroxyvitamin D for several weeks, but
anaesthetic agent. In addition, there are specific occasionally intravenous calcium is required. These
complications, including: complications are avoided by understanding the
• postoperative neck haematoma surgical anatomy of the thyroid gland (Figure 37.1)
• damage to the recurrent laryngeal nerves and by the technique of capsular dissection, care
• damage to the external branch of the superior fully preserving the parathyroid glands and their
laryngeal nerves blood supply and the recurrent laryngeal and exter
• damage to the parathyroid glands. nal laryngeal nerves. If there is devascularisation of
Postoperative haemorrhage causing a neck haema parathyroid glands or inadvertent removal, they
toma is a major surgical emergency requiring should be autotransplanted.
37: Thyroid 337
External branch of
superior laryngeal nerve
Inferior parathyroid
Superior parathyroid
Recurrent laryngeal nerve
Fig. 37.1 Surgical anatomy of the thyroid gland. The left lobe of the gland is elevated and rotated medially exposing the
recurrent laryngeal nerve, the external branch of the superior laryngeal nerve and both parathyroid glands, with their
blood supply arising from the inferior thyroid artery.
b papillary thyroid cancer

Further reading c anaplastic thyroid cancer
d medullary thyroid cancer
Fundakowski CE, Hales NW, Agrawal N et al. Surgical
Management of the recurrent laryngeal nerve in thyroid
e metastases from renal cell cancer
ectomy: American Head and Neck Society Consensus
Statement. Head Neck 2018;40:663–75. 3 The type of thyroid cancer with the worst prognosis
Haugen BR, Alexander EK, Bible KC et al. 2015 American (5‐year survival <1%) is:
Thyroid Association Management Guidelines for adult a papillary thyroid cancer
patients with thyroid nodules and differentiated thyroid b follicular thyroid cancer
cancer: The American Thyroid Association Guidelines c anaplastic thyroid cancer
Task Force on Thyroid Nodules and Differentiated d medullary thyroid cancer
Thyroid Cancer. Thyroid 2016;26:1–133. e thyroid lymphoma
Qian SY, Topliss DJ. Thyroid cancer: how to achieve opti
mal patient outcomes. Medicine Today 2017;18:28–35.
4 Thyroiditis presenting following a viral infection
Ross DS, Burch HB, Cooper DS et al. 2016 American
Thyroid Association Guideline for diagnosis and with an exquisitely tender, enlarged, firm thyroid
management of hyperthyroidism and other causes of gland, and with systemic symptoms of headache
thyrotoxicosis. Thyroid 2016;26:1343–421. and malaise is generally due to:
a Hashimoto’s thyroiditis
b de Quervain’s (subacute) thyroiditis
MCQs c Reidel’s thyroiditis
d acute bacterial thyroiditis
Select the single correct answer to each question. The e non‐specific thyroiditis
at the end of the book. 5 Damage to one recurrent laryngeal nerve during
thyroidectomy generally leads to:
1 Thyroid follicular cells arise primarily from:
a the need for a tracheostomy
a laryngeal cartilage
b inability to sing high notes
b second branchial arch
c inability to project the voice to the back of a hall
c oesophagus
d a falsetto voice
d base of the tongue
e a hoarse voice
e neural crest
2 FNAC may diagnose all types of thyroid cancer

except:
a follicular thyroid cancer
38 Parathyroid
Jonathan Serpell
Victoria, Australia
nerve and above the inferior thyroid artery, whereas

Introduction inferior glands are located anterior to the nerve and
below the inferior thyroid artery. Superior and infe-
There are usually four parathyroid glands, two on
rior parathyroid glands take their name from their
each side, having a posterolateral relationship to
relationship, either above or below, the inferior thy-
the lateral lobes of the thyroid gland. The two supe-
roid artery.
rior parathyroid glands arise from the fourth phar-
A normal parathyroid gland weighs 30–35 mg.
yngeal pouch and ultimobranchial body and
Both superior and inferior glands derive their pri-
migrate medially early in fetal development along
mary blood supply from branches of the inferior
with the C‐cells to meet the developing thyroid
thyroid artery, although superior glands may
gland. They are generally reasonably constant in
receive branches from the superior thyroid artery.
position in relation to the lateral lobe or to the
The parathyroid glands secrete parathyroid hor-
tubercle of Zuckerkandl. The two inferior parathy-
mone (PTH), an 84‐amino acid peptide with a half‐
roid glands arise from the third pharyngeal pouch
life of about 5 minutes. PTH is rapidly broken down
and descend into the anterior neck along with the
into N‐terminal and C‐terminal fragments in the
thymus. Because of their longer course of descent
reticuloendothelial cells of the liver. PTH acts on
they are more variable in position and may be
bone to mobilise calcium by stimulation of osteo-
found in relation to the inferior pole of the thyroid
clast activity, leading to bone resorption. PTH also
gland, in the thyrothymic tract, or within or adja-
acts on the kidney to increase calcium resorption in
cent to the thymus, in its cervical or anterior medi-
the proximal convoluted tubule and inhibit resorp-
astinal components.
tion of both phosphate and bicarbonate. An addi-
Ectopic or supernumerary parathyroid glands
tional renal effect is the production by the proximal
are common, being found in over 10% of the popu-
tubule of activated 1,25‐dihydroxyvitamin D, which
lation. Ectopic inferior parathyroid glands may be
results in calcium absorption by the small intestine.
located in a variety of positions, such as within the
Diseases affecting the parathyroid glands result
carotid sheath or as an undescended para‐thymus
essentially in disorders of function, either excess or
(high in the neck at the level of the submandibular
reduced PTH secretion. These include:
salivary gland) or within the thyroid gland itself.
• primary hyperparathyroidism
Rare ectopic sites include the pericardium and
• secondary and tertiary hyperparathyroidism
aorto‐pulmonary window. If parathyroid glands
• hypoparathyroidism.
enlarge, they may migrate from their original loca-
tion. Superior parathyroid glands, as they enlarge,
often move down along the oesophagus, presuma-
bly aided by peristalsis, and can end up in the pos- Disorders of the parathyroid glands
terior mediastinum in a para‐ or retro‐oesophageal
position. Superior glands tend to move inferiorly Primary hyperparathyroidism
and posteriorly, whereas inferior glands move infe-
Pathology
riorly and anteriorly.
The course of the recurrent laryngeal nerve acts as Primary hyperparathyroidism is due to a parathy-
a marker to the location of the parathyroid glands, roid adenoma, usually solitary (85% of cases). It
with superior glands usually located posterior to the may also be due to parathyroid hyperplasia (up to
339
15%) or, rarely, parathyroid carcinoma (<1%). It Measurement of 24‐hour urinary calcium excre-
may occur as a sporadic phenomenon or may be tion excludes the rare but confounding genetic
associated with one of the familial endocrine syn- autosomal dominant disorder of familial hypocal-
dromes, including multiple endocrine neoplasia ciuric hypercalcaemia, in which an elevated serum
(MEN) 1 and MEN 2A, or familial hyperparathy- calcium may be associated with a marginally
roidism. Hyperparathyroidism is also associated raised PTH level and low urinary calcium excre-
with a history of previous exposure to ionising radi- tion. Magnesium and phosphate should be esti-
ation to the neck, especially in childhood and ado- mated. Vitamin D and serum creatinine are
lescent years. measured to exclude the two common causes of
secondary hyperparathyroidism. A bone density
study should be undertaken as a baseline to docu-
Clinical presentation ment established osteopenia or osteoporosis and
enable assessment of bone remineralisation fol-
Primary hyperparathyroidism occurs predomi-
lowing treatment.
nantly in women, with the highest incidence in the
A careful family history will generally exclude an
fifth to sixth decades. The commonest presentation
association with one of the familial endocrine syn-
is in apparently asymptomatic individuals who are
dromes. If the patient has MEN 1, tumours of the
found to have hypercalcaemia during routine blood
pituitary and pancreatic islet cells need to be
testing, or who present for routine bone mineral
excluded, whereas if they are part of a MEN 2A
density testing and are found to have osteopenia or
family, serum calcitonin and urinary catechola-
osteoporosis. Symptoms specifically associated
mines need to be measured to exclude medullary
with primary hyperparathyroidism include neu-
thyroid carcinoma and phaeochromocytoma.
ropsychological manifestations such as tiredness,
Once a diagnosis of primary hyperparathy-
lethargy and depression, musculoskeletal manifes-
roidism has been confirmed, parathyroid localisa-
tations such as bone pain and muscle weakness and
tion studies should be undertaken. The aim of
myalgia, renal stones, abdominal pain from consti-
localisation studies is to identify or at least lateral-
pation or peptic ulceration, polyuria and polydip-
ise the site of the parathyroid adenoma to allow a
sia, leading to their summary description as ‘bones,
decision to be made as to whether a targeted,
stones, abdominal groans and psychic moans’.
focused, unilateral surgical approach is possible.
However, careful history taking will often elicit evi-
Localisation studies are only undertaken after the
dence of these symptoms in a subtle form, leading
diagnosis is clearly established; they should not be
many to believe that all patients with primary
done to make the diagnosis of primary hyperpar-
hyperparathyroidism are in fact symptomatic to
athyroidism. Further, imaging results should not be
some extent, with the corollary that all should
used to decide whether surgery is indicated, as those
be treated. A careful medication history is impor-
who are not localised by imaging remain candi-
tant, as for example lithium may result in para-
dates for surgery. Ultrasound and nuclear medicine
thyroid hyperplasia, as well as exhibiting renal
scanning are routinely used for localisation.
manifestations.
A 99mTc‐sestamibi parathyroid scan using single‐
photon emission computed tomography (SPECT)
will demonstrate uptake in a single parathyroid
Investigations
adenoma in more than 70% of cases, with neck
The diagnosis of primary hyperparathyroidism is ultrasound providing valuable additional informa-
biochemical and confirmed by the finding of an tion. If localisation is positive, and the two studies
elevated serum calcium level in association with an concordant, targeted exploration is possible; this
inappropriately raised (i.e. non‐suppressed) PTH focused approach is also described as a minimally
level. Occasionally the PTH may be in the normal invasive parathyroidectomy. If localisation is not
range despite the presence of primary hyperparath- achieved, the patient requires bilateral neck
yroidism but nonetheless still inappropriately ele- exploration, aiming to identify all four parathy-
vated. In contradistinction, other secondary causes roid glands. The rationale is that without locali-
of hypercalcaemia (e.g. metastatic malignancy) sation the involved glands are probably smaller,
have an elevated serum calcium but a suppressed and there may be multiple glands involved due to
PTH level. Calcium levels may fluctuate, passing in hyperplasia, hence the need to explore both sides
and out of the normal range, so at least three esti- of the neck. Overall, parathyroid imaging is sig-
mates are required. Further, ionised calcium will be nificantly less accurate for those with multi‐gland
elevated if doubt remains about the diagnosis. disease.
38: Parathyroid 341
Rarely, in patients with recurrent primary hyper- hyperplasia and stimulates PTH secretion. Further,
parathyroidism, other specialised localisation stud- in CKD there is reduced expression of the calcium‐
ies are undertaken, including four‐dimensional CT sensing receptor in parathyroid cells. Increases in
scanning (now undertaken by some for initial local- PTH result in osteodystrophy much greater than
isation) and selective venous sampling. However, that normally seen in primary disease. The parathy-
the radioactivity associated with four‐dimensional roid glands initially undergo hyperplasia and then
CT needs to be considered in a younger patient. develop nodularity, and the process is often asym-
At the same time as localisation, neck ultrasound metrical so that some glands will have greater
will also assess the thyroid gland for significant degrees of enlargement than others. Renal osteod-
abnormalities which may require investigation ystrophy is often a combination of secondary
(thyroid function and cytology of any suspicious hyperparathyroidism and the disturbed vitamin D
nodules) and potential surgery at the same time as metabolism of CKD (osteomalacia). More recently,
the proposed parathyroidectomy. Concomitant thy- the role of increasing fibroblast growth factor
roid disease is common, found in at least 12% of (FGF)23 levels (which parallel PTH levels) and
patients. Klotho deficiency in CKD as biomarkers of osteod-
ystrophy and associated vascular disease has
become an area of active ongoing research in sec-
Treatment
ondary hyperparathyroidism.
The only successful treatment for primary hyper-
parathyroidism is parathyroidectomy. All sympto-
Clinical features
matic patients should undergo surgery. Other
definite indications for surgery are calcium greater The osteodystrophy of secondary hyperparathy-
than 0.25 mmol/L above normal range regardless roidism causes bone, joint and muscle pain and
of whether symptomatic, evidence of renal involve- may lead to pathological fractures. There may be
ment (e.g. nephrolithiasis and nephrocalcinosis), deposition of calcium in soft tissues resulting
osteoporosis and age less than 50 years. There is in skin itch and may be associated with severe
debate about whether asymptomatic patients may skin necrosis (calciphylaxis) and conjunctivitis.
be treated by observation subject to a set of strict Ectopic calcification also occurs in blood vessels,
criteria; however, there is increasing evidence that heart valves and other organs such as lung and
even ‘asymptomatic’ patients obtain significant intestines. Neuromuscular and psychiatric symp-
benefit in relation to improvements in non‐specific toms also occur, as well as anaemia and cardiac
neuropsychological symptoms following normali- failure.
sation of serum calcium levels after surgery. As
such, most patients, unless there are specific con-
Investigations
traindications to surgery, are now offered parathy-
roidectomy as initial therapy. The likelihood of Secondary hyperparathyroidism is characterised by
curing the primary hyperparathyroidism is on the hypocalcaemia, hyperphosphataemia and an ele-
order of 95–98%, with a very low risk of recurrent vated PTH level. Significant bone disease is indi-
disease. Further, surgery is probably more cost‐ cated by elevation of serum alkaline phosphatase.
effective overall than observation. Hypercalcaemia may occur secondary to vitamin D
treatment, or development of tertiary hyperpar-
athyroidism. Radiology may demonstrate much
Secondary hyperparathyroidism grosser changes in the skeleton than is usual in pri-
mary hyperparathyroidism in the modern context,
Pathology
with irregular bone density loss and subperiosteal
Secondary hyperparathyroidism is the result of pro- absorption of bone. Classical appearances include
longed hypocalcaemia and is usually due to chronic ‘pepperpot’ skull, ‘rugger jersey’ spine and the less
kidney disease (CKD), although vitamin D defi- dramatic but more frequent loss of the outer third
ciency and gluten‐sensitive enteropathy must be of clavicle and scalloping of the radial side of the
excluded as causes. The prolonged hypocalcaemia middle phalanges. Metastatic calcification can be
results in chief cell hyperplasia and PTH secretion. seen around vessels and in the capsules of joints.
In CKD this appears primarily to be due to diffi- If surgery is contemplated, localisation with ses-
culty with excretion of phosphate, resulting in tamibi scanning is useful to exclude ectopic loca-
hyperphosphataemia and secondary hypocalcae- tions, especially the mediastinum, and ultrasound is
mia. Hyperphoshataemia leads to parathyroid cell necessary to assess the thyroid.
Treatment appears the most normal parathyroid tissue, usually

of an inferior gland, so if recurrence does occur it
Secondary hyperparathyroidism occurs to some
will be further away from the recurrent laryngeal
degree in all patients with CKD, but especially in
nerve at the time of re‐exploratory surgery. The sub-
those with dialysis‐dependent CKD (stage 5 CKD).
total procedure has theoretical advantages for a
The symptoms can often be ameliorated by oral
patient who is likely to receive a renal transplant, in
calcium‐based and other phosphate binders (aimed at
the hope that the remnant will function normally
reducing intestinal absorption of phosphate), with or
once normal renal function is established. Equally, if
without the administration of 1,25‐dihydroxyvitamin
transplantation not an option, the total procedure
D (active vitamin D, calcitriol). There has also been
seems sensible. However, studies do not indicate
considerable interest in extended‐hour (nocturnal)
which surgical procedure is preferred, and this is
dialysis as a mechanism for controlling hyperphos-
therefore tailored to the individual patient and sur-
phataemia, as short‐hour intermittent dialysis is rela-
geon’s preference.
tively ineffective at removing phosphate.
Cinacalcet, a calcimimetic, acts as a positive
modulator of the calcium sensing receptor located Tertiary hyperparathyroidism
on parathyroid cells. It acts to reduce PTH produc- Tertiary hyperparathyroidism results from the
tion from the cells. It has been a major advance in hyperplasia of secondary hyperparathyroidism
the treatment of secondary hyperparathyroidism when the glands become autonomously hyper-
but is not always available. Cinacalcet had been functioning rather than responsive to the original
shown to reduce the need for parathyroidectomy in stimulus. Thus, tertiary hyperparathyroidism is a
90% of patients. progression of secondary hyperparathyroidism
Although the treatment of secondary hyperpar- accompanied by spontaneous hypercalcaemia. This
athyroidism is therefore largely medical in nature, is most clearly seen after a successful renal trans-
some patients will not achieve satisfactory symp- plant has been performed, where the restoration of
tom or biochemical control (high phosphate and normal renal function and the appropriate produc-
high PTH). The need for parathyroidectomy has tion of 1,25‐dihydroxyvitamin D could be expected
varied in the eras before and after cinacalcet but is to restore normal calcium balance. Most patients
about 10% of those on haemodialysis for more should receive active medical treatment in an
than 10 years. With restrictions on the availability attempt to avoid end‐organ damage and will usu-
of cincalcet, the requirement for parathyroid sur- ally show a return to normal calcium metabolism
gery is likely to increase once more. Indications for within a period of 6 months. In the small number of
surgery include the development of hypercalcaemia patients whose symptoms are not controlled or in
because this is likely to lead to metastatic calcifica- whom the hypercalcaemia persists despite adequate
tion and persistent elevation in alkaline phos- treatment and normal renal function, the glands
phatase, which is an indication of continuing major must be assumed to have developed some degree of
bone disease. Other indications include inability autonomy and parathyroidectomy is required. The
to control serum phosphorus, calcium and PTH extent of surgery is dictated by the operative
within target ranges; intractable subjective symp- findings, with either subtotal or total parathy-

toms including itch or bone pain and muscle roidectomy with cervical thymectomy, and with
weakness; ectopic calcification; calciphylaxis; autotransplantation being undertaken depending
non‐availability of cincalcet or when cincalcet does on the number of glands involved in this process.
not achieve a satisfactory reduction in PTH level;
anaemia resistant to erythropoietin; and dilated
cardiomyopathy.
Hypoparathyroidism
These patients should be treated by parathyroid- Hypoparathyroidism may be due to congenital
ectomy. The options available include subtotal par- absence of the parathyroid glands, idiopathic auto-
athyroidectomy, or total parathyroidectomy with or immune failure of the parathyroid glands or, most
without parathyroid autotransplantation into the commonly, surgical removal or damage to the para-
sternocleidomastoid in the neck or brachioradialis in thyroid glands after total thyroidectomy. Temporary
the forearm. Both the subtotal and total procedures hypoparathyroidism is common (8–12%) after total
should include cervical thymectomy, as rests of parathyroidectomy, due to oedema, bruising and devas-
thyroid tissue are common in the thymus. The subto- cularisation of glands. Temporary hypoparathy-
tal procedure aims to leave a 50‐mg remnant of what roidism is commoner if devascularised parathyroid
38: Parathyroid 343
glands have been autotransplanted during the pro- or total parathyroidectomy with or without neck or
cedure. Such patients may be asymptomatic or may forearm autotransplantation. Both should also
present with paraesthesiae in the fingertips and toes have cervical thymectomy. As the stimuli causing
and around the mouth. This is managed by replace- secondary hyperparathyroidism affect all glands,
ment therapy with oral calcium and/or 1,25‐ the aim of surgery is to identify all glands, and
dihydroxyvitamin D awaiting recovery of the remove the thymus as this contains parathyroid
autotransplanted glands; this usually is a matter of rests of cells. Surgery generally results in a marked
weeks but can take up to 6 months. Most endocrine and sustained reduction in levels of serum PTH,
surgery units have proactive protocols to manage calcium and phosphorus.
hypoparathyroidism following total thyroidectomy,
and this approach has been shown to aid parathy-
roid gland recovery, due to a ‘splinting’ effect, Complications of parathyroidectomy
while the parathyroid glands regain their normal
The complications of parathyroidectomy include
function.
all the general complications of any operation, such
as bleeding, wound infection and reaction to the
anaesthetic agent. In addition, there are specific
Operative management
complications, including:
• damage to the recurrent laryngeal nerves and to
Parathyroidectomy
the external branch of the superior laryngeal
Primary hyperparathyroidism nerves (see Chapter 33)
Patients with primary hyperparathyroidism and • failure to locate abnormal parathyroid tissue
concordant localisation (sestamibi and ultrasound (discussed previously)
showing similar localisation to a single site) can • hypoparathyroidism.
undergo minimally invasive parathyroidectomy. If more than one parathyroid gland is involved,
Patients with primary hyperparathyroidism where subtotal parathyroidectomy may lead to hypopar-
localisation has been unsuccessful may have smaller athyroidism, which may require short‐term admin-
adenomas or may have multiple gland disease and istration of oral calcium and 1,25‐dihydroxyvitamin
should undergo bilateral neck exploration parathy- D. As in thyroid surgery, devascularised normal
roidectomy aiming to identify all four glands in parathyroid tissue should be autotransplanted.
order to assess for a single adenoma or multi‐gland Thus postoperatively, patients require close obser-
disease. vation, evaluating for symptoms of hypocalcaemia
The advantages of minimally invasive parathy- and monitoring serum calcium levels.
roidectomy are unilateral exploration, quicker Cure is defined as normocalcaemia at 6 months.
postoperative recovery and reduced incision length. Elevated postoperative calcium levels indicate per-
However, it is important to note that the magnitude sistent hyperparathyroidism. Cure followed by
of these benefits is small, and most patients still recurrence of hypercalcaemia after 6 months indi-
only require an overnight stay with bilateral neck cates recurrent hyperparathyroidism.
exploration.
The chance of cure is about 95–98% for both
surgical approaches. In the small percentage of
patients in whom the gland is not detected at the Further reading
time of primary surgery, it is likely to lie in an
Norlan O, Wang KC, Tay YK et al. No need to abandon
ectopic position, such as the pericardium or middle
focused parathyroidectomy: a multicenter study of long
mediastinum, and additional localisation studies term outcome after surgery for primary hypoparathy-
such as four‐dimensional CT and selective venous roidism. Ann Surg 2015;261:991–6.
sampling will be required prior to considering a Tominaga Y. Surgical management of secondary and ter-
second operation. tiary hyperparathyroidism. In: Randolph GW (ed.)
Surgery of the Thyroid and Parathyroid Glands, 2nd
edn. Philadelphia: Elsevier Saunders, 2013:639–47.
Secondary hyperparathyroidism Wilhelm SM, Wang TS, Ruan DT et al. American
Association of Endocrine Surgeons guidelines for defin-
Patients with secondary and tertiary hyperparathy- itive management of primary hyperparathyroidism.
roidism require either subtotal parathyroidectomy JAMA Surg 2016;151:959–68.
b parathyroid cancer
MCQs c parathyroid hyperplasia
d multiple parathyroid tumours
e a single parathyroid adenoma
4 The diagnosis of primary hyperparathyroidism is
1 The parathyroid glands arise from: usually confirmed by which of the following
a third and fourth branchial pouches biochemical results:
b base of the tongue a raised serum calcium, suppressed PTH
c first branchial pouch b raised serum calcium, raised or normal PTH
d thyroid parenchyma c normal serum calcium, raised PTH
e a tracheal diverticulum d normal serum calcium, suppressed PTH
e low serum calcium, raised or normal PTH
2 Parathyroid hormone (PTH) has a half‐life of:
a 7 seconds 5 The most common cause of hypoparathyroidism is:
b 5 minutes a congenital absence of the parathyroids
c 1 hour b autoimmune parathyroid failure
d 2 days c parathyroid cancer
e 5 weeks d surgical removal of the parathyroids at total
thyroidectomy
3 Primary hyperparathyroidism is due, in 90% of e acute bacterial infection
cases, to:
a metastatic cancer
39 Tumours of the adrenal gland
Jonathan Serpell
Victoria, Australia
Although the classification has been confusing in

Introduction the past, a consensus is now emerging (Table 39.2).
All such tumours are thought to ultimately be of
The adrenal glands lie superomedial to the upper
neural crest origin. Adrenal phaeochromocytomas
poles of both kidneys. Each adrenal gland com-
are of sympathetic origin. Extra‐adrenal tumours
prises a medulla and a cortex, and each component
may be of sympathetic origin and are located
has a distinct embryological origin. The adrenal
anywhere from the cervical ganglia to the urinary
cortex is of mesodermal origin, whereas the adrenal
bladder. They are classified as extra‐adrenal phae-
medulla arises from neural crest cells along with the
ochromocytoma, although they have also been
sympathetic ganglia. The adrenal medulla produces
labelled as paraganglioma in the past. Extra‐adrenal
catecholamines, including adrenaline, noradrena-
tumours may also be of parasympathetic origin,
line and dopamine, and is under the control of the
comprising mainly head and neck tumours such as
sympathetic nervous system. The adrenal cortex
carotid body tumours. Adrenal phaeochromocyto-
produces glucocorticoids (cortisol, corticosterone),
mas are the commonest hormone‐secreting adrenal
mineralocorticoids (aldosterone) and the sex ster-
tumour. Extra‐adrenal phaeochromocytomas and
oids oestrogen, testosterone and dehydroepiandros-
paragangliomas are rare.
terone (DHEAS). The adrenal cortex is under the
The majority of adrenal phaeochromocytomas are
control of adrenocorticotropic hormone (ACTH), a
benign and functioning, but between 10 and 20% are
hormone produced by the pituitary gland.
malignant. This diagnosis may be difficult to make
on histological examination, as with most endocrine
Adrenal and neural crest tumours tumours, and may not become apparent until the
appearance of distant metastases during follow‐up.
Adrenal masses are common, affecting 3–7% of the Such tumours have a tendency to grow along the
population. Tumours can arise from both the adre- adrenal and renal veins and may extend into the
nal cortex and the adrenal medulla as well as from inferior vena cava. Approximately 10% of phaeochro-
neural crest structures. Tumours of either origin mocytomas are bilateral within the adrenal glands.
may be benign or malignant, functioning or non‐ The majority of extra‐adrenal phaeochromocy-
functioning, and solitary or multiple. Adrenal toma are also functioning, but a greater percentage
tumours can be considered in the following groups: are malignant compared with adrenal tumours.
• tumours of the adrenal medulla/neural crest True paragangliomas only rarely function, and the
(phaeochromocytomas and paragangliomas) rate of malignancy is very low.
• adrenocortical tumours Phaeochromocytomas and paragangliomas may
• adrenal incidentalomas. occur sporadically or in association with a familial
The clinical features and investigation of adrenal disorder such as multiple endocrine neoplasia (MEN)
tumours are summarised in Table 39.1. 2A syndrome (comprising medullary carcinoma of
the thyroid, phaeochromocytoma and hyperparath-
Phaeochromocytoma and paraganglioma yroidism) or von Hippel–Lindau syndrome (retinal,
cerebellar, spinal and medullary haemangioblasto-
Pathology
mas, renal cysts and carcinoma, pancreatic cysts,
Phaeochromocytoma and paraganglioma are tumours phaeochromocytoma and papillary cystadenoma of
arising from the adrenal medulla or neural crest. the epididymis).
345
Table 39.1 Clinical features and investigations for adrenal tumours.
Syndrome or tumour Hormones secreted Symptoms
Adrenal medullary or Phaeochromocytoma Adrenaline Sweating, palpitations, hypertension

neural crest tumours Paraganglioma Noradrenaline (intermittent or sustained, and often severe),
Dopamine headache
Adrenocortical Cushing’s syndrome Glucocorticoids Central obesity, buffalo hump, abdominal
tumours striae, hypertension, proximal muscle
weakness, plethoric rounded facies, thin skin,
easy bruising, hirsutism
Conn’s syndrome Aldosterone Hypertension, hypokalaemia
Virilising/feminising Sex steroids Virilisation in females, feminisation in males
tumours
Adrenal Benign adrenocortical Non‐secreting Asymptomatic (incidental finding on CT or
incidentaloma adenomas ultrasound performed for other reasons)
Adrenal cysts
Adrenal lymphomas
Schwannomas
Myelolipomas
Metastases
Table 39.2 Classification of adrenal medullary and neural crest tumours.
Origin Tumour site Pathology
Sympathetic tissue Adrenal gland Adrenal phaeochromocytoma

Extra‐adrenal Extra‐adrenal phaeochromocytoma
Zuckerkandl remnant: pre‐aortic, below inferior mesenteric artery
Filum terminale tumour
Urinary bladder tumour
Thoracic paravertebral tumour
Cervical ganglia tumour
Parasympathetic tissue Extra‐adrenal Paraganglioma
Carotid body tumour
Vagal paraganglioma
Jugulotympanic paraganglioma
Laryngeal paranganglioma
Aorticopulmonary paraganglioma
Phaeochromocytomas have been termed the infarction or cerebrovascular accident. Paroxysmal

‘10% tumour’, as roughly 10% are malignant, hypertension may be precipitated by invasive pro-
bilateral, extra‐adrenal, extra‐abdominal, inherited cedures such as needle biopsy, angiograpthy, CT
and occur in children. scanning with intravenous contrast, and general
anaesthesia
Phaeochromocytomas present a rare but curable
Investigation
cause of hypertension, with varying combinations
of paroxysmal or sustained hypertension (0.5% of The clinical diagnosis of phaeochromocytoma is
patients with hypertension have a phaeochromo- confirmed in 99% of cases on the basis of elevated
cytoma), headache, sweating and palpitations. catecholamine levels (adrenaline, noradrenaline,
Loss of weight is a common symptom. Up to one‐ dopamine) or their metabolites – metanephrines –
third of cases may be asymptomatic. Some patients in plasma or in a 24‐hour urinary collection.
present as a hypertensive crisis, or even as sudden Collections require careful adherence to protocols,
death due to a complication such as myocardial and a careful medication history is necessary as
39: Tumours of the adrenal gland 347
l‐dopa and some antidepressants for exam- syndrome, Beckwith–Wiedemann syndrome, Carney’s
ple interfere with interpretation of results. The complex or MEN 1. The majority of glucocorticoid‐
catcholamine levels should be elevated greater than producing adrenocortical tumours are benign but
twofold, and the estimate repeated to document at up to 20% may be malignant. As with other
least two abnormal levels. Stress‐related elevations endocrine tumours, a diagnosis of adrenocortical
tend to be marginal and less than twofold. Once a carcinoma is based on the finding of capsular or
biochemical diagnosis is established, the tumour vascular invasion, but again may not be made
can usually be localised by CT or MRI. A nuclear until the later appearance of distant metastases.
medicine scan performed with metaiodobenzyl- These tumours may reach a very large size before
guanidine (MIBG) is useful for confirming the diagnosis, and as the size increases the risk of
functional status of a tumour, and may detect an malignancy also rises.
extra‐adrenal phaeochromocytoma or demonstrate Mineralocorticoid‐producing adrenal tumours
small lesions within the adrenal gland that are not are almost always small (<1 cm) and virtually
apparent on other forms of imaging, or multifocal- always benign. Bilateral nodular hyperplasia may
ity. Adrenal phaeochromocytomas are usually at be difficult to distinguish from a single aldosterone‐
least several centimetres in dimension, and hence producing adenoma.
are usually readily detected by CT scanning. They The majority of sex steroid‐producing tumours
tend to be vascular and may have areas of necrosis; are malignant at presentation. Adrenocortical
as a consequence their appearance on imaging carcinomas are rare and 70% are associated with
may raise suspicion of malignancy, although the hormonal hypersecretion, the most common
majority are benign. being cortisol, but often multiple hormones are
produced.
Treatment
Phaeochromocytoma and paraganglioma are treated Clinical presentation
by surgical excision. Careful preoperative preparation
Glucocorticoid‐producing tumours
is required in order to prevent an intraoperative
Most patients present with features of glucocorti-
hypertensive crisis, due to the massive release of
coid excess (Cushing’s syndrome). Occasionally a
catecholamine with tumour handling, or profound
large tumour may present with local symptoms,
postoperative hypotension. Unprepared patients
such as pain or fullness in the flank.
will have a significantly constricted intravascular
A number of hormone‐secreting tumours are
space due to the unopposed action of catechola-
diagnosed incidentally on CT or ultrasound scan
mines. Hence, following removal of the tumour in
(adrenal incidentaloma), although many such
an unprepared patient, there will be a dramatic fall
tumours have now been shown to be associated
in blood pressure requiring intravenous fluids
with subclinical Cushing’s syndrome (pre‐Cushing’s
and vasopressors. Preoperative preparation is best
syndrome). This syndrome is associated with
undertaken with administration of α‐adrenergic
hypertension, diabetes, obesity and osteoporosis
blocking agents, such as phenoxybenzamine, usually
but without the full biochemical manifestations of
over several weeks, closely supervised by an endo-
Cushing’s syndrome. Often all that is demonstrated
crinologist. This allows control of blood pressure
on investigation is loss of the diurnal rhythm of
and expansion of the intravascular space. Fluid
cortisol secretion and suppression of function of
loading intraoperatively, as well as the availability
the contralateral gland.
of intravenous nitroprusside to lower blood pres-
sure and intravenous noradrenaline to maintain
blood pressure, are essential requirements for safe Aldosterone‐producing adenomas
surgical removal. (Conn’s syndrome)
Most of these tumours present during the investiga-
tion of hypertension but may be suggested by symp-
Adrenocortical tumours toms such as polyuria, polydipsia and muscle
weakness due to the associated hypokalaemia.
Pathology
While hypokalaemia has been used as a screening
These tumours may be non‐functioning or may test for Conn’s syndrome in the past, there is increas-
secrete glucocorticoids, aldosterone or the sex ster- ing evidence that up to 50% of mineralocorticoid‐
oids. They may occur sporadically, or rarely as part producing tumours may be associated with normal
of a hereditary syndrome such as Li–Fraumeni levels of serum potassium.
Sex steroid‐producing tumours steroid‐producing tumour. These tumours are often

Clinical features of these rare tumours will be spe- large and should be detected on CT scanning.
cific to the type of hormone produced, with either Elevated DHEAS levels may suggest malignancy,
virilisation in females or feminisation in males. as carcinomas are often deficient in 3‐hydroxyster-
Many of these patients also have palpable masses oid dehydrogenase, such deficiency inhibiting
and 50% have metastatic tumour at the time of conversion of pregnenolone to cortisol and aldos-
presentation. terone but not inhibiting sex hormone production,
resulting in their elevation as well as their precursor
DHEAS.
Investigations
Initial screening tests used to diagnose Cushing’s
Treatment
syndrome usually involve two of (i) measurement
of a spot salivary cortisol, (ii) a 24‐hour urinary Surgical excision (adrenalectomy) is the only treat-
free cortisol level or (iii) a low‐dose dexamethasone ment for an adrenocortical tumour. For large or
suppression test to assess suppression of cortisol potentially malignant tumours, wide local exci-
overnight. If two of these are normal, Cushing’s sion and local lymph node dissection may be
syndrome is unlikely. If spot salivary cortisol or 24‐ required.
hour urinary free cortisol is elevated, a low‐dose
dexamethasone suppression test will usually be
undertaken to confirm glucocorticoid excess. Once Adrenal incidentalomas
a diagnosis of Cushing’s syndrome is established,
Pathology
further tests are required to establish the aetiology
of the excess glucocorticoid production. This may Any tumour arising in the adrenal gland can
involve measuring serum ACTH, a high‐dose dexa- present as an adrenal incidentaloma, including
methasone suppression test and an abdominal CT adrenocortical tumours, adrenal medullary tumours,
scan. The presence of an adrenal tumour as the schwannomas, myelolipomas, adrenal cysts, adre-
cause of the glucocorticoid excess, rather than a nal lymphomas and adrenal metastases from other
pituitary tumour (Cushing’s disease) or an ectopic malignancies, particularly breast cancer. Incidental
ACTH‐secreting tumour, can generally be made by benign adrenocortical adenomas are common and
measuring plasma ACTH levels and performing can be found at post‐mortem in up to 10% of the
abdominal CT. Adrenal tumours producing cortisol normal population and will be found in about 4%
will suppress ACTH levels to undetectable or very of abdominal CT scans. Metastases are increas-
low levels, whereas Cushing’s disease and ectopic ingly detected in adrenals on positron emission
ACTH‐producing tumours will have elevated tomography.
ACTH levels. A high‐dose dexamethasone suppres-
sion test will help distinguish the latter two (ectopic Clinical presentation
ACTH‐producing tumour will not suppress,
By definition, an adrenal incidentaloma will pre-
whereas Cushing’s disease will suppress). For adre-
sent as an incidental finding, usually on a CT or
nal Cushing’s, a high‐dose dexamethasone suppres-
ultrasound scan. They will not be associated with
sion test will not suppress the already low ACTH.
local symptoms, nor with any of the syndromes of
The rare bilateral nodular adrenal hyperplasia may
hormonal excess.
occasionally be difficult to differentiate from a
single small adrenal tumour.
Investigation
A low serum potassium level will suggest the
possibility of an aldosterone‐secreting tumour. The tumour will already have been demonstrated
Measurement of the ratio of plasma renin and by imaging. Hormonal hypersecretion must be
plasma aldosterone (PRA ratio) will confirm the excluded by screening tests, including measurement
diagnosis of hyperaldosteronism, as primary hyper- of spot salivary cortisol, 24‐hour urinary free corti-
aldosteronism is characterised by low plasma renin sol, PRA ratio, adrenal sex steroids, DHEAS, and
activity. A CT scan may detect an adrenal tumour urinary catecholamines and metanephrines.
but because many of these tumours are very small,
selective adrenal vein sampling for aldosterone may
Treatment
be required to localise the tumour.
Measurement of the sex hormones as well as the Incidental adrenal tumours that do not secrete hor-
17‐ketosteroids will confirm the diagnosis of a sex mones, are not associated with local symptoms and
39: Tumours of the adrenal gland 349
are less than 4 cm in diameter can be treated until the remaining gland recovers, which may take
conservatively, although there are increasing data 4–6 weeks.
to suggest that the potential risk for malignancy
may require that cut‐off to be lower, for example
3 cm. A follow‐up CT scan should be performed Further reading
after 6 months to ensure there is no progressive Clark OH, Duh QY, Kebebew E, Gosnell JE, Shen WT (eds)
increase in size, which would suggest malignancy. Textbook of Endocrine Surgery, 3rd edn. New Delhi:
Large tumours, or those that demonstrate an Jaypee Brothers Medical Publishing, 2016:80–93.
increase in size, should be removed surgically Else T, Kim AC, Sabolch A et al. Adrenocortical carcinoma.
because of the increased risk of malignancy. Endocr Rev 2014;35:282–326.
Operative management: adrenalectomy MCQs
Adrenalectomy can be performed as an open pro- Select the single correct answer to each question. The
cedure, as an anterior laparoscopic procedure or correct answers can be found in the Answers section
as a posterior retroperitoneoscopic procedure. at the end of the book.
Increasingly, the accepted philosophy is to tailor 1 Adrenal masses occur in:
the surgical approach to the tumour size and clini- a <1% of the population
cal situation. b 3–7% of the population
The open approach to the adrenal gland involves c 10–20% of the population
(i) an anterior approach (via a midline, transverse or d 40–50% of the population
oblique incision) through the peritoneal cavity or e >66% of the population
(ii) an extraperitoneal approach, either posteriorly
through the bed of the 12th rib or posterolaterally or 2 Conn’s syndrome is due to a tumour of the adrenal
(iii) combined as a thoraco‐abdominal procedure. cortex secreting excess:
These procedures are now used mainly for very large a cortisol
tumours or those known to be malignant. b adrenaline
Laparoscopic adrenalectomy is associated with c noradrenaline
reduced postoperative pain allowing the patient to d aldosterone
leave hospital after 2 or 3 days, smaller incisions, e sex steroids
reduced blood loss and fewer complications. The
procedure is ideally suited to small benign adrenal 3 Paragangliomas arise from:
tumours, such as those commonly found in Conn’s a adrenal cortex
syndrome, but is also indicated for phaeochromo- b adrenal medulla
cytoma, including bilateral tumours. c carotid bifurcation
The newer posterior retroperitoneoscopic d foregut
approach is increasingly used in centres around the e parasympathetic tissue arising from the neural crest
world as the preferred technique. It has many of the
advantages of the anterior laparoscopic approach, 4 The initial test used to diagnose Cushing’s syndrome
but probably less postoperative pain and shorter is measurement of:
postoperative stay, which may be overnight only, a spot salivary cortisol and 24‐hour urinary free
and reduced incidence of ileus. cortisol levels
Complications of adrenalectomy include all the b serum ACTH
general complications of any open abdominal adre- c serum cortisol after a dexamethasone test
nal operation or laparoscopic or retroperitoneo- d plasma renin/aldosterone ratio
scopic procedure such as bleeding, wound infection e serum catecholamines
and ileus. The particular anaesthetic complications of
phaeochromocytoma surgery have already been dis- 5 Adrenal incidentalomas should be removed when
cussed. Surgery for glucocorticoid‐secreting tumours, they are:
and occasionally for incidentalomas with subclinical a >25 cm
hormone secretion, may potentially lead to a postop- b >10–15 cm
erative Addisonian crisis because of suppression of the c >3–5 cm
contralateral adrenal gland. This should be anticipated d >1 cm
and prevented by prophylactic steroid administration e any size at all
Section 7
Head and Neck Surgery
40 Eye injuries and infections
Helen V. Danesh‐Meyer
Department of Ophthalmology, School of Medicine, University of Auckland, Auckland, New Zealand
• Conjunctiva and sclera: the white of the eye

Introduction should be white. Obvious lacerations or haemor-
rhage may overlay an open globe injury. Dark
Eye injuries can range from the very minor to the
uveal tissue presenting on the white of the eye
catastrophic, resulting in permanent loss of vision
(sclera) may suggest an open globe. If a foreign
or even loss of the eye. Infections can also range
body is suspected, this may be the site of
from conjunctivitis to serious sight‐threatening
penetration.
infections that can cause irreversible damage. A sys-
• Cornea: the cornea should be clear.
tematic approach to these conditions is necessary
• Anterior chamber: blood in the anterior chamber
so that timely and appropriate treatment can be
(hyphaema) indicates severe blunt trauma or
initiated.
penetrating injury.
• Pupil: should be round and respond briskly to
light. It is important to check for a relative affer-
Eye injuries ent pupillary defect using the swinging flashlight
test.
The aim of the approach to a patient with eye • Eye movements: restriction of motility may sug-
injuries is to identify serious sight‐threatening gest orbital fracture, haemorrhage or an open
injuries that require immediate action. The most globe injury.
time‐critical injury is a chemical injury (see later)
in which immediate treatment with irrigation can
significantly impact the long‐term prognosis. Equally Visual acuity testing
important is identifying the ruptured globe or
intraocular foreign body. Therefore, a systematic The visual acuity of all patients with an ocular
approach to the history and examination is injury must be measured and recorded. Each eye
necessary. should be tested separately. In instances of chemical
burns, the priority is irrigation which should not be
delayed under any circumstance.
History and examination
The visual acuity in ocular trauma is often pro-
A careful history of the cause of the injury should foundly impacted. If it is possible, visual acuity
be taken and examination of the eye performed. should be tested using a Snellen acuity chart. The
Specific aspects of the history and examination will patient will need to be positioned the appropriate
assist in determining the severity and nature of the distance from the chart, usually 4 or 6 m, depend-
ocular injury. ing of the chart.
• Face: proptosis may indicate retrobulbar haem- • Instruct the patient to read the letters on the
orrhage, which is an ocular emergency. If not chart from the top down. Each line is num-
treated immediately (usually requiring lateral bered. The number represents the distance in
canthotomy and intravenous acetozolamide or meters at which a person with normal sight can
mannitol) the ischaemia to the optic nerve and read the line.
retina may be irreversible. • The last line the patient reads is recorded, e.g.
• Lids: check lid movement. Lacerations of the lid 6/30. The top line represents the distance from the
tend to increase the risk of having associated chart, and the bottom line the distance from
ocular injuries. the chart at which a person with normal sight
353
354 Head and Neck Surgery
would read that line. Thus, a measure of 6/30 • Prevent emesis.

suggests that the patient reads at 6 m the line a • Biplanar radiographs or CT scan of the head
normal person would read at 30 m. may help to identify a metallic intraocular fragment.
• If no letters on the chart can be seen, bring the
chart closer until the top letter can be identified.
If this occurs at 2 m the acuity is recorded as 2/60 Chemical injuries
(the top letter on the chart can be seen by a per-
Both acids and alkalis produce serious damage to
son with normal sight at 60 m).
the eye. Both penetrate readily into the eye, result-
• If the top letter cannot be identified at any
ing in corneal opacification and inflammation.
distance, then wave a hand in front of the

Long‐term complications include corneal scarring,
eye (with the other eye covered). If the move-
cataract, retinal detachment and glaucoma.
ment is perceived, it is recorded as HM (hand
Acids and alkalis also cause thrombosis of the
movements).
circum‐corneal blood vessels that supply nutrients
• If hand movements cannot be seen, shine a light
to the cornea, resulting in corneal ischaemia and
into the eye. If it is seen, this is recorded as LP
opacification.
(light perception). Shine the light into the eye
The most important aspect of treatment is irriga-
from different directions and instruct the patient
tion, both at the site of injury and in hospital.
to point to the light. If this is performed accu-
rately, the acuity is recorded as ‘LP with accurate
Irrigation
projection’.
• If a bright light cannot be seen, the acuity is Irrigate the eye immediately with saline for at least
recorded as NLP (no light perception). 30 minutes. If non‐sterile water is the only fluid
available, it should be used. Irrigation should not be
delayed. If a speculum is available, it is helpful to
use this along with topical anaesthetic. The victim
Ruptured or open globe should then be transported to specialist care rap-
An open globe may result from either blunt or pen- idly. Evert the upper and lower lids to ensure that
etrating eye injury. Clinical signs that suggest an no solid matter is retained behind the lids. After
open globe include: appropriate irrigation, wait 5–10 minutes and use
• significant visual impairment litmus paper to touch the inferior cul‐de‐sac.
• traumatic hyphaema Irrigation should be continued until neutral pH is
• large subconjunctival haemorrhage with chemosis reached.
• flat anterior chamber Once irrigation is completed, fluorescein may be
• ‘soft’ eye. used to assess the cornea for epithelial defects. It is
important for the patient to be assessed with a slit‐
lamp to provide adequate understanding of the
Examination
extent of the injury. Patients with chemical injuries
Where suspicion of a perforating injury exists, are usually admitted to hospital for intensive treat-
examine the eye carefully after the instillation of ment with antibiotics and steroids.
two or three drops of local anaesthetic. Ask the
patient to open the eyes. It is important not to force Prognosis
the eye apart or examine the eye under a general
Chemical injuries have a poor prognosis.
anaesthetic.
Immediate treatment Blow‐out fracture of the orbit

• If an open globe is suspected, cover the eye with An object larger than the orbital opening will
a shield made with a device that applies forces to compress the orbital contents and may produce a
the bony orbit area instead of the eye. blow‐out fracture of the orbital floor into the max-
• Do not apply pressure on or manipulate the eye, illary antrum or, less commonly, of the medial wall
including ultrasound. into the ethmoidal air cells. These are the thinnest
• Do not apply any topical medications. of the orbital walls and are the most likely to be
• Start oral or intravenous antibiotics. damaged.
• Schedule an urgent referral to an ophthalmologist. Features that suggest a blow‐out fracture of the
• Administer tetanus toxoid if indicated. orbit include the following.
40: Eye injuries and infections 355
• Restricted eye movements, especially upward or • There may be pain on attempted vertical eye
lateral gaze. If visual acuity is good in both eyes, movements, eyelid swelling and creptitus after
the patient will complain of diplopia due to nose blowing.
entrapment of the fascia, usually around the infe-
rior rectus muscle in the fracture in the orbital
Treatment
floor (Figure 40.1).
• Hyperaesthesia of cheek and upper lip (distribu- The treatment is surgical with release of the
tion of infraorbital nerve). entrapped tissues from the fracture site. The appro-
• Enophthalmos because of prolapse of orbital fat priate investigation is CT scan of the brain and
into the antrum. orbit (axial and coronal views, 3‐mm cuts).
(a)
(b)
Fig. 40.1 (a) This patient has a blow‐out fracture of the right orbit and shows absent elevation in that eye. (b) CT scan
of the orbit reveals the blow‐out of the floor of the orbit.
Hyphaema position by applying a layer of Vaseline to the skin

around the orbit to which the plastic film adheres.
Hyphaema is a haemorrhage into the anterior
chamber of the eye (between the cornea and iris).
Corneal abrasion
Clinical features include:
• decreased visual acuity Corneal abrasions can be very painful. Patients pre-
• pupil may not respond to light sent with sharp pain, photophobia and tearing. The
• elevated intraocular pressure, which can be esti- diagnosis is made with the identification of an epi-
mated by gently palpating the eye and comparing thelial defect with fluorescein staining.
with the other eye. Management involves everting the eyelids to
Where the hyphaema occupies less than three‐ ensure that no foreign body is present. Symptoms
quarters of the anterior chamber, treat with bed rest usually resolve instantaneously with topical anaes-
and sedation. However, often it may be necessary to thetic drops. Treatment involves antibiotic drops or
lower intraocular pressure with acetazolamide 500 mg ointment, a short‐acting cycloplegic (for comfort
initially. The patient must be referred immediately with cyclopentolate 1%, as relaxing the ciliary
for specialist treatment because a hyphaema may be muscle decreases pain which may be secondary to
complicated by intraocular damage, which will not ciliary spasm) and eye patching (for comfort).
be apparent on presentation. Arrange expert ophthalmic assessment if there is
any question regarding infection.
Traumatic mydriasis
Corneal foreign body
Following a blow on the eye, the iris muscles may
be paralysed, producing a fixed dilated pupil, which The commonest eye injury is probably a foreign
may recover within a few days. Small tears in the lid body on the cornea. The patient complains of a
margin may involve the sphincter and cause perma- scratching sensation in the eye, and with good light
nent pupil dilatation. and magnification the foreign body can usually be
seen easily.
If it is not immediately obvious, stain the cornea
Choroidal rupture with fluorescein: moisten a fluorescein strip with
Rupture of the choroid occurs in an arc concentric local anaesthetic and touch the inner surface of the
with the optic nerve. It results in disruption of the lower eyelid. Ask the patient to blink to spread the
overlying nerve fibres and hence produces a perma- dye and then illuminate with the blue filter in the
nent visual field defect. If the rupture occurs ophthalmoscope. The site of the foreign body will
between the disc and the macula, central vision is glow bright green.
permanently lost. The foreign body may be adhering to the deep
surface of the upper lid, i.e. a subtarsal foreign
Thermal injuries body. Evert the upper lid and wipe off the foreign
body (Box 40.1).
Thermal injuries cause burns to the eyelids. The
management of the skin burn follows the usual
principles, but particular care must be exercised to Corneal foreign body removal
protect the cornea. Shrinkage of the eyelids in the • Lie the patient down.
healing phase puts the cornea at risk from exposure • Instill local anaesthetic drops: two drops every
and drying. minute for 3 minutes.
Care of the eye
Protect the cornea by the instillation of antibiotic Box 40.1 Tarsal eversion
ointment (chloramphenicol) every hour to provide
a layer of grease, which delays the evaporation 1 Tell the patient to look down, then grasp the lashes
of tears. If this is insufficient to prevent corneal and pull down the upper lid.
drying, the eyelids must be sutured together
2 Push down and back on the upper edge of the
tarsal plate.
(tarsorrhaphy).
3 Fold the lid margin up and the tarsal plate rolls over.
Alternatively, cover the eye with transparent
4 Hold the lid everted by resting a finger on the lid
plastic film. A piece large enough to cover the orbit
margin.
reaching from the forehead to the cheek is held in
40: Eye injuries and infections 357
• Use a focused bright light to illuminate the eye. Trachoma

• Lift off the foreign body with a cotton‐tipped
Of more concern in rural and under‐developed
applicator or needle.
communities is trachoma. This recurrent conjuncti-
• Instill antibiotic drops and apply an eye pad.
vitis is caused by the organism Chlamydia tra-
It is helpful to use a magnifying lens to facilitate
chomatis. The organism replicates intracellularly in
foreign body removal. However, the ideal environ-
the conjunctival epithelium. It is a mild infection
ment is to remove the foreign body through a
but after each attack scarring occurs at the site of
slit‐lamp.
the follicles in which the organism replicated. After
Instill antibiotic drops (chloramphenicol) every
probably 30 or 40 attacks the scarring becomes
2 hours until the cornea heals and the eye is comfort-
serious and causes inversion of eyelashes and subse-
able. If the foreign body is hot, for example from
quent damage to the cornea, causing blindness
using a grindstone, a rust ring may be left in the cor-
(Figure 40.2).
nea after its removal. Instill chloramphenicol oint-
The control of trachoma requires attention to the
ment in the eye four times daily for 2 or 3 days. The
following:
rust ring can then be lifted off with a fine needle.
• Surgery to the inverted eyelids
• Antibiotic treatment with azithromycin
• Fly eradication, the commonest vector
Eye infections
• Environmental upgrade.
This is the SAFE strategy devised by the World
The main defence mechanisms against infection in the
Health Organization. When trachoma is diagnosed,
eye are the tears, which contain lysozyme, and the cor-
all members of the family are treated with a single
neal epithelium. Once these are breached, an infection
dose of azithromycin. Children and young mothers
can be established and will progress rapidly.
are most commonly infected.
Extraocular infections
Intraocular infections
Conjunctivitis
The management of intraocular infection follows
Acute conjunctivitis is common, usually due to a the principles of management of any infection:
staphylococcus and responds rapidly to the instilla- • identify the organism
tion of eye drops every 2 hours. The most com- • treat it with the appropriate antibiotic.
monly used antibiotic is chloramphenicol. Even However, this requires specialist assessment and the
untreated, most acute conjunctivitis resolves in patient should be referred to an ophthalmologist as
about 3 days. soon as possible.
Fig. 40.2 Corneal abscess. The pathological process is visible because of the transparency of ocular structures.
b the denominator expresses the distance acuity in

Further reading the tested eye
Erikitola OO, Shahid SM, Waqar S, Hewick SA. Ocular c the numerator expresses the near vision in the
trauma: classification, management, prognosis. Br J tested eye
Hosp Med 2013;74:C108–11. d Snellen acuity compares a tested eye to a
Nika B, Wajda B, Calvo C, Durani A (eds) The Wills Eye normally seeing eye
Manual: Office and Emergency Room Diagnosis and
Treatment of Eye Disease, 7th edn. Philadelphia:
2 Which of the following is most likely to be found in
Wolters Kluwer, 2017.
a patient with an orbital blow‐out fracture?
Romaniuk VM. Ocular trauma and other catastrophes.
Emerg Med Clin North Am 2013;31:399–411. a proptosis
b horizontal diplopia
c anosmia
MCQs d ptosis
Select the single correct answer to each question. The 3 The most important aspect of management of
correct answers can be found in the Answers section chemical burns is:
at the end of the book. a intravenous steroids
b intensive antibiotic drops
1 The Snellen visual acuity in a patient is noted to be
c intensive irrigation
6/60 in the right eye and 6/18 in the left eye.
d intravenous antibiotics
Which of the following statements is correct?
a Snellen acuity in the right eye is better than the
left eye
41 Otorhinolaryngology
Stephen O’Leary1 and Neil Vallance2
1
University of Melbourne and Royal Victorian Eye and Ear Hospital, Melbourne, Victoria, Australia
2
Monash University and Department of Otolaryngology, Head and Neck Surgery, Monash Health,
tendency for the TM to become retracted and the

Otology mucosal lining to exude a serous or mucoid dis-
charge. Infection may ensue if bacteria are present in
Otologic surgery aims to eradicate aural disease
the middle ear cleft, frequently leading to perforation
and restore hearing in the ear, or gain surgical
of the TM. In the presence of chronic ET dysfunction,
access to the skull base. The proximity to the brain,
the TM perforation will tend not to heal. An infected
major vessels and the facial nerve demands skill in
discharge follows, associated with chronic changes
microsurgery of bone, soft tissues and nerve.
to the middle ear mucosa (including biofilm) and a
Surgical treatment of the hearing apparatus requires
low‐grade osteitis of the temporal bone.
a good working knowledge of auditory physiology
Indigenous populations, such as the Australian
and pathophysiology.
Aborigines or the Inuits in Greenland and Alaska,
have a significantly higher prevalence of COM than
Surgical anatomy of the ear
The tympanic membrane (TM) and the ossicles ET TM Mastoid
(malleus, incus and stapes) collect sound and deliver
them to the inner ear (the labyrinth). The space
behind the TM is in continuity with a system of air
cells extending posteriorly into the mastoid, and
together these constitute the middle ear cleft.
Aeration of the middle ear cleft is maintained by the
eustachian tube (ET), which runs from the nasophar-
ynx to the anterior tympanic cavity (Figure 41.1).
The middle ear cleft is lined with respiratory epithe-
lium (mucosa). The external ear canal and external
surface of the TM are lined by skin. The facial nerve
traverses the middle ear and mastoid. Facial nerve
Chronic otitis media

SCM
Chronic otitis media (COM) is an ear disease
requiring surgical treatment. It presents as aural
discharge with or without hearing loss.
Pathophysiology Fig. 41.1 Schematic anatomy of the ear. The

sternocleidomastoid muscle attaches to the mastoid tip.
Most cases of COM are a consequence of ET dys- The mastoid is a system of air cells within the temporal
function. The ET’s role is to aerate the middle ear bone. The arrows depict the flow of air through the
cleft (see Figure 41.1). Inadequate aeration of the eustachian tube into the middle ear and mastoid. ET,
middle ear leads to negative pressure with respect to eustachian tube; TM, tympanic membrane; SCM,
the atmosphere behind the eardrum. There is a sternocleidomastoid muscle.
359
other populations. The reason(s) are not well (a) (b)

understood, but contributing factors are thought to Central perforation
include post‐nasal colonisation with pathogenic
bacteria at a much younger age (often within
the first 3 months of life), leading to early onset
of otitis media. Socioeconomic disadvantage and
overcrowding also contribute.
(c) Cholesteatoma
(d)
Cholesteatoma
This is an important manifestation of COM.
Acquired cholesteatoma is the invagination of the
TM into the middle ear cleft. This occurs where the
drum is weakest, usually in its posterosuperior seg-
ment. Although causes of cholesteatoma may vary,
most often the invagination is secondary to the Fig. 41.2 Chronic otitis media and surgical treatment.
negative middle ear pressure accompanying ET dys- (a) Chronic otitis media with a central perforation of the
function. The invaginated skin continues to desqua- tympanic membrane. (b) A canal wall‐up mastoidectomy.
mate, but the squames become trapped in the The mastoid air cells have been removed, as indicated by
retracted pocket of skin. It is at this stage that the the thick dashed line. (c) Cholesteatoma presenting as a
‘marginal’ perforation of the tympanic membrane. The
retraction pocket is no longer self‐cleaning and is,
cholesteatoma extends beyond the tympanic membrane
by definition, a cholesteatoma. The desquamated
into the mastoid. (d) A canal wall‐down mastoidectomy.
skin within the retraction pocket will usually The limits of the mastoid cavity, created by removing the
become infected, with the development of an aural mastoid air cells and taking down the posterior and
discharge. The cytokines liberated erode surrounding superior canal walls, is indicated by the thick solid line.
bone, with expansion of the cholesteatoma into
the mastoid, the ossicles and/or the labyrinth.
Complications of this disease can be serious and
include facial nerve palsy, loss of labyrinthine surgery, particularly when medical treatments (such
function and intracranial sepsis. as aural and/or oral antibiotics) and keeping the ear
dry have failed to settle recurrent aural discharge.
However, the condition of the contralateral ear
Clinical findings must be considered. A better hearing ear is a rela-
A history of aural discharge, hearing loss and some- tive contraindication, due to the risk of sensorineu-
times otalgia or tinnitus should be expected. Vertigo ral deafness at surgery. Restoration of hearing is a
suggests erosion of the labyrinth and warrants secondary indication for surgery.
urgent surgical treatment. Non‐cholesteatomatous The overall aim of surgery is to produce a disease‐
COM is associated with a central perforation of the free and hence non‐discharging ear. The surgical
TM, where the edges of the perforation are visible principles include the preservation of vital struc-
and bounded by a rim of drum (Figure 41.2a). tures, including the facial nerve and inner ear, the
A marginal perforation is the hallmark of choleste- eradication of disease and the reconstruction of
atoma, where the perforation extends beyond the the TM and hearing. Eradication of disease involves
edge of the drum and ‘disappears’ behind the pos- the removal of diseased bone and mucosa, and
terosuperior wall of the ear canal (Figure 41.2c). cholesteatoma if it is present.
The facial nerve should always be examined and The appropriate operative procedure depends on
the hearing tested clinically and audiometrically. the extent of the disease and the surgeon’s preferred
Both ears must be examined. High‐resolution CT operative method, either microscopic or endo-
of the temporal bone helps to define the extent of scopic. If disease is confined to the middle ear and
disease. ET function is only moderately impaired, then
grafting the TM (myringoplasty) may be all that is
required. If the mastoid is also infected, the classical
Treatment
microscopic approach is exenteration of the mas-
Cholesteatoma is an absolute indication for surgery, toid air cell system combined with myringoplasty
unless the patient is elderly, when regular aural (a ‘canal wall‐up’ mastoidectomy; Figure 41.2b).
toilet may suffice. COM is a relative indication for The mastoidectomy both removes the disease and
41: Otorhinolaryngology 361
reduces the surface area of the middle ear cleft, thus 60‐dB hearing loss. A ‘mixed’ hearing loss has
decreasing the work done by a compromised ET. both conductive and sensorineural components.
For failed canal wall‐up mastoidectomy, especially
if there is either persistent (‘residual’) or recurrent Treatment
cholesteatoma, a modified radical mastoidectomy
Hearing loss is treated when it impedes an individ-
is performed. This involves performing a mastoid-
ual’s ability to communicate. Surgery is indicated
ectomy, removing the posterior and superior (ear)
when a hearing aid is not helpful or cannot be worn
canal walls, and grafting the TM (a ‘canal wall‐
for medical reasons. For example, occlusion of the
down’ mastoidectomy; Figure 41.2d). Following
external ear canal (by the hearing aid) may cause
this operation, the mastoid cavity is exteriorised so
recurrent otitis externa or persistent aural discharge
that it is now part of the external ear and is lined
if there is also a TM perforation. Hearing restora-
with skin.
tion surgery will also be performed with operations
The endoscopic approach to surgery for COM
for COM as discussed in the previous section.
provides direct visualisation ‘around corners’ with
However, it is usually not possible to reconstruct
angled Hopkins rods, allowing a better view of
the ossicular chain if there is a coexistent TM per-
middle ear structures and more reliable clearance
foration. A better approach is to repair the drum
of pockets of cholesteatoma that cannot be seen
first and perform an ossicular chain reconstruction
directly with the microscope. However, unlike
as a staged procedure. For this reason, ossicular
microscopic surgery, it has the disadvantage of leav-
chain reconstruction is usually a second‐stage pro-
ing only one hand free to manipulate surgical
cedure following surgery for COM.
instruments. This technique does not require large
Conductive hearing loss is amenable to surgical
surgical incisions, so hospitalisation is shorter and
treatment. Glue ear may be treated by performing a
recovery may be more comfortable for the patient.
myringotomy and placing a ventilation tube within
It is an option for disease in the middle ear or for
the TM. A perforated TM may be grafted (myringo-
cholesteatoma extending as far backwards as the
plasty). When the ossicles are disrupted, reconstruc-
lateral semicircular canal.
tion aims to re‐establish a stable link between the
TM and the stapes footplate. The configuration of
Hearing impairment
the reconstruction depends on which ossicle(s)
Pathophysiology remain intact. These procedures do not restore ana-
tomical normality, and this is not required to
Hearing impairment is classified as either conduc-
achieve good hearing.
tive or sensorineural. A conductive loss results
When the middle ear cannot be reconstructed
from an interruption of sound transmission
surgically, bone‐conducting auditory prostheses are
through the TM and the ossicles. It may arise from
indicated. These devices vibrate the bone behind the
an effusion of the middle ear (‘glue ear’) or a TM
ear, and this leads to direct acoustic stimulation of
perforation. Sound transmission through the
the cochlea. Bone‐conducting auditory prostheses
ossicular chain may be interrupted if the ossicles
have become a preferred method of rehabilitating
are no longer in continuity or if the ossicular chain
hearing for children with congenital anomalies of
is fixed. Ossicular discontinuity usually arises
the middle or external ear and are an excellent
from ossicular erosion following COM. The most
choice when a hearing aid cannot be worn, or for
common cause of ossicular fixation is otosclerosis,
end‐stage COM when ossicular reconstruction is
where the bone of the labyrinth is abnormal and
no longer possible.
the stapes footplate becomes fixed to surrounding
labyrinthine bone. Sensorineural hearing loss is
due to cochlear or, rarely, retrocochlear pathology.
Cochlear implantation
The most common causes of sensorineural loss are
hereditary, meningitis, ototoxic, trauma and pro- Severe‐to‐profound sensorineural hearing loss is
gression of unknown aetiology. In this case, it is characterised by loss of clarity of speech, which is
thought likely that the hearing loss arises from a not overcome by the amplification of sound with a
combination of environmental exposure(s) and hearing aid. Eventually, amplification ceases to aid
genetic predisposition. A TM perforation will lead communication and, under these circumstances, a
to a mild‐to‐moderate conductive hearing loss cochlear implant may be of more benefit. A coch-
(20–30 dB). Ossicular chain discontinuity will lear implant is also indicated for congenitally deaf
lead to an additional 20–30 dB loss. Ossicular children, provided that the operation is performed
chain disruption behind an intact drum leads to a before the child is 5 years of age. Up until this age a
child may learn to comprehend speech with the in turbulence of nasal airflow and hence a sensation
implant, even though he or she has no previous of obstruction. Symptomatic septal deviation is
auditory experience. Children implanted before treated surgically. The corrective procedure, septo-
the age of 3 years may learn to speak. The younger plasty, involves elevating mucosal flaps and removal
the child at the age of implantation, the better the of the deviated segment of cartilage or bone.
speech and language outcomes, and it is preferable
to implant well before the child’s second birthday. Rhinorrhoea
The operation for a cochlear implant involves
implanting a prosthesis, the ‘receiver–stimulator’, Rhinorrhea is a clear discharge from the nose. It
which electrically stimulates the auditory nerve may arise from allergic rhinitis or be neural in ori-
within the cochlea. The receiver–stimulator is gin when it is termed vasomotor rhinitis. Rarely, a
placed over the parietal bone. Its electrode array clear discharge from the nose may be cerebrospinal
passes through the mastoid and middle ear into the fluid. This is usually post‐traumatic and may origi-
cochlea. The receiver–stimulator is entirely subcu- nate from a breach of the cribriform plate, a para-
taneous. It communicates via a radiofrequency link nasal sinus (ethmoid, frontal or sphenoid sinus) or
with an external device called the speech processor. from the middle ear space via the ET. The fluid will
The speech processor translates speech into the pat- test positive for β‐transferrin. Surgical repair via an
tern of electrical stimulation to be delivered to the endoscopic approach through the nose or as a com-
auditory nerve. bined procedure with neurosurgeons via the ante-
Cochlear implantation is also considered for uni- rior cranial fossa will usually be necessary.
lateral (single‐sided) deafness because it is now
appreciated that communication in real‐life listen- Epistaxis
ing conditions, where there is usually competing Epistaxis is dealt with in Chapter 77.
background noise, is far easier with two working
ears rather than one.
Sinusitis
Tumours of the ear Acute sinusitis is a bacterial infection of the parana-
sal sinus secondary to obstruction of the sinus ostia.
The most common type of malignant neoplasm of the The obstruction is usually due to swelling of the
ear is a squamous cell carcinoma of the pinna or exter- nasal mucosa caused by a virus, but may also fol-
nal ear canal, followed in incidence by melanoma. low dental infection or dental work, nasal allergy,
Symptoms include otalgia, aural discharge or hearing facial fractures and barotrauma. It is usually due to
loss if the external ear canal is occluded. Treatment is aerobic organisms and manifests as facial pain and
radical surgical excision and radiotherapy. mucopurulent nasal discharge. Initial medical man-
agement requires antibiotics and topical nasal
decongestants. Systemic corticosteroids may also be
Rhinology needed to settle a severe attack. Occasionally, drain-
age of the sinus via an endoscopic antrostomy may
Nasal polyps be required to remove the pus.
Nasal polyps are translucent pedunculated swell- Acute sinusitis can be complicated by spread of
ings arising from nasal and sinus mucosa. They the infection through the paper‐thin bone (the lam-
arise from mucosal inflammation, with or without ina papyracea) between the ethmoidal sinuses and
an allergic association, and result in nasal obstruc- the orbit. Although this infection is usually extraor-
tion and discharge. Although these respond (i.e. bital, it causes proptosis and can if left untreated
shrink) in response to oral steroids, they will usu- compromise vision. If there is pus present it must be
ally rebound rapidly and surgical excision via an drained via an endonasal or an external approach,
endoscopic approach provides better longer‐term but if less severe intravenous antibiotics may suffice.
control. Nasal polyps have a tendency to recur, so Chronic sinusitis may follow poorly treated acute
revision surgery is not unusual. sinusitis or occur in chronic sinus obstruction (e.g.
secondary to nasal allergy or polyps). In this situa-
tion anaerobic organisms play a significant role.
Septal deviation
Antibiotic treatment should be tried, but if the infec-
Deviation of the nasal septum from the midline tion has been present for more than 3 months func-
may be traumatic or congenital. The deviation may tional endoscopic sinus surgery is recommended in
involve the cartilaginous or bony septum. It results order to drain the infection and aerate the sinuses.
Nasal tumours toxicity and trismus and usually a large unilateral

tonsillar swelling. The abscess must be drained by
Benign tumours
an incision in the upper half of the tonsil pillar fol-
Inverted papillomas, squamous papilloma and lowed by admission to hospital and intravenous
juvenile angiofibroma may all result in obstruction, antibiotics for several days. In a history of recurrent
sinusitis and bleeding. Diagnosis is made following tonsillitis, this is an indication for a tonsillectomy,
imaging of the paranasal sinuses (CT or MRI) usually after the acute abscess has settled down.
and, unless a juvenile angiofibroma is suspected, a
transnasal biopsy. (Angiofibromas are not biopsied Epiglottitis
due to a risk of bleeding.) Benign tumours are
best treated with surgical excision, performed Epiglottitis is a peculiar and serious disease often
either transnasally or via an external transfacial affecting children, and occasionally adults. There is
approach. Angiofibromas are embolised before acute bacterial inflammation of the epiglottis and
surgical excision. supraglottic structures with rapid onset and rapid
progression such that the airway may be occluded,
Malignant tumours with death resulting from acute upper airway
obstruction. Intubation in an operating theatre
Squamous cell carcinoma of the maxillary sinus is environment is the treatment of choice in both
the most common paranasal sinus malignancy. The adults and children, with the surgeon standing
most common cancer of the ethmoid sinus in by to perform urgent surgical access to the airway
Australia is adenocarcinoma, which occurs more should intubation fail. After the airway is secure,
commonly in people employed in the hardwood the problem usually settles rapidly with intrave-
industry. Other cancers of the nasal complex nous antibiotics and, on occasion, steroids.
include adenoidcystic carcinoma, sinonasal undif- Haemophilus influenzae is a common casual organ-
ferentiated (small cell) carcinoma, transitional car- ism in the paediatric population. The condition is
cinoma and malignant melanoma. Diagnosis is life‐threatening and must be treated urgently.
made on radiological and histological grounds and
treatment involves surgical excision with adjunc- Benign vocal fold lesions
tive radiation therapy and/or chemotherapy.
Vocal nodules are common benign bilateral swell-
ings at the junction of the middle and anterior third
of the vocal fold. They result from vocal abuse in
Oral cavity, oropharynx and larynx children and heavy vocal use and abuse in adults.
They may be physiological in heavy voice users,
Tonsil and adenoid disease such as singers. There is rarely an indication for sur-
gery as almost all cases will improve or resolve
The tonsils and adenoids are the commonest areas
completely with voice therapy and re‐education of
of infection in the head and neck. They belong to a
vocal habits.
collection of lymphoid tissue called Waldeyer’s ring,
Benign cysts and polyps are less common condi-
which also comprises an aggregate of lymphoid
tions and are usually unilateral and require surgical
tissue at the base of the tongue called the lingual
intervention if the effect on the voice is significant
tonsil and lymphoid tissue around the opening of
enough for the patient to request intervention. The
the ET called the tubal tonsil. The adenoid tissue
lesions are removed with microsurgical techniques
usually atrophies over the second decade of life and
via a direct laryngoscopy under general anaesthesia.
is not a common cause of disease after childhood.
Reflux commonly causes hoarseness, throat dis-
Tonsillectomy and adenoidectomy are performed if
comfort and a variety of laryngeal conditions
the tonsils become recurrently infected. In child-
resulting from chronic inflammation due to reflux-
hood, tonsils and adenoids may become large
ate in the laryngopharynx. Very commonly, heart-
enough to cause significant obstruction, leading to
burn is absent in laryngopharyngeal reflux. The
airway interference and intermittent cessation of
condition responds to anti‐reflux measures and
breathing overnight (obstructive sleep apnoea).
medication, including proton pump inhibitors.
This necessitates removal to re‐establish a normal
airway and breathing pattern.
Tonsillitis may become complicated by abscess
Vocal cord paralysis
formation in the peritonsillar space, commonly Loss of vocal fold movement is caused by loss of
referred to as quinsy. This results in severe pain, function of the recurrent laryngeal nerve. The nerve
is a branch of the vagus nerve. The left arises in the outcomes for patients. These tumours are best treated
thorax, looping around the aorta. On the right side via a multidisciplinary surgical approach in depart-
it arises higher in the thorax, looping around the ments that can make the best use of advances in
right subclavian artery. Both travel in the tracheo‐ tumour biology, imaging modalities, radiotherapy
oesophageal groove superiorly to the larynx, where and chemotherapy, and conservation and organ pres-
they supply the intrinsic muscles that move the ervation techniques. Recent advances in endoscopic
vocal folds. Causes of unilateral paralysis may be laser surgical techniques and transoral robotic sur-
tumours of the thyroid or lung or metastatic depos- gery have led to an improvement in outcomes and
its within mediastinal lymph nodes. Surgical trauma organ preservation for oropharyngeal, laryngeal and
during thyroidectomy may also result in paralysis. hypopharyngeal cancers. Reconstructive techniques
However, the commonest cause of paralysis is idio- and the use of free flaps is well established and con-
pathic and the commonest nerve affected is the left, tinues to provide better outcomes.
probably because of its greater length. The presen-
tation of unilateral paralysis is hoarseness and
breathiness. This may improve as the larynx com-
Squamous carcinomas of the upper
pensates and other muscles assist in phonation.
aerodigestive tract
A common misconception is that the intact vocal Pathogenesis
cord compensates for the palsy, but this is not true,
Most malignant tumours of the upper aerodigestive
as the functioning vocal fold can never adduct fur-
tract are squamous cell carcinomas. A significant
ther than the midline. If both vocal folds are para-
proportion of these cancers can be attributed to a
lysed the voice is often normal, but the airway can
combination of cigarette and alcohol abuse. Their
be severely compromised if the vocal folds both lie
effects are believed to be synergistic, resulting in
well towards the midline. Hence the need to assess
widespread changes in the mucosa and the potential
vocal fold function prior to thyroidectomy to
for multiple tumours (estimated at 15–20%). Over
exclude an asymptomatic old palsy and therefore
the last several years human papillomavirus (HPV)‐
exercise diligence in protecting the intact nerve.
driven cancers have become more common. These
Diagnosis of the palsy is made by indirect mirror
cancers are more common in the oropharynx and
examination or more usually flexible fibre‐optic
are usually very responsive to chemoradiotherapy.
laryngoscopy. A thorough search to exclude tumour,
including CT scan from skull base to thorax, must
Pathology
be made. Treatment is required for unilateral palsy
if the voice is poor and sufficient time has elapsed Most head and neck squamous cancers will metas-
(usually 6 months) to exclude spontaneous recov- tasise to cervical lymph nodes and this factor bears
ery. Such operations may include medialisation of the most significance in terms of prognosis. It is gen-
the vocal fold via laryngeal framework‐type sur- erally accepted that the survival rate of head and
gery or injection of commercially available materi- neck cancer is halved when a positive neck node is
als including the patient’s own fat lateral to the fold present. Head and neck cancer surgeons refer to
to medialise it. There is no longer any place for neck nodes in terms of different levels, I through V.
Teflon injection of the vocal fold. Bilateral vocal Level I comprises the uppermost nodes in the sub-
fold paralysis can present as an upper‐airway emer- mental and submandibular triangles. Levels II, III
gency that may require tracheotomy. In the long and IV correspond to the upper, middle and lower
term, endoscopic laser techniques allow the re‐ cervical lymph nodes, respectively, and level V repre-
establishment of an airway, often with the preserva- sents the nodes in the posterior triangle. On this
tion of good voice. basis, it is now possible to tailor neck dissection
according to the site of primary tumour and the lev-
els of nodes involved. Neck dissections are now
Cancer of the head and neck almost exclusively of a selective nature rather than
the older‐style radical neck dissection, which sacri-
Cancer of the head and neck is relatively uncommon ficed the sternomastoid muscle, the internal jugular
when compared with the frequency of other, more vein and the accessory nerve. It is rare now to sacri-
common tumours such as bowel and breast cancer. fice the accessory nerve in neck dissection as this
Nonetheless, because of the significance of functional often produces significant morbidity, with denerva-
impairment and the potential for disfigurement, it tion of the trapezius muscle and resulting shoulder
is an important management problem. Significant droop. Prognostic variables include the T stage of
advances have seen improvements in survival and the primary tumour (Table 41.1) and the N stage of
Thorough clinical evaluation is essential to

Table 41.1 Tumour staging in squamous carcinoma. exclude a cancer in a site not readily seen, such as
Regional lymph nodes
the tongue base or hypopharynx. Thorough endo-
Nx Regional lymph nodes cannot be assessed scopic evaluation and fine‐needle aspiration cytol-
N0 No regional lymph node metastasis ogy of suspicious nodes (which has not been found
N1 Metastasis in a single ipsilateral lymph to cause recurrent neck disease) should be used to
node, 3 cm or less at greatest dimension investigate these lesions before open biopsy or sur-
N2a Metastasis in single ipsilateral lymph node, gical removal.
>3 cm but not more than 6 cm at greatest Modern CT and MRI are invaluable for the
dimension accurate assessment and staging of head and neck
N2b Metastasis in multiple ipsilateral lymph cancer. It is well demonstrated that they are more
nodes, none more than 6 cm at greatest
sensitive than clinical examination in detecting
dimension
metastatic neck disease. CT scanning is beneficial
N2c Metastasis in contralateral lymph nodes,
none more than 6 cm at greatest in the detection of bone disease and spread of
dimension laryngeal disease beyond the laryngeal framework.
N3 Metastasis in lymph node >6 cm at MRI is particularly useful for investigation of the
greatest dimension tongue and soft‐tissue extension of disease, includ-
Primary tumour ing involvement of the nerves and brain.
Tx Primary tumour cannot be assessed The relatively new technique of positron emis-
T0 No evidence of primary tumour sion tomography (PET) allows imaging of the
Tis Carcinoma in situ metabolic behaviour of the tumour rather than an
T1 Tumour 2 cm or less at greatest dimension
anatomical mass. However, merging these biologi-
T2 Tumour >2 cm but not more than 4 cm at
cal images with CT scans allows a more anatomical
greatest dimension
T3 Tumour >4 cm at greatest dimension perspective.
T4 Tumour invades adjacent structures Guidelines for diagnostic and preoperative work‐
up of a patient with a suspected head and neck
malignancy are given in Box 41.1.
the neck. Usually the greater the T or N stage, the

Treatment
poorer the prognosis. Other poor prognostic factors
are the presence of extracapsular spread in cervical The goals of treatment in head and neck cancer are:
lymph nodes; perineural, lymphatic and vascular • eradication of disease
invasion; and increased depth of tumour invasion. • preservation or restoration of function, particu-
The differentiation of the primary cancer does not larly speech and swallowing
appear to have prognostic significance, with the • minimal cosmetic deformity.
possible exception of the oral tongue. The following general points are relevant.
• For early disease, particularly in the larynx, cure
rates of radiotherapy and surgery are equivalent.
Clinical presentation and investigation
Clinical presentation is dependent on the anatomical
subsite of the disease. In the oral cavity and the Box 41.1 Diagnostic and preoperative
oropharynx, for example, common symptoms include work‐up of the patient with head
a mass or an ulcer with pain and difficulties and neck squamous carcinoma
with speech and swallowing. Painful swallowing
(odynophagia) is a serious symptom which indicates 1 Confirm diagnosis by biopsy of primary lesion and/
the presence of a cancer until otherwise proven. or fine‐needle aspiration cytology of cervical nodes
Likewise, pain referred to the ear is a serious symp- 2 Clinical staging of disease by TNM classification
tom. Vocal fold cancers frequently present with 3 Investigate with CT, MRI or PET for selected cases
hoarseness that does not resolve with adequate treat- 4 Endoscopic evaluation under anaesthesia for more
accurate staging and to exclude a second primary
ment after 2 or 3 weeks. Cancers in the hypopharynx
5 For cervical node with unknown primary, full
may be more subtle in presentation and can reach a
endoscopic evaluation and, if no primary found,
significant size before the primary tumour presents
proceed to open biopsy with frozen section and
problems for the patient. These lesions frequently
neck dissection if squamous cell carcinoma
present with a painless enlarging lump in the neck
confirmed
which represents a metastatic node.
• Chemotherapy on its own has little role to play tumours of the true vocal fold. Cure rates are
in the treatment of squamous cell cancer of the excellent, as are functional outcomes. The disad-
head and neck other than in a palliative sense but vantage is a 5‐week course of therapy.
is used as an adjunct to the use of radiotherapy. Consequently, laser surgery is tending to replace
• The emphasis in treatment is now on organ pres- radiotherapy for these lesions as the outcomes
ervation, particularly with respect to the larynx. are similar and the treatment involves only a
There has been a shift away from radical surgery, 1‐ or 2‐day stay in hospital.
such as total laryngectomy, to the use of proto- • In certain advanced hypopharyngeal and laryn-
cols involving chemoradiation for relatively geal cancers, where combined radiotherapy and
advanced tumours. Partial laryngectomy, par- chemotherapy offers organ preservation and
ticularly with endoscopic laser surgery, often pro- good locoregional control without surgery.
vides organ sparing and successful outcomes. It • For palliation of recurrent disease or advanced
should be remembered, however, that the preser- disease not suitable for surgery or organ preser-
vation of a crippled larynx which does not func- vation through chemoradiotherapy.
tion and aspirates is a poor outcome. • Postoperatively and, less commonly, preopera-
• The combination of surgery and radiotherapy in tively in disease where it is felt prudent to use
advanced disease is superior to single‐modality multimodality therapy. Whether radiation is used
therapy. preoperatively or postoperatively is often deter-
• In planning treatment, it is vital to consider gen- mined by the accepted practices in individual
eral patient factors such as general health and cancer treatment units.
medical condition, fitness for surgery or a chal- • For HPV‐driven oropharyngeal cancers in com-
lenging course of radiation, and nutritional sta- bination with chemotherapy where response
tus, which is often poor in these patients and may rates are often very good.
need attention before treatment. Radiation is delivered by external beam in dedicated
radiotherapy units. Radiation affects both normal
Management of the primary tumour tissue and cancer tissue, and the salivary glands and
Surgical resection is a better option in the following oral mucosa are particularly affected. Dryness is a
situations. common post‐radiotherapy complaint. The mandi-
• Small tumours where the surgical defect is mini- ble is commonly devascularised following radiother-
mal and functional restoration assured. apy and very prone to osteomyelitis and necrosis,
• Large tumours with spread beyond the primary secondary to dental sepsis. Dental consultation and
site to involve bone or cartilage. These tumours management of the teeth are therefore essential if the
rarely, if ever, respond to radial radiotherapy. jaw is to be involved in the radiotherapy field.
Modern reconstructive techniques and the use of
free flaps have allowed many of these tumours to Management of the neck
be successfully resected and reconstructed in a Metastatic disease in the neck may be obvious or
single‐stage procedure. This has allowed a more occult at presentation. Secondary neck disease is a
rapid transition to postoperative radiotherapy, significant factor in determining prognosis and, in
which is essential if all the benefits of multimo- general, the presence of neck disease lowers the sur-
dality therapy are to be achieved. vival by some 50%. Neck disease is often treated by
• Salvage of lesions unresponsive to or recurrent neck dissection unless associated with HPV‐driven
after radiotherapy. Reconstructive techniques oropharyngeal cancers, where responses to chemo-
involving free flaps elicit a better blood supply to radiotherapy alone are often very good. Accepted
the area and have allowed improved healing in poor prognostic indicators with neck disease
previously irradiated tissues where the blood include multiple levels of nodes involved or spread
supply has been diminished by radiation. of tumour beyond the capsule of the lymph node on
• Endolaryngeal and hypopharyngeal disease is now pathology assessment. In these instances, postoper-
being successfully treated with endoscopic laser ative radiotherapy is always used in the neck.
techniques or transoral robotic surgery where pre- The approach to neck dissection has changed
viously external partial procedures, and even total over the years. The mainstay in the past was the
laryngectomy, may have been considered. so‐called radial neck dissection. It is now apparent
Radiotherapy is considered for the following that similar regional control of disease can be
situations. achieved by a more selective approach. These modi-
• As a single‐modality treatment in early lesions. fied or selective neck dissections remove node levels
This was traditionally the case with small which are most likely to contain metastatic disease
from the associated primary. Consequently, fewer Aetiology

than the five levels of nodes are removed and, inher-
Epstein–Barr virus is implicated in the pathogenesis
ent in this approach, is the preservation of various
of nasopharyngeal carcinoma. An elevation of viral
non‐lymphatic tissues, including the spinal acces-
titres can precede the onset of disease. Titres are
sory nerve, internal jugular vein and sternomastoid
useful as tumour markers following treatment.
muscle. This has led to better functional outcomes
Genetic markers have also been investigated
with no sacrifice of disease control.
because of the ethnic predilection of the tumour. An
increased incidence is seen in patients with certain
Tumours of the nasal cavity major histocompatibility complex (HLA) profiles.
and paranasal sinuses The ingestion of preserved foods, especially salted
These are rare tumours. It is worth noting that a fish, duck eggs and salted mustard green, have also
significant aetiological factor is wood‐dust. People been implicated in nasopharyngeal cancer.
with a long history of wood‐dust exposure (cabinet
Presentation and management
makers, sawmill operators) are usually common
among patients diagnosed with ethmoid cancer. Nasopharyngeal cancer often presents late and fre-
This is usually an adenocarcinoma. Efforts have quently as a lump in the neck. It is a very infiltrative
been made to make the woodworking industry cancer with often very little in the way of mucosal
aware of this danger. changes. It frequently invades the base of the skull,
Presentation depends on the anatomical subsite causing cranial nerve involvement and palsies. It is
but, unfortunately, tumours are often very advanced one of the few cancers of the head and neck with a
at diagnosis. It is not unusual to find orbital and predilection to distant metastases, with the bone,
anterior cranial fossa involvement on CT and MRI lung and liver the preferred sites. MRI is the inves-
scanning. tigation of choice and, universally, radiotherapy
The usual treatment principle is surgery com- with concomitant chemotherapy is the treatment of
bined with postoperative radiotherapy. The prog- choice. The tumour is usually radiosensitive and
nosis of these cancers is poor, usually because of the because of the inaccessibility of the site surgery
advanced state of disease at diagnosis and the prox- with clear margins is usually not possible. Neck
imity of the anterior cranial fossa. nodes are always irradiated with the primary site.
Nasopharyngeal carcinoma
Further reading
Nasopharyngeal cancer is the commonest tumour
seen in certain Asian countries (southern China and Chan Y, Goddard JC (eds) KJ Lee’s Essential
Southeast Asian countries with Chinese populations). Otolaryngology Head and Neck Surgery, 11th edn.
In Hong Kong and China, it accounts for about 20% New York: McGraw Hill Education, 2016.
of all malignancies. In southern China, it comprises Probst R, Grevers G, Iro H (eds) Basic Otorhinolary
ngology: A Step by Step Learning Guide, 2nd edn.
approximately 50% of all head and neck cancers.
Stuttgart: Georg Thieme Verlag, 2018.
Wackym PA, Snow JB (eds) Ballenger’s Otorhinolaryngology
Pathology Head and Neck Surgery, 18th edn. Shelton, CT: People’s
Medical Publishing House, 2016.
The nasopharynx is the space behind the nasal cav-
ity and above the oropharynx. The mucosa is strati-
fied, ciliated, columnar epithelium, with a large MCQs
aggregate of lymphoid tissue forming part of
Waldeyer’s ring. Select the single correct answer to each question. The
Nasopharyngeal cancer is classified according to correct answers can be found in the Answers section
the World Health Organization classification. There at the end of the book.
are three types.
• Type 1: keratinising squamous carcinoma. 1 Which modality of treatment is most useful for
• Type 2: non‐keratinising poorly differentiated nasopharyngeal carcinoma?
carcinoma. a chemotherapy
• Type 3: undifferentiated carcinoma. b radiotherapy
Type 3 is by far the more common subtype in c surgery
endemic Asian areas. Type 1 is more common in d immunotherapy
developed countries. e hormonal therapy
2 Which of the following statements concerning 3 Which of the following statements concerning
nasopharyngeal carcinoma is incorrect? parotid gland tumours is incorrect?
a keratinising squamous cell carcinoma is most a a cystic lesion in the lower pole is likely to be benign
common in developed countries b a long‐standing tumour that enlarges and
b examination of the nasopharynx is usually becomes painful suggests malignancy
positive c bilateral tumours in elderly men are usually benign
c in 90% of patients, cervical nodes are involved d facial nerve palsy suggests malignant disease
d there are known aetiological factors e needle aspiration cytology of parotid tumours is
e the tumour tends to infiltrate widely contraindicated
42 Tumours of the head and neck
Rodney T. Judson
anatomy of the region should guide the clinician as

Introduction to the likely diagnosis based on clinical assessment
(Table 42.1). However, treatment planning requires
The concentration of anatomical structures and the
a detailed assessment including endoscopy, accurate
rich traversing lymphatic system, bearing drainage
anatomical localisation with CT or MRI and path-
from all parts of the body, explains the diversity of
ological appraisal utilising the least invasive tech-
primary and secondary tumours found in the head
nique applicable. Fine‐needle aspiration cytology,
and neck region. Exposure of the skin to ultraviolet
preferably ultrasound guided, provides diagnostic
B radiation results in 85–90% of cutaneous carci-
material. Core biopsy or carefully considered open
nomas, the most common human malignancy
biopsy may be required if cytology is inconclusive.
occurring in the head and neck area. Excluding
cutaneous tumours, 90% of head and neck tumours
are squamous cell carcinomas arising from the epi- Characteristics of common tumours
thelium of the upper aerodigestive tract. These
tumours predominantly result from carcinogens Squamous cell carcinoma
released while smoking or chewing tobacco or are
The commonest head and neck malignancy is squa-
secondary to infection with human papillomavirus
mous cell carcinoma (SCC) arising from the upper
(HPV). Primary tumours, malignant and benign,
aerodigestive tract. Full details of this problem are
can arise from all other structures – glandular, vas-
covered in Chapter 41.
cular, lymphatic, neural, muscular, bony or connec-
tive tissue.
Cutaneous squamous cell carcinoma
Metastatic tumours to the head and neck are pre-
dominantly due to lymphatic spread. Metastatic The lips, forehead and ear are the commonest sites
lymph nodes characteristically firm to hard and for SCC of the head and neck due to their exposure
matted and which are confined to the upper third to sunlight. Lesions vary from an area of crusting
of the neck are most commonly the result of tumour through to ulceration and induration. SCC of the
spread from a primary squamous carcinoma of the upper lip has a higher propensity for lymph node
upper aerodigestive tract. Metastatic lymph nodes metastasis than SCC arising at other sites. SCC of
confined to the lower third of the neck are less com- the temple and ear may metastasise to the pre‐
monly from an aerodigestive tract origin and more auricular intraparotid lymph nodes. Such metasta-
likely from primary sites such as skin, thyroid or a sis may appear some time following successful local
malignant focus below the clavicle. Rare blood‐ excision of the primary tumour. Involvement of the
borne metastases are seen in the parotid gland from facial nerve from intraparotid metastases carries a
colon, kidney, breast and lung and in the thyroid very poor prognosis. Metastatic lymph nodes from
from lung and kidney. a cutaneous SCC, like those from an aerodigestive
The common mode of presentation of head and tract origin, often undergo cystic degeneration.
neck tumours is that of a painless neck mass or Rapid growth, redness of the overlying skin and
swelling. The approach to solving the problem of a clinical fluctuance can lead to the mistaken diagno-
neck swelling is dealt with in detail in Chapter 70. sis of a suppurating lymph node. Thorough clinical
An understanding of the characteristic features assessment, noting the absence of pain and the
of the common head and neck tumours and of the presence or history of a primary lesion coupled with
369
Table 42.1 Tumours of the head and neck.
Benign/
Tissue of origin malignant Tumour type Clinical site Common clinical feature
Upper Benign Squamous papilloma Oral cavity mucosa Solitary papillary lesion
aerodigestive Malignant Carcinoma in situ Oral cavity larynx/pharynx White or red mucosal patch
tract mucosa Squamous cell carcinoma Mucosa of upper aerodigestive Ulcerated infiltrative lesion with raised edges
tract
Lymphoepithelial carcinoma Nasopharynx Ulcerated lesion, frequent nodal metastases, nasal symptoms
Salivary gland Benign Pleomorphic adenoma Parotid commonest Painless slow‐growing firm mass
Oncocytic tumour (Warthin’s Parotid grand Soft to firm, occasionally bilateral, mass
tumour)
Malignant Mucoepidermoid carcinoma Parotid commonest Slow‐growing firm mass
Adenoid cystic Minor salivary glands Slow‐growing submucosal nodule in the upper aerodigestive tract
commonest
Acinic cell tumour Parotid gland Slow‐growing nodule
Adenocarcinoma Minor salivary gland Submucosal lump
Thyroid Benign Follicular adenoma Thyroid Slow‐growing smooth thyroid nodule
Hurtle cell adenoma Thyroid Slow‐growing smooth thyroid nodule
Malignant Papillary carcinoma Thyroid gland ± nodes Slow‐growing nodule; 50% of children have associated nodal metastases
Follicular carcinoma Thyroid Slow‐growing smooth thyroid nodule
Anaplastic carcinoma Thyroid Rapidly growing infiltrating mass often arising within a pre‐existing goitre
Medullary carcinoma Thyroid ± nodes Firm thyroid nodule, may be associated with multiple endocrine adenoma
syndrome
Parathyroid cells Benign Parathyroid adenoma Parathyroid glands (impalpable) Commonest cause of primary hyperparathyroidism
Malignant Parathyroid carcinoma Parathyroid ± nodes Progressive hyperparathyroidism, nodule may be palpable
Neuroendocrine Benign Paraganglionoma Carotid body Mass in region of upper carotid sheath
Glomus jugulare
Glomus intravagale Occasional symptoms resulting from noradrenaline secretion
Malignant Olfactory neuroblastoma Olfactory mucosa in nasal vault Bimodal age distribution occurring in adolescents and adults. Epistaxis
and nasal obstruction
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Adipose Benign Lipoma Commonest in subcutaneous Mobile superficial soft mass
layer
Malignant Liposarcoma Neck, larynx, pharynx Rare head and neck tumour. Occurs in elderly patients
Vascular Benign Haemangioma Face, scalp, neck Seen in childhood. Compressible red to purple mass
Lymphangioma Neck Soft, occasionally translucent neck mass in children
Malignant Angiosarcoma Skin of scalp or face Ulcerating cutaneous nodule occurring in elderly white males
Fibrous tissue Benign Fibromatosis Commonly in neck Slow‐growing mass in young females
Dermatofibroma Skin Small plaque in skin
Malignant Fibrosarcoma Face, neck, scalp and paranasal Painless growing mass in adults
sinus
Malignant fibrous Deep tissues of head and neck Infiltrating mass in elderly males. Commonest post‐irradiation tumour
histiocytoma
Neural tissue Benign Schwannoma Cranial nerves VII (rare), VIII, Lateral neck mass
IX, X, XI and XII
Neurofibroma Peripheral nerve sheaths Isolated subcutaneous neck nodule, or multiple nodules and large
plexiform benign neuromas in familial neurofibromatosis
Malignant Malignant schwannoma Cranial and cervical nerve roots Fixed mass, metastases possible
Muscle cell Malignant Rhabdomyosarcoma Orbit, nasal cavity and Commonest soft tissue sarcoma seen in children
paranasal sinuses
Bone Benign Osteoma Bony skeleton of face Smooth mass occurring in paranasal sinuses, multiple osteomas
associated with Gardner’s syndrome
Malignant Osteosarcoma Mandible or maxilla Painless enlarging bony swelling
Skin Malignant Squamous cell carcinoma Sun‐exposed skin Crusting ulcerating lesion
Basal cell carcinoma Skin of central face Translucent nodular lesion. Rarely a deeply ulcerating or erosive lesion
Malignant melanoma Skin of face, mucosa of nasal Pigmented skin lesion or polypoid nasal mass
cavity
Lymphoid tissue Malignant Lymphoma Lymphatic tissue, salivary Rubbery, discrete, multiple neck nodes
glands, thyroid
Dental tissue Benign Ameloblastoma Usually intra‐osseous but may Expanding mass arising in association with mandible. Rarely malignant
Squamous ontogenic tumour involve the gingiva
Ondontoma
Ondontogenic fibroma
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aspiration cytology, should avert the disaster of doing, the facial nerve, for descriptive purposes,
inappropriate incisional drainage. Management divides the gland into the larger superficial lobe
of cutaneous SCCs involves full clinical assessment covered by skin, platysma in part and parotid
of the tumour and draining lymph nodes aided by fascia, and the smaller deep lobe, which lies in the
fine‐cut CT scanning if deep tissue or nodal involve- parapharyngeal space and through which passes the
ment is suspected. Localised small lesions are cured retromandibular vein and external carotid artery.
by excision with clear surgical margins. Larger Saliva drains from the gland via the parotid duct,
lesions may necessitate extensive surgical resection which crosses the masseter muscle and enters the
involving underlying tissues and a planned lymph buccal cavity opposite the upper second molar teeth.
node clearance. Elaborate reconstructive procedures The submandibular glands lie close to the inner
may be necessary, especially for areas of the face to aspect of the mandible lying on the mylohyoid mus-
restore function and attain acceptable cosmesis. cle. The larger superficial lobe is covered by skin,
Cutaneous SCCs are radiosensitive. Radiotherapy platysma and deep cervical fascia, with the mandibu-
as primary treatment, owing to its protracted treat- lar branch of the facial nerve crossing its upper bor-
ment time, is reserved for small primary tumours in der on its way to supplying the depressor anguli oris.
difficult anatomical sites. Radiotherapy is used as The posterior aspect of the submandibular gland is
adjuvant therapy postoperatively in the manage- wrapped around the posterior‐free border of the
ment of advanced infiltrative tumours, especially mylohyoid muscle, and the deep lobe of the gland
with multiple lymph node metastases or perineural passes forward deep to the mylohyoid lying on the
tumour spread. hypoglossus muscle. The submandibular duct drains
from the deep lobe, running a long course in the floor
Cutaneous basal cell carcinoma of the mouth to open at a papilla in the anterior floor
of the mouth just lateral to the lingual frenulum. The
The most common site for basal cell carcinoma of
deep lobe of the gland and the duct are closely related
the head and neck is the central face. The most
to the lingual nerve, which may be involved in patho-
common clinical variant is a translucent nodule
logical processes and damaged during surgical treat-
made clinically more apparent by stretching of the
ment of the gland. The deep lobe is inferolaterally
skin around the lesion. Most tumours run a slow
related to the mylohyoid and supramedially covered
protracted course and nodal metastases are rare.
only by the oral mucosa in the floor of the mouth,
Tumours in areas of embryonal fusion lines may
thus being easily assessed clinically by bimanual
burrow deeply, making surgical clearance difficult.
palpation. Using the gloved left index finger placed in
Local surgical excision is the usual form of
the floor of the mouth and the right fingers applied
treatment.
externally, submandibular glandular swelling may be
differentiated from lymph node swellings.
The sublingual glands, predominantly mucus
Salivary gland tumours
secreting, lie submucosally in the anterior floor of
the mouth, supported by the mylohyoid muscles.
Salivary tissue is found not only in the three pairs of
These glands drain by multiple small ducts opening
major salivary glands (parotid, submandibular and
directly into the floor of the mouth along the sub-
sublingual glands) but also in small submucosal
lingual folds and occasionally into the subman-
glands known as the minor salivary glands, which
dibular duct.
are scattered throughout the upper aerodigestive
tract. The parotid glands are host to a variety of
tumours both benign and malignant, primary and Assessment of salivary gland disorders
secondary.
The diagnosis of salivary pathology can be deter-
mined in a high proportion of cases by a thorough
Anatomy history, clinical examination and the judicious use
The parotid glands, so named because of their ana- of special tests.
tomical proximity to the ear, are the largest salivary
glands and produce a high volume of serous saliva.
Clinical history
The most important anatomical relationship of the
parotid gland is with the facial nerve. This enters A history of a slowly growing lump suggests a
the posteromedial aspect of the gland as a single benign tumour. The rapid growth of a lump with
trunk and divides within its substance to emerge at the development of pain would strongly suggest a
the anterior border as the five main branches. In so malignant process.
42: Tumours of the head and neck 373
Clinical examination Pleomorphic adenoma (mixed salivary tumour)

Clinical examination, including intraoral and man- Approximately 65–75% of mass lesions arising
ual examination noting the site, size, shape, texture, within the parotid gland are benign, slowly growing,
tenderness, fixation, involvement of surrounding firm, smooth, usually asymptomatic tumours called
anatomical structures and the state of the regional pleomorphic adenoma. It is so named because of its
lymph nodes, should not only define involvement histological appearance of a variable mix of glan-
of the salivary gland but also suggest the most likely dular and stromal elements, both of which are
pathological process. Deep lobe parotid masses thought to arise from myoepithelial cells. While the
may be detected by a diffuse bulge in the root of peak incidence is in the fifth decade with a slight
the soft palate or tonsillar fossa region and also female preponderance, this tumour can occur from
may be palpable manually. Facial nerve function childhood to old age. Malignant transformation is
must be assessed with all parotid lesions. Tongue uncommon and rarely reported in those tumours
sensation should be tested in the presence of sub- present for less than 10 years. While initially a
mandibular problems. smooth lump, with time multiple bosselations may
develop. Rapid growth with pain and facial nerve
involvement are the hallmark of advanced malig-
Special tests
nant change. Given the relentless growth pattern,
Computed tomography the chance of malignant change and the inability to
Computed tomography (CT) scans are useful for differentiate this benign tumour clinically from
clarifying anatomical detail and detecting impalpa- slow‐growing malignant parotid tumours, all
ble lymph node metastases in suspected malignant parotid tumours are best treated by complete sur-
processes. gical excision.
Usually no preoperative investigation is necessary
Magnetic resonance imaging after establishing that the mass is mobile within the
Magnetic resonance imaging (MRI) is indicated if parotid gland. Cytology may help treatment plan-
cranial nerve involvement is suspected in malignant ning by deciding the urgency and timing of surgery.
processes, especially those involving the parotid Radiological assessment with CT scanning is only
gland. necessary when malignancy is suspected. Treatment
consists of excision of the lesion with an intact
Fine‐needle aspiration cytology capsule and preservation of the facial nerve.
Cytological assessment of clinically suspected Incomplete excision or capsular rupture at the time
tumours of the salivary glands produces useful of excision predisposes to local recurrence, which
information in treatment planning. This is a safe may be multinodular and exceedingly difficult to
procedure that is not associated with tumour eradicate. Complete excision is associated with a
dissemination or seeding. very low local recurrence rate (usually <2%). The
surgical technique involves identification of the
main trunk of the facial nerve, which is then traced
Parotid tumours through the gland while the tumour with the sur-
rounding parotid tissue is excised. This is known as
The parotid gland is not only the commonest site of
a superficial parotidectomy. For deep tumours, the
primary salivary neoplasms but is also affected by a
superficial lobe is excised first. The facial nerve and
wide variety of infiltrative and inflammatory pro-
branches are then fully mobilised to allow removal
cesses. From a clinical point of view, it is easier to
of the deep lobe, either between or below the facial
consider the presentation of either diffuse parotid
nerve. With careful surgical technique, the risk of
swelling or a mass within the region of the parotid.
permanent facial damage is low, but some degree of
Any mass arising within the region of the parotid
temporary facial weakness due to neuropraxia is
(i.e. from the zygomatic arch superiorly, the upper
not uncommon.
neck inferiorly, the anterior border of the masseter
anteriorly and the mastoid process posteriorly)
should be suspected as arising from within the
Adenolymphoma (Warthin’s tumour)
parotid gland and treated accordingly. An isolated
mass within the parotid is most commonly due to a Approximately 6–10% of parotid masses are due
parotid tumour; 80% of all salivary tumours occur to a benign softer tumour, more commonly found
within the parotid gland, and approximately 80% in males and arising in the inferior pole of the
of parotid tumours are benign. parotid, called an adenolymphoma. This tumour is
so called because of the dense lymphocytic infil- Malignant pleomorphic adenoma

tration. The exact origin of this lesion is uncer- Malignant pleomorphic adenoma is a more aggres-
tain. Approximately 10% of cases are bilateral. sive tumour that can arise either de novo or from a
The cytological picture is usually diagnostic. pre‐existing pleomorphic tumour.
Surgical excision in the form of parotidectomy is
usually recommended, except in the frail and Adenocarcinoma
elderly, in whom clinical observation may be more Adenocarcinoma, otherwise unspecified, may also
appropriate. arise in the parotid and displays a more aggressive
growth pattern.
Malignant parotid tumour
Treatment of malignant parotid tumours
Approximately 15–20% of parotid tumours are Treatment decisions are based on the biological and
malignant. In Australia, the most common malig- histological features of the tumour. Slow‐growing,
nancy involving the parotid is metastatic SCC clinically discrete, low‐grade lesions are usually
from a skin primary arising in the head and neck cured by complete surgical excision with sparing of
region. Such tumours tend to spread to intrapa- the facial nerve. For those tumours demonstrating
rotid lymph nodes. These lesions are often charac- more aggressive histological features, parotidectomy
terised by rapid growth due to tumour necrosis with facial nerve sparing may be followed by radio-
producing a cystic lesion within the parotid. therapy. Clinically aggressive tumours with facial
Treatment of metastatic SCCs involves parotid nerve involvement will require radical surgery
resection, often in association with a neck dissec- with sacrifice of the facial nerve and radiotherapy.
tion and postoperative radiotherapy. The parotid Primary nerve grafting using the sural nerve if pos-
is uncommonly the site of metastases from other sible is performed. Lymph node dissection is usually
tumours, but kidney, thyroid, lung and breast can- only performed for clinically or radiographically
cers may all spread to the parotid and mimic pri- detected nodal metastasis.
mary parotid tumours.
Submandibular tumours
Primary parotid malignancies
Mucoepidermoid carcinoma Unlike the parotid gland, tumours of the subman-
The most common primary malignancy of the dibular gland are relatively uncommon. However,
parotid is mucoepidermoid carcinoma, which can a higher proportion (approximately 40%) of sub-
occur from childhood onwards, with a peak incidence mandibular tumours are malignant. Pleomorphic
in the fifth to sixth decades. Approximately 75% of adenoma is the most common tumour affecting the
mucoepidermoid carcinomas are of low‐grade gland. As with the parotid, most submandibular
histological type and present with a slow‐growing tumours present as slow‐growing asymptomatic
parotid mass. High‐grade tumours have a more lumps. The diagnosis is usually suspected clinically
rapid growth pattern and a poorer prognosis. and based on bimanual palpation. Differentiation
Lymph node metastasis is uncommon in low‐grade from submandibular lymph node pathology can
tumours. usually be confirmed by aspiration cytology.
Submandibular tumours are treated by total gland
excision. Malignant lesions with local spread beyond
Adenoid cystic carcinoma
the submandibular gland may require sacrifice of
Adenoid cystic carcinoma, formerly known as cylin-
the underlying lingual and hypoglossal nerves
droma, also presents with a slow‐growing asympto-
followed by radiotherapy to effect a cure.
matic parotid mass. These tumours are characterised
by early perineural spread and have a propensity for
late recurrence, often to bone or lung, even up to Sublingual tumours
20 years following an apparent cure. Primary tumours of the sublingual gland are rare,
of which 60% are malignant.
Acinic cell tumour
Acinic cell tumour, in which some cells demonstrate
differentiation towards acinar cells, was once Paraganglionomas
thought to be a benign adenoma but has been
reclassified as a malignant carcinoma with a more The extra‐adrenal paraganglia of neural crest‐derived
common low‐grade behaviour. These tumours are cells can be the site of tumours known as paragan-
more common in females. glionomas. These, usually benign, tumours may
release neurotransmitters and produce intermittent the level of the inferior vagal ganglion. The usual
hypertension and facial flushing. Tumours are clinical presentation is that of a neck mass near the
named according to the neurovascular structure origin of the sternocleidomastoid muscle with an
with which they are associated. The common sites associated vocal cord palsy. Multiple cranial nerve
for these uncommon tumours are the carotid body, neuropathies may develop with progressive tumour
the jugular bulb and the vagus nerve. Whilst most growth. Contrast CT scanning demonstrates a vascu-
tumours occur sporadically, 10% represent an lar tumour within the carotid sheath displacing the
autosomal dominant inherited condition often vessel anteriorly. Other neural tumours of the vagus
associated with multiple paraganglionomas. nerve form the differential diagnosis. Malignant
transformation is commoner with glomus intrava-
gale tumours than other parapharyngeal tumours,
Carotid body tumour
with pulmonary metastases present in 20% of cases.
The carotid body paraganglion is a chemoreceptor Treatment consists of either radiotherapy or surgical
situated in the adventitia of the carotid bifurcation. excision based on an assessment of tumour size
Tumours present with a slowly growing, painless, and associated cranial nerve involvement. Although
smooth, firm, deep, lateral upper neck mass with surgical resection necessitates sacrifice of the vagus
limited supero‐inferior mobility. Transmitted pul- nerve, more than 50% of cases present with an
sation may be evident but tumours, although vas- established vocal cord paralysis.
cular, are not truly pulsatile. The intense contrast
enhancement on CT scanning with splaying of the
carotid bifurcation and the typical clinical presen-
tation are usually diagnostic. Surgical excision in Neural tumours
the sub‐adventitial plane with preservation of
the carotid vessels is curative for benign small Schwannomas
tumours. Occasionally, vascular reconstruction Half of the solitary well‐encapsulated tumours aris-
may be necessary for excision of larger and malig- ing from the Schwann cells of peripheral nerve
nant tumours. sheaths occur within the head and neck. Within the
head and neck the common nerves of origin are the
Glomus jugulare acoustic nerve and vagus nerve and, less commonly,
from cranial nerves VII, IX, XI and XII. These
Glomus jugulare tumours arise from the jugular
tumours expand the nerve from which they arise
bulb at the skull base. These deeply placed tumours
and surgical excision with preservation of the nerve
are not clinically apparent until their growth
can occasionally be achieved. The clinical presenta-
impinges on surrounding cranial nerves IX, X, XI
tion is of a slow‐growing, painless, deep, lateral
and XII or the internal auditory canal. Presenting
neck mass with limited mobility. Neurological
symptoms include tinnitus, hearing loss and voice
signs suggesting the nerve of origin are unusual.
and swallowing problems. If bone erosion of the
Radiological examination demonstrates a well‐
hypotympanum occurs, a vascular mass may be
circumscribed mass with some but not marked
clinically apparent medial to an intact tympanic
contrast enhancement. MRI may demonstrate an
membrane. A combination of contrast‐enhanced
associated neural structure suggesting the diagnosis.
CT and MRI should demonstrate the degree of
Tumours arising from a cervical nerve root may
bony erosion and the relationship of the tumour to
extend through the intervertebral foramen, produc-
the surrounding cranial nerves. The optimal treat-
ing a dumb‐bell tumour with a cervical and spinal
ment of these tumours is unresolved. Complete
component. Aspiration cytology showing the
surgical excision with sparing of the facial and
benign spindle cell pattern is usually inconclusive.
lower cranial nerves may be difficult to achieve.
Treatment is determined by tumour extent and the
Post‐surgical recurrent and persistent disease (7 and
clinical picture. Slow‐growing small tumours in
8%, respectively) are usually reported. Radiotherapy
elderly patients may be observed. Tumours arising
leading to tumour fibrosis produces similar imper-
peripherally in the neck may be separated from the
fect results and carries its own morbidity.
associated nerve with minimal morbidity. Surgical
excision of large tumours or those in surgically less
Glomus intravagale
accessible sites or contiguous with important
Glomus intravagale tumours arise from the para- neurological structures such as the brachial plexus
ganglionic tissue within the perineurium of the is associated with the risk of significant neurological
vagus nerve. These tumours are usually situated at morbidity.
Malignant schwannomas the head and neck, with the upper aerodigetive
tract being favoured and less commonly neck and
Less than 5% of schwannonas are malignant. These
salivary glands. The 5‐year survival for these
tumours infiltrate locally, may extend intracranially
aggressive tumours is approximately 50%.
or intravertebrally and can metastasise to the lungs.
Aggressive surgical resection is advocated.
Dermatofibrosarcoma protuberans
Neurofibromas Dermatofibrosarcoma protuberans, which accounts
for approximately 7–15% of soft tissue sarcomas,
Neurofibromas are tumours arising from the
usually presents as an elevated, firm, solitary,
peripheral nerve sheaths and present commonly as
slow‐growing, painless mass in the scalp or neck.
rubbery, fusiform, subcutaneous nodules. Multiple
Metastases are uncommon and an excellent out-
neurofibromas and plexiform neurofibromas are
come is achieved if histologically clear margins are
found along with café‐au‐lait spots and skeletal,
obtained following local excision.
CNS and ocular lesions in the autosomal dominant
inherited disorder of neurofibromatosis. Surgical
excision, with sacrifice of the associated nerve, is Angiosarcoma
definitive treatment for isolated lesions.
Over half of all angiosarcomas present as an ulcer-
ating, nodular or diffuse dermal lesion of the scalp
or face in elderly white males. They are uncommon
Soft tissue sarcomas
tumours, accounting for only 0.1% of all head and
neck tumours.
Soft tissue sarcomas are tumours of mesenchymal
origin that display a wide spectrum of clinical and
biological behaviour. Less than 10% of these Rhabdomyosarcoma
uncommon tumours arise in the head and neck.
Rhabdomyosarcoma is the most common paediat-
A number of genetic abnormalities have been iden-
ric soft tissue sarcoma. This malignant tumour of
tified. Many of these clonal aberrations have the
striated muscle cell origin arises in the nasal cavity,
potential to be applied to the differential diagnosis,
paranasal sinuses, orbit, nasopharynx and middle
in these, often difficult to categorise tumours. Most
ear. Early metastases, both regional and distant,
tumours present as a painless neck mass. Tumours
are common. Treatment usually involves chemo-
arising from the tissues of the upper aerodigestive
therapy and irradiation, with an overall survival
tract or the deep tissue spaces may present with a
of approximately 50%.
variety of symptoms such as epistaxis, otalgia, visual
disturbance or cranial nerve palsies resulting from
local tumour infiltration. A thorough clinical
examination including intraoral, neurological and Bone tumours
endoscopic examination of the upper aerodigestive
tract often forms an impression of the extent of the
Bone tumours may affect the mandible, maxilla or
tumour. Fine‐cut CT scanning and MRI allow accu-
cervical vertebrae, presenting usually as painless
rate anatomical assessment. Fine‐needle aspiration
swellings. Tumours are classified according to the
cytology is simple and safe for accessible tumour and
matrix produced by the tumour cells into chondro-
is helpful in differentiating sarcomas from other
sarcomas if cartilaginous, osteosarcomas if osteoid,
more common tumours but is usually unhelpful in
and fibrosarcomas if they lack a distinct matrix.
the precise diagnosis of tumour type and grade.
Surgical excision with clear margins is associated
Core needle biopsies, radiologically directed, usually
with survival rates of 40–80% independent of the
provide adequate tissue for pathological assessment.
anatomical sites of origin. Distant metastases are
Tumours are staged according to their size and
infrequent.
whether superficial or deep and graded histologically
based on differentiation, cellularity, density of the
stroma, vascularity and degree of necrosis.
Metastatic tumours
Malignant fibrous histiocytoma
The management of neck metastases is outlined in
Malignant fibrous histiocytoma is the commonest Chapter 70. An understanding of the pattern of
soft tissue sarcoma in adults. Less than 3% involve lymphatic drainage should direct the clinician to
the likely site of the primary lesion. Primary

tumours in the tongue base and the tonsil, occa-
MCQs
sionally small and hidden within the tissue convo-
lutions, may thwart attempts at detection.
Melanoma may also present with metastatic nodes
in the absence of a detectable primary lesion,
which may be amelanotic or have undergone 1 The commonest tumour of the head and neck area is:
spontaneous regression. Definitive treatment of a pleomorphic tumour of the parotid gland
the primary tumour and neck metastases arising b squamous cell carcinoma of the larynx
from SCC of the upper aerodigestive tract may be c squamous cell carcinoma of the skin
achieved with radiation often followed by surgery. d basal cell carcinoma of the skin
Palliative radiotherapy may have a role in reduc- e carcinoma of the thyroid gland
ing the local devastating effects of uncontrolled
neck disease arising from a distant incurable pri- 2 The most common paediatric soft tissue sarcoma in
mary tumour. the head and neck area is:
a angiosarcoma
b malignant fibrous histiocytoma
c dermatofibrosarcoma protuberans
Further reading d rhabdomyosarcoma
e chondrosarcoma
Ridge JA, Mehra R, Lango MN, Galloway T. Head and
neck tumors. CancerNetwork. Available at https://www.
3 The highest propensity for lymph node metastasis
cancernetwork.com/cancer‐management/head‐
and‐neck‐tumors
occurs in squamous cell carcinoma of the:
Shah JP, Patel SG (eds) Cancer of the Head and Neck. a ear
Hamilton, Ontario: BC Decker, 2001, chapters b scalp
13–17. c upper lip
Thompson LD, Bishop JA (eds) Head and Neck Pathology, d nose
3rd edn. Philadelphia: Elsevier, 2018. e lower lip
Section 8
Hernias
43 Hernias
Roger Berry1 and David M.A. Francis2
1
2
Department of Urology, Royal Children’s Hospital, Melbourne, Victoria, Australia and
Department of Surgery, Tribhuvan University Teaching Hospital, Kathmandu, Nepal
surgical reduction of the viscera from the hernial

Introduction orifice and closure of the defect. If strangulation
occurs the compromised viscus has to be resected.
A hernia is an abnormal protrusion of a viscus (or
part of a viscus) through a defect either in the con-
taining wall of that viscus or within the cavity in Components of a hernia
which the viscus is normally situated. The ‘wall’
refers to the muscle layers of the abdomen or the Hernias are composed of a sac that protrudes
diaphragm, or the walls of the pelvis. Hernias are through a defect or hernia orifice and envelops the
either external or internal. hernia contents. The sac consists of peritoneum, the
parts of which are described as the neck, body and
External hernias fundus (Figure 43.1). The neck of the sac is situated
External hernias present as an abnormal lump at the defect. The body is the widest part of the her-
which can be detected by clinical examination nial sac, and the fundus is the apex or furthest
of the abdomen or groin; they present externally. extremity. Viscera most likely to enter a hernial sac
The relative occurrence and gender distribution are those normally situated in the region of the
of external abdominal hernias are shown in defect and those which are mobile, namely the
Tables 43.1 and 43.2. omentum, small intestine and colon. Some hernia
contents have been ascribed eponymous names.
Internal hernias
Richter’s hernia
Internal hernias are rare and occur when the intes-
tine (the ‘viscus’) passes beneath a constricting band The sac contains only part of the circumference of
or through a peritoneal window (the ‘defect’) within the bowel, usually the antimesenteric border
the abdominal cavity, or through the diaphragm or (Figure 43.2).
pelvic floor. They present as:
• acute intestinal obstruction, or Littré’s hernia
• chronic recurrent abdominal pain and vomiting
A Meckel’s diverticulum lies within the hernial sac.
due to incomplete and intermittent intestinal
Littré’s hernia occurs most commonly in a femoral
obstruction.
or inguinal hernia (see later section).
Sites of internal herniation include (i) the paradu-
odenal and paracaecal fossae, (ii) the lesser sac
Maydl’s hernia
through the epiploic foramen (foramen of Winslow)
or a defect in the transverse mesocolon, (iii) beneath The hernial sac contains two loops of intestine
congenital bands or adhesions, (iv) through defects (Figure 43.3). The loop of intestine within the
in the small bowel mesentery, (v) between the lat- abdominal cavity may become obstructed or stran-
eral abdominal walls and intestinal stomas, and (vi) gulated, and this may not be recognised unless the
through defects in the diaphragm (hernias of hernia contents are inspected and returned to the
Bochdalek and Morgagni). Treatment consists of abdominal cavity (‘reduced’) completely.
381
382 Hernias
Hernial sac
Table 43.1 Relative occurrence of external
abdominal hernias in adults. Hernial contents
Hernia Percentage
Inguinal 80 Peritoneum
Incisional 10
Femoral 5
Umbilical 4
Epigastric <1
Other <1
Table 43.2 Sex distribution of abdominal hernias.

Obstructed loop of
Male (%) Female (%) intestine within
peritoneal cavity
Inguinal hernia 96 45
Femoral hernia 2 39 Fig. 43.3 Maydl’s hernia.
Umbilical hernia 1 15
Other 1 1 De Garengeot’s hernia
A femoral hernia with the appendix in the hernia sac.
Amyand’s hernia
Fundus of sac An inguinal hernia in which the hernial sac con-
Hernial contents tains a normal or inflamed appendix.
Body of sac Predisposing factors
A hernia occurs because of (i) weakness or defect

Neck of sac
Hernial defect
in the abdominal wall and (ii) positive intra‐
abdominal pressure (IAP), which is often raised,
forces the viscus into the defect.
Abdominal wall
Peritoneum Sites of weakness in the abdominal wall
Weaknesses in the abdominal wall may be due to
the following.
Fig. 43.1 Components of a hernia.
• Congenital (i.e. present at birth), for example
patent processus vaginalis or canal of Nuck, pos-
terolateral or anterior parasternal diaphragmatic
defect, patent umbilical ring in children.
Herniated intestine
• Where a normal anatomical structure passes
Hernial sac
through the abdominal wall, for example
oesophageal hiatus, umbilical ligament in adults,
Skin obturator foramen, sciatic foramen.
• Acquired, for example surgical scar, site of an
Abdominal wall intestinal stoma, muscle wasting with increasing
Peritoneum age, fatty infiltration of tissues because of obesity.
Increased intra‐abdominal pressure

Intestinal lumen
Raised IAP stretches the abdominal wall vertically
and horizontally, thereby increasing the circumfer-
Fig. 43.2 Richter’s hernia. ence of any defect. Also, high IAP forces abdominal
43: Hernias 383
Strangulation
Box 43.1 Causes of sudden or sustained
increases in intra‐abdominal pressure Strangulation occurs when the blood supply of the
contents has ceased due to compression at the her-
• Coughing nial orifice. Initially, lymphatic and venous chan-
• Vomiting nels are obstructed, leading to oedema and venous
• Straining during urination or defecation
congestion but with continued arterial inflow.
• Pregnancy and childbirth
When the tissue pressure equals arterial pressure,
• Occupational heavy lifting or straining, and
arterial flow ceases and tissue necrosis ensues.
strenuous muscular exercise
Strangulation is a serious complication and, if the
• Obesity
intestine is involved, leads to peritonitis (see
• Ascites
• Continuous ambulatory peritoneal dialysis (CAPD)
Chapter 68) which can be fatal. A strangulated her-
• Gross organomegaly nia is both irreducible and obstructed and is very
tense and usually exquisitely tender. Erythema of
the overlying skin is a late sign. A tense, tender, irre-
ducible hernia implies strangulation and requires
urgent surgery.
contents through a defect. There are several causes
of increased IAP (Box 43.1).
Principles of treatment
Complications
Uncomplicated hernias can be managed conserva-
tively with no treatment or support with a truss,
Most hernias are uncomplicated at presentation.
but most will require operative treatment.
The three important complications of hernias are
Complicated hernias always require surgery, often
irreducibility, obstruction and strangulation.
urgently.
Irreducibility
No treatment
A hernia is ‘irreducible’ when the sac cannot be
No treatment may be advised in debilitated patients
emptied completely of contents. Irreducibility is
who are not medically fit for surgery and who have
caused by (i) adhesions between the sac and its
uncomplicated hernias with minimal symptoms.
contents, (ii) fibrosis leading to narrowing at the
Few patients fall into this category. Most external
neck of the sac, or (iii) a sudden increase in IAP
hernias can be successfully repaired surgically with
that causes transient stretching of the neck and
minimal morbidity. If a patient refuses treatment,
forceful movement of contents into the sac, which
then the full implications of this decision must be
cannot subsequently return to their original
explained.
location.
Truss or abdominal binder
Obstruction
A truss or some form of hernia support may be
A hernia becomes obstructed when the neck is suf-
used to provide symptomatic relief. After the hernia
ficiently narrow to occlude the lumen of the intes-
has been reduced, the truss presses on the hernial
tine contained within the sac. The contained bowel
orifice to prevent protrusion. However, it frequently
becomes obstructed by the hernia defect. Obstructed
does not prevent prolapse of the hernia and simply
hernias are nearly always irreducible and, if not
presses on the hernia contents. They can be uncom-
treated, may become strangulated. Often, there is a
fortable to wear.
history of a sudden increase in IAP that has pushed
intestine or other contents into the sac. The patient
Reducing raised intra‐abdominal pressure
presents with symptoms and signs of intestinal
obstruction (abdominal colic, vomiting, constipa- Causes of increased IAP should be corrected.
tion, abdominal distension) (see Chapters 27 and Stopping smoking, investigation and treatment of
32), together with a tender irreducible hernia. prostatism and constipation, weight reduction,
Identifying an external hernia in patients with and effective management of ascites should be
intestinal obstruction may alter the operative attempted where indicated. Changes in occupation
approach. Obstructed hernias need urgent surgical and physical exercise also may have to be
treatment. considered.
384 Hernias
Operation Importance of the integrity

of the inguinal canal
Operation is indicated for all other patients because
of symptoms and the risk of complications. Surgery The inguinal canal passes through the abdominal
aims to (i) reduce the hernia contents, (ii) excise the wall between the deep (internal) and superficial
sac (herniotomy) in most cases, and (iii) repair and (external) inguinal rings. It carries the spermatic
close the defect, either by approximation of adja- cord to the scrotum in the male, or the round liga-
cent tissues to restore the normal anatomy (hernior- ment of the uterus to the labium majora in the
rhaphy) or by insertion of additional material female, together with the ilioinguinal nerve. The
(hernioplasty). canal is a site of weakness and therefore potential
herniation.
Urgent operation In addition to the presence of a patent processus
Urgent operation is indicated when obstruction or vaginalis in an IIH, both IIH and DIH result from fail-
strangulation is suspected. Resuscitation with intra- ure of normal mechanisms that maintain the integrity
venous fluids, antibiotics, analgesia and nasogastric of the inguinal canal, including the following.
aspiration is required before surgery. • ‘Shutter mechanism’ around the deep inguinal
ring: during straining, a U‐shaped condensation
of transversalis fascia which passes under the
Inguinal hernia cord is pulled upward and laterally, closing the
deep ring around the cord and increasing the
Inguinal hernia is the commonest hernia and is obliquity of the inguinal canal.
approximately 10 times more common in males • ‘Shutter action’ of the internal oblique and trans-
than females (see Tables 43.1 and 43.2). Two types versus abdominis muscles: contraction of these
of inguinal hernia are recognised (Figure 43.4), muscles draws them downwards so that the
indirect inguinal hernia (IIH) and direct inguinal inguinal canal tends to close and become more
hernia (DIH), but they can occur together. oblique.
(a) Inferior epigastric artery
Peritoneum
Transversalis
fascia
Conjoint tendon
External oblique
aponeurosis
Spermatic cord
Hernial sac
(b) Inferior epigastric artery
Peritoneum
Transversalis fascia
Conjoint tendon
Spermatic cord
Fig. 43.4 Types of inguinal hernias (right side): (a) indirect inguinal hernia; (b) direct inguinal hernia.
43: Hernias 385
Deep inguinal ring
Hernial sac
Superficial inguinal ring
Testis
BUBONOCELE FUNICULAR INGUINOSCROTAL
Fig. 43.5 Types of indirect inguinal hernias.
• Integrity of the posterior wall of the inguinal Classification of indirect inguinal hernias
canal: weakness of the conjoint tendon reduces
These hernias are classified according to the length
the strength of the posterior wall of the inguinal
of the hernial sac (Figure 43.5).
canal and reduces support behind the superficial
• Bubonocele: the sac is confined to the inguinal
inguinal ring.
canal.
• Oblique direction of the inguinal canal: if the
• Funicular: the sac extends along the length of the
deep and superficial inguinal rings enlarge, they
inguinal canal and through the superficial ingui-
may almost overlie each other and obliquity of
nal ring but does not extend to the scrotum or
the canal is lost.
labium majora.
• Complete, scrotal or inguinoscrotal: the sac
Indirect inguinal hernia passes through the inguinal canal and superficial
inguinal ring and extends into the scrotum or
The hernial sac of an IIH is a patent processus vagi-
labium.
nalis, and the neck of the sac is situated at the deep
inguinal ring, lateral to the inferior epigastric artery.
Direct inguinal hernia
The sac accompanies the spermatic cord along the
inguinal canal towards the scrotum for a varying A DIH protrudes directly through the posterior
distance (see below). The sac lies in front of the wall of the inguinal canal, medial to the inferior
cord and is enclosed by the coverings of the cord. epigastric artery and deep inguinal ring. The essen-
Except in children and infants, the essential cause tial fault with a DIH is weakness of the inguinal
of an IIH is (i) failure of the processus vaginalis to canal and is invariably associated with poor
become completely obliterated to form the ligamen- abdominal musculature. Herniation occurs at a site
tum vaginale, which normally occurs within a few where the transversalis fascia is not supported by
days after birth, and (ii) loss of integrity of the the conjoint tendon or the transversus aponeurosis,
inguinal canal. Even though the sac of an IIH is an area known as Hesselbach’s triangle. The bound-
congenital, herniation may not occur until later in aries of Hesselbach’s triangle are medially the lat-
life, when there is failure of the normal mechanisms eral edge of the rectus sheath, superolaterally the
that maintain the inguinal canal. inferior epigastric vessels, and inferiorly the ingui-
The incidence of IIH is approximately 800–1000 nal ligament. Occasionally, the hernia sac straddles
per million male population. IIH is approximately inferior epigastric vessels and is then known as a
four times more common than DIH, occurs at any ‘pantaloon hernia’.
time during life, and has a male to female ratio of DIH is rare in females and does not occur in chil-
about 10 : 1. dren. It is more common on the right side after
386 Hernias
appendicectomy, suggesting that damage to the pressure medial to the deep inguinal ring. The deep
iliohypogastric and ilioinguinal nerves with subse- inguinal ring lies just above the midpoint of the
quent weakness of the internal oblique and trans- inguinal ligament. The midpoint of the inguinal
versus abdominis muscles is an aetiological factor. ligament lies halfway between the anterior superior
iliac spine and the pubic tubercle; these are the
Clinical features of inguinal hernias attachments of the inguinal ligament to the pelvis.
The midpoint of the inguinal ligament differs from
Inguinal hernias present with inguinal discomfort,
the mid‐inguinal point. The mid‐inguinal point is
with or without a lump. Discomfort is due to
halfway between the anterior superior iliac spine
stretching of the tissues of the inguinal canal and
and the pubic symphysis. The femoral pulse can be
occurs typically when IAP is increased. Pain may
palpated, below the inguinal ligament at the mid‐
also be referred to the testis because of pressure on
inguinal point.
the spermatic cord and ilioinguinal nerve. Severe
To distinguish an indirect from a direct inguinal
inguinal or abdominal pain suggests obstruction or
hernia pressure is applied to the deep inguinal
strangulation. A lump is usually obvious to the
ring (midpoint of the inguinal ligament) and the
patient, is often precipitated by increasing IAP, and
patient is asked to cough; if the hernia is con-
may reduce completely with rest and lying down.
trolled, it is an IIH; if the hernia is not controlled,
The patient initially is examined standing to
it is a DIH.
demonstrate the lump and possible ‘cough impulse’,
and then lying down to allow the hernia to be
reduced. An IIH protrudes along the line of the Sliding inguinal hernia
inguinal canal for a variable distance towards the
A sliding inguinal hernia is a variant in which part
scrotum or labia; a DIH appears as a diffuse bulge
of a viscus (usually the colon) is adherent to the
at the medial end of the inguinal canal. The signifi-
outside of the peritoneum forming the hernial sac
cance of a cough impulse, or sudden bulging of the
beyond the hernial orifice. Thus, the viscus and the
inguinal region with coughing, must be interpreted
hernial sac, which may contain another abdominal
carefully. A generalised weakness in the inguinal
viscus, lie within the inguinal canal (Figure 43.6).
region will result in a diffuse bulge appearing with
Sliding hernias are more common on the left side
coughing, but this condition (known as Malgaigne’s
(where they contain part of the sigmoid colon) than
bulge) is not the same as a hernia, in which the
on the right (where they contain part of the cae-
cough impulse is discrete and confined to the area
cum). Sliding hernias occasionally contain part of
of herniation. Abdominal examination is performed
the bladder or an ovary and ovarian tube. A sliding
to detect organomegaly, a mass or ascites.
hernia may be indirect or direct. They are nearly
always found in males. A sliding hernia should be
Indirect or direct inguinal hernia?
suspected if the neck of the hernia is bulky, or if the
An IIH is prevented from appearing by applying hernial sac does not separate easily from the cord at
pressure over the deep inguinal ring, a DIH by operation.
Colon
Conjoint tendon
Transversalis fascia
Peritoneum
Transversalis
Internal
oblique
External oblique
aponeurosis
Hernial sac
Fig. 43.6 Section through sliding inguinal hernia.

43: Hernias 387
Inguinal hernias in infants and children posterior wall behind the cord and is attached
along the inguinal ligament from the pubic tubercle
Inguinal hernias are always indirect in infants and
to lateral to the deep inguinal ring. Alternatively,
children and are due to a patent processus vagi-
the mesh can be inserted via an extraperitoneal
nalis. The majority (90%) occur in males and more
approach and placed deep to the defect in the pos-
commonly on the right side, presumably due to
terior wall.
the slightly later descent of the right testis.
Approximately 10–20% are bilateral. If the con-
tralateral side is also explored in a child undergoing Laparoscopic hernia repair
unilateral inguinal hernia repair, a patent processus Laparoscopic repair is performed under general
is found in approximately 50% of cases. anaesthesia, using either a transperitoneal or extra-
Irreducibility is common and occurs in about 50% peritoneal approach. The sac is dissected from the
of hernias presenting within the first year of life. spermatic cord (or round ligament) and reduced. A
Strangulation appears to be rare. Testicular infarc- mesh is inserted behind the posterior wall and deep
tion can occur if a large irreducible hernia severely ring to strengthen the area.
compresses the spermatic cord and is more com-
mon than infarction of the hernial contents.
Inguinal hernias in children should be repaired Management after inguinal hernia repair
surgically. The hernial sac is very thin and because
the superficial and deep inguinal rings are almost Patients require analgesia for the first few days.
superimposed upon one another in children, the sac They should avoid straining and lifting for 2 weeks
can be mobilised and ligated through the superficial after surgery, and slowly resume physical activity
inguinal ring. Herniotomy is all that is required. and work over the next 4 weeks. It takes about 6
weeks to fully recover.
Treatment of inguinal hernias Potential complications of inguinal hernia repair

Inguinal hernias are treated surgically and the sur- In addition to the complications of any surgical
gery can be performed open or laparoscopically. procedure (haemorrhage, haematoma, wound and
Open inguinal hernia surgery can be undertaken chest infection, deep vein thrombosis, pulmonary
under general, regional or local infiltration anaes- embolus, anaesthetic complications) there are a
thesia. Open repair is performed through a skin‐ number of potential complications specific to ingui-
crease incision centred over the inguinal canal. The nal hernia repair.
sac is dissected carefully from the cord, opened and • Urinary retention: elderly male patients are par-
the contents returned to the abdominal cavity. In an ticularly susceptible to retention of urine.
IIH, the sac is ligated at the deep inguinal ring and Prostatic symptoms should be identified and
excised (herniotomy), whereas in a DIH the sac is treated before the hernia is repaired.
formed from layers of the posterior wall of the • Scrotal swelling and haematoma: oedema, swell-
inguinal canal and so is not excised. A procedure to ing and bruising of the scrotum are common
strengthen the posterior wall of the inguinal canal (especially with bilateral repairs) and resolve
is performed (herniorrhaphy or hernioplasty). spontaneously. Scrotal support may bring symp-
tomatic relief. Large haematomas require opera-
tive drainage.
Herniorrhaphy
• Wound infection: a deep wound infection which
Herniorrhaphy refers to repair of the posterior wall does not settle with antibiotics requires removal
of the inguinal canal behind the spermatic cord by of the prosthetic mesh.
one of several methods, together with repair of the • Recurrent hernia: recurrence is related to surgical
external oblique aponeurosis in front of the cord. technique and expertise, experience of the opera-
There are a variety of described techniques. tor, postoperative infection and haematoma, and
failure to correct factors predisposing to hernia
formation. Recurrence rates should be less than
Hernioplasty
2%. About 50% of recurrences appear within
Hernioplasty refers to insertion of a prosthetic 5 years after the initial repair, and approximately
mesh (e.g. polypropylene) to cover and support the 50% of recurrences are indirect hernias. A first
posterior wall of the inguinal canal. The mesh recurrence is treated along the principles outlined
encircles the cord at the deep ring, covers the in the previous section.
388 Hernias
• Nerve injury: injury to the ilioinguinal nerve, hernia. Aetiological factors in femoral hernia for-
which lies below the spermatic cord in the mation are:
inguinal canal and passes out through the • localised weakness at the femoral ring
superficial inguinal ring, occurs in 10–20% • factors which increase IAP (see Box 43.1).
of inguinal hernia repairs, resulting in paraes-
thesia or numbness below and medial to the Presentation
wound over the pubic tubercle and proximal
A femoral hernia presents as either discomfort in
scrotum.
the groin together with a lump, or acutely as intes-
• Persisting wound pain: this is uncommon, and
tinal obstruction with or without strangulation.
results from nerve entrapment or damage, neu-
A small hernia may be difficult to palpate, espe-
roma formation, osteitis pubis if sutures have
cially in the obese patient. The hernia is frequently
been inserted into the pubis, displacement of a
irreducible and may not have a cough impulse.
mesh repair, or pressure on the spermatic cord.
On examination, the bulge of a femoral hernia
Pain may be a symptom of recurrent herniation.
appears in the region of the saphenous opening.
Local anaesthetic or phenol injections may help,
The neck of the sac is always located below the line
and surgical exploration is indicated for severe or
of the inguinal ligament, even though the fundus
persistent pain.
may appear to be above the ligament. This is
• Testicular ischaemia and atrophy: interruption of
because once within the femoral canal, the hernial
the testicular arterial supply (testicular artery
sac is prevented from continuing inferiorly down
and indirectly from the cremasteric artery and
the thigh with the femoral vessels because the femo-
the artery of the vas deferens) can occur during
ral sheath (which encloses the femoral vessels and
dissection of an indirect sac from the cord.
the femoral canal) becomes narrow and tapers to a
Ischaemia produces testicular pain, tenderness
point around the vessels. The hernia is therefore
and swelling. Testicular atrophy is observed in
directed forwards through the fossa ovalis and is
1–5% of males.
quite superficial at this point (Figure 43.7). It can-
• Hydrocele: a long‐term complication probably
not continue down the thigh in a subcutaneous
resulting from the repair being too tight or scar-
plane because the superficial fascia of the thigh is
ring, with subsequent compression of lymphatics
attached to the lower border of the fossa ovalis and
of the cord.
is firmer than the superficial fascia above the level
• Injury to the vas deferens: a rare complication
of the foramen ovalis. As the hernia enlarges, it
that is most likely to occur when a recurrent her-
turns upwards into the looser areolar tissue beneath
nia is repaired.
the skin of the groin crease and may be confused
• Visceral injury: viscera in a sliding hernia are at
with an inguinal hernia.
risk for injury when the sac is being dissected
Thus, the direction taken by a femoral hernia is
away from them.
initially downwards through the femoral canal,
then forwards through the fossa ovalis, and then
upwards in the loose areolar tissue of the upper
Femoral hernia
thigh. Therefore, in attempting to reduce the hernia,
pressure is applied in the reverse order, i.e. initially
A femoral hernia occurs when the transversalis fas-
downwards, backwards and then upwards.
cia which normally covers the femoral ring is dis-
rupted, so that a peritoneal sac and hernial contents
pass through the femoral ring into the femoral
Inguinal or femoral hernia?
canal. The femoral canal is the most medial com-
partment of the femoral sheath and lies medial to Inguinal and femoral hernias are distinguished by
the femoral vein. Femoral hernias are two to three their positions relative to the inguinal ligament and
times more common in females than males, and pubic tubercle. The inguinal ligament is identified
occur in the older age group, often after a period of by palpating the anterior superior iliac spine and
weight loss. Femoral hernias are never congenital the pubic tubercle; an imaginary line drawn
and are twice as common in parous as in non‐ between the two points is the line of the inguinal
parous females. Inguinal hernias are more common ligament. The neck of an inguinal hernia is above
than femoral hernias in females (see Table 43.2). the inguinal ligament and pubic tubercle, and the
Approximately 60% of femoral hernias are on the hernia protrudes initially from above the ligament
right, 30% on the left and 10% bilateral. A femo- even though it may descend into the scrotum. The
ral hernia is the commonest site for a Richter’s hernia passes medial to the pubic tubercle as it
43: Hernias 389
Transversalis
Internal oblique
External oblique
aponeurosis
Superficial fascia
Spermatic cord
Cribriform
fascia Superficial fascia
Transversalis
fascia
Pectineal ligament
Extraperitoneal
fat
Peritoneum Superior pubic ramus
Pectineus and pectineal fascia
Fascia lata
Superficial fascia
Fig. 43.7 Sagittal section of a femoral hernia.
descends from the superficial inguinal ring, into the space between the peritoneum and abdominal
scrotum or labia. The neck of a femoral hernia is wall muscles is accessed through an abdominal
below the inguinal ligament and lateral to the pubic incision. The sac is identified and opened to
tubercle, and the hernia protrudes initially from inspect the contents. The intestine is resected if
below the ligament. necessary and the sac is excised. The femoral ring
is repaired from this intra‐abdominal approach.
Treatment
Surgical treatment of a femoral hernia should
always be advised because of the risk of obstruction Incisional hernia
and strangulation. Surgery involves opening and
emptying the sac and performing a herniorrhaphy An incisional hernia is a protrusion of the perito-
to prevent recurrence. Herniorrhaphy aims to neum (the sac) and underlying abdominal contents
reduce the size of the femoral ring and is performed (hernial contents) into the subcutaneous plane
by inserting several sutures between the inguinal through a defect at the site of an abdominal scar.
and pectineal ligaments, thereby effectively closing The true incidence is difficult to ascertain but is on
off the femoral canal. One of two operative the order of 5% at 5 years and 10% at 10 years.
approaches is used. There is a higher preponderance in males. Patients
• A ‘low’ or subinguinal approach is used for small present a bulge at the site of a previous incision.
uncomplicated femoral hernias by making an Incisional hernias increase in size with time and fre-
incision over the hernia below the level of the quently become irreducible.
inguinal ligament. The main predisposing factors for incisional her-
• The ‘high’ or supra‐inguinal approach is recom- nia are poor surgical techniques, local wound com-
mended for large or complicated femoral hernias plications, impaired wound healing and increased
in an emergency situation. The extraperitoneal IAP (Box 43.2).
390 Hernias
Box 43.2 Aetiological factors

in incisional hernias
Poor surgical technique

• Angulated incision Non-absorbable
sutures
• Parallel incisions Inverted
• Devitalised tissue in wound Rectus linea alba
• Tightly sutured wound sheath
• Poor technique of abdominal wound closure
Rectus
• Absorbable sutures of short duration abdominis
The
Local wound factors
‘keel’
• Infection
• Haematoma Fig. 43.8 Keel repair.
• Foreign body
• Wound edges not in apposition
subcutaneous space (on‐lay repair). The mesh can
Impaired wound healing be placed intraperitoneally and the musculo‐
• Malnutrition aponeurotic layer is closed over the mesh (inlay
• Corticosteroids, anti‐proliferative and immunosup- technique). Alternatively, a sub‐lay technique can
pressive drugs be used. The mesh is placed over the closed poste-
• Uraemia rior rectus sheath and peritoneum, with rectus
• Jaundice muscles overlying the mesh and the anterior rectus
• Diabetes sheath closed.
• Anaemia
Raised intra‐abdominal pressure

See Box 43.1 Epigastric hernia
An epigastric hernia is a protrusion of extraperito-

Treatment neal fat, with or without a small sac of peritoneum,
through a defect in the linea alba anywhere
Incisional hernias should be repaired because (i)
between the xiphisternum and the umbilicus. The
they increase in size with time and become more
defect is characteristically small, often about 1 cm
difficult to repair as they become larger; (ii) they are
in diameter, and seen as a transverse split in the
at risk of becoming irreducible, obstructed and
linea alba. The hernia is usually easier to feel than
strangulated, especially if the neck is narrow; and
to see, and is diagnosed by palpation of a small,
(iii) patients request repair because of discomfort
often very tender, lump in the linea alba. Ultrasound
and unsightly appearance. Preoperative weight
may be helpful when a hernia is suspected but
reduction in obese patients aims to facilitate the
cannot be palpated. Epigastric hernias are usually
repair and to reduce postoperative respiratory
irreducible and may be multiple.
problems and likelihood of recurrence. Diabetes
and smoking contribute to higher rates of surgical
Treatment
failure, so patients need good preoperative diabetic
control and should stop smoking. Surgery is undertaken to relieve symptoms. The
Operation involves defining the sac and neck, hernia is marked preoperatively because it may be
returning the contents to the abdominal cavity, and difficult to palpate when the patient is anaesthe-
repairing the hole in the abdominal wall. If the tised. If there are multiple hernias, the linea alba is
edges of the defect can be apposed without tension, exposed through a vertical incision, the extraperito-
the defect is closed directly with strong non‐absorb- neal fat is excised and each defect is repaired. Small
able sutures; if not, the defect is reinforced with defects can be suture repaired by simple closure,
prosthetic mesh. ‘keel’ repair or ‘Mayo’ repair. A ‘keel’ repair is per-
Mesh hernia repairs can be performed open or formed by inserting two or more layers of sutures
laparoscopically. Laparoscopic repairs are used for into the linea alba and anterior rectus sheath, each
small (<5 cm diameter) defects and the mesh is successive layer covering the previous layer so that
placed intraperitoneally. For larger (>5 cm) defects the repaired tissue resembles the keel of a boat
an open mesh repair is favoured. The mesh can (Figure 43.8). A ‘Mayo’ repair (Figure 43.9) is
be placed over the abdominal closure in the where the upper and lower edges of the defect are
43: Hernias 391
Non-absorbable
(a) sutures (b)
Upper edge of defect
Lower edge of defect
Fig. 43.9 Mayo repair. (a) Insertion of two sutures through upper and lower edges of hernial defect. (b) Sagittal section
of linea alba after repair.
overlapped with interrupted sutures (‘pants over hernia is still present at school age. A short trans-
vest’ repair). Large defects are repaired with mesh. verse subumbilical incision is made, the sac is excised,
and the defect is closed by either edge‐to‐edge
apposition or a Mayo repair (see Figure 43.9). The
Umbilical hernia in children umbilical cicatrix is preserved. Recurrence is rare.
An umbilical hernia in a child is a congenital defect

in which a peritoneal sac protrudes through a pat- Para‐umbilical hernia in adults
ent umbilical ring and is covered by normal skin.
Approximately 5–10% of Caucasian infants have A para‐umbilical hernia in an adult is an acquired
an umbilical hernia at birth. About one‐third of condition and quite distinct from the umbilical her-
hernias close within a month of birth, and they nia of childhood. A para‐umbilical hernia protrudes
rarely persist beyond the age of 3–4 years. The hernia through one side of the umbilical ring, while the
is noticeable whenever the child cries, coughs or umbilicus still retains its fibrous character within
vomits, and is a cause of concern for parents. the linea alba, although it becomes effaced by the
Umbilical hernias in children rarely become irre- pressure of the hernial contents and has an eccen-
ducible or strangulate. tric ‘half‐moon’ or crescentic furrow. Para‐umbili-
Umbilical hernia is a separate entity from exom- cal hernias initially contain extraperitoneal fat but,
phalos (omphalocele). Exomphalos is a rare con- as the hernial orifice enlarges, omentum enters the
genital condition in which the midgut fails to return sac. The contents typically adhere to the sac so that
to the abdominal cavity during the first trimester, the hernia becomes loculated and irreducible. Para‐
with subsequent failure of the abdominal wall to umbilical hernias occasionally become very large
close at the umbilicus. At birth, the intestine pro- and contain transverse colon and small intestine.
trudes into the base of the umbilical cord and is
covered by a thin opaque sac of amnion, not nor- Treatment
mal skin.
Para‐umbilical hernias are treated surgically
because of the risk of obstruction, strangulation
Treatment
and, rarely, excoriation and ulceration of the skin
An expectant approach can be adopted as nearly all overlying the hernia. The classic operative proce-
hernias close or greatly reduce in size. Repair is dure is a Mayo repair (see Figure 43.9), but repairs
recommended for unusually large hernias or if the with mesh are performed increasingly.
392 Hernias
Hernias related to intestinal stomas Spigelian hernia
A hernia may occur through the abdominal wall at Spigelian hernias are rare. A Spigelian hernia occurs
the site of an intestinal stoma (see Chapter 25). The through a defect lateral to the rectus muscle through
surgically created defect through which the stoma the semilunar line. The semilunar line marks the
is fashioned enlarges due to raised IAP and allows outer border of the rectus muscle. A Spigelian hernia
protrusion of the peritoneum (the hernial sac) protrudes through a defect lateral to the rectus mus-
through the defect to lie adjacent to the stoma cle, through the Spigelian fascia. The hernia is lim-
(Figure 43.10). ited laterally by the internal oblique muscle fibres
Parastomal hernias eventually occur in about and medially by the insertion of the external oblique
10–30% of patients with colostomies and ileosto- aponeurosis to form the anterior rectus sheath.
mies. Correct surgical technique when fashioning Clinically, the diagnosis of a Spigelian hernia may
intestinal stomas is of paramount importance in be difficult. The patient, who typically is a middle‐
prevention. For example, stomas should be brought aged female, presents with diffuse aching pain in
out through the aponeurotic part of the abdominal the area of the hernia, which is small and may not
wall, not the muscular part, and they should not be palpable. Pain is often present during the day but
be sited in the main abdominal wound or the may recede at night if the hernia reduces and may
umbilicus. be made worse by raising the arm on the affected
side. If a lump is not palpable, the diagnosis may
Treatment be confirmed by ultrasound or CT scanning. The
hernia usually contains omentum but may contain
Surgery is required if the bulge of the hernia causes
small or large bowel. A Richter’s hernia may
poor fitting of the stoma appliance and consequent
occur, and obstruction and strangulation are well‐
leakage from beneath the appliance. Also, intestinal
recognised complications.
obstruction and strangulation may occur. Operation
involves reducing the size of the stomal orifice by
Treatment
closing the abdominal wall tissues around the
stoma, but this method has a high recurrence rate. Spigelian hernias should be treated surgically
Insertion of prosthetic mesh in an extraperitoneal because of the severity of symptoms and the risk of
or extraparietal plane to cover the defect in the complications. An open or laparoscopic technique
abdominal wall generally provides a good repair can be used.
but runs the risk of infection of the mesh. Relocation
of the stoma and complete closure of the previous
stoma site provides the best chance of cure. Lumbar hernias
Lumbar hernias are rare. They occur typically in

Hernial sac individuals with poor muscle tone, either spontane-
ously or following trauma, surgery, or paralysis of
Hernial contents paravertebral muscles secondary to poliomyelitis.
Differential diagnosis includes a lipoma, lumbar
Stoma
abscess or haematoma.
Lumbar hernias occur through two triangular
sites of weakness in the lumbar region of the
abdominal wall.
• Inferior lumbar triangle hernia (triangle of Petit):
herniation occurs between the iliac crest inferiorly,
the posterior edge of external oblique muscle ante-
riorly, and the anterior edge of latissimus dorsi
posteriorly. The ‘floor’ of the triangle through
which the hernia protrudes is formed by the inter-
nal oblique and transversus abdominis muscles.
• Superior lumbar triangle (triangle of Grynfeltt–
Lesshaft): the hernia occurs between the lower-
most edge of serratus posterior inferior muscle and
the 12th rib superiorly, the anterior border of inter-
Fig. 43.10 Parastomal hernia. nal oblique muscle anteriorly, and the lateral edge
43: Hernias 393
of erector spinae muscle medially. Grynfeltt’s trian- laparotomy for intestinal obstruction. The sac is
gle lies superior to Petit’s triangle, and the ‘floor’ is excised but attempts to close the defect run the risk
formed by the quadratus lumborum muscle. The of sciatic nerve damage.
hernia is covered by the latissimus dorsi.
Treatment Further reading

Treatment of lumbar hernias is difficult because of Cheek CM, Black NA, Devlin HB, Kingsnorth AN, Taylor
their anatomical boundaries, their size, the type of RS, Watkin DFL. Groin hernia surgery: a systematic
patient in whom they occur, and because they are review. Ann R Coll Surg Engl 1998;80:S1–S80.
bounded in part by muscle rather than tough Fitzgibbons RJ, Greenburg AO (eds) Nhyus and Condon’s
aponeurotic tissue. Prosthetic mesh repair is required. Hernia. Philadelphia: Lippincott, Williams & Wilkins, 2001.
Obturator hernia MCQs
An obturator hernia is rare. It protrudes through the Select the single correct answer to each question. The
obturator canal or foramen, which is a normal ana- correct answers can be found in the Answers section
tomical structure between the obturator groove on at the end of the book.
the inferior aspect of the superior pubic ramus and 1 The commonest type of hernia is:
superior border of the obturator membrane. The a inguinal
obturator canal carries the obturator nerve and ves- b femoral
sels. When large, the hernial sac passes between the c epigastric
pectineus and adductor longus muscles and pro- d incisional
trudes forwards to produce a diffuse bulge in the e umbilical
femoral triangle, where it can be mistaken for a
femoral hernia. It is more common on the right side. 2 The most serious and urgent complication of a
The hernia occurs most often in elderly females, hernia is:
particularly in those who have become debilitated a pressure on the spermatic cord
and lost weight rapidly. Usually, the patient pre- b irreducibility
sents with intestinal obstruction of unknown cause. c obstruction
An abdominal and pelvic CT scan may make the d strangulation
diagnosis preoperatively. Otherwise, the hernia is e neuralgia
diagnosed at operation. Patients may complain of
diffuse pain in the groin together with pain in the 3 Indirect inguinal hernias:
medial side of the thigh and knee because of pres- a can hardly ever be distinguished from direct
sure on the obturator nerve. The hernia may be felt inguinal hernias by clinical examination
in the femoral triangle and also on vaginal exami- b rarely occur in children
nation. A Richter’s hernia may occur with strangu- c can be treated by herniotomy, herniorraphy and
lation of the entrapped part of the intestinal wall. hernioplasty
d should not be treated laparoscopically
Treatment e arise beneath the inguinal ligament
Laparotomy or laparoscopy is performed and the
entrapped segment of bowel is released. The hernial 4 Femoral hernias:
defect is often found to be small. Care is taken not a may occasionally appear above the inguinal
to damage the obturator nerve when either closing ligament in young children
the defect or covering it with prosthetic mesh. b should always be repaired surgically
c can be treated with a surgical truss
d are caused by a defect in the cribriform fascia
Sciatic hernias e may compress the femoral artery
Sciatic hernias are very rare and occur when a peri- 5 A strangulated hernia:
toneal sac enters the greater (gluteal hernia) or a is easily reducible
lesser sciatic foramina. Pain caused by pressure on b can be observed and treated electively
the sciatic nerve or a palpable swelling and tender- c requires urgent surgery
ness in the buttock suggests the diagnosis. Most d is more comfortable with a truss
commonly, sciatic hernias are discovered at e has a strong cough impulse
Section 9
Skin and Soft Tissues
44 Tumours and cysts of the skin
Rodney T. Judson
Milia are tiny multiple epidermal cysts that occur

Introduction on the face, particularly around the eyes, and can be
shelled out for cosmesis.
The skin has many functions, including the provision
of a physical barrier between the body and the envi-
Dermoid cysts
ronment, and temperature regulation. The skin
structure, of epithelium and appendages with the Dermoid cysts are congenital inclusion cysts that
underlying dermis, forms a complex and interactive occur at points of fusion, particularly in the face.
grouping of tissues and cells to serve these functions. Their structure differs from epidermal cysts in that
It is not surprising that genetically determined pro- they show multiple skin appendages rather than
cesses and external factors can interact to produce epidermis alone. They can be treated by excision
lesions that by their superficial placement are both but are less readily enucleated than epidermal cysts.
obvious and deserving of attention. The common Post‐traumatic dermoid cysts result from implan-
lesions of the skin possibly requiring surgical therapy tation of epidermis and appendages under the skin
will be dealt with under the headings of cysts, benign surface by penetrating injury and occur most com-
tumours, malignant lesions and malignant tumours. monly in the hands and fingers. Such cysts are often
densely adherent to the underlying dermis but are
readily excised.
Cysts of the skin
These are common lesions whose only importance Benign epidermal tumours
is their cosmetic effect and their propensity to
become infected. These are extremely common and arise from the
epidermis itself, or more rarely from the skin
Epidermal or epidermoid cysts appendages.
Epidermal or epidermoid cysts are the most com-
Seborrhoeic keratosis
mon cysts, and are frequently misnamed sebaceous
cysts in the mistaken belief that they arise from Seborrhoeic keratoses are the most common of
sebaceous glands. True sebaceous cysts do occur but these lesions and occur on the trunk or limbs of the
are rare. Epidermal cysts are inclusion cysts lined by middle‐aged or elderly. They develop initially as flat
fully differentiated epidermis. They are filled by plaques with a waxy surface that progressively
laminated keratin, which forms the characteristic, thickens, often with pigmentation due to haemosid-
white, unpleasant‐smelling content. Clinically they erin deposition. Exuberant keratin and parakeratin
are characterised by the presence of a small punc- production results from simple proliferation of
tum or sinus on their surface They occur most com- keratinocytes for unknown cause, without any der-
monly on the face, the scalp, the back and the mal involvement, so that the lesions are said to have
scrotum and may be shelled out under local anaes- a ‘painted on’ appearance. Because of their protrud-
thesia if uninfected or enucleated through small ing nature the lesions are prone to trauma and
incisions to provide optimal cosmetic results. Infected subsequent low‐grade infection. Keratoses can be
cysts should be treated by incision and drainage, removed or shaved under local anaesthesia if
with later excision to avoid recurrence. unsightly or irritated.
397
398 Skin and Soft Tissues
Actinic keratosis that the true progenitor is a potential epithelial cell

in pylosebaceous tissue. Exposure to UVB is
Actinic keratosis represents a progressive dysplas-
believed to be the precipitating factor, and there is
tic change in the epidermis and the underlying
no clear genetic basis for the disease apart from
dermis as the result of exposure to ultraviolet
race, except in some rare conditions such as the
(UV) light. There is a build‐up of keratin and par-
naevoid BCC syndrome, where BCC occurs in
akeratin, with thickened elastic fibres (elastosis)
childhood, often in non‐sun‐exposed areas and
in the dermis due to damaged fibroblasts. The
with associated odontogenic cysts of the mandi-
lesions occur most commonly on sun‐exposed
ble, medulloblastoma and tumours of the repro-
areas, such as the ears in the male, the nose, the
ductive organs.
backs of the hands and f orearms. They appear as
rough crusty areas of thickening that may bleed
when traumatised. Actinic keratoses are unques-
tionably premalignant, in contradistinction to Basal cell carcinoma presents in a wide variety of
seborrhoeic keratosis. They can be managed by forms, but the most common is as a waxy translu-
the application of cytotoxic creams or by surgical cent nodule with a thin overlying epithelium and a
excision if there is any suspicion that malignant fine network of vessels traversing the margins,
change has already occurred. probably the result of tumour‐induced angiogene-
sis. Central regression may lead to depressions in
Keratoacanthoma the centre of the lesion, which may progress to
ulceration to show the classical ‘rodent ulcer’
Keratoacanthoma is a benign lesion that presents on appearance. The tumours may be multifocal and as
the cheek, nose, ear or back of the hand in the elderly they grow tend to become infiltrative and may
as a rapidly growing nodule which develops a charac- involve deeper tissues. They may thus become
teristic central keratin plug. The lesions usually locally aggressive but only rarely metastasise.
develop to several centimetres in diameter over the
course of a few weeks and then regress spontaneously
and rapidly. They can thus be treated expectantly. Treatment
Keratoacanthomas may occur in patients receiv- Optimal treatment for nodular BCC depends
ing immunosuppression, such as transplant recipi- on size. Lesions less than 1 cm in diameter are
ents, and in these circumstances should be treated rarely deeply invasive and can be treated by elec-
as squamous carcinoma because they may behave tro‐desiccation with curettage, by cryosurgery or
aggressively. by excision with a narrow margin in terms of
depth and width. Radiotherapy is an alternative
form of therapy but not in areas close to cartilage.
Malignant epithelial tumours Lesions greater than 1 cm in size are best treated
by excision with perioperative confirmation of
The most common tumours arise from the cells of clear margins of excision, which should not be less
the epidermis in the form of basal and squamous than 1 mm.
carcinomas and melanoma, which will be consid- If treatment has been adequate, recurrence is rare,
ered with pigmented lesions. except in the case of sclerosing BCC, which may
require multiple procedures to achieve control.
Basal cell carcinoma
Basal cell carcinoma (BCC) is the most common
Squamous cell carcinoma
form of skin cancer and occurs almost exclusively
on sun‐exposed areas of the skin in the adult white Squamous cell carcinoma (SCC) is the second most
population over the age of 40 years. They are rare common tumour of the skin. The major aetiological
in the oriental population and almost never occur factor is again exposure to UV light. Although such
in black‐skinned races. lesions are most commonly seen in the elderly, they
Between 75 and 80% of the lesions occur in the are now becoming increasingly frequent in young
head and neck, usually above a line running from adults because of excessive sun exposure in child-
the corner of the mouth to the ear, with the remain- hood. As expected from its aetiology, the lesions are
der being situated on the limbs and a minority on most common in white populations and are seen
the trunk. Although the cell of origin was presumed most frequently on the face and ears, lip, the back
to be the basal cell in the epidermis, it is probable of hands and forearms.
44: Tumours and cysts of the skin 399
Clinical presentation dissection is only indicated when there are enlarged

glands that prove on biopsy to demonstrate
Clinical presentation is initially as an area of crust-
involvement with tumour. Prognosis is good, with
ing that is clinically indistinguishable from solar
at least 95% disease‐free survival at 5 years. Local
keratosis but which on excision shows the cellular
recurrence is rare following pathologically con-
atypia that provides the diagnosis of carcinoma
firmed complete surgical excision.
in situ before the breaching of the basement
membrane at the dermoepidermal junction to

form frank invasive carcinoma. If the lesions are
untreated at this stage, they will progress to form a Pigmented lesions
nodule or plaque that is irregular in shape and may
ulcerate with a pink rolled edge. Unlike BCC, SCC Pigmented tumours of the skin are common. Their
can metastasise, usually to the regional lymph major importance is the propensity of some lesions
nodes but also systemically, although this is unusual to progress to the formation of melanoma, or the
unless the lesions are large or neglected. It should initial clinical differentiation from primary mela-
be noted that immunosuppression is associated noma. A number of lesions that may become
with a much higher incidence of SCC, as for exam- pigmented, such as seborrhoeic keratoses or BCC,
ple in renal transplant recipients in whom the nor- have been dealt with previously.
mal 4 : 1 ratio of BCC to SCC is reversed; BCCs are
also more common in such patients than in the Naevus
normal age‐ and sex‐matched population.
The term naevus should refer by definition to any
congenital lesion of the skin, but by convention is
Treatment used to describe any congenital or acquired neo-
plasm of melanocytes.
Treatment of SCC is primarily surgical with exci-
sion to a margin of at least 0.5 cm in depth and
peripherally, as determined on clinical grounds, Acquired naevus
although this margin may be reduced in the head
Acquired or naevocellular naevi are common. An
and neck to avoid unnecessary cosmetic problems.
Australian survey demonstrated 15 such lesions per
If lesser margins are used, frozen section should be
person in an adult white Caucasian population.
utilised to ensure that complete excision of the
They are most common on sun‐exposed areas of the
lesion has occurred. Tumour thickness is closely
body. They are formed by melanocytes that have
related to outcome. Local recurrence is unusual
been transferred from their usual dendritic single‐
with lesions less than 4 mm in thickness and metas-
cell position among the basal layers of keratinocytes
tasis is more common in lesions which are greater
to form aggregates along the dermoepithelial junc-
than 10 mm in thickness (Table 44.1). Adjuvant
tion. This aggregation of cells forms a junctional
radiotherapy is only used when the margins of
naevus. The cells of such naevi show little individual
excision are compromised by vital structures.
change, and mitotic figures are not numerous.
Radiotherapy as a primary treatment is almost as
The clinical appearance of each form of naevus is
effective as surgery but should be reserved for
thus important, although it must be understood that
those patients not fit for surgery. As nodal involve-
clinical interpretation of any pigmented skin lesion
ment with cutaneous SCC is unusual, prophylactic
is not always accurate and any lesion where there is
lymph node dissection is not used and therapeutic
uncertainty about its nature must be subjected to
excisional biopsy. The junctional naevus is impalpable,
pale to dark brown in colour and is usually small,
Table 44.1 Excision margins related to tumour
rarely being more than 1 cm in diameter. They may
thickness. appear in childhood but usually become obvious
around puberty, growing slowly until the cessation
Thickness of Stage Excision of skeletal growth in late adolescence. In contrast,
melanoma (TNM) margin compound naevi are palpable, because of the size of
the collection of melanocytes in the papillary
In situ pTis 5 mm
dermis. These naevi are usually darker in colour
<1.5 mm pT1, pT2 1 cm
1.5–4 mm pT3 1–2 cm than junctional naevi. The transitional phase
>4 mm pT4 2–3 cm between junctional and compound naevus means
that some lesions show the characteristics of both.
Dysplastic naevus (atypical moles) with the highest incidence being in white popula-
tions living close to the equator who are exposed to
Dysplastic naevi (BK moles) occur as large (>5 mm
UV light during both work and recreation. There
in diameter) flat macules or slightly raised plaques
has been a rapidly increasing incidence in such pop-
that are present in large numbers all over the body
ulations, even in susceptible populations in north-
surface but with a particular concentration on the
ern Europe with a much lower regular exposure to
trunk. These naevi, in contrast to those already
sunlight. It is probable that this is a real increase in
described, are frequent in non‐sun‐exposed areas.
incidence rather than a process of earlier detection,
They commonly have an irregular contour and var-
although public education programs now lead to
iable colour, particularly being darker in the centre
much earlier presentation of the disease. The role of
than on the periphery. Histologically, there is
UV light is well established, with melanoma being
replacement of the normal basal cell layer of the
most common on sun‐exposed skin such as that of
epidermis by naevus cells at the dermoepithelial
the upper back in males and females and also on
junction with elongation of rete ridges. In the
the lower leg in females.
majority of cases there is a strong family history of
Melanoma can be classified into four types: len-
such naevi and sometimes an additional family his-
tigo maligna, superficial spreading, nodular, and
tory of melanoma. Where there is an established
acral lentiginous. As noted previously, a melanoma
family history of melanoma in association with
gene has been mapped to chromosome 1p36, and a
dysplastic naevi, the trait is inherited in an autoso-
second, designated CMM2, to chromosome 9p21,
mal dominant fashion. Dysplastic naevi may be a
with the cell cycle regulator CDKN2A as the candi-
pleiotropic manifestation of the 1p36 familial mel-
date gene. Mutations in this gene are the most com-
anoma gene, designated CMM1.
mon cause of inherited melanoma. The risk of
The management of such patients requires exci-
melanoma in CDKN2A mutation carriers is
sional biopsy of a typical lesion to establish the
approximately 14% by age 50, 24% by age 70 and
diagnosis, with genetic studies where appropriate
28% by age 80 years.
and regular review with photographs and measure-
ment of lesions for comparison, allowing excision
of suspicious lesions at an early stage. Where there
Lentigo maligna
is no family history of melanoma, there is a much
lesser chance of development of melanoma, and Lentigo maligna occurs in elderly patients, usually
review can be less intense. more than 70 years of age, and is more common in
men than in women. It appears as an extensive mel-
Juvenile naevus anotic lesion (Hutchinson’s melanotic freckle) on
the cheek or temple. It is characteristically dark
Juvenile naevus (Spitz naevus) is most common in
brown in colour and develops over many years as a
children and adolescents but may also occur in adults.
superficial impalpable lesion unless malignant
It presents as a pink nodule that rapidly increases in
change occurs. Malignant change is manifested by
size and on excision shows frequent mitoses and cel-
the development of palpable darker nodules with
lular pleomorphism which may raise questions of
an irregular edge, and this change is often multicen-
malignancy. Melanoma is comparatively rare in chil-
tric. Hutchinson’s freckle itself requires no specific
dren and it is probable that some cases reported in
treatment apart from regular observation, but
the past have actually been Spitz naevi, which appear
lesions demonstrating suspicious changes should be
to have no malignant potential. However, this is not
removed by excisional biopsy. If malignant on
to say that melanoma does not occur in children.
biopsy, the entire lesion should be widely excised.
Indeed, when it does occur it may be aggressive in its
Prognosis is good, with at least 95% disease‐free
behaviour and have a poor prognosis.
survival at 10 years. There is a tendency for lateral
and superficial spread of tumours long before verti-
cal invasion occurs.
Melanoma
Aetiology and pathology
Superficial spreading melanoma
Melanomas are composed of malignant cells aris-
ing from melanocytes in the skin but can also arise Superficial spreading melanoma is the most com-
in oral and anogenital mucosa, and in the eye. mon form of melanoma and can occur in any site
Cutaneous melanomas, like naevocellular naevi, are and at any age, although it is most common in mid-
a disorder of white‐skinned Caucasian populations, dle age and commonly arises from a pre‐existing
44: Tumours and cysts of the skin 401
naevus as already discussed. Characteristically, it is Nodular melanoma

slightly raised above the skin surface, is variegated
Nodular melanoma presents as its name suggests with
in colour (often with a dark brown or even black
a protruding lesion usually arising from a pre‐existing
component) and has an irregular edge. Over a
naevus, the nodular form being one component of ver-
variable period, the lesion remains within the epi-
tical invasion. The nodule may be dark or may be
dermis and then involves the reticular dermis. It is
amelanotic. As it is really a particular form of invasive
rare for metastasis to occur at this phase of radial
melanoma, it is treated on its merits in terms of thick-
growth. If untreated, an invasive vertical growth
ness by wide local excision with consideration of ther-
phase supervenes, with progressive involvement of
apeutic lymph node dissection and adjuvant therapy.
the deeper dermis and underlying tissues and the
development of metastatic potential. It is now
possible to use a variety of melanoma antigens to Acral lentiginous melanoma
discriminate between benign melanotic lesions, Acral lentiginous melanoma occurs in all races in
in situ melanoma, the radial and vertical growth non‐pigmented areas, such as the palms of the
phases of invasive melanoma, and finally meta- hands, the soles of the feet, the subungual area and
static melanoma. These tests give clear indica- on mucosal surfaces. They are often pink in colour
tions of differences in cell behaviour at these with little in the way of pigmentation, and there is
various phases. often delay in diagnosis because of this non‐spe-
The treatment for superficial spreading mela- cific appearance. Treatment is as for superficial
noma is excisional biopsy with a margin that varies spreading melanoma, depending on the thickness
with the size of the primary lesion and subsequent of the lesion. Late presentation often means that
assessment of depth of invasion. This is determined there is a significant invasive element and wide
by the use of Clark’s levels of invasion, which define excision with or without adjuvant therapy may be
six levels in terms of the anatomy of the epidermis necessary.
and dermis, or by the thickness of the lesion, as
described by Breslow. Although Clark’s levels have
Adjuvant therapy
some correlation with prognosis, it is clear that sim-
ple measurement of the thickness of the lesion gives Chemotherapy
an even better correlation. For those with a thick- The benefits of combining surgery with adjuvant
ness of less than 0.75 mm, 95% 10‐year survival chemotherapy are now clear in relation to some
can be expected. This contrasts with only 25% sur- cancers. This is undertaken in the belief that metas-
vival at 10 years if the thickness is greater than tasis will often have occurred before patients pre-
4 mm. There has been much controversy about the sent for primary surgery, although this may not be
margins of excision in the past. It had been felt that clinically apparent, and that systemic therapy is
radical excision with at least a 5‐cm margin was most likely to be effective in such patients when the
necessary for all melanomas, but it is clear that with bulk of tumour has been removed by surgery and
superficial spreading melanoma a limited margin is the residual tumour burden is low.
quite adequate.
There is also controversy about the role of elec- Limb perfusion
tive lymph node dissection (ELND). On present evi- For melanoma of poor prognosis confined to a
dence, as nodal metastasis is rare in lesions less than limb, an additional form of treatment aimed at con-
1 mm thick, ELND should not be performed in trolling presumed in‐transit metastasis is perfusion
such cases. As patients with invasive lesions more of the isolated limb at high temperatures through
than 4 mm thick are unlikely to survive in any an oxygenated circuit that contains phenylalanine
event, the operation is superfluous. mustard, which is selectively taken up by melanoma
Of particular interest has been the development cells (at least in theory). The role of isolated limb
of lymphatic mapping following intradermal perfusion as an adjuvant to surgical treatment in
injection of radiolabelled colloids around the
primary treatment remains unclear and is generally
primary site, with removal of ‘sentinel nodes’ and not recommended especially in the light of recent
histological and histochemical examination with advances in immunotherapy.
subsequent full node dissection if positive. This
procedure was examined in a large multicentre Radiation therapy
international trial and found not to provide Radiation therapy has no role as an adjuvant to
any survival advantage and thus is not routinely surgery for localised disease that is treatable by
recommended. wide excision, but is of value in the treatment of
recurrent or inoperable disease with effective local present for 12 months and it bothers him now
control, particularly of nodal metastases. when he presses on that finger. He seems to
remember injuring that finger at work several years
Systemic therapy
earlier. On examination there is a 0.5‐cm nodule
Immunotherapy with anti‐CTLA4 (cytotoxic
and the overlying skin is intact. What is the most
T‐lymphocyte‐associated protein 4) has become a
likely diagnosis?
standard treatment for metastatic melanoma and
a dermoid cyst
BRAF (serine/threonine protein kinase B‐raf) inhib-
b epidermoid cyst
itors have demonstrated a rapid but sometimes
c pyogenic granuloma
short‐lived effect in patients with oncogene‐addicted
d dermatofibroma
BRAF‐mutant metastatic melanoma. The most
e cylindroma
appropriate sequencing of therapeutic agents
remains under investigation as does the role of
3 The parents of a 4‐week‐old boy are con-
these agents as neoadjuvant therapy for high‐risk
cerned about a lump above the infant’s right eye.
locally advanced melanoma.
It has been present since birth and has not
changed in size. The skin over the 1‐cm lump is
intact and the lump appears to be attached to the
Further reading underlying tissues. What is the most likely
diagnosis?
Jakub JW, Racz JM, Hieken TJ et al. Neoadjuvant sys-
temic therapy for regionally advanced melanoma. a dermoid cyst
J Surg Oncol 2018;117:1164–9. b epidermoid cyst
Menzies AM, Long GV. Systemic treatment for BRAF‐ c cystic hygroma
mutant melanoma: where do we go next? Lancet Oncol d branchial cyst
2014;15:e371–e381. e osteoma
Singh B, Shah JP. Skin cancers of the head and neck. In:
Shah JP, Patel SG (eds) Cancer of the Head and Neck. 4 A 75‐year‐old man has what appears to be a 1‐cm
Hamilton, Ontario: BC Decker, 2001, chapter 4. basal cell carcinoma on the side of his nose
immediately below his left eye. What would be the
most appropriate treatment?
MCQs a radiotherapy
b application of 5‐fluorouracil cream
c injection of vinblastine
d excision and split‐skin graft
e excision and full‐thickness graft
1 A 70‐year‐old man presents with a 1‐cm painless
nodule on the side of his nose. This has been 5 A 17‐year‐old girl presents with a painless
present for 3 weeks. The centre of the lesion swelling on the anterior aspect of her right leg.
appears to contain a plug of hard skin. What is the This has been present for about 6 months and
most likely diagnosis? does not bother her much, except that it itches
a squamous cell carcinoma occasionally. The lump is pink and firm, and the
b basal cell carcinoma overlying skin is intact. What is the most likely
c keratoacanthoma diagnosis?
d Merkel cell carcinoma a basal cell carcinoma
e seborrhoiec keratosis b epidermoid cyst
c Bowen’s disease
2 A 45‐year‐old motor mechanic presents with a d dermatofibroma
nodule on the tip of his finger. This has been e malignant melanoma
45 Soft tissue tumours
Peter F. Choong
University of Melbourne, St. Vincent’s Hospital and Peter MacCallum Cancer Centre, Melbourne,
Victoria, Australia
Introduction Benign soft tissue tumours
Primary soft tissue tumours include benign and Lipoma

malignant tumours. Malignancies of skin such as
The commonest benign tumour is the lipoma
basal cell carcinomas, squamous cell carcinomas
(Figure 45.1). Originating from the mesenchyme, fatty
and melanomas are dealt with in Chapter 44. The
tissue is one of the ubiquitous supportive tissues in the
most common soft tissue tumours are benign.
body that separate anatomical parts. In this regard,
Sometimes differentiating these from malignant
lipomas may arise from almost any part of the body.
tumours (sarcoma) can be very difficult because
Typically, lipomas have a long history (years) and may
sarcomas are rare and experience in both identifica-
be characterised by slow growth. Occasionally, there
tion and treating this entity may be lacking.
may be a history of fast growth (months). Often this is
The approach to managing soft tissue tumours is
less a case of exponential growth but more of a large
focused on differentiating benign from malignant
lipoma emerging (herniating) from between muscle
forms. To this end, a good history and examination
fibres, septae or anatomical compartments.
coupled with appropriate investigations and biopsy
Lipomas are slow‐growing, thus allowing the
are essential to avoid the complications of inad-
adjacent fascial tissue to expand and adapt around
vertent excision of sarcoma. Important characteris-
it. Rather than being fixed and constraining, the
tics on history include the temporal nature of
membranous capsule around a lipoma adapts and
tumour occurrence and the presence of symptoms
is the reason why lipomas are often soft and pliable.
(pain and compression). The tumour’s physical
Lipomas are often solitary but may be multiple.
characteristics should be described in terms of size,
Dercum’s disease is a syndrome of multiple painful
site, shape, consistency, border, underlying struc-
lipomata.
tures, and overlying structures. Cystic structures
Atypical lipomas are a variant of lipomas where
may be transilluminated and vascular sturctures
there is a mild cellular atypia. These are thought to
may be pulsatile.
have malignant potential leading to the formation
Investigations include ultrasound, anatomic and
of well‐differentiated lipoma-like liposarcoma.
functional imaging. Anatomic imaging includes
CT often shows a well‐encapsulated lesion with a
computed tomography (CT) and magnetic reso-
predominance of fatty attenuation. What should
nance imaging (MRI). The latter is the most accu-
raise suspicion is the presence of obvious fibrous stri-
rate means of characterising the anatomy and nature
ations running through the substance of the tumour.
of soft tissue tumours because it provides unparal-
Histology is the key to making the diagnosis, with the
leled soft tissue contrast. Ultrasound, although very
presence of cells with size differences and some level
easy to obtain, is prone to misdiagnosis and is best
of atypia. Lipoblasts tip the diagnosis towards sar-
reserved solely for determining whether the lesion is
coma. More recent investigations include molecular
solid or cystic. Differentiating the malignant poten-
profiling, which has identified MDM2 gene amplifi-
tial based on ultrasound is fraught.
cation as a hallmark of sarcomatous change.
Most benign tumours may be excised alone and
Lipomas may be excised if large or cosmetically
rarely require adjuvant therapy. Sarcomas, in con-
unacceptable. Sometimes, lipomas may recur and
trast, require expert centre‐based multidisciplinary
intramuscular varieties have a greater likelihood
care.
for this.
403
(a) (b)
Lipoma
Normal Fat
Fig. 45.1 (a) Lipoma of the flank: MRI showing typically encapsulated lesion (arrows) with signal attenuation identical
to surrounding normal fat. (b) Surgical specimen is encapsulated, greasy and yellow in colour.
Nerve sheath tumour Haemangiomas comprise tortuous channels of

blood vessels often embedded in lipomatous tissue.
Nerve sheath tumours comprise schwannomas and
They may be predominantly arterial or, more com-
neurofibromas. Schwannomas are peripheral nerve
monly, low‐flow venous types. When deep, hae-
sheath tumours that arise from the myelin‐produc-
mangiomas may be first noticed as a lump that
ing supporting cells (Schwann cells) that surround
increases and decreases in size. Other times, the
the nerves and their fibrils. They usually occur as
lump may be heralded by acute pain and swelling
solitary lesions, lying along the line of skin or motor
caused by thrombosis and pain.
nerves. They may vary in size from small pea‐sized
Haemangiomas of the skin are often referred to
tumours to much larger tumours that can occupy
as birthmarks. They may be very localised and
whole anatomic compartments. These tumours are
small like the strawberry naevus seen on the fore-
associated with hypersensitivity when touched or
heads of young babies that often involute with age,
knocked. Neurofibromas are small benign tumours
or the wide permanent areas often referred to as
that also arise from peripheral nerves. In almost all
port wine stains. When on the face, these may fol-
cases (90%), these are sporadic. However, the
low a dermatomal pattern.
remainder may be associated with an abnormality of
Haemangiomas may be associated with a num-
the neurofibromatosis (NF1) gene.Neurofibromatosis
ber of well‐described syndromes, including Sturge–
is an autosomal dominant inherited abnormality
Weber syndrome, Klippel–Trenaunay syndrome,
characterised by a constellation of cutaneous, vis-
Bean syndrome and Proteus syndrome.
ceral and musculoskeletal abnormalities as well as
Deep‐seated haemangiomas which cause a mass
pain syndromes and occasionally cognitive deficits.
can be excised if well circumscribed. If the haeman-
The key investigation here is MRI, which classi-
gioma is more extensive without clear boundaries,
cally demonstrates a round encapsulated lesion
repeated embolisation may help to reduce its size.
with a ‘rat’s tail’ appearance of the nerve entering
Surgery for this variety is more challenging.
and leaving the mass (Figure 45.2).
Nerve sheath tumours can usually be left alone
Angiomyoma
unless they are symptomatic (exquisitely tender). If
they arise from important sensory or motor nerves, Angiomyomas are small painful tumours often
careful intraneural dissection may be required to found near joints. They are mostly in a subcutane-
preserve the continuity of the affected nerve. ous position and the knee and ankle are common
sites. They arise from the tunica media of blood
vessels and present as discrete firm nodules or
Haemangioma
lumps. They are exquisitely tender when touched
Haemangiomas are a variety of vascular malforma- and can mimic neuromas. They are often well cir-
tion and are common (Figure 45.3). They may cumscribed. Angiomyomas are easily excised and
occur in any tissue and may be superficial or deep. rarely recur.
(a) (b)
Rat’s tail
Target sign
Fig. 45.2 (a) MRI of schwannoma (S) of the upper arm demonstrating ovoid lesion in the line of the radial nerve
(arrows) which give the characteristic ‘rat’s tail’ appearance. (b) Axial MRI showing characteristic concentric light–
dark–light rings within schwannoma giving rise to the ‘target’ sign.
(a) (c)
(b)
H
Fig. 45.3 (a) MRI showing haemangioma (H) in proximal vastus lateralis (arrows). Note the large cavernous spaces
within the haemangioma. (b) MRI showing vascular supply to the haemangioma (arrowheads). (c) MRI angiogram
demonstrating vascular tree with tributary (arrows) to haemangioma.
Myxoma because of the poor response, but other agents such

as hormonal/antihormonal drugs and other novel
An intramuscular myxoma is a mucin‐producing
agents have been tried with some success. Predicting
tumour that is found deep within muscle. Although
which tumour is likely to respond is difficult.
it is poorly encapsulated and merges with the sur-
Occasionally, desmoid may behave in an idiosyn-
rounding musculature, its defining characteristic
cratic fashion and disappear after needle biopsy
is its mobility within muscle and it is sometimes
alone. This has led to one option which is to merely
likened to the ‘breast mouse’ (fibroadenoma).

observe desmoid until such time as it becomes a
Generally paucicellular, this entity produces abun-
problem, then a choice of surgery or surgery plus
dant myxoid tissue and can grow to large sizes. This
adjuvants may be exercised.
can sometimes be difficult to differentiate from a
low‐grade myxoid sarcoma.
Excision of a myxoma, once confirmed from Primary malignant soft tissue tumours
biopsy, is not associated with any recurrence, (sarcomas)
despite the surgery often leaving residual tumour
behind because of its embedment within muscle. Soft tissue sarcoma (STS) is of mesenchymal origin
and may arise in any tissue layer of the body.
Desmoid Despite being rare, over 70 subtypes exist, attesting
to the complexity of diagnosis and confusion that
Desmoid tumours arise from the fibroblast lineage
may sometimes arise in identifying the nature of a
and are characterised by a craggy hard mass. The
soft tissue lump. Fewer than 1% of all soft tissue
condition is also known as fibromatosis. They are
tumours and only 0.1% of all cancers are sarcomas,
usually solitary but may be multiple. As they arise
meaning that the lack of familiarity of pathologists
from the mesenchyme, they may occur in any loca-
and clinicians with this entity often leads to incor-
tion. They commonly occur in women between 20
rect or delayed diagnoses and care. Modern sar-
and 40 years of age and are found on the nape and
coma management is best conducted in expert
flank. They may also occur in the limbs.
centres where multidisciplinary care may be pro-
They are often slow‐growing, although their
vided by clinicians with a specialist interest in sar-
growth pattern may be irregular and unpredictable.
coma treatment, and in this setting patients with
A sudden acceleration during or after pregnancy
sarcoma are afforded the best outcomes for local
and their predominance in women suggest a corre-
and systemic control of disease. Surgery is the
lation with hormonal regulation. Although benign,
mainstay of sarcoma management and is often
desmoid tumours may grow in critical localities
combined with radiotherapy in a neoadjuvant or
compromising vital structures such as organs, ves-
adjuvant setting. Chemotherapy is sometimes used
sels and nerves. At worse, desmoid tumours may
in combination with surgery, although this is not
also prove fatal because of impingement on these
regarded as conventional and depends on institu-
vital structures.
tional preferences.
Desmoid tumours may also be syndromic, such
as in Gardner’s syndrome, a variant of familial ade-
Incidence
nomatous polyposis (FAP). FAP is an autosomal
dominant inherited condition characterised by mul- Soft tissue sarcomas arise in 2–4 per 100 000 popu-
tiple colonic polyps with a predisposition to colonic lation and are more common than primary bone
carcinoma. In Gardner’s syndrome, there is also the sarcomas. There is a male predominance (1.4 : 1)
presence of multiple extracolonic abnormalities and the median age of occurrence is approximately
including osteomas, fibromas, thyroid malignan- 60 years. STS have a bimodal presentation with
cies, epidermoid cysts and desmoid tumours. peaks in the fifth and eighth decades. Specific
The treatment of desmoid tumours may be chal- tumour types are associated with each of these
lenging. The presence of peripheral microscopic peaks. For example, synovial sarcoma and myxoid
extensions make recurrence of the tumour highly liposarcoma arise in younger patients whereas
likely if resected with close margins. Adjuvant radi- undifferentiated pleomorphic sarcoma is mainly
otherapy has been shown to reduce the likelihood found in middle‐aged and older adults.
of recurrence if combined with resection, although STSs occur most commonly in the limbs, with
radiotherapy alone may result in size reduction to lower limb tumours being twice as common (28%)
the point where surgery may not be required. as upper limb tumours (12%). The thigh is by far
Conventional chemotherapy is not normally used the most common site for STS. Over 50% of STSs
45: Soft tissue tumours 407
occur deep to the deep fascia and may grow to regimens. The most significant change to the clas-
substantial sizes if they arise in the thigh and pel- sification since the 2000s has been to drop the
vic cavity. The median size of an STS is approxi- entity ‘malignant fibrous histiocytoma’ and its vari-
mately 8 cm. ants, which was previously the most frequent diag-
nosis made. This term was used to describe a
Behaviour grab‐bag of tumours that could not otherwise be
classified into distinct histological types according
Soft tissue sarcomas grow in a centrifugal manner
to the most differentiated cell type observed. Today,
and displace adjacent tissue. More aggressive
an STS that cannot be classified according to histol-
lesions may show an ‘invasive’ character rather
ogy is referred to as undifferentiated pleomorphic
than a ‘pushing’ character. STSs may be mistaken
sarcoma (UPS) and this is often a diagnosis of
for lipomas, which are by far the most common soft
exclusion. Newer modalities of pathological inter-
tissue lumps. While lipomas may grow to enormous
rogation, including molecular, chromosomal and
sizes, they are often soft and pliable which reflects
immunohistochemical techniques, have aided in
their slow rate of growth and adaptation of the sur-
refining the diagnostic process and accuracy.
rounding tissue to their slow growth. STSs, on the
other hand, are often firm or hard, which reflect
their rapid growth within the confines of a tissue Tumour grade
boundary or the tumour’s pseudocapsule. The pseu-
The grade of a tumour relates to its histological
docapsule is a boundary of compressed normal tis-
appearance, which also correlates with its clinical
sue or inflammatory adventitia that forms due to
behaviour. A variety of grading systems exist.
the growth of the tumour and the stimulation of an
Increasing cellular pleomorphism, hyperchroma-
inflammatory response at the periphery of the
tism, spontaneous tumour necrosis, intratumoral
tumour by tumour cytokines. STSs are known to
vascular invasion, mitotic activity and lack of cel-
have satellite lesions within the inflammatory zone
lular differentiation are hallmarks of higher‐grade
at the periphery of the tumour. This is an important
tumours. Higher‐grade tumours are associated with
characteristic of a STS that mandates appropriate
a higher risk of local and systemic recurrence of dis-
surgical margins and adjuvant treatment.
ease. A four‐grade (I–IV) histological system to
STSs recur locally or systemically. The reason for
grade tumours is commonly used. Grades I and II
local recurrence is the existence of residual tumour
may also be referred to as low grade, while grades
after resection or local metastasis in the setting of a
III and IV may be referred to as high grade.
very aggressive tumour. Control of local recurrence
is achieved through adequate surgical margins in
the first instance. Diagnosis
STSs may also metastasise and these occur most
Diagnosis relies on a high index of clinical suspicion,
commonly to the lungs. Pulmonary metastases
and the judicious use of appropriate investigations
account for 50% of all metastases and may be uni-
(anatomical, functional) that culminate in biopsy.
lateral or bilateral. Often pulmonary metastases are
solitary or low in numbers and are amenable to
resection (pulmonary metastasectomy). Metastases History
occur via the haematogenous route but may also
Soft tissue sarcomas undergo a regular and rapid
occur via lymphatic spread in rare cases. Examples
doubling rate. Therefore, patients often report the
of tumours that may metastasise to the lymph
presence of a lump that appeared spontaneously
nodes include synovial sarcoma, alveolar soft part
and which seemed to remain a certain size before
sarcoma and epithelioid cell sarcoma.
rapidly increasing its dimensions over a period of
months. The rapid increase is due to tumour cells
Classification
reaching the exponential phase of growth. The
The World Health Organization Classification of lump is often painless and because of this there is
Tumours of Soft Tissue and Bone is an attempt at often a delay in presentation. It is surprising, how-
developing a common nomenclature to describe ever, the number of patients who present with enor-
this rare tumour (Table 45.1)and is based on the mous tumours. Synovial sarcoma is one that has
most differentiated cell type within the array of contrasting behaviour to other STSs. It is often
malignant cells. Its adoption allows more meaning- detected at a younger age, smaller size and a hall-
ful comparisons of tumour types and treatment mark of presentation is pain.
Table 45.1 Primary soft tissue tumours.
Tissue type Subtype
Adipose Benign Lipoma

Malignant Well‐differentiated lipoma‐like liposarcoma
Myxoid liposarcoma
Round cell liposarcoma
Pleomorphic liposarcoma
Fibrous Benign Desmoid (fibromatosis)
Nodular fasciitis
Malignant Fibrosarcoma
Myxofibrosarcoma
Cartilage Benign Enchondroma
Osteochondroma
Malignant Central chondrosarcoma
Dedifferentiated chondrosarcoma
Clear‐cell chondrosarcoma
Mesenchymal chondrosarcoma
Bone Benign Osteoma
Malignant Conventional osteosarcoma
Parosteal osteosarcoma
Periosteal osteosarcoma
Low‐grade central osteosarcoma
Skeletal muscle Benign Myoma
Malignant Alveolar rhabdomyosarcoma
Embryonal rhabdomyosarcoma
Smooth muscle Benign Leiomyoma
Malignant Leiomyosarcoma
Vascular Benign Haemangioma
Malignant Haemangioendothelioma
Haemangiopericytoma
Angiosarcoma
Nerve sheath Benign Neurofibroma
Schwannoma
Malignant Malignant peripheral nerve sheath tumour
Neuroepithelioma
Malignant granular cell tumour
Synovial Benign Pigmented vilonodular synovitis (giant cell tumour of tendon sheath)
Malignant Synovial sarcoma
Unclassified Malignant Undifferentiated pleomorphic sarcoma
All lumps greater than 5 cm (golf ball size) or suspected of being a sarcoma should be referred to
deep to the deep fascia should be considered a sar- a tumour centre specialising in sarcoma manage-
coma until proven otherwise. ment for definitive investigation and treatment.
Plain radiography
Investigations
Plain radiography is seldom indicated as an initial
All lumps suspected of being a sarcoma must investigation for STS. However, this modality may
undergo appropriate anatomical and functional be useful for differentiating a soft tissue mass from
imaging prior to biopsy. The reason for biopsy fol- a bony protruberance such as an osteochondroma.
lowing imaging is that imaging modalities such as Plain radiography may also detect ossification
MRI may be difficult to interpret in the setting of a within a soft tissue mass and this may be character-
biopsy‐induced imaging artefact (e.g. inflamma- istic of myositis ossificans, heterotopic ossification,
tion, haematoma, altered anatomy). To avoid phleboliths within a haemangioma or a synovial
unnecessary or inadequate imaging, all lumps sarcoma.
Magnetic resonance imaging extremely useful for delineating adjacent neurovas-

MRI provides unsurpassed soft tissue contrast and cular structures and the involvement of specific
is essential for evaluating soft tissue tumours muscular compartments. Such anatomical informa-
(Figure 45.4). MRI scans can be used to accurately tion assists in determining tumour resectability and
characterise the site, size, shape, consistency, and the anticipated quality of surgical margins.
relation of the mass to adjacent structures. Fine
detail provided by MRI may also allow evaluation Computed tomography
of invasion of the tumour into adjacent bone and CT scans are ubiquitous and are easily obtained
soft tissue structures. Peritumoral oedema is an where MRI is either not available or contraindi-
important finding which reflects the possibility of cated such as in patients with pacemakers, vascular
tumour extension. Spontaneous tumour necrosis stents or embedded metal shrapnel. These scans are
may also be suggested by a heterogeneous MRI sig- particularly good for detecting fine calcifications
nal reflecting a high‐grade tumour. and this modality may be useful when evaluating
The most viable tumour tissue is present in the the nature of periosteal reactions, bone destruction
more solid areas and at the periphery of the tumour. or soft tissue calcification (Figure 45.5).
These areas should be targeted for biopsy. Centrally CT scans of the lungs are essential for assessing
necrotic or haemorrhagic areas should be avoided the systemic spread of disease because the lungs are
in order to prevent a false‐negative diagnosis. These the commonest site for metastases.
features are readily identifiable on MRI, which can Percutaneous CT‐guided core needle biopsy is
be used to plan the approach to biopsy. Because now the standard for obtaining tissue for diagnosis.
MRI is so sensitive to any soft tissue perturbation, This modality allows accurate placement of the
it is essential that these scans are performed prior to biopsy needle, planning of the biopsy tract, and a
biopsy to avoid confounding signals generated by scan to be obtained of the needle in position to con-
biopsy or surgical artefact that may make interpre- firm adequacy and appropriateness of the biopsy.
tation difficult leading to under‐ or over‐diagnosis.
The entire tumour‐bearing compartment should Functional scans
be scanned to ensure that any satellite lesions Functional scans are used to evaluate the metabolic
are detected so that these can be included as part of activity of a tumour. Highly metabolic lesions are
the resected specimen. Moreover, MRI scans are more likely to be malignant; in the context of a con-
firmed STS, a highly metabolic tumour is likely to
be a higher‐grade lesion. Functional scans are inval-
uable for identifying the most metabolically active
location within a tumour and this location may
then be co‐registered with a CT scan and used to
QM STS QM
V
QM B
MO
Fig. 45.4 MRI provides unsurpassed soft tissue contrast.

Fatty tissue (blue arrows) around soft tissue sarcoma
(STS) within the quadriceps musculature (QM) provides
different signal characteristics from the tumour and is
invaluable for determining the boundary of
the tumour. MRI clearly demonstrates important
neighbouring structures such as the femoral vessels
(V) and the uninvolved cortex and intramedually canal Fig. 45.5 CT scan of foot demonstrating calcification of
of bone (B). myositis ossificans (MO) on plantar aspect.
up thallium when activated. Such tissues that take

up 201Tl on a thallium scan stand out as a ‘hotspot’.
Glucose is also used as an energy source by highly
metabolically active tumours. This characteristic is
exploited in PET scans where radioactively labelled
glucose is used as the nuclear tracer.
Both types of scan may be used effectively for
tumours of the limbs. However, PET is more useful
for intra‐abdominal and pelvic STSs as the high
amount of visceral uptake of 201Tl can sometimes
obscure any tracer‐avid tumour.
Biopsy
Biopsy is essential for the appropriate treatment of
STS. No soft tissue tumour should be excised with-
out an accurate diagnosis and biopsy is the most
H effective way of obtaining this. Biopsy should be
performed at the completion of all other anatomi-
cal and functional investigations. This is because
biopsy may confound the findings of anatomical
N
STS and functional scans if done before imaging,
because of the post‐biopsy imaging artefact. In
addition, imaging provides an ideal resource for
targeting the optimal site for biopsy in order to
obtain the most representative and highest‐grade
component of a tumour.
Biopsy may be performed in a number of ways,
namely fine‐needle aspiration biopsy, percutaneous
core needle biopsy, open biopsy and excisional
biopsy. Fine‐needle biopsy requires a highly skilled
cytologist who is expert in sarcoma pathology for
interpretation of cellular findings and these indi-
Fig. 45.6 PET scan of a soft tissue sarcoma (STS) within viduals may not be readily available in all institu-
the quadriceps muscle. Note high metabolic activity tions. For optimal care, open biopsy should be
(H) in tracer‐avid region of tumour, and low tracer undertaken at a tumour centre where experts in
avidity in area of central tumour necrosis (N). This sarcoma surgery are available to plan the biopsy
helps to demonstrate both response to treatment and entry site in relation to the definitive procedure.
also areas that should be targeted or avoided during This is because the biopsy tract will need to be
image‐guided biopsy.
excised en bloc with the tumour mass to ensure
local control of disease. The placement of the
target the biopsy. Functional scans may also be used biopsy site is critical for appropriate surgical man-
to evaluate the tumour’s response to neoadjuvant agement because errors in biopsy placement or pro-
treatment such as radiotherapy or chemotherapy. cedure may compromise subsequent surgery or
Functional scans may be used to differentiate recur- reconstruction. At worse, an error in biopsy may
rent tumour from postoperative granulation. If a lead to amputation of the affected limb. Excisional
patient is referred after inadvertent resection of an biopsy should never be done except in a tumour
STS, functional scans may be useful for identifying centre where appropriate multidisciplinary discus-
gross residual tumour. sion can occur prior to the procedure and all the
Two types of functional scan in use include the relevant imaging modalities scrutinised. Image‐
thallium scan and positron emission tomography guided core needle biopsy is now a standard method
(PET) (Figure 45.6). Thallium‐201 (201Tl) is a radio- for obtaining biopsy material (Figure 45.7). Image
active chemical analogue of potassium and its guidance allows accurate targeting of representa-
uptake by metabolically active tissue relies on the tive tissue and the procedure is less invasive or
sodium potassium pump. Cardiac muscle, bowel harmful than open biopsy, where the complications
and active muscle are examples of tissue that take of haemorrhage and infection are a finite risk that
(a) (b)
Fig. 45.7 (a) Heterogeneous area (H) within lipomatous tumour raising suspicions that this ‘lipoma’ may be atypical.
(b) Image‐guided biopsy can target suspicious areas.
may affect subsequent treatment. Image‐guided Chemotherapy is sometimes provided as an institu-

core needle biopsy requires skill and experience in tional preference.
this field, and the modality is best sought from a
centre specialising in sarcoma care. Surgery
The most important goal of surgical care is to
Staging of tumours achieve adequate surgical margins. Doing so
Staging of tumours is the process whereby exten- ensures the lowest risk of local recurrence of dis-
sive data are collected on tumours. Preoperative ease. Surgical margins are planned preoperatively
local staging includes all the imaging modalities with the use of the staging studies. MRI provides
described to better understand the local extent of unsurpassed soft tissue contrast and is critical for
the tumour. Systemic staging includes a CT scan of planning surgical margins. Surgery should be per-
the chest and functional scans in order to assess the formed with oncological goals and not with the
occurrence of metastatic spread. Preoperative stag- view to reducing reconstruction (aesthetic goals).
ing studies also include the biopsy. Surgical margins may be classified as intrale-
Restaging studies after neoadjuvant treatment sional, marginal, wide or radical margins
and prior to surgery include these same tests but (Figure 45.8). Intralesional margins are seen when
without the need for a second biopsy. The purpose the excision passes through the tumour capsule.
of the restaging studies is to evaluate the response Marginal margins are seen when the excision passes
of the tumour to neoadjuvant treatment, whether through the inflammatory zone around the tumour.
metastases are visible after the treatment or whether This zone contains satellite lesions or extensions of
there has been any change in lesions suspected of the tumour which may be responsible for the high
being metastases. The features of response may rate of local recurrence should a resection pass
include a change in size, shape, number, consistency, through this zone. Wide margins include a cuff of
presence of intratumoral haemorrhage or cystic normal tissue around the tumour itself. This can be
change, and the appearance of a true capsule achieved when there is a named anatomical layer of
around the tumour. Functional scans are valuable normal tissue around the tumour in the radial
for assessing the metabolic response to neoadjuvant direction and there is 2–5 cm of normal tissue in the
treatment and is a measure of tumour ‘kill’. longitudinal axis of the tumour. Radical margins
are achieved when the entire tumour‐bearing com-
partment is excised.
Treatment
Intralesional or marginal margins are inadequate
The mainstay of treatment is surgical resection. surgical margins. Occasionally, marginal margins
This is usually combined with radiotherapy. are required to preserve vital structures such as
(b) (c)
(a)
Femur
I M
Femoral artery & vein
STS
S (d) (e)
Sciatic nerve
W R
Fig. 45.8 (a) MRI of soft tissue sarcoma (STS) within adductor magnus muscle. Note adductor compartment (green),
hamstring compartment (orange) and quadriceps compartment (blue). (b) Intralesional margin (dotted line) passes
through the capsule of the tumour. (c) Marginal margin (dotted line) passes through the inflammatory pseudocapsule of
the tumour. (d) Wide margin (dotted line) passes outside the inflammatory zone through a cuff of normal tissue.
(e) Radical margin (dotted line) includes the entire tumour‐bearing compartment, which in this case is the adductor
compartment.
nerves, vessels and viscera. In this scenario, radio- is particularly important where the margin has to
therapy is often used to upgrade the quality of the be close because of an attempt to preserve vital neu-
margin and when combined with marginal margins rovascular structures or viscera.
is equal to wide margins alone. Intralesional mar- Radiotherapy is usually given to a total dose of
gins should never be knowingly employed. 50.4 cGy and delivered over 5–6 weeks. During this
Resection of an STS usually leaves a large dead time, the patient may develop skin reactions in the
space or exposed soft tissue defect. In both cases, field of radiotherapy and this may be characterised by
soft tissue reconstructions are required to diminish erythema, desquamation or blistering. Surgery is usu-
dead space and provide skin cover or to provide a ally performed 4–5 weeks after completion of radio-
functional reconstruction. If following resection therapy to allow the soft tissue reaction to settle.
a limb is not expected to be functional or if the
defect cannot be closed, then amputation should be
considered. Chemotherapy
Inadequate surgery should be avoided where
There is debate as to the role of chemotherapy in
possible. Inadvertent resection with positive mar-
the management of primary STS. It is not conven-
gins is associated with a higher risk of death from
tionally used, but some institutions do prescribe
disease, inferior survival and local recurrence.
chemotherapy and cite a local control advantage.
Surgery for STS should be performed at a tumour
Some suggest the use of chemotherapy in the setting
centre specialising in sarcoma care.
of a high‐risk tumour (large and high grade).
Chemotherapy does have a role in metastatic dis-
ease. In a palliative setting, chemotherapy may con-
Radiotherapy
trol growth for a period of time and may be able to
The combination of radiotherapy and surgery pro- provide some relief for patients with symptomatic
vides better local control of disease than either sur- disease.
gery or radiotherapy alone. Radiotherapy is able to There is growing interest in next‐generation
upgrade the quality of the surgical margins and this sequencing for identifying genetic aberrations that
may be linked with mechanisms for tumour pro- 3 Which of the following is an indication for removal
gression. Identifying these aberrations may pave the of a lipoma?
way for novel therapy in appropriate candidates. a a 3‐cm lipoma in the tibialis anterior
b a 3‐cm lipoma in the subcutaneous fat of the
anterior abdominal wall
Further reading c a 3‐cm lipoma in the subcutaneous fat of the
buttock
Trieu J, Sinnathamby M, Di Bella C et al. Biopsy and the
diagnostic evaluation of musculoskeletal tumours: criti- d a lipoma of many years standing which has not
cal but often missed in the 21st century. ANZ J Surg changed in size
2016;86:133–8. e a lipoma on CT scanning of heterogeneous
Vodanovich DA, Choong PF. Soft‐tissue sarcomas. Indian density
J Orthop 2018;52:35–44.
4 Desmoid tumours:
a are commoner in women as they age
MCQs b occur in the root of the mesentery in association
with FAP syndrome
Select the single correct answer to each question. The c cause death by metastasis
correct answers can be found in the Answers section d tend not to recur locally
at the end of the book. e metastasise to regional lymph nodes
1 Soft tissue sarcomas are commonest in:
a abdomen and retroperitoneum 5 Soft tissue sarcomas:
b head and neck a are often greater than 5 cm
c lower limb b often engage the deep fascia
d upper limb c should be treated at a sarcoma centre
e thorax d need to be investigated and biopsied at a
sarcoma centre
2 The commonest site of metastasis for soft tissue e all the above
sarcomas is:
a regional lymph nodes
b liver
c bone
d lungs
e brain
46 Infection of the extremities
Mark W. Ashton1 and David M.A. Francis2
1
2
Department of Urology, Royal Children’s Hospital, Melbourne, Victoria, Australia and Department
of Surgery, Tribhuvan University Teaching Hospital, Kathmandu, Nepal
Tinea pedis
Introduction
This is probably the most common fungal infection
Infections of the extremities may be broadly in the extremities and may be caused by either a
grouped into those arising from fungal and those mould or a yeast. The moist occluded areas of foot-
arising from bacterial organisms. Bacteria may sec- wear, particularly in the presence of sweat, provide
ondarily infect fungal disease. Whilst most patients an ideal environment for fungi. These fungi also
will have no underlying medical problems, particu- thrive in the warm humid atmosphere of public
lar care needs to be taken in treating patients with showers, saunas, spas and steam rooms, and conse-
a compromised immune system, especially those quently transmission between individuals can occur
with diabetes, immunosuppression and alcoholism. readily in these environments.
Tinea pedis appears in three ways.
• In the interdigital skin, where it appears as white
Fungal infections of the extremities macerated soggy skin that may or may not be
accompanied by an odour.
Fungal infections are probably the most common • As patches of recurrent vesicular eruptions that
of the infections involving the extremities, particu- are itchy and red, commonly on the instep of
larly the lower limb. Almost everyone has either the foot.
experienced personally or knows someone who has • On the soles of the foot, where it appears as dry
had a fungal infection. Fungi thrive in warm, moist, and scaly skin that is frequently itchy; there may
dark environments, and are broadly divided into be cracking, fissuring and thickening of the skin.
two groups, yeasts and moulds. Yeasts are unicel- The treatment of tinea pedis initially involves
lular and round or oval in shape whereas moulds changing the environment in which the fungi are
are multicellular and filamentous or threadlike in growing. These measures are aimed at reducing the
shape. Both yeasts and moulds can infect humans. amount of available moisture, and include proper
The most common types of fungi causing disease drying of the feet after bathing, open footwear, and
in humans are called dermatophytes. These are aer- using natural fibres such as cotton or wool to
obic fungi that require keratin for growth and reduce sweating. Patients are advised to avoid con-
hence they invade and infect the skin, hair and tact with high‐risk areas by the use of sandals.
nails. In general, these infections are superficial Conservative treatment may be combined with
and the fungi do not cause invasive disease except antifungal agents. These may be administered either
in immunocompromised patients. Dermatophytes topically or systemically. Topical treatment with
are usually spread by direct contact from other tolnaftate or micronazole creams, for example, is
people, animals or soil. However, they can also be best used in superficial infection, as these agents are
spread via non‐living objects that are capable of unable to penetrate thick keratin layers such as
transferring infection. These objects are called those found on the heel. These topical treatments
fomites and common examples are skin cells, hair, usually need to be applied daily for a minimum of
clothing, bedding and mattresses. 6 weeks. Recurrence of tinea pedis is often due to
The clinical disease varies by the type of organ- patients discontinuing the treatment once the symptoms
ism, the site of infection and the host response. disappear.
415
In severe or chronic cases, oral treatment with

griseofulvin may be considered. The newer genera-
Bacterial infection of the extremities
tion of oral treatments have shorter treatment times
Bacterial infection of the extremity may arise
and higher cure rates with fewer side effects.
following injury to the arm or leg or may arise as a
manifestation of a systemic infection. Bacterial
Onychomycosis
infection may rapidly progress and can lead to
This is a fungal infection of the nail. In general, it is significant loss of tissue, the amputation of the limb,
much more difficult to treat than tinea pedis. or death. Patients particularly at risk are those with
It is broadly grouped into four distinctive types. a compromised immune system, such as those with
• Distal or lateral side of the nail: this is the most diabetes, alcoholism or HIV infection, and therefore
common. any history obtained from a patient must specifi-
• Proximal: this is often chronic. cally question the individual’s immune status. In
• Superficial: the nail plate becomes white. It usu- almost every case, bacterial infection of the extremi-
ally develops from distal to proximal. ties will respond to rest and elevation of the affected
• Total: the whole nail is affected and may result limb, and indeed this is the mainstay of the treat-
from any of the above. ment of bacterial infection of the extremities.
In all these categories the nail takes on a character- Bacterial infection of the extremities covers a
istic appearance. The nail becomes white and thick- diverse range of disease, extending from the minor
ened, there may be white or yellow vertical to the rapidly progressing infection that is life‐
striations, and the nail plate may lift off the under- threatening. The most common infections involve
lying nail bed. organisms that are usually seen on the skin surface
The treatment of fungal infection of the nail of otherwise healthy individuals. The most com-
depends on number of nails involved, the clinical mon of these are Staphylococcus aureus and group
type and the severity of infection. In general, distal A Streptococcus. Streptococcus species are particu-
and superficial disease can be treated with a topical larly important as they produce an enzyme called
agent whereas systemic treatment is always required streptokinase that breaks down the body’s defence
in proximal infection. Topical treatments are usu- systems and allows rapid spread of Streptococcus
ally unable to cure proximal nail infection because (and other bacteria) significantly beyond the origi-
of inadequate nail penetration. In general, mono- nal site of contamination.
therapy tends to be less effective than combination Usually these organisms are sensitive to simple
therapy, and daily application for a long period of antibiotics. However, in environments where there
time is usually required, sometimes up to a year. is a high usage of penicillin antibiotics, a resistant
In severe or chronic cases, oral or systemic treat- form of Staphylococcus aureus (the most common
ment may be considered. As with the treatment of of which is meticillin‐resistant Staphylococcus
tinea pedis, the newer generation of oral treatments aureus or MRSA) is able to proliferate, and hence
have replaced the older treatments. These agents normal penicillins and β‐lactam antibiotics are not
have shorter treatment times and higher cure rates effective, and more sophisticated antibiotics may be
with fewer side effects. In severe cases oral treat- required. The environments in which these MRSA
ments may be combined with nail removal and bacteria are found include, but are not limited to,
topical agents. hospitals, nursing homes, emergency departments
Despite these newer agents, the rate of recurrence and doctors’ surgeries. Therefore, in treating bacte-
in proximal disease remains high, and therefore rial infection acquired in these environments the
alternative treatments such as photodynamic ther- practitioner should consider MRSA infection, par-
apy may represent future treatment options. ticularly if the wound is not responding to tradi-
tional antibiotic therapy.
Ringworm
Ringworm is a fungal infection of the skin. Typically, Simple contained bacterial infections
it results in a red, itchy, scaly circular rash. It may of the hand and foot
be associated with hair loss and multiple areas of
Felon
skin can be affected simultaneously. About 40 dif-
ferent types of fungi can cause ringworm. Treatment A felon is an abscess of the pulp space of the digit or
is the same as for tinea pedis and involves keeping the toe (Figure 46.1). It usually occurs after trauma
the area clean and dry, reducing moisture and the to the pulp in which bacteria are introduced beneath
use of topical antifungal creams. the skin surface. Treatment involves drainage of the
46: Infection of the extremities 417
Distal phalanx
Pulp space abscess
Fig. 46.1 Longitudinal section of the finger tip with a pulp space abscess. Source: courtesy of Mr David M.A. Francis.
abscess, removal of any retained foreign body (such Synovial sheath infection
as a splinter of wood), copious lavage, elevation
In certain circumstances, infection may extend into
and splinting of the digit to limit movement, and
the synovial sheath surrounding the flexor tendons.
antibiotics.
This is more common in the hand and usually
involves a penetrating injury. When this occurs a
Paronychia classic combination of signs appears, called Kanavel’s
four cardinal signs of flexor sheath infection:
Paronychia, sometimes called a whitlow, is an
• sausage‐shaped fusiform swelling of the digit
abscess of the nail fold and nail bed (Figure 46.2).
• stiffness of the finger in a semi‐flexed position
The infection is usually due to Staphylococcus
• tenderness of the sheath extending proximally
aureus or Staphylococcus epidermidis and most
into the palm
commonly follows minor injury to the nail fold. Pus
• pain when the finger is passively extended.
forms around the nail fold and may extend under
This diagnosis is important because if the infection is
the nail to involve the nail bed or proximally to
left untreated the tendon may rupture, or the inflam-
involve the subcutaneous tissue between the nail
mation may lead to adhesions forming between the
fold and distal interphalangeal joint. In rare cir-
tendon and its sheath, leading to limitation of move-
cumstances, the infection may extend into the joint,
ment and compromised hand function.
causing a septic arthritis.
Treatment involves surgical washout or lavage of
Treatment consists of elevation and splinting of
the tendon sheath, usually on multiple occasions,
the finger or hand, antibiotics and, if pus is present,
elevation and splinting of the hand, antibiotics and,
surgical drainage.
once the infection is treated, aggressive hand ther-
apy to prevent adhesion formation and mainte-
nance of hand function.
Absess
Nail fold
Infection of the metacarpophalangeal joint
This infection is common after bare‐fisted fights
and results from a clenched fist striking the teeth
Nail
and mouth. The mechanism of injury is a tooth lac-
erating the skin and extensor tendon overlying the
joint and entering the joint capsule of the metacar-
pophalangeal joint (MCPJ). This is a surgical emer-
gency as the infection and septic arthritis may
Distal phalanx destroy the joint cartilage, resulting in permanent
damage to the joint itself. Because the patient invar-
iably presents with their hand in a flat or open posi-
tion, the communication between the laceration
and the joint is usually not immediately apparent, and
the diagnosis may be missed. It is only when the
patient is asked to remake a clenched fist and flex
Fig. 46.2 Transverse section of acute paronychia with the MCPJ to 90° that the direct continuation of the
subungual extension. Source: courtesy of Mr David M.A. laceration into the joint cavity becomes clear. On
Francis. examination, the soft tissue around the joint is
Box 46.1 Organisms most commonly

isolated in bite wounds to the hands
Human bites: these are the most dangerous

• Staphylococcus
• Streptobacillus
• Eikenella corrodens
• Anaerobes
Dog bites
• Pasteurella multocida
• Streptobacillus
• Staphylococcus
• Anaerobes
Cat bites
• Pasteurella multocida
In its early stages, the offending segment of the

nail can be cut back or the sharp edge of the nail
plate lifted with a splint so that the underlying soft
tissue of the nail bed is protected. In more advanced
cases, the entire nail may need to be surgically
Fig. 46.3 This laceration overlying the proximal
removed. Treatment of an associated abscess
interphalangeal joint needs to be explored to ensure the
laceration does not communicate with the joint. This is involves removing the nail and draining the under-
best done by asking the patient to make a fist to lying infection. For recurrent or chronic ingrown
reproduce the joint position at the time of injury. toenails, a lateral matricectomy is performed in
which the germinal matrix from which the nail
grows is surgically removed.
usually swollen and movement of the MCPJ is

Disseminated bacterial infections
painful. A history of recently being involved in a
of the extremities (Box 46.2)
fight is helpful but is not always given. Treatment is
similar to that of flexor tendon sheath infection and Impetigo
involves multiple surgical washouts of the joint,
Impetigo is a highly contagious common superficial
elevation and splinting of the hand, and antibiotic
skin infection caused by Staphylococcus aureus or
therapy. An injury overlying an interphalangeal
Streptococcus pyogenes (group A Streptococcus). It
joint is shown in Figure 46.3 and the organisms
typically appears as yellow crusts on the face, arms
most commonly isolated in bite wounds to the
or legs, but may also develop into superficial b
listers.
hands are listed in Box 46.1.
It is spread by direct contact and hence is common
in schools, day care facilities, nursing homes and
Ingrown toenail (onychocryptosis)
areas in which crowding occurs. Left alone the
This is a painful condition that occurs when the infection usually clears in 2–3 weeks, but the infec-
sharp corner or the edge of the toenail cuts into the tion can be treated with topical or systemic antibiot-
skin at the distal end or side of the toe. Whilst pain ics. Patients should keep the sores clean and dry and
and inflammation are common, occasionally the should avoid spreading the fluid of the sores onto
condition can progress to infection and then abscess unaffected skin or other non‐affected people.
formation. The disorder is particularly common in
adolescents and young adults. Whilst any toenail
Cellulitis
can become involved, it is most common in the
great toe. It is thought that tight shoes and high Cellulitis is a bacterial infection of the skin and is
heels are risk factors as they force the toes to be one of the most common infections of the extremi-
compressed. Particular care should be taken in ties. Typically, the skin progressively becomes red,
treating people with diabetes and those who are swollen and painful. It takes on a shiny glossy
immunosuppressed. appearance and may begin to weep, particularly in
system is compromised such as diabetics and

Box 46.2 How to treat bacterial
alcoholics. There may or may not be a history of
infection of the extremities
trauma to the leg or hand, and diabetics or people
• Rest and elevation of the limb (critically important) with venous hypertension in the lower legs may
• Debridement of non‐viable tissue and cleansing of notice that cellulitis seems to appear for no obvious
the wound reason. Patients at risk are those with immune com-
• Antibiotic therapy targeted to the organism promise, diabetes, eczema, tinea and other fungal
• Frequent review to ensure the treatment is effective infections, and venous insufficiency.
and the infection is subsiding Cellulitis can spread proximally, particularly in
the presence of group A Streptococcus, and it may
enter the lymphatics where it induces inflammation
characterised by linear red streaks extending up the
arm or leg to the cubital fossa, axilla or groin lymph
nodes (lymphangitis) (Figure 46.5). In severe cases
cellulitis is associated with systemic signs such as
fever, fatigue, sweating, aches, chills and shaking.The
immediate treatment is to rest and immobilise the
affected limb, preferably with a splint made from
plaster of Paris or fibreglass, so that the splint closely
contours the limb and is therefore more comfortable
and patient compliance is better. It is important that
the hand is placed in a neutral position, or position
of function (Figure 46.6) to avoid contracture of the
ligaments and short muscles of the hand. In the
lower limb, it is important to place the ankle at 90°
to avoid contracture of the Achilles tendon and mus-
cle flexors of the ankle joint (Figure 46.7). The limb
should be elevated and the patient confined to bed.
The most common organisms are sensitive to the
penicillins and cephalosporins. This antibiotic
therapy should be commenced immediately,
either through intravenous or oral administration.
Usually, once the exact organism is subsequently
identified, the antibiotic therapy is modified
depending on the sensitivities obtained from micro-
biology. Importantly, the treatment of lower leg cel-
lulitis should also include antithrombolytic therapy
such as enoxaparin sodium or heparin to minimise
the risk of subsequent deep venous thrombosis in
the setting of extended bed rest.
Once the cellulitis is controlled, the underlying
cause should be identified and treated. This may
involve referral to an endocrinologist to treat and/
Fig. 46.4 Significant cellulitis of the lower leg. The skin or better control the patient’s diabetes, a dermatol-
is red, shiny and oedematous. ogist to treat the fungal infection or eczema, or a
vascular surgeon to treat the venous insufficiency.
the lower leg (Figure 46.4). Most infections are Occasionally, in severe cellulitis there may be loss of
caused by bacteria that are normally present on the skin and the patient will need referral to a plastic
individual’s skin surface, and of these the most surgeon for skin grafting.
common organisms are Staphylococcus aureus and
Streptococcus species.
Hidradenitis suppurativa
Whilst it usually only affects the superficial
tissues of the leg, sometimes the infection may
This is an infection of the apocrine sweat glands
extend to involve the deeper tissues of fat and fas- and is most common in the axillae, groin, external
cia, particularly in individuals whose immune genitalia and perianal areas. The apocrine sweat
Fig. 46.6 The ideal splinting position for the hand. Note
that the wrist is extended and the metacarpophalangeal
joints are at 90°.
Fig. 46.7 The ideal splinting position for the foot and
lower leg.
Bairnsdale ulcer (also known as Buruli ulcer)

This unusual infection caused by Mycobacterium
ulcerans tends to occur in the cooler months,
particularly in maritime or coastal environments.
It was first described in Bairnsdale in eastern
Victoria, Australia in the 1930s, but has been
Fig. 46.5 The infection in the little finger has spread and
described in coastal areas from far northern
has resulted in lymphangitis along the ulnar border of Queensland to Adelaide. Interestingly, it is quite
the forearm. variable as to who contracts the disease and it is not
clear how it is spread. There is some evidence to
suggest the mosquito may be the vector. The infec-
glands produce a thick secretion and easily become tion’s hallmark is a non‐healing shallow ulcer, usu-
blocked, particularly at adolescence. The secretions ally on the extremities, that slowly enlarges over
subsequently become infected with staphylococci, weeks to months and is not responsive to antibiot-
Gram‐negative and anaerobic organisms leading to ics. It is usually single, and often starts as a small
abscesses, cellulitis and sinuses. The infections are red lump. Treatment involves good wound care and
often recurrent, leading to significant scarring. dressings. Heat therapy in which the ulcer is treated
Unfortunately, antibiotics alone are often unable to with a heat lamp has been shown to be beneficial
control recurrent infection and surgery may be
required to excise the infected and scarred tissue.
Necrotising fasciitis
In severe cases the entire area may need to be
removed and replaced with either a skin graft or This is a rapidly progressive and dangerous bacte-
skin flap (see Chapter 47). rial infection that can affect any part of the body,
but most commonly the extremities. It often has an

Box 46.3 What is gangrene?
insidious onset and may result from the most trivial
damage to the skin. It is followed by rapid progres- Gangrene is the death of tissue due to either:
sion of infection that occurs below the skin surface, • lack of blood flow, or
and hence the extent of the infection may be far • serious bacterial infection.
greater than is initially clinically apparent. It often The difference between these two causes can often be
involves the deep fascia and may lead to muscle determined by whether the gangrene is ‘wet’ or ‘dry’.
necrosis. The rapid spread is due to the presence of • Wet indicates a bacterial cause: there is usually
β‐haemolytic Streptococcus, usually in association swelling and blistering. It often has a rapid onset.
with other organisms particularly mixed anaerobes. • Dry indicates lack of blood flow (ischaemia): there
It is most commonly seen in patients who are is usually minimal swelling and no blistering. The
immunocompromised such as diabetics, alcoholics onset is slow. Note that ischaemic gangrene can
and patients with HIV. The diagnosis is notoriously become infected.
difficult in the early stages, as the skin and soft
tissues appear relatively normal. The key to an early
diagnosis is the presence of severe pain out of keep- Box 46.4 Flesh-eating bacteria
ing with the skin appearance, and the presence of
associated signs such as tachycardia, fever, sweats Flesh‐eating bacteria is a misnomer: the bacteria do
and occasionally episodic hypotension. Interestingly, not eat the tissue but rather destroy tissue by
the majority of infections are caused by organisms releasing toxins.
that normally reside on the individual’s skin.
Most infections manifest more than one type of
intravenous antibiotics and urgent surgical explora-
bacteria, the most common organisms being group
tion and debridement of dead muscle and soft tissue
A Streptococcus, Staphylococcus aureus and MRSA,
with copious lavage of the wounds. The debridement
Klebsiella, Clostridium, Escherichia coli and Aerom
and lavage is repeated on a daily basis until all the
onas hydrophila.
infected and necrotic tissue is removed. This is usu-
Treatment involves aggressive early surgical
ally associated with an improvement in the patient’s
debridement and lavage, often on multiple occa-
systemic condition and can serve as a monitor that
sions. Frequently, large areas of skin and soft tissue
the surgical debridement is adequate. Because soft
are removed and hence most patients require some
tissue loss is frequently extensive, a skin graft is often
form of skin grafting or flap repair. Amputation of
required. Most patients are critically ill and will need
either part or all of the limb is not uncommon.
support in an intensive care unit to treat their renal
Untreated, the infection rapidly leads to death.
failure, severe shock and multiple organ failure.
Gas gangrene
Meningococcal septicaemia
This is a life‐threatening, rapidly progressive bacte-
rial infection classically associated with Clostridium Meningococcal septicaemia is the systemic disease
perfringens (Boxes 46.3 and 46.4). Clostridia are caused by Neisseria meningitidis. It is a life‐threat-
anaerobic, spore‐forming, Gram‐positive bacilli found ening, rapidly progressive bacterial infection and
in soil, manure and decaying plants and a nimals. systemic disease that in addition to causing
They produce potent exotoxins such as haemolysin, systemic shock and multiple organ failure also

collagenase, hyaluronidase and other proteolytic leads to multiple areas of skin, muscle and bone
enzymes that break down tissue and facilitate the necrosis in the extremities. The loss of tissue in the
spread of bacteria. In a similar manner to necrotis- extremities may be severe and frequently involves a
ing fasciitis, the infection spreads along deep muscle segment or whole compartments of tissue. These
and fascial tissue planes and the overlying skin may segments of tissue loss are usually multiple and
appear relatively normal and apparently unin- distributed over the entire body. Amputation of
volved. Gas gangrene derives its name from the limbs is common, and death inevitable without
presence of small bubbles of gas within the integ- aggressive early treatment.
ument, which give the soft tissue a ‘crackling’ In the early stages of infection, patients complain
sound when the skin is pressed. Mortality is high of severe lethargy and tiredness. There may not be
(25–40%). any skin manifestations. Indications of septicaemia
Treatment involves resuscitation from the shock and progressive severe infection include the devel-
that frequently accompanies this infection, high‐dose opment of a blotchy and then purpuric rash, and
high fever. Patients rapidly become shocked. This c frequent changing of the dressings
infection is a life‐threatening emergency. Patients d ensuring the patient is not a diabetic or is
should be given high doses of penicillin or cephalo- immunosuppressed
sporin immediately, by whatever means available, e minimising any causative factors such as
and urgently transferred to hospital. It is important recurrent trauma
not to wait until a rash appears before commencing
treatment if a diagnosis is suspected. 2 Fungal infection:
Neisseria meningitidis is endemic, with up to a is not usually transferred by direct contact
20% of the population carrying the bacteria at any b is not able to be transferred by a non‐living object
one time without ever becoming ill. It normally c is uncommon in warm moist environments
resides in the nose and throat and is transmitted d of the proximal nail is best treated with topical
between individuals via mucus and saliva. The antifungal creams
mechanism by which a bacterium that may harm- e usually requires a combination of conservative
lessly reside in one individual but which becomes measures and antifungal medication for a
life‐threatening when transferred to another is prolonged period
not well understood. The meningococcal disease
accompanying septicaemia is most common in 3 Which of the following statements about hand
young children and adolescents. It is thought this is infection is correct?
because the transfer of saliva and mucus is more a following a fist fight, MCPJ joint involvement
common in these age groups through mouthing of and infection is easy to diagnose
objects and kissing. There are five main strains of b paronychia is not linked with septic arthritis
the organism and vaccines protecting against them c the mainstay of treatment of bacterial hand
are available. infection is rest, elevation and splinting in a
neutral position
d flexor tendon sheaths can become infected, but the
Further reading signs are not characteristic and are highly variable
e patients should be encouraged to return to work
Australian Government National Health and Medical and use their hand as much as possible so that it
Research Council. Therapeutic Guidelines, Antibiotic does not stiffen up
Version 15 (2014). Available at http://www.tg.org.au/
index.php?sectionid=41
Neligan PC (ed.) Plastic Surgery, 4th edn. Elsevier, 2017.
4 Meningococcal septicaemia is:
Royal Australasian College of Surgeons. Infection Control a not associated with a purple rash
in Surgery. Prevention of healthcare associated infection b usually seen in elderly patients, while healthy
in surgery. Ref. No. FES‐PST‐009 Available at https:// young adolescents are safe
www.surgeons.org/media/297157/2015‐05‐20_pos_ c is not life‐threatening and is slowly progressive
fes‐pst‐009_prevention_of_healthcare_associated_ d is caused by a bacterium that harmlessly resides in
infection_in_surgery.pdf the nasopharynx of up to 20% of the population
Weinzweig, J (ed.) Plastic Surgery Secrets Plus, 2nd edn. e not an indication to urgently administer penicillin
Philadelphia: Mosby Elsevier, 2010.
or cephalosporin antibiotics, and it is best to wait
Williams JD, Taylor EW (eds) Infections in Surgical
until the patient gets to hospital and let the
Practice. London: Hodder Arnold Publication, 2003.
emergency doctors do microbiological cultures first
5 Which of the following features are shared by

MCQs necrotising fasciitis and gas gangrene?
a both are very easy to detect in their early stages
b both are relatively harmless
c skin overlying the infection is usually red, shiny
and weeping
1 Which of the following measures is the mainstay d surprisingly, the patient is otherwise quite well
for treatment of cellulitis? e an early diagnosis is made by the dichotomy of a
a bed rest and elevation of the affected limb gravely ill patient, with fever, shock and fatigue, in
b antibiotics the presence of relatively normal‐looking soft tissue
47 Principles of plastic surgery
Mark W. Ashton
Introduction units to be ingenious, in an unheralded way, by

inventing and developing new techniques of tissue
Despite its name, plastic surgery has nothing to do transfer. (In recognition of the uncertainty of out-
with plastic. Both the surgical specialty, and the come, and the adventurous nature of the surgery,
malleable compound that we all know, derive their one of these units in the Second World War became
name from the Greek word plastikos and the Latin affectionately known as the Guinea Pig Club.)
word plasticus. Both words refer to the capacity to Many operations were multi‐staged and it was not
‘mold’ or ‘transform’. The application of these terms uncommon for a patient to undergo 10, or even 20,
to the now ubiquitous ‘plastic’ material makes sense. individual operations (Figure 47.1). Unsure of what
The relevance to plastic surgery requires a little to call themselves, these new surgeons coined the
more explanation. term ‘plastic surgery’ as they were molding and
Plastic surgery, as a specialty, developed in the transforming tissue. One could also say they were
First World War. This war, unlike others before it, molding and transforming the soldiers themselves,
was characterised by trench warfare using high‐ giving them, for the first time, a real chance to re‐
powered but relatively low‐velocity guns, heavy integrate back into society.
artillery that released huge amounts of shrapnel on At its most basic core, plastic surgery involves the
detonation, and a developing air war using the transfer of tissue from one part of the body to the
new aeroplanes made of highly flammable wood, other. It may be very close (local) or far away (dis-
canvas, lacquers and paint. These planes had no tant). The tissue that is transferred may remain
parachutes. attached to the body, in which case it is called a
Surviving casualties of this war fell roughly into flap, or it may be completely detached and there-
two broad groups: those suffering grossly disfigur- fore must gain access to a new blood supply at the
ing compound wounds to the face and limbs and recipient site into which it is inset. These tissue
those with severe full‐thickness burns. In the transfers are called grafts.
unlikely event these soldiers and airmen could be A special situation exists in which the tissue to be
saved, they returned home with horrific disfiguring transferred is isolated on its specific blood supply.
injuries. They were outcast, stared at and excluded. The artery and vein supplying the tissue is identi-
Re‐assimilation into mainstream society was fied and tagged. At the recipient site, a separate
uncommon and suicide rates were high. artery and vein of the same calibre are also identi-
In an effort to help these young men a series of fied and tagged. Using a microscope and fine micro-
special units initially comprising ear nose and surgical instruments and sutures, the artery and
throat surgeons, oral and maxillofacial surgeons, veins are divided and the tissue transferred to the
neurosurgeons and general surgeons were devel- new site, completely free of its original blood sup-
oped to reconstruct and restore these men’s horrific ply. The vessels are then re‐anastomosed and the
injuries. The task was enormous. Whilst well‐ blood supply re‐established. These flaps are called
known historical methods of transferring tissue ‘free flaps’ and were first described in Melbourne,
around the body were utilised as much as possible, Australia. The advantages of these flaps are that the
these proved somewhat limited in being able to tissue can be transferred over great distances in a
provide adequate reconstruction. The sheer com- single operation and that the surgeon is able to cus-
plexity and severity of injury required these new tomise, or choose, what components are in the
423
(a) (b)
Fig. 47.1 (a) Captain J.G.H. Budd was admitted to hospital in May 1919 missing most of his nose. (b) His appearance
in December 1919 after six operations at Sidcup. Source: gilliesarchives.org.uk. Reproduced with permission of Royal
College of Surgeons London.
flap – skin only, muscle only, nerve, bone or a com- Plastic surgeons talk of two important concepts –
bination, all these permutations are possible. ‘like with like’ and a ‘reconstructive ladder’ – in
Integral to every successful plastic surgical proce- repairing defects. In essence, these two principles refer
dure is a comprehensive understanding of blood to matching the donor tissue as closely as possible to
supply. Much of the disappointment in the early the defect, and using the most simple and straightfor-
plastic surgical procedures resulted from tissue ward technique that will achieve the reconstructive
being transferred that did not have a reliable circu- outcome. As the term ladder implies, the initial tech-
lation. Despite all the hard work and long hours of niques to be considered are the most straightforward,
surgery, the surgeon and patient would subse- graduating in complexity to microsurgical free tissue,
quently watch on in despair as the tissue that was which is considered the most complex. With increas-
transferred went purple, and then black, as it died. ing complexity comes an increase in demands on
Many of the advances in plastic surgery have there- staff, infrastructure and the patient, but the capacity
fore come from a new understanding of the blood to individualise the reconstruction is unparalleled.
supply of tissue, and in particular the volume, type These techniques are discussed in the following
and extent of tissue that may be safely transferred on sections.
a single artery and vein. Through a thorough knowl-
edge of soft tissue blood supply, plastic surgeons are
now able to safely transfer large volumes of complex Direct closure
tissue predictably and reliably. As an example,
patients suffering from head and neck cancer can This is the most simple of the techniques of wound
now have their jaw, tongue and mouth removed and closure, but has a number of pitfalls for the unwary.
then replaced using the fibula bone and skin and soft The technique involves directly suturing or oppos-
tissue of the leg on the peroneal artery and vein in a ing the wound edges together. This may be done at
single operation. Patients having a mastectomy for the time of injury, which is called primary closure,
breast cancer can have the breast reconstructed using or some days or weeks later, when it is called
skin and fat tissue from the lower abdomen trans- secondary or delayed closure. This latter technique
ferred on the deep inferior epigastric vessels. And is incredibly useful in contaminated or infected
patients suffering severe mutilating gunshot wounds wounds, or in wounds in which the viability of
to the face can have a face transplant using donor the wound edges is in question. If ever in doubt, a
soft tissue transferred on the facial artery and vein. surgeon is well advised to delay closure. Delaying
47: Principles of plastic surgery 425
closure for up to 72 hours does not affect wound The disadvantage of a split‐thickness skin graft
healing or the final scar. In contrast, prematurely is that the harvested skin does not contain all the
closing a wound by direct suture may result in elements of normal skin, and in particular the
infection, abscess formation, wound breakdown lack of deep dermal structures means that it is
and further tissue loss. quite fragile and does not tolerate friction or
The principles of direct wound closure are to shearing forces. These grafts are intimately
excise the wound edges back to clean, healthy, non‐ dependent on the vascularity and quality of the
infected tissue. The wound edges are then opposed tissue bed onto which they are laid, and hence
using sutures that may pass vertically through the should not be used to cover infected wounds, bare
skin surface as a series of interrupted sutures, or bone or tendon, or tissue in which the vascularity
horizontally just below the surface of the skin in the is poor such as irradiated tissue. Split‐thickness
dermis, either in an interrupted or continuous fash- skin grafts also contract as they heal and there-
ion. It is important to eliminate dead space and fore should not be used on the face, as this con-
hence additional sutures may be employed to traction will lead to distortion of mobile structures
oppose fat, fascia or muscle in the depths of the such as the eyelid, mouth or lip.
wound. An important principle is that the wound is
closed without tension. Full‐thickness skin grafts
A clean dressing should be applied to absorb any
If the skin is harvested deeper, below the lowest
fluid and draw it away from the wound edges. The
part of the dermis, all layers of the skin are included
wound should then be splinted and the patient
in the graft. This is called a full-thickness skin graft.
rested. Depending on the degree of contamination,
There is no possibility of regeneration of the donor
additional antibiotics may be prescribed for a week
site as all the sweat glands and hair follicles con-
following wound closure. Tetanus prophylaxis is
taining the epithelial cells are also included in the
mandatory.
graft. The donor site must therefore be closed by
If the wound edges are unable to be opposed with-
direct suture. The advantage of full-thickness skin
out excessive tension, then the surgeon should move
grafts is that they are more durable and resistant to
up the ‘reconstructive ladder’, and there are now
shear forces. Because all the components of the skin
two quite different techniques that may be used to
are included, these grafts are able to maintain nor-
achieve closure of the wound. Again, wound closure
mal skin colour and are less like to fade or go pale.
may be primary (at the time of injury) or secondary.
Full-thickness skin grafts are therefore the graft
of choice for facial defects, particularly the eyelid
and nose. Because the donor site must be sutured
Skin grafts directly, there is a limit to the possible sites availa-
ble for harvesting. In general, skin that is closest to
Split‐thickness skin grafts the wound will provide the best colour match and
hence the skin behind the ear or the neck is used for
The first technique involves the harvesting of a thin
the face, and the inguinal groin crease used for
layer of skin, called a split‐thickness skin graft,
other parts of the body.
from somewhere else in the body. It is called ‘split
thickness’ because the thickness is such that only
Other grafts
the top layers of the epidermis and dermis are
included in the tissue harvested, and deeper struc- In much the same way that skin may be harvested
tures in the dermis such as the sweat glands and as a graft to replace skin that is missing following
hair follicles are left behind. This is important an injury or surgery, other tissues may also be trans-
because these structures are lined with epithelial ferred as a graft. The most common of these is
cells, and it is the epithelial cells within these struc- nerve tissue and tendons, but bone and cartilage
tures that proliferate to re‐epithelialise the donor can also be transferred. Combinations of tissue can
wound and re‐establish the epithelial lining, thereby also be grafted and these are called composite
healing the donor site. grafts. The limiting factors are the volume of the
Split‐thickness skin grafts have the advantage of graft and the tissue bed into which the graft is inset.
allowing for very large areas of skin to be harvested, As the graft does not have its own blood supply it
and because the epithelial cells regrow over the is initially dependent on oxygen and nutrients dif-
donor site, the skin graft harvesting may be repeated fusing into the cells composing the graft from the
many times. Not surprisingly, this is the method of recipient bed. Over time, blood vessels grow
choice for closing large full‐thickness burn wounds. into the graft and re‐vascularise it; however, this
ingrowth of blood vessels takes somewhere between being further transferred to the final destination,
3 days and a week. The graft cells are therefore and cross leg or arm flaps, in which tissue from one
entirely dependent on oxygen diffusion until revas- leg or arm is transferred to the other. With increased
cularisation occurs, and subsequently there is a understanding of the blood supply to tissue, there
limit as to the volume or dimensions of tissue that has been a refinement in flap transfer. It is now pos-
can be safely and reliably transferred. sible to preoperatively determine what tissue is
required, what artery and vein supply that tissue,
and then harvest that desired tissue on its specific
Flaps blood supply. If the targeted donor tissue is adjacent
to the surgical defect, it may be transferred directly.
Flaps are the second alternative for closing a wound If the defect is at a distance from the donor site,
when the wound edges will not meet to close the the artery and vein are divided and re‐anastomosed
defect. Flaps differ from grafts in that they carry to vessels at the defect site with the aid of a
with them their own blood supply. Because flaps microscope.
are not reliant on the initial diffusion of nutrients As with grafts, flaps may be composed of skin
and oxygen from the recipient bed for their sur- only, muscle only, nerve, bone, cartilage or tendon.
vival, they are less dependent on the vascularity and It is usual for the flap to contain more than one
characteristics of the recipient bed and may there- type of tissue. These flaps are called composite
fore be used to close a greater variety of wounds. flaps. As with all plastic surgery, the best aesthetic
Flaps may be broadly categorised into those that result is achieved when the transferred tissue
are close, or local, and those that are distant. As matches as closely as possible the tissue that was
with grafts, flaps may be composed of skin, fat, lost at the time of injury or surgical resection.
muscle, nerve or bone. Because they have their own
blood supply, much greater volumes of tissue can be
safely transferred, and hence it is not uncommon Cosmetic surgery
for a composite flap comprising all types of differ-
ent tissue to be included in a single transfer. The key It quickly became apparent that the plastic surgical
principle here is an understanding of which tissues techniques used to repair injury could also be used
derive their blood supply from the identified source to repair congenital defects such as cleft lip and pal-
vessel supplying the flap and then ensuring that this ate, and also to reverse the signs of ageing or to
blood supply is included in the transfer. change someone’s appearance. Cosmetic surgery
Several surgical techniques have been described may therefore be defined as:
for transferring flaps, and this has allowed a further
classification. The principle in planning a flap is an Any invasive procedure where the primary intention
assessment of skin laxity and working out which is to achieve what the patient perceives to be a more
tissue can be safely harvested for transfer without desirable appearance and where the procedure
involves changes to bodily features that have a nor-
significant distortion of the remaining body con-
mal appearance on presentation to the doctor.
tour. This tissue is then selected as the flap. The
most simple is a rotation flap (Figure 47.2) but oth- It is understood that ‘normal appearance’ is a sub-
ers, such as transposition, V–Y (Figure 47.3) and jective notion, and what appears normal to the sur-
Z‐plasty (Figure 47.4), are regularly used. More geon may not in fact appear normal to the patient.
complicated flaps have been extensively used, such In contrast, surgery performed with the goal of
as the tubed pedicle, in which the flap is attached to achieving a normal appearance, where bodily
an intermediate site for a period of 3 weeks before
(a) (b) (c)
Fig. 47.2 Rotation flap. (a) Design of flap. Lesion/defect triangulated and flap designed as semicircular arc from apex
of defect. (b) Flap incised, elevated and rotated into defect. (c) Flap sutured into position with secondary defect closed
directly.
47: Principles of plastic surgery 427
(a) (b) (c)
Fig. 47.3 A V–Y advancement flap.
(a) (b) A B
A B
B1
C1
D C D
C
(c) (d)
AC1
DB1
Fig. 47.4 A Z-plasty flap.
features have an abnormal appearance on presenta- The principle is to achieve an outcome that is nor-
tion due to congenital defects, developmental abnormal in appearance and where possible aesthetically
malities, trauma, infections, tumours or disease, pleasing or even beautiful.
does not fall under the definition of cosmetic sur- The most common cosmetic operations are
gery. This is best described as reconstruction of the breast reduction, breast enlargement, abdomino-
whole. plasty and facial plastic procedures such as face‐
An important principle is that there is a contin- lifting, eyelid reduction and rhinoplasty. These
uum between reconstruction and cosmetic surgery, operations all use the same plastic surgical tech-
and that at its very core reconstruction aims to niques of flap repair, and are also critically depend-
make the patient at least the same, if not more ent on a robust and reliable blood supply. Advances
attractive than they would otherwise be. Any prac- in our understanding of tissue perfusion and vascu-
titioner operating within reconstructive surgery lar anatomy has revolutionised all aspects of plas-
must have a clear understanding of what is ‘nor- tic surgery, and cosmetic surgery has benefited
mal’, but must also possess an appreciation of the from this increased understanding. As an example,
nuance of beauty and attractiveness. In this respect, breast reduction surgery can now be performed
one may argue that an arbitrary distinction between reliably and predictably, and even very large breasts
reconstructive and cosmetic surgery is somewhat causing back and neck pain can be safely made
simplistic, as the two are intimately intertwined and smaller without the need for nipple grafting. An
surgical techniques shared extensively across the advanced understanding of nipple and areolar
two aspects of plastic surgery. It is often said that blood and nerve supply means that the nipple is
the hallmark of a master reconstructive surgeon is a now transferred on a neurovascular pedicle that
beautiful cosmetic result. This is clearly apparent in remains attached to the underlying breast tissue. It
the field of breast reconstruction after mastectomy, has the advantage that nipple sensation is pre-
but could equally be applied to facial reconstruction served, and that patients are able to breastfeed
after cancer or hand reconstruction after trauma. after surgery.
In face‐lifting surgery, an increased understand- b advances in plastic surgery have come from a
ing of the blood supply of the face and what tissues reappraisal and increased understanding of blood
can be safely moved has resulted in facial tissue supply to tissue
being tightened at a deeper, relatively avascular sur- c it is not possible to breastfeed after a breast
gical plane below the superficial muscles of facial reduction
expression. This results in less bruising and swell- d ‘non‐surgical’ cosmetic procedures are entirely
ing, and the ability to place tension on deeper struc- safe and carry no risk
tures, and not on wound edges, means that the very e grafts differ from flaps in that they carry with
tight appearance that plagued traditional tech- them their own blood supply
niques is avoided. These are just two examples, but
the principle underlying these operations, and plas- 2 Closing a wound at the time of injury with a
tic surgery in general, remains the same: the tissue split‐thickness skin graft:
that is to be transferred must have a robust blood a is best described as direct closure
supply, and the morbidity associated with harvest- b is best described as secondary closure
ing that tissue must be minimised. c is best described as primary wound closure
Finally, is not possible to eliminate risk, and all d can be safely and reliably performed in the
surgery, even so‐called non‐surgical cosmetic sur- presence of contamination
gery, can go wrong. This is critically important in
elective cosmetic procedures that are not medically 3 A composite graft or flap may contain:
required. Any decision to proceed to surgery must a skin
be based on a sound understanding of the risks b fat
involved in surgery and the other forms of treat- c bone
ment that may be available. The surgeon at all times d muscle
needs to ensure that full informed consent of the e all of the above
outcome of surgery, and the risks involved, is clearly
and carefully explained. 4 Which of the following describes how split‐
thickness skin grafts differ from full‐thickness
skin grafts?
Further reading a hair follicles and sweat glands are harvested
with the graft
Neligan PC (ed.) Plastic Surgery, 4th edn. Elsevier, 2017.
Weinzweig, J (ed.) Plastic Surgery Secrets Plus, 2nd edn. b can only be harvested from the donor
Philadelphia: Mosby Elsevier, 2010. site once
c are best used in areas of friction and shear,
such as the sole of the foot
MCQs d do not contract and are therefore the graft of
choice for eyelid reconstruction
Select the single correct answer to each question. The e none of the above
1 Which of the following statements is correct?
a plastic surgery developed in the 1970s as a
response to breast augmentation
Section 10
Trauma
48 Principles of trauma
management
Scott K. D’Amours1, Stephen A. Deane2 and
Valerie B. Malka1
1
University of New South Wales and Department of Trauma Services, Liverpool Hospital, Sydney,
New South Wales, Australia
2
Macquarie University, Sydney, and University of Newcastle, Newcastle, New South Wales, Australia
It needs to be recognised that for every patient

General principles who dies from injury, 10 more are admitted to
hospital with serious injury and two will suffer

Good trauma management recognises the impor-
significant long‐term disability.
tance of a number of key issues (Box 48.1).
Trauma system planning

Trauma as a disease
When examining deaths due to injury, there has been
Injury is a major economic burden to societies such
a fairly consistent finding worldwide that where sys-
as Australia. Recent estimates suggest a massive
tems of trauma care have not been specifically organ-
total economic burden on Australia’s economy
ised, 15–30% of the deaths can be deemed to have
annually of A$27 billion (an increase from the
been potentially preventable. In addition, approxi-
1990 estimate of A$13 billion), including both
mately two‐thirds of deaths in the absence of serious
direct and indirect costs. Injury is the most frequent
head injury have been deemed to be potentially
cause of death in Australians less than 45 years of
preventable. Much has been done to improve this
age, and is a major cause of death in all age groups.
situation with respect to education, standardised care
Most importantly, it accounts for more years of
and reorganisation, but more progress is still needed.
productive life lost than cancer and heart disease
Considerable attention has been given interna-
combined. The major impact of injury deaths and
tionally in recent years to the appropriate design of
disability is borne by the young adult segment of
regional systems of trauma care that enable patients
the population and disproportionately by males.
with potentially serious injuries to access a process
Although road traffic‐related injuries account for
that minimises the time from injury to definitive
only 30% of injury admissions to major trauma
care. The aim is to ‘get the right patient to the right
services, importantly this group accounts for 75%
hospital in the right time’. The essential compo-
of those with serious multi‐trauma and about 75%
nents of such a plan are outlined here.
of those who die in hospital from injury.
Many of the advances in trauma care in recent
Pre‐hospital triage
years have been derived from experience with inju-
ries suffered in war or with penetrating injuries Triage is the process of grouping injury victims
resulting from interpersonal violence, particularly according to risk of death or other adverse out-
in the USA. However, the proportion of patients come. Pre‐hospital care providers are trained to
admitted to hospitals in Australia with injuries carry this out using a criteria‐based system usually
resulting from gunshot wounds or stabbings is low, employing four simple groups of factors.
varying between 2 and 7%. Even within this popu- • Physiology: the vital signs, such as pulse over
lation, stabbings predominate. 120/min, systolic blood pressure less than
431
432 Trauma
hospital: the pre‐hospital triage process should

Box 48.1 General principles of good
identify patients who need to bypass the nearest
trauma management
hospital for one that has the resourcing and exper-
• The importance of injury as a public health issue tise to care for all types of serious injuries.
including surveillance, prevention, economic impact
and functional outcomes. Categorisation of hospitals
• The importance of the injury mechanism in
The role of a hospital within a regional system of
predicting actual injuries.
trauma care is designated by the appropriate health
• The differing implications of blunt and penetrating
authority. A major trauma service (level 1) has the
injury.
facilities and internal organisation to support its
• The importance of triage and a team‐based approach.
role as the most appropriate primary destination
• The importance to the triage process of:
⚬⚬ injury mechanism
for patients with potentially serious injuries. Some
⚬⚬ physiological status patients can be appropriately triaged to level 2 and
⚬⚬ evident injuries. 3 centres in the urban environment if the above
• The differing risk exposures and injury patterns in criteria are not met. In semi‐rural, rural and remote
children, young adults and the elderly. environments, strategically located regional trauma
• The patterns of associated injuries that are services (levels 2–4) are required. These smaller
commonly observed. trauma services must have strong links with a major
• The commonly documented deficiencies in acute trauma service. Even in remote environments
injury management. trauma care education, trauma service planning,
• The importance of an integrated trauma treatment and strong links with the rest of the regional
service in a hospital. network need to be continuously promoted.
• The value of clinical practice guidelines for the
assessment and management of acute injury. Hospital trauma response and trauma teams
• The importance of regional systems of trauma care
that link injury prevention activities, pre‐hospital Initial assessment of trauma patients requires an
care, acute care hospitals with differing roles, organised trauma response that aims to minimise
rehabilitation services and the overall return to the time from injury to definitive care (Box 48.2).
premorbid functioning. Such trauma responses or teams have a predeter-
mined multidisciplinary membership, a triage
device to trigger mobilisation, predetermined roles
for members, and standardised approaches to
90 mmHg, Glasgow Coma Scale (GCS) score less
the performance of primary survey, resuscitation,
than 15, point‐of‐care testing (e.g. blood gases).
• Anatomy: the immediately evident injuries such
as fractured long bones, pelvic fractures, spinal
Box 48.2 Goals of trauma assessment
cord injury, flail chest, positive FAST (focused
and resuscitation
assessment using sonography for trauma).
• Mechanism of injury: for example fall of more General goals
than 2 m, injury to two or more body regions, The sequence of goals in the initial assessment of an
vehicle crash with ejection, penetrating injury, individual trauma patient is as follows.
significant burns. 1 Save life: this requires knowledge of the causes
• Patient factors: extremes of age, use of anticoagu- of death
lants, pregnancy. 2 Prevent major disability: this requires knowledge of
the causes of disability
Pre‐hospital treatment and transport decisions 3 Diagnose and appropriately manage all injuries
4 Avoid unnecessary investigations or interventions
On the basis of the triage process, certain predeter-
mined decisions are made that attempt to direct the Achieve by:
transport of patients to the most appropriate hospi- 1 Minimise the time from injury to definitive care
tal. Pre‐hospital care providers are trained to recog- 2 Do not allow obvious injuries to distract from
diagnosing other, less obvious injuries
nise and treat life‐threatening problems in the field,
3 Follow the principles of ABCDE
including airway interventions, chest decompres-
4 Always have a clear management plan
sions, application of splints and pelvic binders
5 Assess response to intervention by re‐evaluation of
and administration of blood products. The most
the patient
appropriate hospital is not necessarily the nearest
48: Principles of trauma management 433
secondary survey and investigations. Most impor- investigation and surgical exploration in the presence
tantly the presence of a senior surgeon has been of gunshot wounds than with stab wounds.
shown to facilitate timely decision‐making, investi-
gations and both operative and non‐operative man- Deaths
agement resulting in better patient outcomes.
Deaths from injury can be broadly divided into
four groups that link the cause of death to the time
Disaster management
from injury to death: death at the scene; death
Certain natural and human disasters, as well as terror‐ within ‘minutes’; death within ‘hours’; and death
related incidents, can result in multiple casualties that over ‘days’ (some examples are given in Box 48.3).
may overwhelm otherwise well‐resourced hospitals. Many patients in the fourth group are recognised as
The increasing incidence of these events requires pre‐ ‘late septic complications’ or ‘multiple organ fail-
planned disaster responses, training of personnel and ure’. However, the foundations for these late com-
simulation exercises to ensure that the principles of plications are often laid in the first hour or two
acceptable injury management are applied. The prin- following injury; they relate to the extent and dura-
ciples of disaster management are designed to achieve tion of physiological disturbance. It is therefore
the best outcomes for the greatest possible number of clear that they can also relate to the promptness
casualties using standardised approaches. and completeness of early assessment and resuscita-
tion measures. Prevention of death can be linked
broadly to the principles in Box 48.4.
Blunt and penetrating mechanisms Disability
of injury
Disability principally relates to:
The patterns and severity of injury differ dramati- • cognition
cally between blunt and penetrating injury. The • locomotion
severity of injuries relates to the amount of energy • manipulation skills
transferred in the injury process and the amount of • chronic pain.
the body across which the energy is transferred. While definitive care of the actual injuries plays a
Serious injury from blunt trauma is typified by major role in preventing these categories of disabil-
victims of traffic‐related injury or by falls from a ity, it must be recognised that ensuring adequate
significant height. In these situations, large amounts oxygen delivery to brain and to muscle groups also
of energy are often transferred across broad and plays a major role, especially in the first hour or
multiple regions of the body without breaching the two after injury. As with death, prevention of disa-
walls of the body cavities. Accordingly, certain bility is linked to specific measures (Box 48.5).
injury patterns can only be broadly anticipated and
occult injuries are not uncommon.
Penetrating injuries are divided into those that Initial assessment
result from gunshot wounds and those from stab-
bings. A further small group are patients who suffer Efficient initial assessment of a trauma patient
impalement. It is important to recognise that inter- derives from the broad principles outlined previ-
personal violence can combine mechanisms (gunshot ously in Box 48.1, a clear understanding of the pat-
wounds, stabbings and blunt injury from a fist or a terns of death and disability (Boxes 48.3, 48.4 and
boot). Possible injuries from stab wounds can often 48.5) and recognition of the following factors.
be fairly confidently predicted as energy transmission • Trauma patient assessment is different from that
and tissue disruption is limited to the penetrating of the usual patient. The traditional approach of
tract. However, gunshot wounds can pose additional taking a full history, doing a full physical exami-
difficulties because the missile path may not be pre- nation, determining a provisional diagnosis and a
dictable and energy transmission and tissue disrup- list of differential diagnoses, and deriving a logi-
tion can cause gross destruction of surrounding soft cal plan for investigation and treatment needs to
tissues through cavitation and other aspects of be laid aside in order to first ensure a patient’s
ballistics and the physical features of the missile such survival and then to ensure the smallest possible
as velocity, size, mass and impact surface. Because of risk of major complications (see later).
the uncertainties posed by these features and the • Minimise the time from injury to definitive care,
potentially serious nature of possible injuries, a
with special attention to recognition and man-
lower threshold usually exists for comprehensive agement of haemorrhage.
434 Trauma
Box 48.3 Causes of death from injury Box 48.4 Prevention of death
Deaths at scene/incompatible with life General measures

• Brainstem transection • Optimise oxygenation (A, B)
• High spinal cord transection • Optimise perfusion acutely (C)
• Decapitation • Meticulous continuing fluid management
• Major thoracic vascular injury with free intrapleural • Thrombosis prophylaxis
bleeding • Adequate nutrition by appropriate route
• Major tracheobronchial disruption
Local measures
• Liver avulsion
• Arrest or minimise bleeding (C)
• Cardiac rupture
• Correct raised ICP (D)
Death within minutes • Control ‘leaks’ (tracheobronchial, oesophageal,
• Hypoxia: airway obstruction, tension pneumotho- abdominal hollow viscera, pancreas, urinary)
rax, open pneumothorax, massive flail chest • Decompress or revascularise ischaemic tissue promptly
• Major bleeding: external (amputation), thoracic • Debride dead tissue aggressively
(haemothorax), abdominal (spleen, liver, mesen- • Debride and clean contaminated wounds
tery, major vessels), pelvic fracture
• Pericardial tamponade (cardiac rupture)
• Rapid tentorial herniation: rapid rise in intracranial
pressure (ICP) Box 48.5 Prevention of disability
Death within hours General measures

• Hypoxia: severe pulmonary contusion, tracheo- • Optimise oxygenation (A, B)
bronchial rupture, diaphragm rupture • Optimise perfusion (C)
• Sepsis: perforated hollow viscus (e.g. thoracic • Protect spine (A and following measures)
oesophagus, abdominal viscera) • Correct raised ICP (D)
• Bleeding: external (face, massive wounds); thoracic
Local measures
aortic rupture; lungs, chest wall (haemothorax);
• Reduce dislocations as soon as possible
liver, spleen, retroperitoneum; pelvis fracture;
• Realign fractures as soon as possible
long‐bone fractures
• Correct local ischaemia early
• Coagulopathy
• Diagnose and decompress compartment syndromes
• Brain: increasing ICP (haematoma, swelling)
early
Death over days • Prevent secondary damage to nerves (iatrogenic
• Brain: high ICP from brain swelling, no cerebral injury, ischaemia, compression, e.g. dislocations)
perfusion • Debride ischaemic tissue early
• Respiratory failure: pneumonia, severe pulmonary • Debride contaminated wounds early
contusions, fat emboli, type 2 respiratory failure in • Find the ‘minor injuries’ to ligaments, joints and
elderly (i.e. hypoxaemia in setting of hypercapnia) small bones (tertiary survey)
• Renal failure: crush injury, acute on chronic,
contrast nephropathy
• Gastrointestinal failure, especially liver, gut mucosal • The concept of the ‘golden hour’ is important, a
barrier 1–2 hour period during which all opportunities
• Sepsis: pulmonary, abdominal, wound need to be taken to discover injuries that may
• Ischaemia: muscle groups, liver, gut cause death within minutes and then to discover
• Myocardial infarction injuries that may cause death within hours.
• Pulmonary embolus • Pre‐planned protocols or evidence‐based guide-
lines help to prevent errors in care.
Figure 48.1 outlines a well‐accepted approach to
• Any single measurement of physiology (e.g. pulse, the first 24 hours of injury management. The term
respiratory rate, GCS and blood pressure) is of lim- ‘initial assessment’ applies particularly to the ele-
ited value. Overall trends and specific tests (blood ments of primary survey, resuscitation, secondary
gases, viscoelastic testing) are more informative. survey, monitoring/reassessment and specific inves-
• Life‐threatening injuries may be occult, multiple tigations. The term ‘definitive care’ relates to spe-
life‐threatening injuries may coexist in different cific treatment (operative or non‐operative) aimed
body regions, and the injuries that appear most dra- at establishing the optimal conditions for the heal-
matic may not be those that pose the greatest risk. ing of specific injuries.
PRIMARY SURVEY
X-RAYS – CHEST
RESUSCITATION PELVIS + FAST MONITORING/
REASSESSMENT
INITIAL
ASSESSMENT
SECONDARY SURVEY
SPECIFIC INVESTIGATIONS
DEFINITIVE CARE
TERTIARY SURVEY
REHABILITATION AND DISCHARGE
Fig. 48.1 Acute trauma management procedure.
Primary survey and resuscitation primary survey requires awareness of a limited

number of life‐threatening entities, rapid and sim-
The strategy for primary survey and resuscitation is
ple systems of physiological assessment, and
outlined in Figure 48.2. The ABCDE sequence
awareness of a menu of interventions that can be
prioritises the importance of specific injuries and
applied to correct the identified problem. Some
assists clinical performance. Primary survey is the
aspects of care during the primary survey need
process used to assist the recognition of acutely life‐
special emphasis.
threatening injuries and should proceed concur-
rently with resuscitation. As the primary survey
Imaging
assessment scheme is followed, intervention should
be taken immediately to correct the problems that The only appropriate imaging at the time of the
are identified with each step. Note the emphasis primary survey should be directed towards proving
given to using simple measures to protect the cervi- or excluding a source for haemorrhage leading to
cal spine when attending to the adequacy of the haemodynamic instability. These include a chest
airway. External bleeding must be controlled; direct X‐ray, a pelvic X‐ray and a FAST examination.
pressure is usually effective. Lateral C‐spine X‐rays (previously routine) are not
In a hospital with a major trauma service and an required in initial patient assessment given the
effective trauma‐team response there will be enough primacy of haemorrhage identification and con-
team members to perform some parts of the trol. In major trauma patients, spinal injuries are
primary survey concurrently, together with the nec- presumed until excluded by further assessment and
essary resuscitative interventions. However, when CT scanning (with or without MRI). It is impor-
resources are limited the framework illustrated in tant to minimise movement of the cervical and
Figure 48.2 assumes even greater importance. thoracolumbar spine until after the completion of
Table 48.1 provides further detail regarding the primary survey or later if other injuries or
primary survey and resuscitation. Effective unstable physiology take priority.
436 Trauma
ASSESS INTERVENE
A—AIRWAY Obstructed
No problem
Protect C-SPINE
Secure patient airway

Protect C-SPINE
B—BREATHING Inadequate Exclude Tension pneumo thorax

(FAST, CXR or clinical examination)
No problem
Secure adequate ventilation

MONITOR AND REASSESS
C—CIRCULATION Inadequate
IV access – large × 2
Careful warmed fluid and balanced
blood product resuscitation
ARREST EXTERNAL BLEEDING (pressure)
No problem
Response No response
Tension Pericardial Significant

pneumothorax? tamponade? active
bleeding?
Decompress Decompress
Plan urgent IMMEDIATE SURGERY TO

D—DISABILITY (CNS)
thoracotomy ARREST HAEMORRHAGE
E — EXPOSURE (Complete)
—ENVIRONMENT CONTROL (Preserve Heat)
Fig. 48.2 Outline of strategy for primary survey and resuscitation.
Table 48.1 Primary survey and resuscitation.
Problem Assess Intervene
Airway Direct trauma: Cyanosis Gloved finger, light, suction

disruption/oedema Tachypnoea Laryngoscope, forceps
Obstruction: Voice Oxygen
Foreign bodies Stridor Chin lift/jaw thrust
Blood and vomitus Confusion Oropharyngeal airway
Soft tissue oedema ‘Respiratory distress’ Nasopharyngeal airway
Deteriorating Air movement Orotracheal tube
consciousness Supraglottic airway
Video‐assisted laryngobronchoscopy
Surgical airway:
Cricothyroidotomy
Urgent tracheostomy
Table 48.1 (Continued)
Problem Assess Intervene
C‐spine Unstable fracture Assume if: Protect C‐spine/limit mobility

Unconscious Collar
Head injury Sandbags
Face injury
Breathing Tension pneumothorax Cyanosis Oxygen
Massive haemothorax Tachypnoea Ventilation
Open pneumothorax Confusion Needle or finger thoracostomy
Massive flail ‘Respiratory distress’ Tube thoracostomy
Reduction in level of Shallow respiration Tracheal intubation
consciousness/poor effort Poor expansion Cover open wound: three‐sided dressing
High spinal cord injury Asymmetric expansion
Hyperinflation
Hyperresonance
Breath sounds
Tracheal shift
Diaphragmatic breathing
Circulation Bleeding: Pale, clammy, cool Haemorrhage control (direct pressure or
External (scene, bed, Peripheral cyanosis surgery)
floor) Confusion Oxygen
Chest (X‐ray) Tachycardia Intravenous access (large‐bore ×2)
Abdomen (FAST or Low pulse volume Warmed crystalloid/blood products
DPA/DPL) Slow capillary refill (packed red blood cells, fresh frozen
Pelvis (X‐ray) Neck veins plasma or plasma concentrate, platelets,
Femurs (clinical Heart sounds (muffled) cryoprecipitate)
examination) Blood warming
Combination Gastric tube
Surgery
Urinary catheter
Heart: Needle/finger tube thoracostomy
Tension Resuscitative thoracotomy
pneumothorax Cross‐clamp aorta/REBOA
Pericardial tamponade
Contusion
Infarction
Disability Secondary brain injury Alert A, B, C
(CNS) Intracranial haematoma Voice response C‐spine protection
Brain: Pain response Limited hyperventilation (aim Paco2
Compression Unresponsive low end of normal)
Contusion Lateralising signs Osmotic agents:
Laceration Pupils Hypertonic saline
Swelling Mannitol
Exposure Concealed injuries Prepare for secondary Remove all clothes
survey
Environment Hypothermia Warm fluids
control External warming devices (bear hugger,
warmed blankets)
Ambient room temperature
DPA/DPL, diagnostic peritoneal aspiration or lavage; FAST, focused assessment using sonography for trauma;
REBOA, resuscitative endovascular balloon occlusion of the aorta.
Shock
interruption of oxygen supply (airway). The next
A primary goal in minimising death and disability most urgent threat is interference with alveolar
is to ensure adequate oxygen supply to peripheral oxygen exchange (breathing). The third most
tissues. The most urgent threat to achieving this is important threat is failure of peripheral delivery of
438 Trauma
oxygen (via the circulation). The adverse effects of Gastric tube

shock occur at the microcirculation level, and early
Insertion of a gastric tube can be a life‐saving
recognition of shock depends on clinical observa-
manoeuvre if it is used to decompress a full stomach
tions of:
and avoid aspiration of gastric contents. A gastric
• the microcirculation of the skin (pale, cold, clammy)
tube should be inserted, usually towards the end of
• the brain (level of consciousness: confusion, agi-
the primary survey, in all trauma patients with major
tation, anxiety, etc.)
abdominal injury, major chest injury, spinal injury,
• the kidneys (timed urinary output via urinary
brain injury, major burns and shock. Gastric disten-
catheter).
sion is particularly common in injured children. In
The acid–base status of the patient, as manifested in
most situations the gastric tube can be placed
the results of arterial blood gases, gives an indica-
through the nasal route; however, in patients with a
tion of the magnitude of the microcirculatory fail-
high likelihood of basal skull or cribriform plate
ure and is an invaluable tool for assessing shock
fractures it should only be placed by the oral route.
and the response to resuscitation in a critically
injured patient. Urinary catheter
There is no great urgency to insert a urinary catheter
Cardiac arrest but it is helpful if used in patients with potentially
From time to time, injured patients present in actual serious injury and is inserted at the end of the pri-
or impending cardiac arrest. It is generally agreed mary survey. The observation of gross haematuria or
that attempted resuscitation of patients who have documentation of microscopic haematuria may have
no vital signs at the scene of injury will not restore important diagnostic implications. However, once
life except in some circumstances where hypother- the bladder is empty, monitoring of the hourly urine
mia is extreme. output is an important part of assessing the response
When patients who have arrived with recordable to intravenous fluid resuscitation. In nearly all
vital signs deteriorate rapidly so that cardiac arrest patients a urinary catheter can be placed by an expe-
is imminent, there is no time even to carry out a rienced operator. If it cannot be gently advanced, it is
rapid systematic primary survey. Management is advisable to seek urologist support or suprapubic
simplified by rapidly instituting the maximum catheter placement needs to be considered.
response to potential problems with airway and
breathing and circulation. This involves endotra- Secondary survey
cheal intubation and controlled ventilation with The emphasis in secondary survey is on identifying
100% oxygen, insertion of bilateral intercostal anatomical injuries and providing clinical informa-
catheters and insertion of at least two large‐bore tion that will determine the need for plain X‐rays
intravenous cannulas to facilitate infusion of and other special investigations. It is a careful and
warmed blood. External bleeding must be rapidly methodical physical examination from head to toe.
controlled by direct pressure. It requires close inspection, careful palpation and
Although victims of blunt trauma who arrive at appropriate auscultation. Common omissions
hospital without vital signs are unlikely to be sal- resulting in delayed identification of injury include
vaged by the most aggressive resuscitation, patients examination of the entire scalp, careful inspection
with sub‐diaphragmatic haemorrhage and circula- of the back (always needing a log‐roll), inspection
tory collapse may be salvageable with limitation of of the perineum and inspection of the axillae.
systemic circulation (resuscitative endovascular Table 48.2 outlines a useful sequence for the exe-
balloon occlusion of the aorta, thoracic aortic cution of the secondary survey. It also indicates the
cross‐clamping via left anterolateral thoracotomy), common general abnormalities that may be
volume resuscitation and immediate definitive sur- observed and highlights some simple procedures
gical intervention. that assist with pain relief, reduce the risk of infec-
In the setting of penetrating injury leading to car- tion and lead into the definitive‐care phase of early
diac arrest, there is greater opportunity for patient trauma management.
salvage. These patients require immediate resuscita-
tive thoracotomy with or without pericardotomy
Monitoring
and/or aortic cross‐clamping in the emergency
department to restore central perfusion (heart and Injuries may be multiple and occult and therefore
brain). Patients will then need definitive surgical repeated examination and close monitoring are
management in the operating room. essential, particularly in the first 24 hours following
the respiratory system, chest X‐rays, pulse oxime-

Table 48.2 Secondary survey: look! listen! feel!
try, capnography, arterial blood gases and ventila-
Head‐to‐toe tion pressures.
Monitoring of the circulation may include pulse
Glasgow Coma Scale Assess for the following rate, blood pressure, skin colour and temperature,
Scalp Tenderness level of consciousness, urinary output, assessment
Ears (including Lacerations (including
of volume status and cardiac function, serial
tympanic membranes) entry, exit wounds)
haemoglobin, arterial blood gases, drain outputs

Eyes (including pupils, Swelling (including
acuity, fundoscopic haematoma)
(e.g. chest tube), as well as repeated physical exami-
exam) nation of the abdomen and wound dressings.
Facial bones Structural deformity (i.e. Monitoring of the central nervous system relies
bones) heavily on physical examination and serial CT scans.
Mouth (including Discoloration (e.g. When CT scans reveal significant injury, an intracra-
teeth) bruising) nial pressure monitoring device may be required.
Neck (C‐spine, soft Crepitus (including Serial documentation of the GCS score is imperative
tissues, trachea) subcutaneous) in patients who are not sedated and paralysed.
Clavicles Ischaemia (i.e. limbs) Early detection and treatment of sepsis are
Chest: Functional impairment:
important. Temperature regulation and avoidance
Chest wall Visceral (lungs, heart,
of extremes are important in limiting adverse con-
Chest movement bowel)
Lungs Musculoskeletal sequences such as coagulopathy with hypothermia
Heart neurological or secondary brain injury with hyperthermia.
Abdomen Proceed with the following
Pelvis Take photos of wounds
Hips Sterile pad on wounds Definitive care
Thighs Pressure on bleeding sites
Knees Splint fractures: traction Definitive care is the phase of early trauma manage-
where indicated ment when particular injuries receive their specific
Legs Application of pelvic
treatment. Much of this takes place in the operating
binding device if indicated
theatre, and in situations of multiple major injuries
Ankles Pain relief
Feet Tetanus prophylaxis a number of surgical subspecialty teams may be
Upper arms Antibiotics if indicated involved. Figure 48.1 emphasises the need for
Elbows resuscitation to be continuing, and for monitoring
Forearms and reassessment of a patient’s responses to resusci-
Wrists tation to be conducted, throughout this and all
Hands other phases of care. Any deterioration in a patient’s
Fingers physiological status should lead to urgent reassess-
Back and flanks ment of the primary survey priorities and immedi-
(log‐roll)
ate intervention when acutely life‐threatening
Perineum, genitalia
events are identified.
Rectal examination
Urinalysis
Definitive care continues through any necessary
stay in the intensive care unit (ICU) and through
early convalescence on the hospital ward. As our
injury. Injuries may also progress to become life‐ or systems of trauma care improve, the interface
limb‐threatening, and recognition of these possible between acute care and rehabilitation should
patterns of progression are essential. Table 48.3 become progressively more invisible.
identifies some common injury progression patterns
to be wary of.
The monitoring strategy varies with the known Tertiary survey
injuries, comorbidity and age factors, other antici-
pated injuries and the potential consequences or The tertiary survey is a repeat clinical examination
complications of the known injuries or their along the lines of the primary and secondary sur-
management. veys. It is performed with the aim of identifying
Monitoring of oxygenation (airway and breath- injuries that have been missed during initial assess-
ing) may include skin colour, level of consciousness, ment. It is best performed after the early phase of
respiratory rate and depth, physical examination of definitive care and is most likely to be done if viewed
440 Trauma
Table 48.3 Common injuries and potentially dangerous sequelae.
Finding Beware
Fractured mandible: patent airway when Acutely obstructs if the patient lies down
patient sitting upright
Small pneumothorax: patient not Enlarges to become life‐threatening complete pneumothorax
compromised or develops tension
Small pulmonary contusions: patient well Progression of oedema or haemorrhage resulting in major
alterations to pulmonary compliance and oxygen exchange
Small intracranial haematoma: GCS >13 Enlarges leading to GCS drop, increased intracranial pressure
Contained arterial vascular disruptions: Free rupture and massive haemorrhage
haemodynamics normal
Arterial intimal injuries: no distal organ/ Thrombotic or embolic events, e.g. stroke, gut or limb
tissue compromise ischaemia, renal infarction
Crushed or reperfused extremity muscles Compartment syndrome, rhabdomyolysis, renal failure
as the first routine clinical task on the morning after prompt. Application and extension of the principles
admission of the patient to hospital. In addition to outlined for prevention of death will also succeed in
clinical examination, all X‐rays and CT scans should minimising disability.
be reviewed (along with final consultant radiologist
reports) and new X‐rays or other tests organised as Trauma registries and performance
indicated from the physical examination. improvement
Injuries that may not have been identified during It is critical that any mature or maturing trauma sys-
primary survey often have great functional impor- tem has a functional trauma registry that incorporates
tance and impact the return of the patient to normal information on injuries sustained and specific criteria
occupational, family and social functions. They usu- of initial assessment and management that can also be
ally pose little threat to life but often would lead to used as markers indicating adequate or inadequate
locomotor or manipulative disability if undetected care. Additionally, it is important that details of com-
and untreated. Examples include cervical spine plications and information on outcomes and lengths
injury without neurological deficit, fractures of of stay are included. It is only with this information
small bones in the hands and feet, ligamentous that objective comparisons can be made and assess-
injuries to the knee or ankle, dislocated acromiocla- ments of adequacy of care undertaken.
vicular joint and peripheral nerve injuries. Review Performance improvement refers specifically to a
of previous X‐rays will sometimes result in a new process whereby care is objectively assessed and strat-
diagnosis of pneumothorax, widened mediastinum, egies are implemented to either better the process of
pelvic fracture or rib fractures that require specific care or result in better patient outcomes. This
management. Visceral injury (solid organ or hollow approach requires objective collection of information,
viscus) may not be appreciated on clinical examina- a robust system of review or audit, strategies to ame-
tion or even on CT imaging, and must be considered liorate demonstrated deficiencies, and repeated collec-
especially in patients who then develop subtle signs tion of data to assess efficacy of changes. It is only
(e.g. mild tachycardia, change in abdominal exami- with repeated cycles of assessment and change that
nation). In addition, mild traumatic brain injury better overall results and outcomes can be achieved.
may have no initial signs other than amnesia. These
patients should be formally assessed using a test
such as the post‐traumatic amnesia test, which is Further reading
administered in the hours to days following injury.
Boffard KD (ed.) Manual of Definitive Surgical Trauma
Care incorporating Definitive Anaesthetic Trauma Care,
Outcomes 5th edn. Boca Raton, FL: CRC Press, 2019.
Gabbe BJ, Simpson PM, Sutherland AM et al. Improved
Prevention of deaths and disability functional outcomes for major trauma patients in a
regionalized, inclusive trauma system. Ann Surg 2012;
In accordance with these strategies, deaths that are 255:1009–15.
avoidable can usually be prevented. Diagnosis of Mattox KL, Moore EE, Feliciano DV (eds) Trauma, 7th
any problems must be early. Surgery must be edn. NewYork: McGraw‐Hill, 2013.
3 A restrained 32‐year‐old male involved in a head‐on

MCQs motor vehicle collision presents with chest pain and
the following vital signs on arrival in the emergency
department: heart rate, 120/min; blood pressure,
86/50 mmHg; GCS score, 10; and oxygen saturation,
92%. Which of the following takes first priority?
1 Which of the following critical determinants of a urgent CT scan of the head to rule out an
patient outcome following injury is incorrect? extradural haemorrhage with midline shift
a time from injury to definitive care b rapid resuscitation with two large‐bore intrave-
b presence of a well‐organised regional system of nous cannulas and warmed fluids
trauma care c ECG and an echocardiogram to eliminate cardiac
c protocols and guidelines when clinical experience contusion as the cause of his hypotension
is limited d obtaining an urgent cross‐match
d early mobilisation of teams led by doctors to e elimination of tension pneumothorax as a cause
most scenes of injury of his symptoms/signs
e thrombosis prophylaxis
4 Which of the following is not considered an
2 Which of the following does not result in hypovol- immediate threat to life?
aemic shock? a fracture of T6 with a complete spinal cord
a pulmonary laceration transection
b extradural haemorrhage b splenic injury with ongoing bleeding
c pelvic fracture c open pneumothorax
d femur fracture d rapidly rising intracranial pressure
e laceration to scalp e aspiration
49 Burns
Ioana Tichil and Heather Cleland
Victorian Adult Burns Service, Alfred Health, Melbourne, Victoria, Australia
the commonest cause of burns in the elderly, and

Introduction have a high mortality rate. Chemical and electrical
injuries are much less common than thermal inju-
Burns are common. From sunburn to scald injuries
ries (for more information see Burns Registry of
to major flame burns, anyone can be affected due to
Australia and New Zealand, www.branz.org).
the accidental and often unpredictable nature of the
injuries. Most are minor and will heal on their own
with little or no medical intervention. However,
Skin anatomy and physiology
severe burns are a life‐changing event, with
potentially devastating consequences for physical,
Skin is the largest human organ, comprising 16%
emotional, psychosocial and economic function.

of total body weight. Its main role is to protect
Therefore, burn treatments have been an area of
the body from the environment and to facilitate
interest and research in medicine from ancient
interaction via sensory input, to insulate and
times, and have principally involved the use of
thermoregulate, and to aid in immune defence
various topical applications applied in the hope of
and vitamin D production.
aiding spontaneous healing. More recently, the
Skin is composed of two layers, the epidermis and
acute surgical management of even massive burns,
the dermis, which rest on the panniculus adiposus
made possible by improvements in critical and sup-
(known as the hypodermis) and sometimes consid-
portive care, has resulted in significantly better
ered to be the third layer of the skin (Figure 49.1).
prognoses for burn‐injured patients.
The epidermis is a stratified squamous epithelium
containing keratinocytes in progressive stages of dif-
Epidemiology and aetiology of burns ferentiation, designated from deep to superficial lay-
ers as stratum basale, stratum spinosum, stratum
Incidence, cause, pattern, gender and age groups granulosum, stratum lucidum and stratum corneum.
affected by burns vary greatly between low‐ and Among the keratinocytes are melanocytes, antigen‐
middle‐income countries and high‐income coun- processing Langerhans cells and pressure‐sensing
tries. In Australia and New Zealand, it is estimated Merkel cells. Dermis contains collagen, elastic fibres,
that every year 1% of the population suffers a burn blood vessels, sensory structures, appendages and
that requires medical attention. Of these, 10% will fibroblasts. It is composed of two layers: a superfi-
require hospitalisation and of these 10% will have cial layer, the papillary dermis, and a deep layer, the
life‐threatening injuries. Thus, severe burns are rela- reticular dermis. The papillary dermis contains vas-
tively uncommon in Australia and New Zealand, cular plexuses, free nerve endings and Meissner’s
where adults and children alike are most likely to be corpuscles and the reticular dermis contains hair
injured at home in the kitchen or in the bathroom. follicles, sebaceous glands, sweat glands, hair folli-
For adults, workplace injuries and burns sustained cles, Pacinian corpuscles and Ruffini’s endings.
during recreational activities are also frequent. The capacity of a burn to heal without the need
Scalds are the third most common cause of injury in for surgical intervention is largely determined by
the general population and the most frequent form the depth of burn: the epithelial elements of the
of injury amongst the paediatric population. For dermis are destroyed by deep burns and therefore
adults requiring admission to burn units, flame is cannot heal by proliferation of epithelial stem cells
the commonest cause of injury. However, scalds are remaining in the wound bed.
443
444 Trauma
Epidermis
Sebaceous gland Partial

Thickness
Dermis Burns
Sweat gland
Hair follicle
Subcutaneous Full
Thickness
fat Burns
Fig. 49.1 Burn depth in relation to skin structure.
not require specialised care. Severe sunburn is a

Classification of burns typical superficial burn.
Burns are classified by extent (percent body sur-

face area involved and depth) and by cause. It is Superficial dermal (partial‐thickness) burns
important to accurately assess a burn injury, as Superficial dermal (partial‐thickness) burns extend to
extent determines treatment (transfer, resuscitation, involve the papillary dermis. They are very painful
surgical management) and prognosis. because of the exposed nerve endings. Capillary return
is brisk as dermal vasculature is intact. Serous blisters
are characteristic. The skin covering the blister is
Assessment of extent of burn
dead and is separated from the base by inflammatory
Size of burn is expressed as a percentage of total oedema fluid (Figure 49.4). When the blister ruptures
body surface area (TBSA) and is best assessed with the underlying papillary dermis is exposed, which pre-
the assistance of diagrams. For adults, the ‘rule of sents as pink, moist and shiny. These burns heal spon-
nines’ is used (Figure 49.2). Each arm is approxi- taneously by epithelialisation within 14 days.
mately 9% TBSA, the head 9% TBSA, each leg
18% TBSA, and the front and back of the torso Deep dermal (partial‐thickness) burns
18% TBSA each. The palmar surface of the hand
Deep dermal (partial‐thickness) burns extend into
(including fingers) is approximately 1% TBSA. For
the reticular dermis, i.e. the epidermis, papillary
children, who depending on age have a relatively
dermis and reticular dermis are affected. Blisters
larger head and smaller legs relative to torso, use
may be present on examination but have typically
the Lund and Browder chart (Figure 49.3) or equiv-
burst and sloughed very early (Figure 49.5).
alent. These are guidelines only and are less accu-
Exposed dermis is pale, or red due to red cell
rate in the morbidly obese. Superficial burns should
extravasation, and capillary refill is very slow. Some
not be included in extent estimates.
nerve endings may be intact so the burn can be sen-
sate but are generally less painful than more super-
ficial burns. They tend to be dry. These burns have
Assessment of burn depth the potential to heal through a combination of
Depth of burn is classified according to anatomy granulation, wound contraction and epithelialisa-
(Table 49.1). Superficial burns involve the epider- tion from deep dermal appendages and the wound
mis only. They clinically manifest as painful ery- edges with conservative management, but typically
thema and late blistering (‘peeling’ or dry scaling). take 3 weeks or more to heal and are at high risk of
They heal spontaneously within a few days and do hypertrophic scarring if allowed to do so.
49: Burns 445
4.5%
4.5%
18%
18%
4.5% 4.5% 4.5% 4.5%
1%
9% 9% 9%
9%
Fig. 49.2 ‘Rule of nines’ for estimating extent of burns in adults.
Mid‐dermal (partial‐thickness) burns Electrical injuries

Mid‐dermal partial‐thickness burns are burns that Electrical injuries are classified into high and low
present as neither superficial nor deep partial thick- voltage. Sources of low‐voltage current (<1000 V)
ness. It is not possible to predict soon after injury include domestic power supplies (240 V Australia
whether these will go on to heal within 3 weeks, and New Zealand), motor vehicle batteries (12 V)
and generally this will become evident only after and industrial switchboards (415 V). They can
5–7 days, as the burn wound evolves. result in significant usually localised tissue damage,
and less commonly other effects such as cardiac
Full‐thickness burns arrhythmias. High voltage is defined as greater
than 1000 V and is related to electrical distribution
Full‐thickness burns extend to the hypodermis. All systems, including high‐tension power lines
layers of the skin are affected, no dermal structures (11 000–33 000 V), power stations and substations.
are preserved and underlying hypodermic fat may be Tissue damage is, in simple terms, the result of
implicated. There is no blistering; the wounds are dry heat generated by resistance to current transfer.
with a charred leathery appearance, known as eschar, However, the precise mechanism of tissue damage
and underlying thrombosed blood vessels. These may be multifactorial, especially in high‐voltage
wounds do not heal with conservative management. injuries: electrical field changes can damage cell
membranes (a cause of rhabdomyolysis).
In high‐voltage injuries, in addition to damage
Burn mechanism due to current flow, arcing over a distance may pro-
duce a flash type of burn without direct contact
Most burns are due to thermal injury and are the with the current source. Arcs may also ignite cloth-
result of flame, hot liquids (i.e. scalds), contact with ing and result in flame burns. In high‐voltage injury,
hot objects, or radiant heat. Chemical and electrical current may be conducted according to a composite
injuries are uncommon. resistance across all tissues: limbs (especially at
446 Trauma
Lund and Browder chart

Plot burnt areas on chart below — do not include areas of erythema Region % Circ
A A Head
Neck
1
1
Ant. Trunk
13 13
Post. Trunk
2 2 2 2
Right arm
1½ 1½ 1½ 1½ Right hand
2½ 2½ Left arm
1
1½ 1½ 1½ 1½
Left hand
B B B B
Buttocks
Genitalia
Right leg
C C C C
Left leg
Total burn
1¾ 1¾ 1¾ 1¾
Time of assessment :
Superficial/partial thickness Full thickness Date / /
Circumferential YES NO Areas: Name of assessor
Airway Burn YES NO Signature
Designation
Age (years) 0 1 5 10 15 Adult Relative

A – ½ of head 9½ 8½ 6½ 5½ 4½ 3½ percentage of
B – ½ of one thigh 2¾ 3¼ 4 4¼ 4½ 4¾ areas affected
C – ½ of one leg 2½ 2½ 2¾ 3 3¼ 3 by growth
Fig. 49.3 Lund and Browder chart for estimating extent of burns in children. Source: Shutterstock.
Table 49.1 Assessment of burn depth.
Superficial partial thickness dermal burn Deep partial thickness dermal burn Full‐thickness burn
Colour Pink Pale/red White/red

Blisters Late Early Epidermis destroyed
Circulation Present Sluggish Absent
Sensation Hypersensitive: painful Decreased Anaesthetic
Healing <2–3 weeks >3 weeks No
joints, where there is localised increased resistance)

Chemical burns
will be more damaged than the torso. High‐voltage
injuries tend to cause extensive deep tissue damage Most chemical burns occur as a result of the
and are associated with high amputation and mishandling of household cleaners and other

mortality rates. chemicals. Because of occupational health and
49: Burns 447
Fig. 49.4 Superficial partial‐thickness burn at 24 hours with intact blister. Note hyperaemic underlying dermis.
Fig. 49.5 Mixed depth predominantly deep partial‐ and full‐thickness burns. Note necrotic epidermis which has largely
sloughed.
safety standards in Australia and New Zealand, of action. There is a wide variety of chemicals that
industrial exposures are rare. However, when they can damage tissues in many ways. Two broad cate-
occur they can be life‐threatening due to the high gories are acids and alkalis. As a general rule, acids
concentrations of toxic chemicals used in these such as sulphuric, hydrochloric and hydrofluoric
settings. produce injury by coagulation necrosis and precipi-
The severity of a chemical burn depends on tation of proteins, while alkaline substances such as
the agent’s concentration, quantity, manner and potassium hydroxide, sodium hypochlorite (bleach)
duration of exposure, penetration and mechanism or cement lead to liquefying necrosis that allows
448 Trauma
further penetration into the tissues resulting in

deeper, more severe and more extensive burns. In
Emergency management of burn patients
addition to direct tissue damage, chemical com-
The principles of initial management of a patient
pounds injure by various mechanisms including
with a severe burn consist of immediate first aid, fol-
exothermic reaction and tissue dehydration. In
lowed by primary and secondary survey, with institu-
some cases, additional systemic manifestations may
tion of simultaneous resuscitation. Burns are obvious
be associated with exposure (which can occur by
but should not distract from the possibility of coex-
inhalation as well as direct contact with skin),
istent other trauma, especially in patients who have
including metabolic acidosis and alkalosis, hypoc-
been involved in motor vehicle accidents or have
alcaemia, and liver or kidney damage.
suffered a high‐voltage electrical or blast injury.
First aid is aimed at removing the offending
agent, removing affected clothing, and application
of copious water irrigation for a minimum of
First aid at the scene
30 minutes. Irrigation should be prolonged if pain First aid should always be aimed at stopping the
persists. The use of specific neutralising agents is burning process and cooling the burn with running
generally not indicated for most agents, although water, ideally for 20 minutes within the first 3 hours
hydrofluoric acid exposure should be managed from injury, while avoiding hypothermia. Ice or
with calcium gluconate applied topically or injected iced water should never be used, as the subsequent
subcutaneously or intra‐arterially. Diphoterine® is vasoconstriction will deepen burns and increase the
a neutralising solution effective against a wide risk of hypothermia. The patient should not be
range of chemicals (but not hydrofluoric acid), in allowed to become hypothermic during irrigation.
addition to acids and alkalis, and is used for first Children especially are susceptible to the develop-
aid in industrial settings, although is not generally ment of hypothermia, and irrigation should be
available in hospital emergency departments. discontinued if this occurs. It is important to
Cutaneous chemical burns are often deep and remember to cool the burn and warm the patient.
require surgical management. Patients with major burns have suffered signifi-
cant trauma, and in addition to assessment of the
Inhalation injury burn wound should undergo a routine primary and
Inhalation of the toxic products of combustion may secondary survey in order to identify all injuries.
occur in association with burn injury, and is likely if Features of particular relevance with respect to
burns are sustained in enclosed spaces. Damage can burn‐injured patients are discussed in the following
be due to thermally or chemically induced injury to sections.
the upper and lower respiratory tract and may be
classified into three groups. Primary survey
• Most fire‐related deaths result not from cutane- A: Airway maintenance and cervical spine control
ous burns but from inhalation of toxic combus-
Patients with upper airway swelling due to inhala-
tion products. Carbon monoxide and other toxic
tion injury may present with a hoarse voice or (a
gases produce hypoxia that can result in altered
late sign) stridor, which is an emergency and an
conscious state and death.
indication for intubation.
• Heat and chemical damage to the upper airway
produces swelling and respiratory obstruction B: Breathing, ventilation and oxygen
over a period of hours after injury. supplementation
• Inhalation of irritant chemicals such as hydrogen
chloride, nitrogen oxide and aldehydes cause Circumferential full‐thickness chest and abdomen
acute pulmonary oedema and chemical pneumo- burns may impede ventilation and are an indication
nitis and may progress to adult respiratory dis- for escharotomy. Be aware of the possibility of
tress syndrome, with secondary infection. carbon monoxide poisoning where ‘cherry‐red’
Bronchoscopy is a useful diagnostic and therapeutic appearance can mask tissue hypoxaemia.
tool, but chest X‐ray has been shown to be an insen-
C: Circulation with haemorrhage control
sitive diagnostic investigation for inhalation injury.
Treatment starts with administration of 100% oxy- Circumferential full‐thickness limb burns can, espe-
gen. Where upper airway injury is suspected, early cially with fluid resuscitation, produce constriction
intubation is indicated to protect the airway, espe- of limbs and distal ischaemia. This is an indication
cially if the patient is to be transported. for escharotomy.
49: Burns 449
Patients with extensive burns rapidly become signs are the primary determinants for the ongoing
hypovolaemic due to fluid losses. Insert two rate of intravenous fluid resuscitation. Therefore,
large‐bore intravenous lines preferably through urinary catherisation is strongly recommended for
unburnt tissue, take bloods and start fluid all children receiving fluid resuscitation, as this pro-
resuscitation. vides the most accurate measure of urine output
and its response to changes in fluid rates.
D: Disability and neurological status The preferred choice of fluid resuscitation is no
different from that of adults (i.e. crystalloid) and
Altered consciousness may be due to inhalation
both Hartmann’s solution and normal saline (0.9%
injury.
NaCl) are in common use. Colloid has no current
routine place in fluid resuscitation for paediatric
E: Exposure with environmental control
burns, albeit the crystalloid versus colloid debate
Remove clothing and jewellery, log roll to assess the continues in the paediatric literature as it does in
posterior surface, keep patient warm and estimate the adult burns literature. The differences in burn
the percentage of burn area in relation to total body fluid management with respect to children versus
surface area. adults include the following.
• Definition of major burn: resuscitation fluids are
Resuscitation commenced for children with burns in excess of
10% TBSA.
Before proceeding to the secondary survey certain
• Optimal urinary output: 1 mL/kg per hour.
therapeutic steps must be taken. In adults with
• Cerebral oedema risk: children receiving exces-
burns of more than 15–20% TBSA, early fluid
sive resuscitation fluids are at increased risk of
resuscitation should be started in order to reduce
cerebral oedema, especially in the setting of
the risk of irreversible organ damage due to hypop-
hyponatraemia. This risk can be mitigated by
erfusion. Delayed or inadequate replacement of
careful monitoring of fluid rates and keeping the
intravascular volume in the setting of major burns
child ‘head up’ in the first 24 hours.
results in suboptimal tissue perfusion associated
• Maintenance fluids: these are given in addition to
with end‐organ failure and death. Multiple resusci-
any resuscitation fluids. Fasting children require
tation formulas are available but are a guide only
maintenance fluids to meet their physiological
to resuscitation, and should be titrated based on
requirements. They are particularly susceptible to
clinical parameters.
hypoglycaemia due to limited hepatic glycogen
A commonly used effective formula is the
stores. Therefore, the maintenance fluid must
Parkland Formula, which uses intravenous warmed
contain glucose (or dextrose), and the child’s
crystalloids (Hartmann’s solution) as follows:
blood glucose should be checked regularly during
3 – 4 mL weight kg %TBSA burn initial stabilisation and transport.
As with resuscitation fluid choices, the ideal
Half is administered in the first 8 hours after maintenance fluid for the injured child remains an
injury and the remainder in the subsequent area of controversy. There is consensus that hypo-
16 hours. The efficacy of fluid resuscitation is tonic fluids, such as 0.18% NaCl with 4% dex-
monitored primarily by urine output: a rate of trose, should not be used as they expose children to
0.5 mL/kg per hour should be the aim in risks of severe iatrogenic hyponatraemia. Recent
adults. A urinary catheter should be inserted evidence supports increased use of isotonic mainte-
for monitoring. nance fluids such as normal saline or PlasmaLyte to
avoid hyponatraemia.
Maintenance rates are calculated according to a
Fluid management in paediatric burns standard and internationally recognised paediatric
formula. This formula, commonly referred to as the
Fluid management in children with burns is both
‘4:2:1 rule’, can be summarised as follows:
similar to and different from that of adults with
burns. Intravenous fluid resuscitation is reserved
4 mL /h for the first 10 kg of body weight
for children whose total body surface burned
exceeds the definition for a major burn, and volumes 2 mL /h for each kg of body weight over 10 kg
and rates are commenced in accordance with the and less than 20 kg body weightt
modified Parkland Formula. Once fluid resuscita- 1 mL /h for each kg of body weight over 20 kg
tion is commenced, optimal urine output and vital of body weight
450 Trauma
Secondary survey s ubcutaneous fat along the mid‐axial lines of limbs,

and incision of chest and abdominal burns in order
This consists of two components: history and head‐
to relieve constriction caused by unyielding eschar
to‐toe examination.
over swelling deeper tissues.
History
Salient points of the history can be summarised by Indications for transfer to a burns unit
the mnemonic AMPLE.
Small superficial burns can be managed in an
A Allergies
outpatient setting with appropriate dressings and
M Medications
follow‐up. Patients with deep burns that will not
P Past medical illness
heal within 3 weeks are likely to require surgical
L Last meal
treatment and should be referred for operative
E Events and circumstances related to injury
management. Indications for referral and transfer
Of particular importance in the history is to
to a burns unit include:
ascertain when the injury occurred, and what
• more than 10% TBSA burn (adults) and more
treatment, including fluid resuscitation, has been
than 5% TBSA burn (children)
administered since. The mechanism and place of
• electrical burn
occurrence are also relevant in helping to assess
• chemical burn
the likely severity of the burn and likelihood of
• associated inhalation injury
inhalation injury.
• circumferential deep burns
• special areas (perineum/hand/face)
Examination • poor‐risk patient (comorbidities/pregnancy)
• Head and neck: check for corneal burns using • non‐accidental injury (suspected child or elder
fluorescein staining. Look for indications of pos- abuse)
sible inhalation injury, such as burns or blistering • associated trauma.
of the nose and mouth, singeing of nasal hairs,
soot in the mouth or pharynx, and blisters or
oedema of the tongue. Carefully check for signs
of cervical spine injury. Burn wound care
• Chest: examine the whole chest, assessing the
burn and noting whether it is compromising For patients with significant injuries who require
respiration. transfer to a burns unit, simple temporary dressings
• Abdomen: assess if abdominal burns are restrict- for transfer are recommended, such as plastic cling
ing respiration, especially in children who are film wrap, hydrogel or paraffin gauze dressings.
predominantly diaphragmatic breathers. Superficial dermal and some mid‐dermal burns that
• Perineum: check for perineal burns and other are expected to heal by epithelisation within 2–3
injuries. weeks with minimal scarring should be managed
• Limbs: assess the burns to determine if they are conservatively with dressings (Figure 49.6).
full‐thickness and circumferential. Such burns A burn wound should be cleaned and loose devi-
may cause constriction as swelling occurs and talised tissue removed. The ideal burn dressing will
impair venous return from the limb, leading to promote moist wound healing, protect against
further swelling and eventual cessation of arterial infection and assist in pain management. Non‐stick
inflow, producing tissue ischaemia and necrosis. dressings that can be kept intact for several days are
Ensure adequate analgesia, as burns are often particularly useful when treating burns in a paedi-
very painful injuries. Make sure the patient does atric population, where the aim is to minimise dis-
not become hypothermic. Ascertain adequate teta- tress brought about by changes of dressings and to
nus prophylaxis. avoid infection.
In order to minimise swelling, affected limbs and It should be noted that burn wounds evolve over
the head and neck region should be elevated. time and require dressings with different character-
Patients with deep circumferential burns that istics as they progress to healing. Early after injury,
impair circulation and ventilation may require burns produce significant amounts of exudate, and
escharotomy prior to transfer. Escharotomy is an dressings should be absorptive. The necessity for
emergency damage control procedure that entails this capacity decreases after the first few days. Even
incision of circumferential deep burns down to relatively minor burns are not ‘set and forget’
49: Burns 451
Fig. 49.6 Healing superficial burn 10 days after injury. Note that more superficial periphery of injury has healed, and
the islands of regenerating epithelial cells which will proliferate to resurface the rest of the wound.
injuries and require regular review to ensure they Major burns affect multiple organ systems. They
are progressing to healing. Silver‐impregnated elicit a hypermetabolic response characterised by
dressings are widely available in a variety of tachycardia and hyperthermia leading to protein
forms, but evidence for their value in superficial breakdown and muscle wasting. Adequate nutri-
non‐contaminated injuries is lacking. Principles tional support is required for all burns exceeding
for informing choice of definitive dressing and 20% TBSA. Immune system compromise due to
alternative types of dressing can be found at
inhibition of the humoral and cellular pathways
www.vicburns.org.au. contributes to susceptibility to infection, which is
Deep dermal and full‐thickness burns do not heal the leading cause of mortality in these patients.
spontaneously: their natural progression is to gran- Gut barrier function may be affected and result in
ulate, contract and epithelialise from the edges. bacterial translocation, which may be ameliorated
This may take several weeks or months, during by early enteral feeding. Patients with extensive
which time wounds are susceptible to infection. burns are also at increased risk of gastric ulcera-
Subsequent scarring is very often hypertrophic and tion. Acute respiratory distress syndrome (ARDS)
contracted and may lead to distorted local anatomy can manifest in the absence of inhalation injury as
and significant functional impairment. This is why part of the body’s SIRS response to injury.
treatment of deep burns is primarily surgical and Various systemic effects can persist for months
aimed at early excisional debridement and wound and even years after all wounds have healed and
closure using autologous skin grafting. range from central disposition of fat to decreased
muscle growth and bone mineralisation. In children
this can lead to a permanent reduction in growth.
Systemic effects of burn injury
Cutaneous burns larger than 20% in adults and Management of the major burn wound
10% in children can have an impact on the entire
body. A systemic inflammatory response syndrome Early excisional debridement of burn eschar, prefer-
(SIRS) consequent on a massive surge of inflamma- ably within 24 hours of injury, may result in benefits
tory mediators is characteristic of extensive burns. such as decreased SIRS response, decreased blood
The most notable early effect of this is ‘burns loss, decreased length of stay, and decreased risk of
shock’, characterised by hypovolaemia secondary invasive wound infections, particularly in massive
to fluid losses and oedema formation, and is a result burns. Tangential excision, whereby successive thin
of generalised increased capillary membrane per- layers of tissue are removed until healthy well‐per-
meability. Decreased cardiac contractility also confused tissue forms the wound bed, is preferred to en
tributes to burns shock. Prior to the recognition of bloc fascial debridement (Figure 49.7). Several
this phenomenon and the consequent need for methods are used to minimise blood loss during sur-
active fluid resuscitation in the early twentieth cen- gery, such us tourniquets, infiltration of tumescent
tury, many people with severe burns died from adrenaline solutions, use of topical diluted adrena-
shock secondary to fluid losses. line, diathermy and various fibrin‐based tissue glues.
452 Trauma
It is rarely a good idea to excise an extensive

burn wound and close the wound with autologous
split‐skin graft at the same sitting, especially in the
setting of acute excision, when the patient is still
undergoing resuscitation. After the burn is excised,
the wound should be closed with a skin substitute
until such time as the patient is stable, when wound
closure can be performed in a semi‐elective, and fre-
quently staged, manner. This is especially the case
when donor sites are insufficient for total wound
coverage.
There are different surgical algorithms for man-
aging such wounds (Figure 49.8). It is essential to
have a consistent and structured approach to
wound closure in patients with major burns, as sur-
Fig. 49.7 Excised burn wound of mixed full and partial vival ultimately depends on timely wound healing.
thickness depth showing preservation of deep dermis in Donor skin can be harvested as a split‐thickness
areas of deep partial thickness depth and hypodermis graft with the use of an electrical dermatome from
(fat) in areas of full‐thickness burn excision.
most sites of the body; thighs are preferred, but in
Early
excisional
debridement
BIOBRANE
Adhered
Not adhered
Patient resuscitated and stable
Remove
(Staged) Re-debride
removal Treat infection
Skin substitute
Dermal template Cadaver skin
Donor sites available
Split skin graft
Fig. 49.8 Surgical algorithm for large burn wound management.

49: Burns 453
Fig. 49.9 Skin mesher.
case of major burns any unburned skin can poten- in acute burns is due to their ability to temporarily
tially be used. Donor sites heal by epithelialisation close extensive wounds while patients are stabilised
from epithelial stem cells in dermal appendages and and donor sites for skin grafts become available.
may be reharvested when healed; depending on For example, Biobrane™ is an epidermal substitute
patient factors and thickness of grafts, this may be consisting of a nylon woven mesh coated with pig
as soon as 7–10 days. Skin grafts can be used as collagen and sealed with a thin silicone membrane.
sheets when repairing functional or aesthetic areas This adheres to open wounds and produces physi-
such as hands, face, neck and upper chest and they ological wound closure, until removed and replaced
can also be meshed to allow for expansion and cov- with an autologous skin graft. Other products are
erage of larger areas (Figure 49.9). This technique is designed to act as dermal templates and are gener-
useful in large burns where donor sites are limited. ally also bilayered constructs. The deeper layer
Widely meshed skin grafts rely on epithelial migra- is composed of animal collagen and supports
tion to fill the gaps in the mesh, which will take ingrowth and vascularisation from the wound bed.
longer to heal and result in suboptimal aesthetic When this has occurred, the superficial sealing layer
outcomes. In the case of large burns with very lim- is removed and the vascularised deeper layer now
ited donor sites, specialised centres may employ an composing the wound bed is skin grafted.
alternative to skin grafting by using tissue engineer-
ing techniques to produce cultured epithelial auto-
grafts (CEA). Otherwise, temporising measures to Teamwork in burn care
close the wound prior to skin grafting, in the form of
various epithelial or dermal substitutes or cadaver Specialised burn care is a complex undertaking,
allografts, can be life‐saving procedures because of delivered in burn units by a multidisciplinary team
their ability to close excised burn wounds (thereby of healthcare professionals. Burns surgeons work
decreasing the risk of wound infection) until donor closely with nursing staff, emergency physicians,
sites heal and become available for reharvesting. anaesthetists, pain specialists, infectious disease
Several skin substitutes are currently commer- physicians, intensivists, physiotherapists and occu-
cially available in Australia. Their main advantage pational therapists, speech pathologists, dietitians,
454 Trauma
psychologists and social workers to deliver care to 4.5% 4.5%

this complex patient group.
Conclusion
Knowledge of burn pathophysiology, and in par- 18%

ticular the systemic effects of burn injury, is a rela-
tively recent achievement, and most major
1%
developments in burn care have been made in the
last 60 years. Improvements in resuscitation, infec- 18%
tion control, nutritional support, treatment of inha-
lation injuries, wound management with early
debridement and coverage of wounds, and a multi-
disciplinary approach to treatment have signifi-
cantly lowered, and continue to lower, the mortality
rate for patients with severe burns, and improve
scarring outcomes and quality of life for survivors.
The future holds great promise for further improve-
ments through scientific developments in the areas
of skin tissue engineering and wound healing, and a 60%
that improved understanding of the pathophysiol- b 54%
ogy of contractures and hypertrophic scar forma- c 40%
tion produces better treatments. d 25%
e 36%
Acknowledgement 2 With regard to the patient in question 1, what would

adequate first aid consist of?
The authors are grateful to Warwick Teague, a wrap the affected area with a cold, wet towel/
Paediatric Surgeon and Director, Trauma Service, flannel
Royal Children’s Hospital, Melbourne for his b cool using ice or ice water, wrap in cling film and
advice on paediatric burn resuscitation. transport to hospital
c cover with silver‐based dressings and see GP for
follow‐up
Further reading d cool running water for 20 minutes within the first
3 hours
Burns Registry of Australia and New Zealand, www. e aloe vera cream
branz.org
Herndon, D. Total Burn Care, 5th edn. Elsevier, 2018. 3 With regard to the patient in question 1, what is
Klasen HJ. History of Burns. Rotterdam: Erasmus, 2004. the correct amount of resuscitation fluid that he
Victorian Adult Burns Service, www.vicburns.org.au requires within the first 8 hours?
a 5000 mL
b 4500 mL
MCQs c 4000 mL
d 5500 mL
e 10 000 mL
4 Surgical management may include:
1 A 49‐year‐old male, weighing 70 kg, suffers a a formal scrub in theatre
scald burn from freshly boiled water while handling b early excision of burns
a pot in the kitchen. The distribution of the burns c use of dermal substitutes
mostly affects the anterior limbs and truck as shown d temporised skin grafting
in the figure below. All of it is blistered and the e all of the above
epidermis is peeling off. What is the approximate
affected TBSA?
Section 11
Orthopaedic Surgery
50 Fractures and dislocations
Peter F. Choong
University of Melbourne and St. Vincent’s Hospital, Melbourne, Victoria, Australia
• Intra‐articular: fractures that extend to the artic

Fractures ular surface of a joint
• Special fractures:
Definitions ◦◦ Pathological fracture: fracture through an
abnormal bone
A fracture is a loss in the normal continuity of bone ◦◦ Stress fracture: fracture through repeated
following the application of a direct or indirect minor trauma to a normal bone (Figure 50.1)
force to that bone. A fracture may involve a part or
the entire circumference of the cortex.
Classification of fractures All fractures are painful. There is normally a history
of trauma except in pathological fractures where
Closed minimal trauma or no trauma is the rule. Fractures
A closed fracture is one that is not associated are tender, swollen, occasionally deformed, mobile
with a breach in the overlying skin or mucous at the fracture site, and associated with loss of limb
membrane. function.
Open
Investigations
An open fracture is one where there is direct com
munication between the fracture and the externa
Radiography
through a breach in the overlying skin or mucous
membrane. Open fractures are at significant risk All suspected fractures should be X‐rayed in two
for infection. planes (anteroposterior, lateral) (Figure 50.2).
Bone scans
Types of fractures Suspected fractures that are not obvious on plain
radiographs may be identified by bone scan, which
• Transverse
show increased isotope uptake corresponding to
• Oblique
the site of the fracture. This may be less apparent in
• Spiral
the geriatric group where an osteoblastic response
• Comminuted (more than two fragments)
may be less prominent. In the elderly, a delay of
• Displaced
1 week before bone scanning is usually required to
• Angulated
show a positive scan. Bone scans are useful for
• Impacted
detecting femoral neck and pelvic fractures in the
• Rotated
elderly and carpal injuries in younger patients.
• Distracted
• Greenstick: this occurs when only one cortex of
Computed tomography
the bone is seen to be fractured on the X‐ray, and
there is usually minimal deformity. This most Computed tomography (CT) is excellent for delin
commonly occurs in the paediatric age group eating cortical and trabecular bone. The plane of
457
458 Orthopaedic Surgery
Transverse Oblique Spiral Comminuted Displaced Angulated
Impacted Rotated Distracted Greenstick Intra-articular Pathologic
Fig. 50.1 Types of fractures.
(a) (b)
Fig. 50.2 Colles fracture. (a) Anteroposterior X‐ray of comminuted distal radial metaphyseal fracture. Note shortening
and slight radial angulation of the fracture. An important sign that denotes a fracture are overlapping cortices (arrow).
(b) Lateral X‐ray of comminuted distal radial fracture. Dorsal displacement, dorsal tilt and shortening is typical of a
Colles fracture.
50: Fractures and dislocations 459
the CT should be perpendicular or oblique to the • immobilisation of the fracture

fracture line to detect the fracture. CT is good for • protection until the fracture has consolidated
demonstrating periosteal new bone formation and • rehabilitation of the muscles and joints of the
may be valuable for diagnosing subtle stress frac affected limb.
tures such as minimally displaced femoral neck
fractures, pelvic ring fractures and rib fractures. Closed reduction
Magnetic resonance imaging Under appropriate anaesthesia (local, regional, gen

eral) the fracture fragments should be manipulated
Limited magnetic resonance imaging (MRI) in the and reduced into normal alignment. In reducing the
coronal or surgical plane is excellent for demon fracture, combinations of distraction, increasing
strating fractures which are suspected but not and then reducing the deformity of the fracture,
readily apparent on plain X‐rays. T1‐weighted and holding the reduction with three‐point fixation
MRI is able to detect the fracture immediately are employed. This technique of reduction is also
after injury and T2‐weighted images can differen used with open fractures (Figure 50.3).
tiate soft tissue inflammation from intraosseous
oedema. MRI scans are excellent for early detec
tion of undisplaced scaphoid and femoral neck Open reduction
fractures. Open reduction is indicated when closed manipula
tion of bone fragments has failed to reduce the frac
ture into a satisfactory position, if reduction is
Treatment impossible or if reduction is lost after initial closed
reduction. Open reduction may be indicated to sta
Closed fractures bilise fractures securely to allow safe and effective
The principles of management of a closed fracture management of the patient with multiple other
include: bone or soft tissue injuries, or if movement of the
• correction of the deformity (reduction) adjacent joint is paramount.
(a) (b)
Periosteum
Traction
Torn periosteum
(c) (d)
Reduction & 3 point fixation

Increase deformity
Fig. 50.3 Principles of the technique of fracture reduction. (a) Most fractures are displaced, impacted and shortened. It
is common that the periosteum on one side of the fracture is intact, while that on the other side is torn. (b) The first step
in reducing a fracture is disimpaction, where traction is applied along the axis of the bone to draw the fracture ends
apart. In young patients, this may be difficult because of the very thick and resilient periosteum. (c) The next step is to
increase the deformity so that the opposing ends of the fracture may be approximated. (d) The final step of reduction
once the fracture ends are opposed is to correct the deformity and to apply three‐point fixation to hold the fracture
reduction (arrows). The arrows point to areas where pressure must be applied while shaping the plaster‐of‐Paris cast.
Open fractures (a)

Open fractures are at risk of developing infections
(acute and chronic osteomyelitis). The principles of
management include the following.
• Cleaning of contaminated tissue. This is usually
accomplished by irrigation with copious amounts
of sterile irrigation solution. In heavily contami
nated wounds, pulsatile irrigation devices are
used to agitate the wound to assist in dislodging
and diluting foreign debris. The use of soaps or
iodinated solutions has been shown to reduce the
bacterial load in contaminated wounds.
• Debridement of traumatised wound edges and
tissue. This step is important for removing
necrotic or ischaemic tissue, which may become (b)
foci for infection if colonised by infective organ
isms. Careful surgical handling of the tissue is
mandatory to prevent extension of tissue injury.
• Stabilisation of fractures. Stability of the fracture is
important for protecting the surrounding soft tissue
from further injury, which may occur if the sharp
fracture ends were allowed to move. The method of
stabilisation is important and will depend on the
extent of the soft tissue injury (see later section).
• Closure of exposed bone by adequate soft tissue
cover. On completion of wound debridement, the
soft tissue defect may be closed either by direct
suture or tissue grafts. Tissue grafts may be in the
form of split‐skin grafts or tissue flaps. The deci
Fig. 50.4 (a) Large pelvic wound after amputation
sion regarding closure will depend on the degree
requiring multiple debridements prior to definitive
of contamination and size of the defect. closure. (b) Vacuum‐assisted dressing facilitates drainage
• Temporary wound closure using vacuum‐assisted of serous collections, enhances local vascularity and
dressings helps to minimise serous collections granulation, and assists wound closure by drawing in
within the wound defect, stimulate granulation wound edges to reduce the size of the actual skin defect
tissue, maintain a closing tension on the wound through suction.
to reduce skin edge retraction, and prepares the
wound for subsequent primary or graft closure Surgical considerations of open fractures
(Figure 50.4).
• Type 1 and 2 open fractures that can be thor
oughly debrided and cleansed with copious
Classification of open fractures
amounts of fluid (6 L) may be able to be fixed
Open fractures are classified according to the sever with internal fixation devices. Such injuries are
ity of the injury and the modality of injury. also treated with prophylactic perioperative anti
• Type 1: puncture of overlying of skin or mucous biotics for 48 hours, such as cefazolin 2 g i.v.
membrane by a bony spike from within. 8‐hourly.
• Type 2: laceration less than 1 cm overlying the • Type 3 open fractures are usually fixed with
fracture. external fixation devices after thorough debridement,
• Type 3: laceration greater than 1 cm overlying a cleansing and fracture reduction. Frequently, soft
fracture. tissue reconstruction is required to provide clo
• Type 3A: raising of a soft tissue flap around the sure of the wound. Administer cefazolin 2 g i.v.
fracture. 8‐hourly.
• Type 3B: absolute skin loss around a fracture. • Type 3C injuries are associated with a poor prog
• Type 3C: deep and highly contaminated wound nosis and amputation may be required in up to
such as after a farm injury, gunshot injury and 60% of cases. A course of antibiotics is usually
fractures associated with neurovascular injury. prescribed and the selection of antibiotic will
depend on the type of contamination introduced

into the wound, for example vancomycin 1 g i.v.
Outcome
12‐hourly (adjusted to pre‐administration levels)
and ceftriaxone 1 g i.v. 12‐hourly.
Fracture union
Fractures treated with closed reduction are said to
have united when no mobility occurs at the
Fracture immobilisation fracture site. Early union is normally associated
with some tenderness on stressing of the frac
Splintage ture, whilst complete union and consolidation is
Minor fractures such as those affecting the phalan said to be evident when there is no tenderness of
ges of the fingers may be treated using small metal the fracture site and stressing does not reproduce
or plastic splints. symptoms of pain. Radiographic assessment of union
is made by observing the development of fracture
callus and the gradual disappearance of the
Plaster of Paris cast fracture line.
Plaster of Paris cast immobilisation is a conven Rigid internal fixation with internal fixation
tional method of immobilising the fracture follow devices may reduce the amount of callus formation
ing closed reduction. This may be either a completely and because of the rigidity of the fracture immobi
encircling moulded cast or an incompletely encir lisation may make clinical assessment of union dif
cling cast (plaster slab). ficult. When fractures have been openly reduced
and internally fixed, the union is assessed using
Traction radiography to demonstrate the disappearance of
the fracture line.
Some fractures, particularly those involving the
lower limb, may be treated temporarily or defini
Fracture protection
tively by the application of traction along the
line of the limb. Traction encourages normal align All healing fractures must be protected against re‐
ment of the fracture and the increased tension of fracture by gradually permitting stresses along the
the surrounding soft tissue helps to provide internal fractured bone that is commensurate with the
splintage of the fracture. strength of that healing bone. In the lower limb, this
may be undertaken as a combination of graduated
External fixation weight bearing of the fractured limb and the use of
external supports such as crutches, splints and
External fixation is the application of transfixing braces after 6–8 weeks of non‐weight bearing. In
pins and bars to create a construct that lies exter the upper limb, weighted activity may commence
nal to the limb and acts to hold the fracture follow after 4–6 weeks.
ing either open or closed reduction. This method
of immobilisation is selected if unstable fractures
cannot be held using traditional non‐operative
Complications
techniques. External fixation is also indicated
when an open and contaminated fracture is at risk
Haemorrhage
of infection and therefore must be held immobi
lised by a system which does not introduce into the Bleeding may occur from laceration of adjacent soft
wound any foreign material such as metal plates tissue, vascular structures or through fracture ends.
and screws. Significant amounts of bleeding may occur into soft
tissue depending on the bone fracture, for example
Internal fixation closed femoral fractures may lose up to 2 L of
blood into the thigh, and pelvic fractures up to 4 L
Internal fixation is indicated when closed reduction into the pelvic cavity.
has failed, when further displacement is anticipated,
when closed non‐operative immobilisation consti
Infection
tutes a risk to the patient, or when internal fixation
allows earlier mobilisation, rehabilitation and earlier Infection is a risk for all open injuries. Adequate
return to normal function. Internal fixation includes prophylactic measures must be taken to prevent
the use of transfixing wires, inter‐fragmentary screws, infection in the setting of an open fracture or when
metal plates and intramedullary rods. internal fixation is employed.
Intra‐articular extension
Rehabilitation
Some fractures extend from bone into the joint.
Displacement of articular fragments must be treated On removal of a plaster cast, the joints adjacent to
by anatomical reduction to reduce the risk of post‐ a fractured limb require rehabilitation to prevent
traumatic arthritis. or treat stiffness. This involves passive and active
range of motion exercises and proprioception exer
Vascular compromise cises to improve the sense of balance in the recover
ing joint. In addition, it is important to return the
Excessive bleeding or swelling into the soft tissue
strength and endurance of the muscles in the injured
may induce a compartment syndrome where exces
limb by a regime of exercises.
sive pressures within the tissue compartment pre
Limbs treated with internal fixation may undergo
vent adequate blood flow to that compartment.
earlier mobilisation because the fracture is usu
Unless this is treated expediently necrosis of soft
ally more stable than those treated by plaster
tissue and subsequent scarring may cause loss of
immobilisation.
limb function or loss of the limb itself. The signs of
a compartment syndrome are dominated by pain
that is not responsive to analgesia. Increasing pain
Dislocations
following limb surgery mandates an examination
to exclude a compartment syndrome. Other signs
Definition
of limb ischaemia include pallor, paraesthesia,
paralysis, poikilothermia and pulselessness.
Dislocation is a complete loss of contact between
the articular surfaces of the bones forming a joint.
Late complications Subluxation is displacement of the joint with loss of
normal congruity but the articular surfaces remain
Delayed union in partial contact with each other (Figure 50.5).
Delayed union occurs when a fracture has not united

in a period of time that is at least 25% longer than Clinical presentation
the expected average time for fracture union at that
site. The causes of delayed union include inadequate Subluxations and dislocations normally follow
immobilisation, infection, avascular necrosis of direct or indirect trauma. These conditions may
bone, and soft tissue interposition between fracture also occur voluntarily in patients with ligamentous
ends. Delayed union is assessed radiographically. laxity. Dislocations may also follow an epileptic sei
zure or electrocution, and the classic injury is a pos
Non‐union terior shoulder dislocation. Patients complain of
Non‐union is said to have occurred when no evi pain, deformity and loss of function. Examination
dence of union is seen on sequential X‐rays over a demonstrates loss of normal contour of the joint,
6‐month period. Non‐union is associated clinically marked restriction of movement and pain on
with movement or pain at the fracture site. If there attempted passive motion of the joint.
is copious callus formation but without bridging of
the fracture, a state of hypertrophic non‐union is
said to exist and requires rigid internal fixation for Investigations
cure. If there is no evidence of callus formation,
then a state of hypotrophic non‐union is said to Radiography
exist and bone grafting and internal fixation is
Plain radiographs are sufficient to demonstrate dis
required for treatment.
locations and subluxations. Radiography in two
planes (anteroposterior and lateral) are essential for
Malunion
confirming the diagnosis. Occasionally, associated
Malunion occurs when the fracture unites with fractures may be seen and care should be taken not
a loss of anatomical alignment. Malunion by to displace these fractures in an attempt to reduce
shortening may be acceptable but angulation the dislocation.
and rotation of the bone following union may It is wise to obtain plain radiographs of all sus
not be acceptable and may interfere with normal pected dislocations to avoid the complication of
function. attempting closed reduction of a fracture or
(a) (b)
Fig. 50.5 (a) Fracture subluxation of the ankle. (b) Fracture dislocation of the ankle.
unwittingly converting an undisplaced crack into a

complete and displaced fracture.
Physiotherapy
Movement of the joint following reduction may

Treatment be encouraged after an adequate period of
time where healing of the soft tissues has occurred.
The principles of treatment are to reduce the dislo Supervised movement by a physiotherapist is normally
cation, immobilise the joint and to rehabilitate the encouraged to prevent re‐dislocation. The purpose
joint. of physiotherapy is to strengthen the periarticular
Closed reduction of the joint under adequate musculature to provide joint stability and also
anaesthesia and analgesia is undertaken with the to improve the range of motion that is normally
combination of traction, rotation and angulation. restricted because of capsular scarring. Streng
At all times forceful manipulation of the joint thening exercises of the joint are only encouraged
should be avoided in order to prevent fracture of after full range of motion has been achieved.
adjacent bones or neurovascular trauma.
Open reduction is undertaken when closed
reduction has failed. This may occur because of the Complications
interposition of tissue or the entrapment of the dis
located bone by capsular or ligamentous attach • Neurovascular injury
ments. Open reduction may also be undertaken if • Joint stiffness
the dislocation is associated with a complex frac • Recurrent dislocation
ture or neurovascular injury that requires explora • Fracture
tion and repair.
Chronic dislocations, i.e. joints that have been
dislocated for more than 1 week, are usually treated
by open reduction because soft tissue scarring and Further reading
fibrosis within the joint would normally prevent
normal reduction. Strudwick K, McPhee M, Bell A, Martin‐Khan M, Russell
T. Review article: Best practice management of of neck
pain in the emergency department (part 6 of the muscu
loskeletal injuries rapid review series). Emerg Med
Immobilisation Australas 2018;30:754–72.
Strudwick K, McPhee M, Bell A, Martin‐Khan M, Russell
Immobilisation of the joint may be performed using T. Review article: Best practice management of closed
a sling or splints. The purpose of immobilisation is hand and wrist injuries in the emergency department
to rest the joint to allow capsular and ligamentous (part 5 of the musculoskeletal injuries rapid review
healing. series). Emerg Med Australas 2018;30:610–40.
Strudwick K, McPhee M, Bell A, Martin‐Khan M, 2 In assessing the severity of an acute fracture, one
Russell T. Review article: Best practice management must always:
of common shoulder injuries and conditions in the a examine for subcutaneous emphysema
emergency department (part 4 of the musculoskeletal b examine for evidence of gangrene
injuries rapid review series). Emerg Med Australas
c examine the status of the neurovascular system
2018;30:456–85.
of the fractured part
d examine for a temperature and arrhythmia
T. Review article: Best practice management of com
mon knee injuries in the emergency department (part 3 e examine for evidence of a fat embolism
of the musculoskeletal injuries rapid review series).
Emerg Med Australas 2018;30:327–52. 3 The cardinal feature of a compartment syndrome is:
Strudwick K, McPhee M, Bell A, Martin‐Khan M, Russell a pain
T. Review article: Best practice management of com b hyperthermia
mon ankle and foot injuries in the emergency depart c rubor
ment (part 2 of the musculoskeletal injuries rapid d punctate ecchymosis
review series). Emerg Med Australas 2018;30:152–80. e limb hyperactivity
T. Review article: Best practice management of low
4 When a plaster cast is applied for a fractured wrist,
back pain in the emergency department (part 1 of the
musculoskeletal injuries rapid review series). Emerg care must be taken to instruct the patient on
Med Australas 2018;30:18–35. symptoms of:
a pulmonary embolism
b fat embolism
MCQs c air embolism
d compartment syndrome
Select the single correct answer to each question. The e Choong–Baker syndrome
at the end of the book. 5 Dislocation may be missed in which of the
following circumstances?
1 Radiological evidence of an acute fracture
a posterior dislocation of the hip
includes:
b posterior dislocation of the shoulder
a loss of continuity in cortical bone
c posterior dislocation of the elbow
b osteoporosis
d posterior dislocation of the sternoclavicular
c sclerosis of bone
joint
d reduced adjacent soft tissue markings
e posterior dislocation of the knee
e gas in the surrounding muscle
51 Diseases of bone and joints
Peter F. Choong
University of Melbourne and St. Vincent’s Hospital, Melbourne, Victoria, Australia
infarction of the involved bone. The necrotic bone

Infections is referred to as a sequestrum. In time, the elevated
periosteum generates new bone that surrounds the
Acute osteomyelitis sequestrum. The new tube of bone that is formed is
Acute osteomyelitis is an acute bacterial infection referred to as an involucrum. A communication
of bone. It occurs more commonly in paediatric and from the intramedullary abscess through the skin to
geriatric patients, and in those who are immuno- form a sinus is referred to as a cloaca, which may
compromised. Infection may also follow trauma discharge pus and necrotic debris. The presence of a
that is associated with major contamination of sequestrum, involucrum and cloaca is referred to as
bone or joints. chronic osteomyelitis.
Organism Clinical presentation

The commonest organism involved is There is often a history of minor trauma to the
Staphylococcus aureus. Other organisms include affected part. Trauma may give rise to a haema-
Streptococcus pneumoniae, Streptococcus spp., toma which then forms a locus of decreased resist-
Haemophilus influenzae, Gram‐negative organisms ance to infection (locus minoris resistentia). Several
and mycobacteria. days later the patient presents with a painful and
swollen limb where pressure over the infected area
Aetiology elicits marked tenderness. Children may be reluc-
tant to use the affected limb. With progression of
Bacteria pass from a distant source (e.g. dental
infection the patient becomes constitutionally
infections, open sores, urinary tract infections)
unwell (fever, rigors, sweat, nausea, vomiting, ano-
via the bloodstream to the metaphysis of bone
rexia). Fluctuance denotes the development of a
(haematogenous spread). Manipulation of infected
subperiosteal abscess.
areas (e.g. tooth extractions, urethral catheterisa-
tion) may cause a bacteraemia that can lead to
Investigations
osteomyelitis. Here the entrapped organisms
multiply to create an acute inflammatory, then
Blood tests
suppurative lesion in metaphyseal bone. Spread Full blood examination reveals elevated white cell
of infection from the intramedullary canal count, left shift, increased band forms, and elevated
through to the cortex may cause a subperiosteal erythrocyte sedimentation rate (ESR) and C‐reac-
abscess. Involvement of the adjacent joint may tive protein (CRP).
cause a suppurative arthritis while spread of
the infection across the growth plate in the paedi- Blood cultures
atric age group may cause growth abnormalities Blood should be taken for aerobic and anaerobic
(Figure 51.1). cultures on diagnosis (two sets of cultures 1 hour
Elevation of the periosteum by the abscess apart) and at times of high fevers (>38.5°C). Blood
together with intraosseous pressure caused by cultures should be obtained prior to the commence-
the metaphyseal abscess may result in a vascular ment of antibiotic therapy.
465
Growth plate
Joint capsule
Haematogenous spread Transepiphyseal

• Generalised sepsis extension
• Urinary tract infection
• Dental sepsis/manipulation
• Skin infections Subperiosteal extension
• Infected ingrown toenail
Direct inoculation
• Trauma
• Surgery
Fig. 51.1 Mechanisms of entry of infective organisms into bone and joints.
Radiography • secondary bone tumour, e.g. breast, lung,

Radiographs early in disease commonly demon- prostate
strate soft tissue swelling or an associated joint • haematological malignancy, e.g. lymphoma,
effusion but no bone changes. After 10–14 days, myeloma
radiographic changes include periosteal new bone • fracture, e.g. stress fracture.
formation, which signifies elevation or inflamma-
tion of the periosteum by oedema or infective mate-
rial and regional osteopenia. Treatment
Bone scans Antibiotic therapy

Infections induce a marked inflammatory response Intravenous antibiotics are initiated after blood
with hyperaemia of bone and increased bone turno- cultures have been taken (flucloxacillin 2 g i.v.
ver. Nuclear bone scans, using technetium‐99 meth- 4‐hourly and cefazalin 2 g i.v. 8‐hourly) and con-
ylene diphosphonate (99mTc‐MDP) or gallium‐67, tinued until the organism(s) has been identified
demonstrate increased tracer uptake at the affected and antibiotic sensitivities known. There is u
sually
site (hot scan). Indium white cell scans demonstrate a rapid response to the initiation of antibiotics
acute white cell collections (abscess). with an improvement in constitutional symptoms
and signs.
MRI is a very sensitive test for inflammation and Immobilisation
bony oedema. Marked marrow and soft tissue The affected limb should be immobilised and ele-
changes on TI‐ and T2‐weighted films can be vated to reduce oedema and pain.
expected. The sensitivity of MRI sometimes con-
founds the interpretation of marked bone and soft Analgesia
tissue oedema, where bone oedema arising as a Combination of oral and intramuscular analgesia
sympathetic response to overlying cellulitis may be may be required.
interpreted as osteomyelitis.
Surgery
Surgery is indicated if:
Differential diagnosis
• there is evidence of a subperiosteal or soft tissue
Important differential diagnoses for a painful swol- abscess
len bone include: • the patient’s condition deteriorates despite adequate
• primary bone tumour, e.g. osteosarcoma, Ewing’s antibiotics therapy, and there is radiological evi-
sarcoma dence of an intramedullary collection.
51: Diseases of bone and joints 467
Outcome cultures should be obtained prior to the commence-

ment of antibiotic therapy.
Modern antibiotic therapy is associated with
good and often complete resolution of infection.
Radiography
Occasionally a remnant nidus of infection will
Radiographs early in disease commonly demon-
cause repeated flare‐ups for which repeated courses
strate soft tissue swelling or an associated joint
of antibiotic therapy will be necessary. If a seques-
effusion with elevation of the extra‐articular fat
trum develops and is colonised, a state of chronic
pad. There are usually no bone changes.
osteomyelitis may develop.
Bone scans
Infections induce a marked inflammatory response
Acute septic arthritis
with hyperaemia of bone and increased bone
This is an acute bacterial infection of a joint. It is turnover. Nuclear bone scans (e.g. 99mTc‐MDP,
commonly monoarticular but may occasionally gallium‐67) demonstrate increased tracer uptake
affect several joints concurrently. at the affected site (hot scan). Indium white cell
scans demonstrate acute white cell collection
Organism (abscess).
The commonest organism involved is Staphylococcus Ultrasound

aureus. Other organisms include Haemophilus and Joints that are difficult to palpate (e.g. shoulder,
Neisseria species. hip) may be examined with ultrasound scans.
Aetiology
Joint aspiration
Septic arthritis may arise from haematogenous An experienced doctor should perform a joint
spread, direct inoculation, transepiphyseal spread aspiration under sterile conditions with a large‐
of osteomyelitis or direct spread from a subperi- bore needle and the fluid should be submitted for
osteal collection of pus (see Figure 51.1). microbiological examination, culture and antibi-
otic sensitivities. Ultrasound or CT guidance can
Clinical presentation be valuable.
The patient is often febrile and toxic. Any move-

ment of the joint causes extreme pain. In the elderly, Differential diagnoses
symptoms may be less dramatic than in younger Important differential diagnoses for an acutely
patients and the diagnosis may be missed. The swollen and painful joint include:
elderly are also prone to multifocal infections, with • gout
several joints being affected at the same time. The • haemarthrosis, e.g. post‐traumatic, haemophilic,
joint is swollen, tender and warm. The joint need coagulopathic
not be erythematous. An antecedent history of • trauma, e.g. osteochondral injury or fracture,
trauma to the limb may exist, or acute septic arthri- intra‐articular ligament injury
tis may follow as a complication of a local skin or • inflammatory arthritis
bone infection. Examination of the cardiac valves is • degenerative arthritis.
necessary to ensure that these are not the source of
infections (bacterial endocarditis) or a consequence Treatment
of septic arthritis.
Surgery
Arthrotomy, irrigation and drainage of the joint.
Investigations
Blood tests Antibiotic therapy
Full blood examination shows elevated white cell Antibiotics are instituted following blood cultures
count, left shift, increased band forms, and elevated and culture of joint fluid (flucloxacillin 2 g i.v. 4‐
ESR and CRP. hourly and ampicillin 1 g i.v. 6‐hourly) until an
organism is identified and sensitivities known.
Blood cultures
Blood should be taken for aerobic and anaerobic Immobilisation
cultures on diagnosis (two sets of cultures 1 hour The limb should be immobilised in a splint and
apart) and at times of high fevers (38.5°C). Blood elevated until symptoms resolve.
Physiotherapy Treatment
Gradual physiotherapy should be prescribed after
• Arthrotomy, irrigation and drainage of the joint
symptoms resolve to regain joint motion.
if the infection is in its acute phase.
• Immobilisation of the limb until the disease is
Outcome quiescent.
Early and adequate treatment is important to • Commence anti‐tuberculous medication follow-
prevent cartilage destruction (chondrolysis) that
ing joint and tissue culture.
may lead to stiffness and arthritis. • Commence physiotherapy after the disease has
become quiescent.
Chronic infective arthritis Outcome
Chronic infective arthritis is uncommon and is Anti‐tuberculous therapy is usually successful in

usually seen following Mycobacterium tuberculosis controlling or eradicating the infection. However,
infections. complications include:
• stiffness from intra‐articular fibrosis
• deformity from destruction of the growth plate
Pathology • degenerative arthritis from cartilage destruction
Joint infection usually follows seeding from a dis- • osteomyelitis from local spread
tant site such as the lung or kidneys. In addition, • haematogenous dissemination.
chronic tuberculosis osteomyelitis may also extend
from the metaphysis or epiphysis into the articular
cavity.
Arthritides
Pain in the joint is variable and may be extreme or Degenerative arthritis
slight. Typically, this is most severe at night when Degenerative arthritis is one of the commonest
the patient relaxes and joint movement during conditions in orthopaedics and a major cause of
sleep causes severe attacks of pain (night cries). life years lost through disability. The commonest
Constitutionally, the patient is unwell with fever, joints involved include the hip, knee, shoulder and
lassitude and loss of weight. lumbar spine. Other joints less commonly involved
Affected joints are swollen with a doughy syno- include the carpometacarpal joint, elbow and
vial thickening, effusion and gross muscle wasting. ankle. Degenerative arthritis is a progressive con-
There is restriction and pain with movement, but dition that is initiated by an acute or chronic repet-
this is not as severe as in acute suppurative arthritis. itive insult.
There may be joint sinuses and marked stiffness
(fibrous or bony ankylosis).
Causes
Investigations • Idiopathic
Blood tests • Trauma
Full blood examination demonstrates an elevated • Infection
lymphocyte count, elevated ESR and anaemia of • Inflammation
chronic infection. • Metabolic, e.g. gout, pseudogout
• Avascular necrosis, e.g. steroid induced, osteo-
chondritis dissecans
Mantoux test
Mantoux test is positive; however, in overwhelming
disease there may be no reaction. Clinical presentation
Pain
Joint aspiration and culture Pain typically occurs with movement or with weight
Joint aspiration and culture may demonstrate acid‐ bearing (mechanical pain). This may radiate to
fast bacilli. More recent tests using polymerase involve the whole limb if it is advanced. Referred
chain reaction (PCR) techniques can demonstrate pain is common, for example knee pain in severe
the characteristic DNA pattern of mycobacteria. hip arthritis.
Stiffness Treatment
Patients note a restricted range of motion, develop
Non‐operative
a limp and are unable to function normally, such as
This usually consists of pain relief with oral
to run, climb stairs or twist their leg to put their
analgesics and anti‐inflammatory medication. The
shoes on.
use of a walking aid such as a walking stick for
lower limb arthritis and splints for upper limb
Deformity
arthritis may also be helpful. Physiotherapy to
With progressive loss of motion and the develop-
maintain range of motion and to prevent further
ment of contractures the patient loses symmetry of
loss is valuable. A mobile arthritic joint is better
the joints. This results in an abnormal gait or pos-
than a stiff arthritic joint.
ture (Figure 51.2).
Operative
Investigations • Prosthetic joint replacement: this is usually rec-
ommended in the advanced stages of arthritis
Radiography
when the severity of symptoms of functional loss
The four main radiological features of arthritis
has reduced the quality of life to an intolerable
include loss of joint space, subchondral sclerosis,
state. The commonest sites of arthritis requiring
osteophyte formation and cyst formation
joint replacement are the hip, knee, shoulder and
(Figure 51.3).
elbows. It is a very successful procedure, with the
survival of joint replacements approaching 95%
at 15 years from initial surgery.
• Osteotomy: this is the division of bone and may
be used to correct the deformity of arthritis and
realign the limb biomechanically to allow pas-
sage of forces through less‐affected parts of the
joints, thus reducing the pressure across the
arthritic part of the joint. Osteotomy has an
important role in managing knee arthritis and
may provide the patient with many years of pain
relief before joint replacement, which in many
cases is inevitable. Osteotomy is also used with
good success for the management of hallux
valgus.
• Arthrodesis: this is the surgical fusion of a joint,
which is usually undertaken in the smaller joints
of the feet or hands or in very young patients.
Fusion results in permanent loss of motion but a
successful fusion can also result in complete pain
relief because the arthritic joint is no longer
mobile.
Outcome
Arthritis is a progressive disease characterised by
remissions and relapses. Non‐operative treatment
may slow the rapidity of symptoms. Whilst X‐rays
demonstrate the extent of arthritis, symptoms may
not always correlate with the severity of radiologi-
cal features.
Fig. 51.2 Typical varus deformity in a patient with

osteoarthritis of the knees where that part of the limb Inflammatory arthritis
distal to the joint is deviated towards the midline. This
contrasts with the knees of a patient with rheumatoid This is a spectrum of seropositive and seronegative
arthritis where that part of the limb distal to the joint is arthritides characterised by acute and subacute
deviated away from the midline (valgus). chronic and relapsing joint inflammation. Joint
(a) (b)
Fig. 51.3 The radiological features of (a) osteoarthritis include joint space narrowing (dotted arrow), subchondral cyst
formation (solid arrow), osteophyte formation (dashed arrow) and subchondral sclerosis (double body arrow).
Compare this with (b) a normal joint.
involvement is part of a clinical picture that may joints of hand, wrist and feet, and triggering of
manifest in multiple large and small joints at the tendons. Eventually involvement of the hips,
same time or be limited to only one or a few joints. knees, shoulders and ankles are noted. Valgus
Inflammatory arthritis may also affect bones, ten- deformities of the knee or a ‘windswept’ appear-
dons and other organs. ance with varus deformity of one knee and valgus
of the other are typical. Ulnar deviation and swan‐
Pathology neck and boutonniere deformities of the fingers
are characteristic.
The cause of inflammatory joint disease is thought
Patients with seronegative arthritis usually pre-
to be an autoimmune process beginning with a syn-
sent with monoarticular arthritis involving the
ovitis that causes articular cartilage destruction,
large joints such as the knee and hip, although
disruption of the joint capsule and a proliferative
small joint involvement of the hand with nail
synovitis.
changes are also seen in psoriatic arthritis. These
patients also present with low back pain. Progressive
Types
vertebral stiffness, kyphosis and sacroiliitis are typi-
• Rheumatoid arthritis (seropositive) cal of advancing ankylosing spondylitis. Visceral
• Psoriatic arthritis (seropositive and seronegative involvement of the heart, lungs, liver, spleen, bowel
varieties) and eyes may occur.
• Ankylosing spondylitis (seronegative)
• Reiter’s disease (seronegative)
• Inflammatory bowel disease (seronegative) Investigations
• Behçet’s disease (seronegative)
Blood tests
Full blood examination reveals elevated white cell
Presentation
count and elevated ESR.
Typically, patients complain of stiffness, pain and
joint swelling. Characteristic exacerbations and Serological tests
remissions are noted, and constitutional symptoms • Rheumatoid factor
may be present, with acute joint involvement. • Anti‐nuclear antibody
Patients with rheumatoid arthritis may present • Anti‐double‐stranded DNA antibody
with bilateral symmetric involvement of the small • HLA‐B27
Radiography definition of the metaphyseal region of bone. The

• Seropositive disease: radiographs demonstrate costochondral junctions may be expanded (rickety
soft tissue swelling, osteopenia, joint erosions or rosary).
narrowing, and symmetric bilateral joint deform-
ity of the hands and feet. Treatment
• Seronegative disease: monoarticular involve-
ment, sacroiliitis, syndesmophytes, bamboo • Correction of malabsorption syndromes
spine, enthesopathy, and ossification of the cap- • Supplementation of vitamin D and calcium.
sular margins. • Surgical correction of long‐standing bone
deformity
Bone scans
Generalised uptake around joint. Increased uptake
Osteomalacia
in arterial phase demonstrating active synovitis. This is a condition of the adult skeleton character-
Bone scans are useful for identifying stress fractures ised by inadequate bone mineralisation. The main
from associated or steroid‐induced osteoporosis. causes of this include vitamin D deficiency, vitamin
D resistance (renal failure), impaired vitamin D
Treatment synthesis (liver failure, renal failure) and other met-
abolic disturbances.
• Rest and immobilisation of affected joints.
• Analgesia, anti‐inflammatory medication and
Presentation
corticosteroids.
• Disease‐modifying medication such as metho- Patients present with pathological fractures or radi-
trexate, penicillamine and gold. ological evidence of bone loss (Looser’s zones), and
• Splints or braces to prevent or correct deformities. muscle aches and pains. There is no growth abnor-
• Surgery to correct deformities or joint destruc- mality because osteomalacia is a condition of the
tion (osteotomy, arthrodesis, joint replacement). mature skeleton.
• Synovectomy is the removal of inflamed syn-
ovium. This is usually indicated in early disease Investigations
and may be performed by open surgery, arthros-
copy, or radiotherapy with intra‐arterial instilla- Blood tests
tion of a radioisotope. • Elevated serum alkaline phosphatase
• Reduced serum calcium
• Reduced serum vitamin D
Metabolic conditions of bones
Radiography
Rickets • Looser’s zones in areas of stress, e.g. pubic rami,
femoral neck
Rickets is an uncommon condition of the immature • General osteopenia
skeleton characterised by poor mineralisation of
osteoid. It is caused by a dietary lack of calcium and Bone biopsy
vitamin D or a lack of exposure to sunlight. It is Bone biopsy shows deficient mineralisation with
usually seen in malnourished patients such as those widened unossified seams of osteoid.
in developing countries. Rickets may also be seen in
malabsorption syndromes. Treatment
• Correction of metabolic irregularity
Presentation
• Supplement calcium and vitamin D
Joint tenderness, swelling and deformity. Bones • Fixation of fractures if appropriate
typically involved include the tibia (genu varum)
and ribs (rickety rosary).
Hormonal conditions of bones
X-rays Hyperthyroidism (see Chapter 37)

Gradual deformation of long bones is seen. In addi- A reduction of thyroid hormone produces growth
tion, there is expansion and loss of cortical abnormalities in infant and paediatric patients.
There is stunted growth, a delay in walking and The fragility leads to bone deformity and/or frac-
cretinism. The late appearance of secondary ossi- tures and soft tissue abnormalities.
fication centres suggests hypothyroidism. Early
treatment with thyroid hormone supplementation Classification
is important to prevent mental retardation.
Type Inheritance Clinical features
Hyperparathyroidism (see Chapter 38) I Autosomal Childhood fractures, hearing

dominant loss, blue sclera ± opalescent
Hyperparathyroidism is due to increased secretion teeth, commonest
of parathyroid hormone. This may be caused by II Autosomal Lethal, multiple fractures, flattened
hypersecretion by a parathyroid adenoma or a sec- recessive vertebrae, blue sclera, very rare
ondary response to chronic renal failure. Increasing III Autosomal Birth fractures and progressive
the secretion of parathyroid hormone raises serum recessive deformity; short stature, ±
calcium through bone resorption. Bone resorption opalescent teeth; white sclera,
spinal deformity and
results in a bone‐softening condition wherein path-
costovertebral anomalies
ological fractures are frequent.
IV Autosomal Skeletal fragility, no hearing
dominant loss, moderate growth failure,
Clinical picture white sclera, may have
opalescent teeth
Nausea, vomiting, weight loss, abdominal pain,
bone pain and muscular weakness.
Presentation
Investigations
Patients with the severe form of osteogenesis imper-
Radiography fecta die at or soon after birth with multiple frac-
There is a generalised reduction in bone density. tures. Patients who survive at birth may present as
Late in the disease bone resorption manifests as an abnormality of development with a typical glob-
bone cysts. Mottling of the skull and subperiosteal ular‐shaped head, frontal bossing, stunted growth,
erosions of the phalanges are commonly seen. kyphoscoliosis and hypermobility of joints. There is
Other manifestations of hypercalcaemia such as commonly a history of multiple fractures following
renal calculi or heterotopic calcification are seen. minimal trauma. If presentation occurs during ado-
lescence, normal skeletal development is seen and
Blood tests fracture incidence declines with increasing matu-
• Elevated serum calcium rity. Fracture healing is normal but remodelling is
• Decreased serum phosphate abnormal, giving rise to bone deformities. Many
• Elevated urinary phosphate survivors have blue sclera, which is due to the
• Elevated parathyroid hormone abnormally thin and translucent sclera highlighting
the dark choroid behind it.
Treatment
• Correction of metabolic irregularity Radiography
• Surgical removal of adenoma or partial removal
Radiographs show multiple healing or old frac-
of the parathyroid glands
tures, bone deformities, ribbon‐shaped ribs and
Wormian bones in the skull and a trefoil pelvis.
Congenital/developmental conditions
Pathology
Osteogenesis imperfecta The condition is characterised by marked cortical
Osteogenesis imperfecta is an extremely rare condi- thinning and attenuation of trabeculae. There may
tion characterised by bone fragility. be persistence of hypercellular woven bone.
Pathology Treatment
This is an inherited condition, and results from an Patients require protection from injury particularly
abnormality in the metabolism of type 1 collagen. when young. Treatment is aimed at correcting limb
deformities by multiple osteotomies and a transfix- that usually presents in childhood and affects the
ing pin or rod. Fracture healing is excellent. growing ends of long bones. Occasionally, ribs,
vertebrae and the pelvis may also be involved.
Dyschondroplasia
Also known as Ollier’s disease, or multiple enchon- Pathology
dromata, dyschondroplasia is characterised by the
development during youth of multiple asymmetric There is an aberration in physeal regulation with
intraosseous cartilage masses. the development of cortical exostoses at the grow-
ing end of bones with a cartilage cap of varying
thickness. This is an autosomal dominant condition
Pathology
in which abnormalities of chromosomes 18, 11 and
There is an abnormality of metaphyseal bone organ- 19 have been identified.
isation. Although metaphyseal growth ceases after
puberty, enchondromata may continue to grow.
Clinical presentation Patients present with problems of:
• impingement
Patients present with metaphyseal swelling that
• deformity
may be particularly severe in the fingers. This may
• limb length discrepancy
affect joint function and the length of the bone.
• malignant transformation to chondrosarcoma.
Limb length discrepancies are not unusual.
Investigations Investigations
Radiography Radiography
Radiographs show areas of lucency with central Exostoses are sessile or pedunculated. Trabecular
calcific stippling and endosteal scalloping. bone of the diaphysis is confluent with that of the
Shortening, angulation and expansion of bone can exostosis and the cortex of the osteochondroma is
be seen. continuous with that of the bone from which it
arises.
Bone scans
Increased 99mTc‐MDP uptake in the lesions implies Bone scans
ongoing growth and remodelling of surrounding Increased 99mTc‐MDP uptake in the lesions implies
bone. Activity in the lesions itself can be demon- ongoing growth and remodelling of surrounding
strated by avidity for thallium or pentavalent bone. Activity in the lesions itself can be demon-
dimercaptosuccinic acid (DMSA). strated by avidity for thallium or DMSA.
Treatment Computed tomography

CT scans are excellent for demonstrating cortical ero-
Troublesome lesions may be excised or curetted. The sion, endosteal scalloping and the large cartilage cap.
prognosis is good. Rarely, transformation to low‐
grade chondrosarcoma may occur. This should be Magnetic resonance imaging
suspected in lesions that show a recent increase in size MRI is excellent for demonstrating the soft
and pain, and radiographs that demonstrate lysis, tissue component, intramedullary changes and the
expansion/remodelling of bone, endosteal erosion thickness of the cartilage cap (if >1 cm, suspect
and cortical breach. Wide resection is recommended. malignancy).
Outcome
Treatment
A normal life expectancy is usual.
Simple excision of the lesion at its base should
suffice. Occasionally, correction of angular

Hereditary diaphyseal aclasis deformities is required. Malignant transformation
Also known as multiple cartilaginous exostoses, is uncommon but when it occurs transformation
hereditary diaphyseal aclasis is a skeletal condition to a low‐grade chondrosarcoma is noted. Like
the sarcomatous transformation noted in dys-

chondroplasia, removal of the tumour requires
Bone conditions of unknown origin
wide resection.
Paget’s disease
Outcome Paget’s disease is a condition of adults in middle
age and onwards. It is a deforming condition char-
A normal life expectancy is usual.
acterised by disorganised bone formation and bone
resorption. Two stages exist, an acute hyperaemic
and bone‐softening phase and a chronic brittle
Achondroplasia phase.
This is an autosomal dominant condition charac- Pathology

terised by abnormalities in limb length in the pres-
ence of a normal‐sized trunk and an enlarged head. It is thought to be of viral origin, as viral inclusion
It is the most common skeletal dysplasia. bodies have been noted within osteoclasts from
affected bones.
Pathology
Presentation
It is a hereditary defect of cartilage modelling,
caused by a mutation in the gene for fibroblast Patients may complain of a painless deformity of a
growth factor receptor protein. Normal chondral long bone such as the femur and tibia. Alternately,
calcification does not occur. Periosteal bone forma- patients may also complain of pain, which is
tion is normal. This causes thickening of bone but usually dull and constant and not related to activ-
not lengthening of bone. Membranous bones are ity. Pain may be due to Paget’s disease, stress frac-
not affected. tures or malignant change. Common bones to be
involved include the skull, pelvis, femur, tibia
Clinical presentation and single vertebrae. Patients may also develop
symptoms of nerve compression, pathological/
The classic achondroplastic dwarf has short limbs, stress fractures, and high‐output failure from the
a normal trunk, a large head with frontal bossing regional hyperaemia which may act like an arteri-
and a flattened root of the nose. Patients develop ovenous shunt.
the typical bow‐legged appearance and an increase
in lumbar lordosis. Lumbar canal stenosis is com-
Investigations
mon because of short pedicles and the increased
lordosis. Blood tests
Elevated serum alkaline phosphatase.
Radiography
Radiographs show short tubular bones with wide Urinary tests
metaphyses. Elevated urinary calcium and hydroxyproline
excretion.
Treatment
Bone biopsy
Corrective osteotomies may be required for Biopsy demonstrates abundant disorganised woven
abnormality in joint alignment, and limb‐length- bone with abnormal cement lines and abnormal‐
ening surgery may be useful for increasing height shaped lamelli, so‐called crazy pavement.
and reach. Limb bowing may lead to degenerative
knee arthritis where osteotomy or joint replace-
Radiography
ment may be required. Canal stenosis may be
Radiographs show coarse trabeculae, thickened
severe enough to cause significant nerve root
cortices, flame‐shaped lysis, stress fractures, bone
impingement symptoms that may require surgical
deformity, enlarged bone and malignant change.
decompression.
Bone scans
Outcome
Bone scans show markedly increased uptake of
A normal life expectancy is usual. radioactive tracer in active Paget’s disease.
Treatment may be seen in the pubic rami, sacrum, medial tibia

and sometimes the distal tibia. The shafts of bone
• Pain relief: oral analgesia, non‐steroidal anti‐
may look washed out with a pencilled‐in cortex.
inflammatory drugs
• Anti‐osteoclastic drugs: bisphosphonate, calcitonin
Bone mineral density scans
• Surgery: joint replacement, correction of deformity
Bone mineral density scans show low mineralised
bone content. Results are compared to age‐ and
Outcome sex‐matched control data to determine the risk of
fracture.
Paget’s may become burnt out with established
deformities and hard, brittle and pain‐free bone.
Bone biopsy
Fractures through this bone are not uncommon
Bone biopsy may be required if the diagnosis and
because of their brittle nature. Abnormality in bone
cause for apparent bone loss is unclear. Tetracycline
architecture may predispose to arthritis. Sometimes,
labelling protocol is required to determine the rate
differentiation between the pain of Paget’s disease
and amount of bone formation within a given time.
and arthritis may be difficult. Rarely malignant
transformation may occur, which carries a very
Treatment
poor prognosis.
• Correction of metabolic deficiencies
• Correction of the underlying medical condition
Osteoporosis • Reduction of bone resorption (bisphosphonates)
• Oestrogen supplementation
Osteoporosis is an absolute loss of bone mass with
• Vitamin D supplementation
an increase in fracture risk.
Pathology
Fibrous dysplasia
There is normal mineralisation of osteoid, but the
absolute amount of bone is decreased. Osteoporosis This is a deforming condition of bone that may
may be associated with calcium deficiency, second- begin in young adulthood. It is characterised by
ary hyperparathyroidism, excess alcohol intake, abnormal development of cysts and fibrotic areas
immobilisation, steroid use and malignancy. within bone associated with gradual deformation.
When associated with McCune–Albright syndrome,
fibrous dysplasia is associated with precocious
puberty, hormonal dysfunction and pituitary
Osteoporosis has an insidious onset characterised abnormalities.
by a gradual loss of height with increasing age, the
development of kyphoscoliosis and a predisposi- Presentation
tion to fracture after minor trauma or falls. Specific
The patient may complain of pain or the condition
areas prone to fracture include vertebrae, the pelvis
may be an incidental finding on X‐ray.
and radius. Stress fractures of the tibia and pelvis
are common.
Investigations
Radiography
Investigations
Radiographs demonstrate thickened bone, with
Blood tests lytic areas containing matrix with a typical ground‐
Primary osteoporosis has a normal blood profile. If glass appearance. Bone deformities include ‘shep-
associated with other causes, blood derangements herd’s crook’ abnormality of the proximal femur,
may be typical of those other conditions. thickened cortices and expanded diaphysis.
Radiography Biopsy
Lumbar vertebrae are bioconcave with herniation Biopsy demonstrates normal trabeculae of bone
of the disc into and through the endplate of the ver- broken up into tiny islands of bone by fibrous
tebrae (fish‐shaped). There may be osteoporotic stroma and bland cells giving a ‘Chinese character’
wedge fractures of the vertebrae. Stress fractures type appearance.
Outcome reduction in the excretion of uric acid. Deposition

of urate crystals and the subsequent inflammatory
There may be gradual deformity in a weight‐bear-
response elicits painful joint symptoms and other
ing bone. Pathological fractures may also occur.
visceral complications. Pseudogout is a replica of
Malignant change occurs rarely.
gout, but the crystals are rhomboid and positively
birefringent and the major abnormality is that of
Conditions of joints high levels of calcium pyrophosphate in the joint.
Charcot’s disease Clinical features

Charcot’s disease is the consequence of conditions Patients present with acutely painful swollen and
that result in denervation or loss of proprioceptive tender joints. If severe, there may be constitutional
sense, predisposing to bone and joint destruction symptoms. Joint symptoms can be mistaken for
(neuropathic joint). septic arthritis. Typically, the metatarsophalangeal
joint of the big toe is affected. In chronic gout,
Pathology deposits of urate crystals in the soft tissue (tophi)
are common and these can be seen on the ear and
Repeated trauma leads to fracture, poor healing and
on the phalangeal joints of the fingers and toes.
joint derangement. Predisposing causes include dia-
Other associated conditions include cardiac dis-
betes, alcoholism, syringomyelia, syphilis and trauma.
ease, hypertension and renal failure.
Presentation
Investigations
Patients present with painless, deformed and swol-
len joints. The ankle and knee are the most com- Radiography
monly affected joints. Syringomyelia should be Radiographs may show peri‐articular erosions,
suspected with Charcot’s disease of the shoulder. joint deformities and soft tissue calcifications.
Patients may also present with the complications of
deformed joints (e.g. chronic non‐healing ulcers Blood tests
overlying bone prominences). Elevated serum uric acid. This may be normal in
30% of patients. The white cell count is elevated, in
Radiography addition to elevated ESR and CRP.
Typical radiographic signs include dense bone, Joint aspiration

destruction of joint, para‐articular bone debris, and Joint aspirations should be performed under sterile
deformity. conditions and fluid submitted for biochemical and
microbiological examination including culture.
Treatment Typically, negatively birefringent needle‐shaped
crystals are noted.
Bracing
Deranged joints may be stabilised with external
braces or splints. The purpose of this is to prevent Treatment
further deformity rather than to correct it, which is
usually permanent. • Rest immobilisation and elevation of joint
• Oral and intramuscular analgesia
Surgery • Anti‐inflammatory medication
Surgery to correct the deformity or to arthrodese • Colchicine
the joint is usually met by failure. Amputation is • Allopurinol
considered if the joint becomes useless and is an • Dietary control
impediment to limb function or is complicated by
persistent infection.
Outcome
Gout
Patients with gout often have recurring attacks.
Gout is an abnormality of purine metabolism char- Uncontrolled gout may lead to joint destruction
acterised by excess production of uric acid or a and renal tubular failure.
Pigmented villonodular synovitis Magnetic resonance imaging

MRI demonstrates cartilage very well and is excel-
This is a rare condition characterised by localised
lent for detecting intra‐articular loose bodies.
nodular or papillary overgrowth and inflammation
of the synovium. This may cause bone erosions,
subchondral cysts and large soft tissue masses. Treatment
There is controversy as to whether this is an inflam-
• Synovectomy
matory or true neoplastic process.
• Removal of loose body
• Joint replacement in severe disease with associ-
Clinical presentation ated articular degeneration
Patients may present with a range of symptoms
including recurrent joint swelling and pain, soft tis- Osteochondritis dissecans
sue masses and osteoarthritis. Osteochondritis dissecans is a condition of adoles-
cence and young adulthood that is characterised by
local avascular necrosis of epiphyseal bone causing
Investigations
fracture and/or separation of an osteoarticular
Radiography fragment.
Radiographs show generalised joint narrowing if
the diffuse form of the disease is present. Typically,
subchondral cyst are large and situated at a dis- Clinical presentation
tance from the joint. The commonest joints involved are the knee, elbow
and ankle. It presents initially with pain on weight‐
Magnetic resonance imaging bearing activity. Repeated joint effusions or clicking
MRI demonstrates an articular soft tissue or locking of the joint may be noted.
haemosiderin‐laden carpet of synovium, or a well‐
circumscribed mass. Synovitis is well demon-
strated by this scan. Investigations
Radiography
Treatment Early in the condition this may be normal. Late in
the condition a defect of bone may be seen and a
• Synovectomy loose fragment may be noted. Typical areas include
• Radiation synovectomy with intra‐articular the lateral side of the medial femoral condyle,
isotopes superomedial corner of the dome of the talus, the
• Joint replacement head of the second metatarsal and the capitellar
surface.
Synovial chondromatosis Bone scans

Bone scans may show increased focal activity.
This is a metaplastic condition of the synovium
resulting in the formation of numerous intra‐articu- Computed tomography
lar cartilaginous loose bodies. CT scans are excellent for demonstrating a sub-
chondral fracture.
These may cause painful catching or locking or
MRI is excellent for demonstrating lesions that are
osteoarthritis of the joint.
not visible on radiography or CT scans. MRI can
detect oedema and inflammation surrounding the
Investigation area of necrosis.
Radiography
Radiographs demonstrate intra‐articular loose
Treatment
bodies if they are calcified. If the loose bodies
remain cartilaginous, they may not be detectable on • Acute pain may be treated by rest, partial weight
radiographs. bearing and use of crutches.
• Arthroscopy and drilling of the fragment may Computed tomography

assist and encourage a new blood supply and CT scans provide excellent imaging of cortical and
thus healing of the fragment. trabecular destruction. Pulmonary scans are man-
• Open reduction internal fixation is indicated if datory for determining systemic spread.
the osteochondral fragment is large.
• Ex vivo autogenous chondrocyte culture and Magnetic resonance imaging
reimplantation is a new and exciting technique MRI provides excellent multiplanar imaging with
for treating this condition. unsurpassed soft tissue contrast. MRI is important
for determining the site, size, shape, consistency
and vascularity of a tumour, and the relationship of
Outcome
adjacent structures. This modality is extremely
Lesions that remain attached usually proceed to important for assessing surgical margins.
heal. Detached lesions may heal after internal fixa-
tion, but if too small may simply be discarded. The Nuclear scans
residual defect does not heal normally and may pre-
99m
Tc‐MDP bone scans are excellent for demonstrat-
dispose to osteoarthritis if it is large and on the ing multicentric bone involvement. Such scans are
weight‐bearing surface of bone. also important for determining response to treat-
ment. More recently, functional nuclear scans (e.g.
thallium, positron emission tomography) allow an
assessment of tumour activity (Figure 51.4).
Orthopaedic malignancies
Biopsy
Malignant primary tumours of bone Biopsy is important for confirming the diagnosis
and for determining histological subtype. Biopsy
Sarcomas are primary malignancies of bone and
may be performed percutaneously with fine‐ or
soft tissue. The cells of origin arise from mesenchy-
wide‐bore needles, or through a formal incision.
mal and neuroectodermal tissue. Two peak inci-
More invasive methods carry a higher risk of com-
dences exist (<20 years and >55 years). Males are
plications and contamination of tissue planes. Each
more commonly affected. The commonest site for
year 30% of limbs are lost through inappropriate
bone sarcomas is the lower limb, particularly
biopsy site and technique. In principle, biopsies
around the knee.
should be performed at a tumour centre by a mus-
culoskeletal specialist in tumour surgery.
Sarcomas present with a mass. Bone sarcomas are Treatment
painful; characteristically, the pain is constant,
Chemotherapy
unremitting, nocturnal and responds poorly to
All osteosarcomas and Ewing’s sarcomas are
oral analgesia. It is important to note that bone
treated with protocols of preoperative chemother-
pain that is unremitting and not responsive to
apy unless the patient’s renal or cardiac function
simple analgesia should raise suspicions of a
prohibits the use of chemotherapy. Chondrosarcoma
tumour.
is resistant to chemotherapy.
The most frequent bone sarcomas are osteosar-
coma, Ewing’s sarcoma and chondrosarcoma. Radiotherapy
Radiotherapy is usually indicated for soft tissue
Investigation sarcomas and is also combined with chemotherapy
in certain cases of Ewing’s sarcoma. This may be
All investigations must be completed prior to provided preoperatively or postoperatively. The
biopsy because biopsy can produce imaging benefit of preoperative radiotherapy is the smaller
artefacts that may confound the final histological target of irradiation. Postoperative radiotherapy
definition. Inappropriate biopsy site or procedure requires targeting of the entire operative field. The
may jeopardise limb‐sparing surgery. complications of preoperative versus postoperative
radiotherapy are comparable.
Radiography
All suspected bone tumours should be radio- Surgery
graphed. Typical patterns are recognised for most Surgical margins may be classified as intralesional
tumours. (tumour capsule is transgressed), marginal
(a) (b) (c) (d)
Fig. 51.4 (a) Radiograph of a distal femoral osteosarcoma showing typical areas of mixed lytic and blastic changes
within the tumour. Note the periosteal new bone formation (arrow). (b) MRI clearly shows the intraosseous and
extraosseous extension of the tumour. (c) Bone scanning shows the activity of new bone formation stimulated by the
tumour. The changes before and after chemotherapy on bone scanning may indicate response to treatment. (d)
Functional metabolic imaging (thallium or positron emission tomography) shows the metabolic activity of the tumour
itself before chemotherapy (upper panel) and after chemotherapy (lower panel), where a good response is noted by the
marked reduction in nuclear tracer activity.
(pericapsular inflammatory zone is transgressed), Clinical presentation

wide (surrounding cuff of normal tissue) and radi-
Patients present with pain, pathological fracture or
cal (entire tumour‐bearing compartment is excised).
loss of limb function, or as an incidental finding on
All sarcomas should be excised with at least wide
other imaging. Solitary metastases are uncommon.
margins. Intralesional and marginal margins are
Up to 30% of bone metastases are the initial pre-
regarded as inadequate and are associated with the
senting feature of carcinoma.
highest local recurrence rates.
Outcome Investigations
The 5‐year metastasis‐free survival for osteosar- Radiography
coma is 75%, for Ewing’s sarcoma 50% and for Radiographs of the affected limb are vital for deter-
chondrosarcoma 80%. All patients should follow a mining the extent of disease and the likelihood of
regular program of surveillance with clinical exam- fracture.
ination, pulmonary CT scans and imaging of the
operated area.
Bone scans
Bone scans are important for determining multicen-
Secondary malignancies tricity of bone disease. All hotspots should be
Metastatic carcinomas are the commonest malig- radiographed.
nant tumours of bone. Carcinomas that commonly
metastasise to bone include breast, prostate, lung, Magnetic resonance imaging
kidney and thyroid. The majority are osteolytic MRI may be important for assessing the quality
although prostate is unique because 95% of bone and extent of bone involvement if reconstruction is
lesions are osteoblastic. being considered.
Computed tomography
CT is helpful for determining cortical destruction. CT
MCQs
scans of the chest, abdomen and pelvis are important
for identifying the site of the primary tumour.
Blood tests
Routine blood tests may indicate the extent of mar- 1 Degenerative arthritis is a common condition
row involvement. Elevation of specific markers characterised by:
such as prostate‐specific antigen (prostate), carci- a joint pain, stiffness, contracture and deformity
noembryonic antigen (gastrointestinal), alpha‐feto- b recurrent haemarthroses, joint swelling and a
protein (gastrointestinal) and ESR (myeloma) may Charcot joint
assist diagnosis. c high temperature, exquisite joint pain and
constitutional symptoms
Treatment d flitting arthralgia, skin rash and sore throat
e single joint swelling, conjunctivitis and urethritis
• Radiotherapy is very useful for controlling pain,
lysis or growth of the tumour. 2 Which of the following radiological features of
• Chemotherapy has an important role in specific degenerative arthritis is correct?
carcinomas. a syndesmophytes, bamboo spine
• Surgery is indicated for the prevention of impend- b joint narrowing, subchondral sclerosis,
ing pathological fracture, or the treatment of osteophyte formation, cyst formation
fracture. In almost all cases, pain is a major rea- c joint debris, density, derangement and destruction
son for surgical intervention. d osteoporosis, valgus knee, marked joint synovitis
e soft tissue swelling, fracture, fluid–fluid levels
Outcome and gas in soft tissue
In general, the surgical treatment of metastatic dis-

3 Crystal arthropathy may be seen in which of the
ease of bone is palliative. On occasion, resection of
following conditions?
solitary renal or thyroid disease may affect cure.
a hyperuricaemia
b chondrodysplasia
c haemochromatosis
Further reading
d Osgood–Schlatter disease
Allen KD, Choong PF, Davis AM et al. Osteoarthritis: e osteochondritis dissecans
models for appropriate care across the disease continuum.
Best Pract Res Clin Rheumatol 2016;30:503–35. 4 Septic arthritis is associated with which of the
Clark JC, Dass CR, Choong PF. Current and future treat- following features?
ments of bone metastases. Expert Opin Emerg Drugs a exquisite pain with attempted joint motion
2008;13:609–27. b minimal constitutional symptoms
Hatzenbuehler J, Pulling TJ. Diagnosis and management c low incidence in children
of osteomyelitis. Am Fam Physician 2011;84:1027–33. d low incidence in the elderly
Kalunian KC. Current advances in therapies for osteoar-
e never associated with trauma
thritis. Curr Opin Rheumatol 2016;28:246–50.
Ta HT, Dass CR, Choong PF, Dunstan DE. Osteosarcoma
5 Septic arthritis should be managed urgently with:
treatment: state of the art. Cancer Metastasis Rev
2009;28:247–63. a amputation
Trieu J, Sinnathamby M, Di Bella C et al. Biopsy and the b arthrodesis
diagnostic evaluation of musculoskeletal tumours: criti- c arthrocentesis
cal but often missed in the 21st century. ANZ J Surg d arthrocutaneous fistula
2016;86:133–8. e arthroplasty
Section 12
Neurosurgery
52 Head injuries
Andrew H. Kaye
Department of Surgery, University of Melbourne and Royal Melbourne Hospital, Melbourne,
Victoria, Australia
injuries the energy from the impact has a wide-

Introduction spread effect on the brain.
Trauma is the leading cause of death in youth and

Cerebral contusion
early middle age, and death is often associated with
major head trauma. Head injury contributes signifi- Cerebral contusion may occur locally, under the
cantly to the outcome in more than half of trauma‐ position of the impact, but often occurs at a dis-
related deaths. There are approximately 2.5 deaths tance from the area of impact as a result of a con-
from head injury per 10 000 population in Australia tracoup injury. As the brain is mobile within the
each year and road traffic accidents are responsible cranial cavity, sudden acceleration/deceleration will
for about 65% of all fatal head injuries. result in the opposite ‘poles’ of the brain being
Head injury may vary from mild concussion to forced against the cranial vault. A sudden blow to
severe brain injury resulting in death. Management the back of the head will cause the temporal and
of patients requires careful identification of the frontal lobes to slide across the skull base, causing
pathological processes that have occurred. contusion to the undersurface of the brain and
to the temporal and frontal poles of the brain as
they are jammed against the sphenoid ridge and
Pathophysiology of head injury frontal bones, respectively.
Most head injuries result from blunt trauma, as dis- Intracerebral shearing
tinct from a penetrating wound of the skull and
Intracerebral shearing forces result from the differ-
brain caused by missiles or sharp objects. The path-
ential brain movement following blunt trauma,
ological processes involved in a head injury include:
causing petechial haemorrhages, and tearing of
• direct trauma
axons and myelin sheaths.
• cerebral contusion
• intracerebral shearing
Cerebral swelling
• cerebral swelling (oedema)
• intracranial haemorrhage Cerebral swelling occurs either focally around an
• hydrocephalus. intracerebral haematoma or diffusely throughout
In addition, it is likely that following the initial the brain. The process involves a disturbance of
injury there is a ‘secondary injury’ leading to further vasomotor tone causing vasodilatation and cerebral
tissue damage, involving a complex series of destruc- oedema.
tive biochemical events. These include the possible
release of excitotoxic neurotransmitters such as Intracranial haemorrhage
glutamate, and lipid peroxidation initiated by free
Intracranial haemorrhage following trauma may be
oxygen radicals originating from the injured tissue,
intracerebral, subdural or extradural. Intracranial
which leads to a cascade of oxidative damage.
haematoma or cerebral swelling may cause cerebral
herniation. The medial surface of the hemisphere
Direct trauma may be pushed under the falx (subfalcine), the uncus
In penetrating injuries the direct trauma to the and parahippocampal gyrus of the temporal lobe
brain produces most of the damage, but in blunt herniate through the tentorium causing pressure on
483
484 Neurosurgery
the third nerve and midbrain (Figure 52.1), or there The exact definition of concussion remains a
may be caudal displacement of the brainstem contentious issue. The American National Football
and/or cerebellum herniating into the foramen League established a Committee on Mild Traumatic
magnum. Brain Injury (MTBI) that has established a much
broader definition for concussion as follows: altera-
Hydrocephalus tion of awareness or consciousness including being
‘dazed’, ‘stunned’ and with features of a ‘post‐concussion
Hydrocephalus occurs occasionally early after a
syndrome’ that include headache, vertigo, light‐
head injury and may be due to obstruction of the
headedness, loss of balance, blurred vision, drowsiness
fourth ventricle by blood or swelling in the poste-
and lethargy. This definition is particularly relevant in
rior fossa, or a result of a traumatic subarachnoid
the sports injury context where it informs the timing
haemorrhage causing a communicating hydroceph-
of commencing physical activity and returning to
alus. This is also an uncommon but important
the sporting activity. Most sporting codes now have
cause of delayed neurological deterioration.
strict guidelines regarding the return to activity after a
concussion. In addition, there is increasing concern
Concussion
regarding the likelihood of the cumulative effects of
Concussion usually involves an instantaneous loss multiple concussions resulting in delayed permanent
of consciousness as a result of trauma. The term serious neurological consequences such as cognitive
concussion is not strictly defined in respect to the decline and possibly other neuropsychiatric disorders.
severity of the injury. However, a minimum crite-
rion is that the patient will have had a period of Associated injuries
amnesia. The retrograde amnesia of most cerebral
Cranial nerves
concussion is usually short term, lasting less than
1 day. The initial retrograde amnesia may extend The cranial nerves may be injured as a result of
over a much longer period but gradually dimin- direct trauma by the skull fracture, cerebral swell-
ishes. A more reliable assessment of the severity of ing, brain herniation or the movement of the brain.
the head injury is the post‐traumatic amnesia. The The olfactory nerves are most commonly affected.
concussion is regarded as being severe if the amne- Eighth nerve damage is often associated with a frac-
sia following the head injury lasts more than 1 day. ture of the petrous temporal bone and deafness may be
Fig. 52.1 Brain herniation: 1, subfalcine; 2, herniation of the uncus and hippocampal gyrus of the temporal lobe into
the tentorial notch, causing pressure on the third nerve and midbrain; 3, brainstem caudally; 4, cerebellar tonsils
through foramen magnum. Source: adapted from Kaye AH. Essential Neurosurgery, 3rd edn. Oxford: Blackwell
Publishing, 2005. Reproduced with permission of John Wiley & Sons.
52: Head injuries 485
conductive, due to a haemotympanum, or sensorineu-

ral, as a result of injury to the inner ear or nerve itself.
Traumatic intracranial haematomas
Facial paralysis is usually associated with a frac-
Intracranial haematoma formation following head
ture through the petrous temporal bone. It may be
injury is the major cause of fatal injuries in which
either immediate, as a result of direct compression
death may potentially have been avoidable. Delay
of the nerve, or delayed, due to bleeding and/or
in the evacuation of the haematoma may also
swelling around the nerve.
increase morbidity in survivors.
The sixth cranial nerve has a long subarachnoid
The general classification of traumatic intracra-
course and is easily damaged by torsion or hernia-
nial haematoma depends on the relationship of the
tion of the brain.
haematoma to the dura and brain. They are classi-
The third cranial nerve may also be damaged by
fied as extradural, subdural or intracerebral.
direct trauma or by brain herniation, with the her-
niated uncus of the temporal lobe either impinging
on the midbrain or directly stretching the nerve.
Extradural haematoma
Extradural haematomas are more likely to occur in
Skull fractures the younger age group because the dura is able to
strip more readily off the underlying bone. Although
Trauma may result in skull fractures that are classi-
an extradural haematoma may occur in the pres-
fied as simple (a linear fracture of the skull vault),
ence of a severe head injury and coexist with a
depressed (when bone fragments are depressed
severe primary brain injury, its important feature is
beneath the vault; Figure 52.2) or compound (when
that it may occur when the injury to the underlying
there is a communication with the external envi-
brain is either trivial or negligible.
ronment, usually from a laceration over the frac-
The most common sites of extradural haematoma
ture). A fracture of the base of the skull may have
are the temporal region followed by the frontal area.
a direct connection outside the vault, via the air
Posterior fossa and parasagittal extradural haemato-
sinuses.
mas are relatively uncommon. In most cases the
haemorrhage is from a torn middle meningeal artery
Scalp lacerations
or its branches, but haematomas may also develop
The extent of the scalp laceration does not necessar- from haemorrhage from extradural veins or the
ily indicate the degree of trauma to the underlying venous sinuses. A fracture overlies the haematoma in
brain. nearly all (95%) adults and most (75%) children.
Fig. 52.2 Depressed skull fracture.

486 Neurosurgery
Clinical presentation A change in vital signs shows the classical

Cushing response to increased intracranial pressure
Frequently, extradural haematoma occurs follow-
(ICP), i.e. bradycardia accompanied by an increase
ing a head injury that has resulted in only a tran-
in blood pressure. Disturbances in respiration
sient loss of consciousness, and in approximately
will develop into a Cheyne–Stokes pattern of
25% of cases there has been no initial loss of con-
breathing.
sciousness. In these patients the most important
symptoms are:
• headache Radiological investigations
• deteriorating conscious state
• focal neurological signs (dilating pupil, hemiparesis) A computed tomography (CT) scan will show the
• change in vital signs (hypertension, bradycardia). typical hyperdense biconvex haematoma with com-
Headache is the main initial symptom in patients pression of the underlying brain and distortion of
who have either not lost consciousness or who have the lateral ventricle (Figure 52.3).
regained consciousness. The headache is often
followed by vomiting.
Treatment
A deteriorating conscious state is the most impor-
tant neurological sign, particularly when it devel- The treatment of extradural haematoma is urgent
ops after a ‘lucid’ interval. It is essential that the craniotomy with evacuation of the clot.
drowsiness that occurs in a patient following a As soon as an extradural haematoma is suspected
head injury is not misinterpreted as just the patient clinically, the patient should have an urgent CT
wishing to sleep. scan. In some cases the rate of neurological deterio-
Focal neurological signs will depend on the posi- ration may be so rapid that there is not sufficient
tion of the haematoma. In general, a temporal hae- time for a CT scan and the patient should be trans-
matoma will produce a progressive contralateral ferred immediately to the operating theatre.
spastic hemiparesis and an ipsilateral dilated pupil. Infusion of mannitol (25% solution, 1 g/kg) or fru-
Further progression will result in bilateral spastic semide (20 mg i.v.) may temporarily reduce the ICP
limbs in a decerebrate posture and dilated pupils during transfer to the operating theatre. If uncon-
related to uncal herniation. Occasionally, the hemipa- scious, the patient should be intubated and hyper-
resis may initially be ipsilateral due to compression of ventilated during the transfer. It is essential that
the contralateral crus cerebri of the tentorial edge, there should be no delay in evacuating the haema-
but only rarely is the opposite pupil involved first. toma. An extradural haematoma is a surgical
Fig. 52.3 Extradural haematoma with typical biconvex configuration.

emergency because the haematoma will result in A CT scan will show the characteristic hyper-
death if not removed promptly. dense haematoma, which is concave towards the
brain with compression of the underlying brain and
distortion of the lateral ventricles (Figure 52.4).
Subdural haematoma More than 80% of patients with acute subdural
Subdural haematomas have been classified depend- haematomas have a fracture of either the cranial
ing on the time at which they become clinically evi- vault or base of skull.
dent following injury: acute (<3 days), subacute
(4–21 days) and chronic (>21 days). However, a CT Chronic subdural haematoma
scan enables a further and clinically more relevant
classification depending on the density of the hae- Chronic subdural haematoma may follow some
matoma relative to the adjacent brain. An acute time after a significant and often severe head injury,
subdural haematoma is hyperdense (white) and but in approximately one‐third of patients there is
a chronic subdural haematoma is hypodense. no definite history of preceding head trauma. The
Between the end of the first week and the third aetiology of the subdural haematoma in this non‐
week the subdural haematoma will be isodense traumatic group is probably related to rupture of a
with the adjacent brain. fragile bridging vein in a relatively atrophic ‘mobile’
brain. A relatively trivial injury may result in move-
ment of the brain, like a walnut inside its shell, with
Acute subdural haematoma
tearing of the bridging vein. The majority of patients
Acute subdural haematoma frequently results from in this group are more than 50 years of age.
severe trauma to the head and commonly arises If the patient is being treated in hospital for a
from cortical lacerations. head injury, the presence of a chronic subdural hae-
An acute subdural haematoma usually presents matoma should be considered if the neurological
in the context of a patient with a severe head injury state deteriorates. Alternatively, a patient may
whose neurological state is either failing to improve present without the history of a significant head
or deteriorating. The features of a deteriorating injury in one of three characteristic ways.
neurological state (decrease in conscious state and/ • Raised ICP with or without significant localising
or increase in lateralising signs) should raise the signs such as a hemiparesis or dysphasia.
possibility of a subdural haematoma. Headache, vomiting and drowsiness, even in the
Fig. 52.4 Acute subdural haematoma with compression of ventricles.

488 Neurosurgery
absence of focal neurological signs, indicate the

possible differential diagnosis of a cerebral neo-
Initial management
plasm or chronic subdural haematoma.
The key aspects in the management of patients
• Fluctuating drowsiness.
following head injury are:
• Progressive dementia.
• clinical assessment of the neurological and other
Chronic subdural haematoma will be diagnosed on
injuries
CT scan as a hypodense extracerebral collection caus-
• determination of the pathological process
ing compression of the underlying brain (Figure 52.5).
involved
In 25% of cases the haematoma is bilateral. The
• recognition that a change in the neurological
chronic subdural haematoma can usually be drained
signs indicates a progression or change in the
through burr holes, but a small craniotomy is some-
pathological processes.
times necessary, especially if there is evidence of sub-
Immediate treatment at the site of the accident is
dural membranes indicating the presence of multiple
critical to the outcome and involves rapid restora-
loculated chronic subdural haematomas.
tion of an adequate airway and ventilation, circu-
latory resuscitation, first‐aid treatment of other
Intracerebral haematoma
injuries, and the urgent transfer of the patient
Intracerebral haematomas occur as a result of a to hospital. It is essential to avoid hypoxia and
penetrating injury (e.g. missile injury), a depressed hypotension because both will cause further brain
skull fracture or following a severe head injury. injury.
They are frequently associated with a subdural
haematoma.
Clinical assessment
An intracerebral haematoma should be suspected
in any patient with a severe head injury or a patient In the management of head injury, it is essential to
whose neurological state is deteriorating. A CT scan know the type of accident that caused the head
will show the size and position of the haematomas. inujury and whether the neurological condition
A large intracerebral haematoma usually needs to is deteriorating. An assessment of the patient’s
be evacuated. Small intracerebral haematomas are initial neurological condition can be obtained from
not removed but should be monitored because the bystanders at the site of the accident or from the
haematoma may expand and require evacuation. ambulance officers.
Fig. 52.5 Chronic subdural haematoma (SDH): (a) CT showing SDH; (b) T1‐ and T2‐weighted MRI showing bilateral
SDH; (c) MRI FLAIR showing bilateral SDH.
Neurological examination In fact in older patients (>60 years) a GCS score of

12 indicates a serious injury, with the possibility of
Neurological examination will help to determine
poor outcome.
the type and position of the pathological process
Careful evaluation of the pupil size and response
and provide a baseline for comparison with subse-
to light is essential at the initial clinical assessment
quent examinations. Although a full neurological
and during further observation. Raised ICP causing
examination should be undertaken, special empha-
temporal lobe herniation will cause compression of
sis should be given to:
the third nerve, resulting in pupillary dilatation that
• the conscious state
nearly always occurs initially on the side of the
• pupillary size and reaction
raised pressure. The pupil will initially remain reac-
• focal neurological signs in the limbs.
tive to light but will subsequently fail to respond to
An assessment should be made of the retrograde
light in any way. As the ICP increases, this same
amnesia and post‐traumatic amnesia, if possible.
process commences on the opposite side.
There is a continuum of altered consciousness
Neurological examination of the limbs will assess
from the patient being alert and responding appro-
tone, power and sensation. A hemiparesis will result
priately to verbal command to those who are deeply
from an injury of the corticospinal tract at any
unconscious. Drowsiness is the first sign of a
point from the motor cortex to the spinal cord.
depressed conscious state. As the level of conscious-
Following a severe brain injury the limbs may adopt
ness deteriorates, the patient will become confused.
an abnormal ‘posturing’ attitude. The decerebrate
The use of the words ‘coma’, ‘semi‐coma’ or ‘stu-
posture consists of the upper limbs adducted and
porose’ should be avoided because they convey
internally rotated against the trunk, extended at the
different meanings to different observers. The

elbow and flexed at the wrist and fingers, with the
assessment is more accurate and reproducible if the
lower limbs adducted, extended at the hip and knee
Glasgow Coma Scale (GCS) is used (Table 52.1).
with the feet plantar flexed. Less frequently the
This scale gives a numerical value to the three most
upper limbs may be flexed, probably due to an
important parameters of the level of consciousness:
injury predominantly involving the cerebral white
eye opening, best verbal response and best motor
matter and basal ganglia, corresponding to a posture
response. The exact response can be shown on a
of decortication.
chart or the level of consciousness can be given as a
Particular attention must be given to the patient’s
numerical score (the sum of the three parameters of
ventilation, blood pressure and pulse. At all times it
the GCS). A score of 8 or less indicates a severe
is essential to ensure the patient’s ventilation is ade-
brain injury. However, it is essential to realise that
quate. Respiratory problems may result either as a
following a head injury the neurological state can
direct manifestation of the severity of the head
deteriorate rapidly and there must be no compla-
injury or due to an associated chest injury.
cency even in patients with a GCS score of 14 or 15.
Table 52.1 Glasgow Coma Scale.
Parameter Response Numerical value
Eye opening Spontaneous 4

To speech 3
To pain 2
None 1
Best verbal response Oriented 5
Confused 4
Inappropriate 3
Incomprehensible sounds 2
None 1
Best motor response to painful stimulus Obeys commands 6
Localises to pain 5
Flexion to pain (withdrawal) 4
Flexion (abnormal) 3
Extension to pain 2
None 1
Total 3–15
490 Neurosurgery
Pyrexia frequently occurs following a head injury.

Box 52.1 Minimum criteria for
A raised temperature lasting more than 2 days is
obligatory admission to hospital after
usually due to traumatic subarachnoid haemor-
head injury
rhage or may occur in patients with a severe brain-
stem injury. • Loss of consciousness (post‐traumatic amnesia) for
more than 10 minutes
General examination • Persistent drowsiness
Careful assessment must be made of any other inju- • Focal neurological deficits
ries. Chest, skeletal, cardiovascular or intra‐abdom- • Skull fracture
• Persisting headache, nausea or vomiting after
inal injury must be diagnosed and the appropriate
4 hours’ observation
management instituted. Hypotension or hypoxia
• Lack of adequate care at the patient’s home
may severely aggravate the brain injury.
Radiological assessment
observations should be recorded on a chart display-
Radiological assessment following the clinical eval- ing the GCS scores.
uation will be essential unless the injury has been Should the patient’s neurological state deterio-
minor. A CT scan will show the macroscopic intrac- rate, an immediate CT scan is essential to re‐evaluate
ranial injury and should be performed if: the intracranial pathology. Further treatment will
• the patient is drowsy or has a more seriously depend on the outcome of the scan.
depressed conscious state
• the patient has a continuing headache Severe head injury
• there are focal neurological signs
The management of a patient following a severe
• there is neurological deterioration
head injury depends on the patient’s neurological
• there is cerebrospinal fluid (CSF) rhinorrhoea
state and the intracranial pathology resulting from
• there are associated injuries that will entail pro-
the trauma. In general, the following applies.
longed ventilation so that ongoing neurological
The patient has a clinical assessment and CT scan
assessment will be difficult.
as described previously. If the CT scan shows
The indications for a skull X‐ray have diminished
an intracranial haematoma causing shift of the
since the introduction of CT, especially as the bony
underlying brain structures, then this is evacuated
vault can be assessed by the CT scan using the bone
immediately.
‘windows’.
Following the operation, or if there is no surgi-
It is important to note that radiological assess-
cal lesion, the patient should be carefully observed
ment of the cervical spine is essential in all patients
and the neurological observations recorded on a
who have sustained a significant head injury, par-
chart with the GCS scores. Measures to decrease
ticularly if there are associated facial injuries.
brain swelling should be implemented, including
Radiological assessment of the full spine is neces-
management of the airway to ensure adequate
sary in all patients who are unconscious and should
oxygenation and ventilation (hypercapnia will
be considered in all patients who have focal spinal
cause cerebral vasodilatation and so exacerbate
pain or tenderness depending on the mechanism of
brain swelling), elevation of the head of the bed to
injury.
20°, and maintenance of fluid and electrolyte bal-
ance. Normal fluid maintenance with an intake of
3000 mL per 24 hours is optimum for the average
Further management
adult. Blood loss from other injuries should be
replaced with colloid or blood, not with crystal-
Following the clinical and radiological assessments,
loid solutions. Pyrexia may be due to hypotha-
subsequent management will depend on the sever-
lamic damage or traumatic subarachnoid
ity of the injury and the intracranial pathology.
haemorrhage, but infection as a cause of the fever
must be excluded. The temperature must be con-
Minor head injury
trolled because hyperthermia can elevate ICP, will
Any patient who has suffered a head injury must be increase brain and body metabolism, and predis-
observed for at least 4 hours. The minimum criteria poses to seizure activity. Adequate nutrition must
for obligatory admission to hospital are given in be maintained as well as routine care of the uncon-
Box 52.1. Further management of these patients scious patient, including bowel and bladder care,
will be by careful observation, and neurological and pressure care.
More aggressive methods to control ICP are Skull fractures

advisable if the patient’s neurological state contin-
Simple fracture
ues to deteriorate and the CT scan shows evidence
of cerebral swelling without an intracranial haema- There is no specific management for a simple skull
toma, there is posturing (decerebrate) response to fracture without an overlying skin injury, although
stimuli, or the GCS score is less than 8. it is an indication that the trauma was not trivial
An ICP monitor will also be useful in patients and it should provide a warning that a haematoma
requiring prolonged sedation and ventilation as a may develop beneath the fracture.
result of other injuries. Measurement of ICP will pro-
vide another useful monitoring parameter, and any Compound fracture
sustained rise in the pressure will be an indication for
careful reassessment and, if necessary, CT scan. A skull fracture may be compound because of an
The techniques used to control ICP include con- overlying scalp laceration or if it involves an air sinus.
trolled ventilation maintaining Paco2 at 33–38 The scalp wound should be debrided and closed.
mmHg, CSF drainage from a ventricular catheter, A short course of prophylactic antibiotics should be
and diuretic therapy using intermittent administra- administered to reduce the risk of infection.
tion of mannitol or frusemide. Mild hypothermia,
achieved by cooling the patient to 34°C, is possibly Depressed skull fracture
of benefit. Other techniques such as administration
If the depressed skull fracture is compound, pro-
of barbiturates (to reduce cerebral metabolism and
phylactic antibiotics and tetanus prophylaxis
ICP) and hyperbaric oxygen have been advocated
should be administered. Surgery, usually requiring a
in the past but have not been shown to have any
general anaesthetic, should be performed as soon as
proven benefit. Steroid medication is of no proven
possible.
benefit in head injury.
The role of a large decompressive craniectomy,
involving removal of a large component of the
Cerebrospinal fluid rhinorrhoea
skull, in severe brain injury remains controversial.
Whilst some studies have shown possible benefit, a A fracture involving the base of the anterior cranial
large prospective study (the DECRA study reported fossa may cause tearing of the dura, resulting in a
in the New England Journal of Medicine in 2011) fistula into the air sinuses. This type of fistulous
showed no advantage and even possible detrimen- connection should also be suspected if the patient
tal outcome. At present most neurosurgeons would suffers an episode of meningitis or if the radiologi-
advise its use only in carefully selected patients in cal investigations show a fracture in the appropri-
whom the ICP continues to rise despite using the ate site. An intracranial aerocele is proof of a
measures described here. fistulous connection. CSF rhinorrhoea may also
occur as a result of a fistula through the tegmen
tympani into the cavity of the middle ear and leak-
Management of associated conditions
age via the eustachian tube.
Surgery should be performed if CSF leakage per-
Scalp injury
sists, if there is an intracranial aerocele or if there
A large scalp laceration may result in considerable has been an episode of meningitis in a patient with
blood loss. When the patient arrives in the emer- a fracture of the anterior cranial fossa.
gency department, ‘spurting’ arteries should be con-
trolled with haemostatic clips prior to a sterile
bandage being applied to the head. After initial Rehabilitation
assessment and stabilisation the wound should be
closed without delay. The hair should be shaved Some form of rehabilitation is essential following
widely around the wound, which should be meticu- any significant head injury. If the injury has been
lously cleaned and debrided. The closure should be relatively minor, then the rehabilitation necessary
performed in two layers if possible, with careful may involve only advice and reassurance to the
apposition of the galea prior to closing the skin. patient and family. Following a severe head injury,
If the scalp wound has resulted in loss of soft tis- rehabilitation will also usually involve a team of
sue, the wound may need to be extended to provide paramedical personnel, including physiotherapists,
an extra ‘flap’ of healthy tissue so that the skin occupational therapists, speech therapists and social
edges can be approximated without tension. workers.
492 Neurosurgery
b patients with a GCS score less than 8 are usually

Further reading intubated and ventilated
American Academy of Neurology. Practice parameter. The c antibiotics are routinely used
management of concussion in sports. Neurology d pyrexia is nearly always due to severe infection
1997;48:581–5. e severe fluid restriction is necessary
American Congress of Rehabilitation Medicine. Definition
of mild traumatic brain injury. J Head Trauma Rehabil 2 Which of the following is the best investigation for
1993;8:86–7.
patients with severe head injury?
Collins M, Grindal S. Relationship between concussion
a CT scan
and neuropsychological performance in college football
players. JAMA 1999;282:964–70. b skull X‐ray
Hsiang JNK, Yeung T, Yu ALM, Poon WS. High‐risk mild c EEG
head injury. J Neurosurg 1997;87:234–8. d ultrasound
Kaye AH. Essential Neurosurgery, 3rd edn. Oxford: e MRI
Blackwell Publishing, 2005.
Sahuquillo J, Poca M‐A, Arridas M, Garnacho A, Rubio E. 3 Traumatic intracerebral haematomas following
Interhemispheric supratentorial intracranial pressure blunt trauma:
gradients in head‐injured patients: are they clinically a can usually be diagnosed by skull X‐ray
important? J Neurosurg 1999;90:16–26.
b are usually associated with severe brain injury
Zhao W, Alonso OF, Loor JY, Busto R, Ginsberg MD. Influence
c always need to be drained
of early posttraumatic hypothermia therapy on local
cerebral blood flow and glucose metabolism after fluid‐

d should be treated with fluid restriction
percussion brain injury. J Neurosurg 1999;90:L510– L519. e are always associated with a skull fracture
4 An acute subdural haematoma:

MCQs a shows a characteristic hyperdense extracerebral
mass
Select the single correct answer to each question. The b is often associated with only a minor head
correct answers can be found in the Answers section injury
at the end of the book. c virtually never needs surgical excision
d can always be managed with diuretic therapy
1 In the treatment of head injury, which of the
e usually causes an ipsilateral hemiparesis
following is correct?
a steroids are regularly used
53 Intracranial tumours, infection
and aneurysms
Andrew H. Kaye
Department of Surgery, University of Melbourne and Royal Melbourne Hospital, Melbourne,
Victoria, Australia
of the tumour cell, including those of brain tumours.

Introduction These include alterations in the genes (such as the
receptor tyrosine kinases) that control the numerous
This chapter provides a brief overview of three
complex cell signalling pathways that regulate cell
important neurosurgical conditions: intracranial
proliferation, survival and migration. It is also clear
tumours, cerebral aneurysms and intracranial infec-
that numerous epigenetic mechanisms, such as meth-
tion. A brief description of each of these patholo-
ylation and microRNA, play a vital role in gene
gies will be given and the principles of treatment
expression. Tumour suppressor genes are normally
discussed.
present in the genome and act as a ‘brake’ on cell
transformation. Mutations in the TP53 tumour sup-
pressor gene are the most common gene abnormality
BRAIN TUMOURS
found in tumours to date and have been shown to
occur in both astrocytomas and meningiomas.
Brain tumours are responsible for approximately
2% of all cancer deaths. However, central nervous
system (CNS) tumours comprise the most common
Cerebral glioma
group of solid tumours in young patients, account-
ing for 20% of all paediatric neoplasms.
Gliomas comprise the majority of cerebral tumours
The general brain tumour classification is related
and arise from neuroglial cells. There are four dis-
to cell of origin and is shown in Box 53.1. Table 53.1
tinct types of glial cells: astrocytes, oligodendroglia,
shows the approximate distribution of the more
ependymal cells and neuroglial precursors. Each of
common brain tumours, some of which are described
these gives rise to tumours with different biological
in this chapter.
and anatomical characteristics.
Aetiology Astrocytoma
Epidemiological studies have not indicated any par- The most common gliomas arise from the astro-
ticular factor, either chemical or traumatic, that cytes, which comprise the majority of intraparen-
causes brain tumours in humans. Generally, there is chymal cells of the brain. The tumours arising from
no inherited genetic predisposition to brain tumours, the astrocytes range from the relatively benign to
but many specific chromosome abnormalities the highly malignant. The term malignant for brain
involving chromosomes 10, 13, 17 and 22 have tumours differs from its usage for systemic tumours,
been noted in a wide range of CNS tumours. There in that intrinsic brain tumours very rarely metasta-
is considerable conjecture regarding the role of sise (except for medulloblastoma and ependymoma)
trauma, electromagnetic radiation and organic sol- and instead refers to the aggressive biological char-
vents in the development of brain tumours, but as acteristics and poor prognosis.
yet no convincing evidence has been forthcoming. There are many classifications of brain tumours
Molecular biology techniques have enabled the in general and gliomas in particular. The World
identification of a variety of alterations in the genome Health Organization (WHO) classification of
493
494 Neurosurgery
cerebral gliomas recognises four grades. Grade I is

Box 53.1 General classifications of brain
assigned to the pilocytic astrocytoma, an uncom-
tumours
mon tumour that is very slow‐growing and biologi-
Neuroepithelial tumours cally distinct from the diffuse astrocytomas, which
Gliomas are classified as astrocytoma (WHO grade II), ana-
Astrocytoma (including glioblastoma) plastic astrocytoma (WHO grade III) and glioblas-
Oligodendrocytoma toma multiforme (WHO grade IV) and which
Ependymoma comprise over 50% of the astrocytoma tumours.
Choroid plexus tumour The most recent 2016 revision of the WHO classifi-
Pineal tumours cation includes the use of both histological appear-
Neuronal tumours ance and molecular features, such as isocitrate
Ganglioglioma dehydrogenase (IDH) mutation and 1p/19q status
Gangliocytoma to classify glioma.
Neuroblastoma
Medulloblastoma Pathology
Nerve sheath tumour The hallmark of the pathology of cerebral gliomas is
Acoustic neuroma invasion of tumour cells into the adjacent normal
Meningeal tumours
brain. Although in certain areas the margin of the
Meningioma
tumour may seem to be macroscopically well defined
Pituitary tumours
from the brain, there are always microscopic nests of
Germ cell tumours
tumour cells extending well into the brain. The histo-
Germinoma
logical appearance of the tumour varies with the
Teratoma
Lymphomas
tumour grade, with increasing cellular atypia,
Tumour‐like malformations mitoses, endothelial and adventitial cell proliferation
Craniopharyngioma and necrosis with increasing grade of the tumour.
Epidermoid tumour
Dermoid tumour Clinical presentation
Colloid cyst The presenting features of all intracranial tumours
Metastatic tumours can be classified under:
Local extensions from regional tumours • raised intracranial pressure (ICP)
(e.g. glomus jugulare, carcinoma of ethmoid) • focal neurological signs
Source: Kaye AH. Essential Neurosurgery, 3rd edn. Oxford: • epilepsy.
Blackwell Publishing, 2005. Reproduced with permission of The duration of symptoms and the evolution of the
John Wiley & Sons. clinical presentation will depend on the grade of the
tumour (i.e. rate of growth). A patient presenting
with a low‐grade astrocytoma (grade I or II) may
have a history of seizures extending over many years
antedating the development of progressive neuro-
logical signs and raised ICP. Patients with the more
Table 53.1 Incidence (%) of common cerebral
common higher‐grade tumour present with a shorter
tumours.
history, and glioblastoma multiforme is character-
Neuroepithelial 52 ised by a short illness of weeks or a few months.
Astrocytoma (all 44 Raised ICP is due to the tumour mass, surround-
grades including ing cerebral oedema and hydrocephalus due to
glioblastoma) blockage of cerebrospinal fluid (CSF) pathways.
Ependymoma 3 The main clinical features of raised ICP are head-
Oligodendroglioma 2 aches, nausea and vomiting, drowsiness and
Medulloblastoma 3 papilloedema.
Metastatic 15 • Headache associated with increased ICP is usu-
Meningioma 15
ally worse on waking in the morning and is
Pituitary 8
relieved by vomiting. ICP increases during sleep,
Acoustic neuroma 8
probably as a result of vascular dilatation due to
Source: Kaye AH. Essential Neurosurgery, 3rd edn. carbon dioxide retention.
Oxford: Blackwell Publishing, 2005. Reproduced with • Nausea and vomiting are usually worse in the
permission of John Wiley & Sons. morning.
53: Intracranial tumours, infection and aneurysms 495
• Drowsiness is the most important clinical feature

of raised ICP. It is the portent of rapid neurologi-
cal deterioration.
• Papilloedema is the definitive sign of raised ICP.
The early features of increased pressure on the
optic nerve head are those of dilatation or failure of
normal pulsations of retinal veins. As the ICP rises,
the nerve head becomes more swollen and the disc
margins become blurred on fundoscopic examina-
tion. Flame‐shaped haemorrhages develop, particu-
larly around the disc margins and along the
vessels.
• Sixth nerve palsy causing diplopia may result in
raised ICP owing to stretching of the sixth cra-
nial nerve by cordal displacement of the brain-
stem. This is a so‐called false localising sign.
• Focal neurological signs are common in patients
presenting with cerebral gliomas, and the nature
of the deficit will depend on the position of the
tumour.
Patients presenting with tumours involving the
Fig. 53.1 Low‐grade glioma with decreased density on
frontal lobes may sometimes have pseudo‐psychiat-
T1‐weighted MRI.
ric problems, with personality change and mood
disorders. Limb paresis results from interference of
the pyramidal tracts, either at a cortical or subcorti-
cal level, and field defects are associated with
tumours of the temporal, occipital or parietal lobes.
Dysphasia, either expressive or receptive, is a par-
ticularly distressing symptom in patients involving
the relevant areas of dominant hemisphere.
Investigations
Computed tomography (CT) and magnetic reso-
nance imaging (MRI) of the brain are the essential
radiological investigations and an accurate diagno-
sis can be made in nearly all tumours on MRI.
Low‐grade gliomas show decreased density on CT
and T1‐weighted MRI, with minimal surrounding
oedema and usually no enhancement with contrast
(Figure 53.1). Calcification may be present. High‐
grade gliomas are usually large and enhance vividly
following intravenous injection of contrast material
and have extensive surrounding oedema (Figure 53.2).
MRI, particularly when used with gadolinium
contrast enhancement, improves the visualisation
of cerebral gliomas. Gadolinium enhancement is Fig. 53.2 High‐grade glioma (glioblastoma multiforme)
more likely to occur in high‐grade tumours. The use showing vivid enhancement after intravenous injection of
of MRI spectroscopy to measure biochemical contrast material.
changes in the tumour and surrounding brain as
well as blood flow and blood volume helps to fur- Surgery
ther define the exact diagnosis. The aim of surgery is to:
• make a definitive diagnosis
Management • reduce the tumour mass to relieve the symptoms
Following the presumptive diagnosis of a glioma, of raised ICP
the management involves surgery and radiation • reduce the tumour mass as a precursor to adju-
and chemotherapy. vant treatments.
496 Neurosurgery
There is still some debate regarding the oncological

benefit of tumour resection in the treatment of
glioma as complete resection of high‐grade (and
most low‐grade) gliomas is not possible and the
high‐grade glioma will inevitably recur despite
what is considered by the surgeon as a ‘complete’
resection. Nevertheless, it is advisable to resect as
much tumour as possible provided that the patient
is not inflicted with a neurological deficit.
Radiotherapy and chemotherapy
Postoperative combined radiation therapy and
temozolomide chemotherapy (known as the Stupp
protocol) is often used as an adjunct to surgery in
the treatment of high‐grade gliomas, especially in
patients under 70 years of age.
The adjuvant treatment for low‐grade astrocy-
toma is more controversial as these tumours are less
responsive to adjuvant therapies. However, studies
have shown possible survival benefit with radiation
and chemotherapy, although the long‐term compli- Fig. 53.3 Oligodendroglioma that is highly calcified.
cations, especially cognitive decline associated with
radiation effects on the normal brain, remain a con- the requirement for these tumours to have an IDH
cern and has tempered the use of these treatments mutation and 1p/19q deletion for the diagnosis.
routinely. However, radiation and possibly chemo- The clinical presentation is essentially the same
therapy are usually advised for the larger tumours as for the astrocyte group, but as these tumours are
in patients over 40 years of age as these patients more likely to be slow‐growing, epilepsy is more
have a poorer prognosis. common.
Oligodendroglioma is more responsive to chem- The principles of treatment are the same as for the
otherapy than other types of glioma and adjuvant astrocytoma group. Surgery is necessary to make a
treatment may be considered either following the definitive diagnosis and debulking the tumour will
initial resection or when there is evidence of tumour relieve the features of raised ICP as well as reducing
recurrence or progression on MRI. the tumour burden for adjuvant therapies.
Radiotherapy is probably helpful in reducing the
Prognosis rate of growth of any remnant tumour. Chemotherapy
At present there is no satisfactory treatment for cer- has been shown to be more beneficial in helping to
ebral glioma. In a large prospective study of the control those tumours with an oligodendroglial
treatment of high‐grade glioma (glioblastoma mul- component, especially those tumours with proven
tiforme), the median survival following surgery and loss of heterozygosity on chromosome 1p or 19q.
the Stupp protocol of combined radiation and
temozolomide chemotherapy was 14.6 weeks, with Metastatic tumours
a 2‐year survival of 26% and 5‐year survival of
Metastatic tumours are responsible for 15% of brain
10%. However, most series report significantly less
tumours in clinical series, but up to 30% of brain
promising survival results.
tumours reported by pathologists. Approximately
30% of deaths are due to cancer and 20% of these
will have intracranial metastatic deposits at post‐
Oligodendroglioma
mortem. The metastatic tumours most commonly
Oligodendrogliomas are much less common than the originate from:
astrocytoma group, being responsible for approxi- • carcinoma of the lung
mately 5% of all gliomas. Oligodendrogliomas have • carcinoma of the breast
the same spectrum of histological appearance as • metastatic melanoma
astrocytomas but, as distinct from the astrocytoma • carcinoma of the kidney
series, are more likely to be slow‐growing. Calcium • gastrointestinal carcinoma.
deposits are found in 90% of these tumours In 15% of cases a primary origin is never found.
(Figure 53.3).The 2016 WHO classification includes Most metastatic tumours are multiple and one‐third
are solitary. In about half of the solitary tumours, • there is a solitary metastasis in a surgically acces-
systemic spread is not apparent. The incidence of sible position
tumours in the cerebrum relative to the cerebellum • there is no systemic spread.
is 8 : 1. Metastatic tumours are often surrounded Excision of multiple metastases may occasionally
by intense cerebral oedema. be indicated if the tumours are causing symptoms,
and are in a surgically accessible position and espe-
Clinical presentation cially if the tumour is known to be resistant to radi-
The interval between diagnosis of the primary can- ation therapy.
cer and cerebral metastasis varies considerably. In Removal of a metastasis is preferable if the pri-
general, secondary tumours from carcinoma of the mary site of origin has been, or will be, controlled.
lung present relatively soon after the initial diagno- Excision of a single or even multiple metastases will
sis, with a median interval of 5 months. Although provide excellent symptomatic relief and conse-
cerebral metastases may present within a few quently may be indicated even if the primary site
months of the initial diagnosis of malignant mela- cannot be treated satisfactorily.
noma or carcinoma of the breast, some patients Radiotherapy, together with steroid medication
may live many years before an intracranial tumour to control cerebral oedema, is often used to treat
appears. patients with multiple cerebral metastases and may
The presenting clinical features for cerebral be advisable following excision of a single metasta-
metastasis are similar to those described for other sis. Stereotactic radiosurgery, which uses a highly
tumours, namely raised ICP, focal neurological focused beam of radiation, can be used to treat sin-
signs and epilepsy. gle and multiple cerebral metastases if the tumour is
less than 3 cm in diameter, especially if the tumour
Radiological investigations is known to be radiation sensitive.
CT or MRI will diagnose metastatic tumour and
show whether or not the deposits are solitary or Prognosis
multiple. Most metastatic tumours are isodense on The survival for patients who have undergone sur-
unenhanced scan and they enhance vividly after gical excision of a metastatic deposit depends on
intravenous contrast material. MRI following gad- control of the primary tumour and the effectiveness
olinium contrast may demonstrate small metastatic of oncological therapies.
tumours often not visible on a CT scan (Figure 53.4).
Treatment Paediatric brain tumours

Steroid medication will control cerebral oedema
Intracranial tumours are the most common form of
and should be commenced immediately if there is
solid tumours in childhood, with 60% of tumours
raised ICP.
occurring below the tentorium cerebelli. The most
Surgery to remove the metastasis is indicated if:
common supratentorial tumours are astrocytomas,
followed by anaplastic astrocytomas and glioblas-
toma multiforme.
Posterior fossa paediatric tumours

Of paediatric brain tumours, 60% occur in the pos-
terior fossa. The relative incidence of tumours is:
• cerebellar astrocytoma, 30%
• medulloblastoma (infratentorial primary neuroe-
ctodermal tumour), 30%
• ependymoma, 20%
• brainstem glioma, 10%
• miscellaneous (choroid plexus papilloma, hae-
mangioblastoma, epidermoid, dermoid, chor-
doma), 10%.
The presenting clinical features of posterior fossa
neoplasms in children are related to raised ICP and
Fig. 53.4 Multiple metastatic tumours. focal neurological signs.
498 Neurosurgery
Raised intracranial pressure (a)

Raised ICP is the most common presenting feature.
It is due to hydrocephalus caused by obstruction of
the fourth ventricle and is manifest by headaches,
vomiting, diplopia and papilloedema. The raised
ICP may result in a strasbismus causing diplopia
due to stretching of one or both of the sixth (abdu-
cens) cranial nerves (a false localising sign).
Focal neurological signs

Focal neurological signs are due to the tumour
invading or compressing the cerebellum, brainstem
and cranial nerves. Truncal and gait ataxia result
particularly from midline cerebellar involvement.
Horizontal gaze paretic nystagmus often occurs in
tumours around the fourth ventricle. Vertical nys-
tagmus is indicative of brainstem involvement.
Disturbance of bulbar function, such as difficulty in
swallowing, with nasal regurgitation of fluid, dys- (b)
arthria and impaired palatal or pharyngeal reflexes,
result from brainstem involvement. Compression
or tumour invasion of the pyramidal tracts may
result in hemiparesis or sensory disturbance.
Investigations
CT and MRI will confirm the position of the tumour
and whether there is hydrocephalus (Figure 53.5).
Management
The treatment of posterior fossa tumours involves
surgery, radiotherapy and chemotherapy.
A CSF shunt may need to be performed to con-
trol raised ICP due to hydrocephalus. The CSF
diversion can be achieved with either an external
drain or ventriculoperitoneal shunt. The shunt will
provide immediate and controlled relief of intracra-
nial hypertension and the subsequent posterior
fossa operation can be performed as a planned elec-
tive procedure. A criticism of preoperative ventricu-
loperitoneal shunt is that it may promote the
Fig. 53.5 (a) Posterior fossa cystic astrocytoma
metastatic spread of these tumours.
with small tumour nodule and large cyst.
In general, the treatment of medulloblastoma (b) Enhancing midline posterior fossa tumour
and ependymoma involves surgery to excise the (medulloblastoma).
tumour, followed by radiation therapy, which may
be to the whole neuraxis as the tumour may spread
throughout the CNS, followed by chemotherapy. Many cerebellar astrocytomas have a small single
The survival of patients with medulloblastoma nodule surrounded by a large cyst. These tumours
depends on the genetic subtype of the tumour, the can often be cured by excision of the nodule alone,
spread of the tumour at the time of diagnosis, the and adjuvant therapy is not necessary. In contrast,
extent of resection and the age of the patients. the treatment of brainstem glioma usually involves
Overall 5‐year survival is 70–80%, for children only a biopsy of the tumour to confirm the diagno-
with high‐risk disease 50–60%, and for infants sis, possibly followed by radiotherapy and/or chem-
30–50%. The prognosis for ependymoma depends otherapy. These tumours usually cause death within
on similar factors and overall 5‐year survival is 24 months of diagnosis, although some patients
70–75%. with low‐grade tumours will live longer.
Benign brain tumours (a) Basal
The most common benign brain tumours are: Olfactory groove

• meningioma
Sphenoidal wing Tuberculum sella
• acoustic neuroma
• haemangioblastoma Clivus
Posterior fossa
• dermoid and epidermoid tumours Foramen magnum
• colloid cysts
• pituitary tumours
• craniopharyngioma. (b) Parasagittal section
Parasagittal/falcine
Meningiomas
Meningiomas are the most common of the benign Clivus
Olfactory groove
brain tumours and constitute about 15% of all Posterior fossa
intracranial tumours, comprising about one‐third the Tuberculum sella Foramen magnum
number of gliomas. However, the true incidence of
meningioma is much higher, as many are small Fig. 53.6 Classical positions of meningiomas.
asymptomatic meningiomas that are only diagnosed
on CT or MRI undertaken for investigation of head-
of the tumour (Figure 53.6) will determine the fea-
ache or other neurological symptoms. Although they
tures of the clinical presentation. The tumours often
may occur at any age, they reach their peak incidence
grow slowly and there is frequently a long history,
in middle age and are very uncommon in children.
often of many years, of symptoms prior to
Unlike gliomas, where the classification system is
diagnosis.
based on the histological appearance of the
• Parasagittal tumours often arise in the middle
tumours, meningiomas are usually classified
third of the vault, and the patient may present
according to the position of origin rather than his-
with focal epilepsy and paresis, usually affecting
tology. The reason for this is that, in general, the
the opposite leg and foot, as the motor cortex on
biological activity of the tumour, presenting fea-
the medial aspect of the posterior frontal lobe is
tures, treatment and prognosis all relate more to the
affected. Urinary incontinence is occasionally a
site of the tumour than the histology (Table 53.2).
symptom for a large frontal tumour, especially if
Whilst there are numerous histological subtypes
it is bilateral.
of meningioma, approximately 10–15% are
• Convexity tumours often grow around the posi-
regarded as showing ‘atypical’ features, which indi-
tion of the coronal suture. Patients present with
cate a much higher risk of recurrence. Only 2% are
raised ICP, and more posterior tumours will
regarded as being malignant.
cause focal neurological symptoms and epilepsy.
• Inner sphenoidal wing meningioma will cause
compression of the adjacent optic nerve and
Meningiomas present with features of raised ICP,
patients may present with a history of uniocular
focal neurological signs and epilepsy. The position
visual failure.
• Olfactory groove meningioma will cause anos-
mia, initially unilateral and later bilateral. The
Table 53.2 Position (%) of intracranial meningioma. presenting features may include symptoms of
raised ICP. Large frontal tumours, especially
Parasagittal and falx 25 those arising in the midline and causing compres-
Convexity 20 sion of both frontal lobes such as tumours arising
Sphenoidal wing 20 from the olfactory groove, may present with cog-
Olfactory groove 12 nitive decline.
Suprasellar 12
• Suprasellar tumours arise from the tuberculum
Posterior fossa 9
sellae and will cause visual failure with a bitem-
Ventricle 1.5
Optic sheath 0.5
poral hemianopia.
• Posterior fossa tumours may arise from the cere-
Source: Kaye AH. Essential Neurosurgery, 3rd edn. bellar convexity or from the cerebellopontine
Oxford: Blackwell Publishing, 2005. Reproduced with angle or clivus. Tumours arising in the cerebello-
permission of John Wiley & Sons. pontine angle or extending into the basal cisterns
500 Neurosurgery
around the brainstem (such as petro‐clival men- (a)

ingiomas) may initially present with cranial nerve
abnormalities, such as hearing loss or facial sen-
sory disturbance before the development of
ataxia or hemiparesis related to brainstem
compression.
Radiological investigations
CT and MRI show tumours that enhance vividly
following intravenous contrast (Figure 53.7).
Hyperostosis of the cranial vault may occur at the
site of attachment of the tumour, and these bony
changes may often be seen on plain skull X‐ray or
better on the bone windows of the CT scan.
Treatment
The treatment of clinically significant meningiomas
is surgical excision, if possible including oblitera-
tion of the dural attachment. Although this objec-
tive is often possible, there are some situations
where complete excision is not possible because of
the position of the tumour. Surgery may be pre-
ceded by embolisation of the main vascular supply (b)
of the tumour.
Incomplete resection carries the possibility of
tumour recurrence, especially in those tumours that
show ‘atypical’ histological features. In these
tumours postoperative radiation therapy may be
recommended to reduce the risk of recurrence.
Small asymptomatic meningiomas may be man-
aged conservatively and followed with regular
MRI.
Acoustic neuroma
Acoustic schwannomas arise from the eighth cra-
nial nerve and account for 8% of intracranial
tumours. The tumours are schwannomas, with
their origin from the vestibular component of the
eighth cranial nerve in or near the internal auditory
meatus.
The clinical presentation of an acoustic schwan-
noma will depend on the size of the tumour at the
time of diagnosis. The earliest symptoms are associ- Fig. 53.7 (a) Axial and (b) coronal MRI showing
ated with eighth nerve involvement. Tinnitus and meningioma with vivid contrast enhancement arising
from floor of anterior carnial fossa (olfactory groove)
unilateral partial or complete sensory neural hear-
and growing into superior frontal lobes.
ing loss are the earliest features. With extension
into the cerebellopontine angle, the tumour will
compress the trigeminal nerve, resulting in facial contralateral hemiparesis, and a large tumour will
numbness, and the cerebellum, causing ataxia. also cause obstructive hydrocephalus. Smaller
Compression of the pyramidal tracts due to a large tumours can cause a communicating hydrocepha-
tumour causing brainstem compression will cause a lus due to raised protein in the CSF.
Fig. 53.8 Acoustic neuroma showing extension to Fig. 53.9 Colloid cyst of third ventricle.
tumour into internal auditory canal.
Pituitary tumours
Radiological investigations Pituitary tumours account for 8–10% of all intrac-
MRI will show an enhancing tumour usually in the ranial tumours.
internal auditory canal and with extension into the
cerebellopontine angle. The internal auditory mea- Pathology
tus and canal will be widened, indicating the tumour Historically, three main types of pituitary tumours
has arisen from the eighth cranial nerve (Figure 53.8). were defined by their cytoplasmic staining character-
This is often best appreciated on CT scan that shows istics: chromophobic, acidophilic and basophilic. The
bone structures better than the MRI. development of immunoperoxidase techniques and
electron microscopy have provided a more refined
Treatment classification of pituitary adenomas based on the spe-
The treatment of a large acoustic neuroma is surgi- cific hormone produced. This classification is shown
cal. Stereotactic radiosurgery has been advocated in Table 53.3. The tumours can be further classified
by some for smaller tumours (<2 cm diameter), by size, with microadenomas (<1 cm diameter) and
with tumour control rates being in excess of 90%. macroadenomas (>1 cm diameter) being confined to
However, the risks of surgery are higher in those the sella or with extrasellar extension (Figure 53.10).
patients in whom radiation fails to control the
tumour and there remains a concern regarding the Clinical presentation
possible carcinogenic effects of radiation in the The presenting clinical features of pituitary tumours
long term, especially in younger patients. are due to the size of the tumour and endocrine dis-
Intracanalicular or small tumours in the elderly turbance. Headache occurs principally in patients
may be just observed and treatment advised only if with acromegaly and is uncommon in other types
there is evidence of tumour growth. of pituitary tumours.
Visual failure
Colloid cyst of third ventricle Suprasellar extension of the pituitary tumour
causes compression of the optic chiasm resulting in
A colloid cyst of the third ventricle is situated in the bitemporal hemianopia. Optic atrophy will be evi-
anterior part of the ventricle and applied to the roof dent in patients with long‐standing compression of
just behind the foramen of Munro. As the cyst grows the chiasm. Extension of the tumour into the cav-
it causes bilateral obstruction to the foramen of ernous sinus may cause compression of the third,
Munro resulting in raised ICP from hydrocephalus. fourth or sixth cranial nerves.
Radiological investigations include MRI and CT,
which show a round tumour in the anterior third Endocrine disturbance
ventricle that usually enhances following intrave- Endocrine disturbance is due to either hypopituita-
nous contrast (Figure 53.9). The treatment is surgi- rism or excess secretion of a particular pituitary
cal excision. hormone.
502 Neurosurgery
Table 53.3 Classification of pituitary adenomas.

is severe episodic confusion occurs and the patient
will become drowsy.
Hormone secreted Percentage of tumours
Pituitary apoplexy
Prolactin 40 Pituitary apoplexy results from sudden spontane-
Growth hormone 20
ous haemorrhage into the pituitary tumour. It is
Null cell and endocrine 20
characterised by sudden severe headache followed
inactive tumours
ACTH 15 by transient and more prolonged loss of conscious-
Prolactin and growth 5 ness, with features of neck stiffness or vomiting and
hormone photophobia. Extension into the suprasellar cistern
FSH/LH 1–2 may cause visual failure and diplopia, but extension
TSH 1 laterally into the cavernous sinus may cause com-
Acidophil stem cell (no 1–2 pression of the nerves controlling ocular motility
hormone) (third, fourth and sixth cranial nerves).
FSH, follicle‐stimulating hormone; LH, luteinising

Prolactinoma
hormone; TSH, thyroid‐stimulating hormone.
Prolactin‐secreting tumours may be a microade-
Source: Kaye AH. Essential Neurosurgery, 3rd edn.
Oxford: Blackwell Publishing, 2005. Reproduced with
noma or a macroadenoma. Patients with microad-
permission of John Wiley & Sons. enomas are usually women who present with
infertility associated with amenorrhoea and galac-
torrhoea. These tumours can usually be treated
with dopamine agonists such as bromocriptine or
cabergoline, which have a direct inhibitory effect
on the lactotroph cells via stimulation of dopamine
D2 receptors. Very large macroadenomas may
occur in males who present with features of hypo-
pituitarism and visual failure due to suprasella
extension.
Acromegaly
Acromegaly is caused by growth hormone‐secreting
pituitary adenomas. Growth hormone (GH) is a
191‐amino acid single‐chain polypeptide whose
secretion is under the control of GH releasing and
inhibiting factors transported via the hypotha-
lamic–pituitary portal system. The anabolic effects
of GH are mostly mediated through the production
Fig. 53.10 Large pituitary tumour with marked of insulin‐like growth factor (IGF)‐1 in the liver.
suprasellar extension causing compression of the optic The clinical features of acromegaly are numerous
chiasma. and include bone and soft tissue changes, as evi-
denced by an enlarged supraciliary ridge, enlarged
Hypopituitarism frontal sinuses and increased mandibular size,
Hypopituitarism results from failure of the hor- which causes the chin to project (prognathism), and
mone secreted by the adenohypophysis. The endo- severe arthritis (especially in weight‐bearing joints)
crine secretions are not equally depressed, but there and arthralgias. The hands and feet enlarge, and the
is selective failure and the order of susceptibility is skin becomes coarse and greasy and sweats pro-
as follows: growth hormone, gonadotrophin, fusely. The voice becomes hoarse and gruff. Systemic
corticotrophin, thyroid‐stimulating hormone.
problems include hypertension, cardiac hypertro-
Hypopituitarism initially results in vague symp- phy and diabetes. The clinical diagnosis must be
toms including lack of energy and tiredness, sexual confirmed by laboratory investigations that include
impairment, undue fatiguability, muscle weakness measurement of both GH and IGF‐1.
and anorexia, and when prolonged or severe will
cause low blood pressure. Clinical hypothyroidism Cushing’s disease
is manifest by physical and mental sluggishness and Cushing’s disease is due to adrenocorticotropic hor-
a preference for warmth. When the hypopituitarism mone (ACTH)‐producing pituitary adenomas. Over
80% of the tumours are microadenomas and there Pineal region tumours
is a marked female predominance. The onset is
Tumours arising in the pineal region are relatively
often insidious and the disease may affect children
uncommon, accounting for 0.5% of all brain
or adults. Severe obesity occurs, the skin is tense and
tumours, although they are much more common in
painful, and purple striae appear around the trunk.
China and Japan where their incidence is 5%. Most
Fat is deposited, particularly on the face (moon-
occur in the age group 10–30 years. The two major
face), neck, cervicodorsal junction (buffalo hump)
groups of tumours are germ cell tumours and pin-
and trunk. The skin becomes purple due to vasodil-
eal cell tumours. Germinomas are the commonest
atation and stasis. Spontaneous bruising is com-
pineal region tumour, and teratoma the next most
mon. The skin is greasy, acne is common and facial
common germ cell tumour. These most frequently
hair excessive. Osteoporosis predisposes to sponta-
occur in children and adolescents. Pineocytoma and
neous fractures and there is wasting of the muscles.
pineoblastoma more commonly occur in young
Glucose tolerance is impaired and hypertension
adults.
occurs. Laboratory investigations are vital to con-
Patients with pineal region tumours present with
firm the diagnosis and to differentiate Cushing’s
the following.
disease due to a pituitary ACTH‐producing tumour
• Raised ICP due to obstructive hydrocephalus.
from either an adrenal tumour or ectopic source of
• Focal neurological signs: compression of the
ACTH production such as small cell carcinoma of
superior quadrigeminal plate causes limitation of
the lung.
upgaze, convergence paresis with impaired reac-
tion of the pupils to light, and accommodation
Treatment
(Parinaud’s syndrome).
The treatment of patients with pituitary tumours
• Endocrine disturbances are uncommon but
depends on whether the patient has presented with
include precocious puberty (nearly always in
features of endocrine disturbance or with problems
males) and diabetes insipidus.
related to compression of adjacent neural
The diagnosis is made by MRI and shows an
structures.
enhancing tumour in the pineal region (Figure 53.11)
Surgical excision will be used as the primary
and the likely associated hydrocephalus. The tumour
method of treatment for the following.
markers alpha‐fetoprotein and β‐human chorionic
• Large tumours (other than prolactin tumours)
gonadotrophin are specific for malignant germ cell
with extrasellar extension and especially if caus-
elements. If present, biopsy may not be necessary
ing compression of adjacent neural structures,
and the tumour can be managed with radiation and
particularly the visual pathways.
chemotherapy.
• Growth hormone‐secreting tumours causing
If hydrocephalus is present, this is best treated by
acromegaly.
an endoscopic third ventriculostomy, at which time
• ACTH‐secreting tumours causing Cushing’s
a biopsy of the tumour can also be obtained.
disease.
Germinomas are very radiosensitive and may be
• The occasional treatment of a prolactin‐secreting
treated with radiation, but the other tumours with
adenoma when medical treatment using a dopa-
negative tumour markers will require resection.
mine agonist is not tolerated or is ineffective in
reducing the size of the tumour.
Most tumours can be excised via the trans‐sphenoi-
dal approach to the pituitary fossa. SUBARACHNOID HAEMORRHAGE
The treatment of patients with persistent acro- AND CEREBRAL ANEURYSM
megaly or Cushing’s disease following surgery now
involves pharmacological therapies, all of which The sudden onset of a severe headache in a patient
have variable effectiveness. Dopamine agonists and should be regarded as subarachnoid haemorrhage
somatostatin analogues (e.g. octreotide and lanreo- until proven otherwise. The most common cause of
tide) are used in acromegaly. The most effective subarachnoid haemorrhage in adults is rupture of a
agents for Cushing’s disease are those that inhibit berry aneurysm. Subarachnoid haemorrhage in chil-
adrenal steroidogenesis, such as ketoconazole, and dren is much less common than in the adult popula-
those that inhibit cortisol synthesis, such as tion, and the most common paediatric cause is
metyrapone. Radiotherapy may be indicated if the rupture of an arteriovenous malformation. Cerebral
endocrine abnormality persists after trial of phar- aneurysm as a cause of subarachnoid haemorrhage
macological agents and if there is tumour recur- becomes more frequent than arteriovenous malfor-
rence in non‐secreting tumours. mation in patients over the age of 20 years.
504 Neurosurgery
Fig. 53.11 T1‐weighted MRI with enhancement showing pineal tumour.
Subarachnoid haemorrhage haemorrhage is often misdiagnosed as migraine.

Confirmation of the clinical diagnosis of subarach-
noid haemorrhage should be undertaken as soon
Headache
as possible by CT scanning (Figure 53.12). If there
The sudden onset of a severe headache of a type not
is any doubt that subarachnoid blood is present on
previously experienced by the patient is the hall-
the CT scan, as may occur following more minor
mark of subarachnoid haemorrhage. A relatively
haemorrhages, a lumbar puncture is essential. The
small leak from an aneurysm may result in a minor
presence of xanthochromia (yellow staining) in the
headache, sometimes referred to as a ‘sentinel head-
CSF will confirm subarachnoid haemorrhage. This
ache’, and this may be the warning episode of a sub-
can be assessed visually, by examining the superna-
sequent major haemorrhage from the aneurysm.
tant following centrifugation of the CSF sample, or
by spectrophotometry.
Diminished conscious state
Cerebral angiography (Figure 53.13) will con-
Most patients have some deterioration of their con-
firm the cause of the subarachnoid haemorrhage
scious state following subarachnoid haemorrhage.
and will determine the subsequent treatment.
This varies from only slight change, when the haem-
orrhage has been minor, to apoplectic death result- Cerebral aneurysm
ing from massive haemorrhage.
Cerebral aneurysms are the most common cause of
Meningismus subarachnoid haemorrhage in the adult population.
Blood in the subarachnoid CSF will cause the fea- The great majority of aneurysms arise at branch
tures of meningismus (headache, neck stiffness, points of two vessels and are situated mainly on the
photophobia and fever or vomiting). circle of Willis, about 85% on the anterior half of
the circle and 15% in the posterior circulation
Focal neurological signs (Box 53.2). Aneurysms occur in more than one
Focal neurological signs may occur in subarach- position in approximately 15% of cases.
noid haemorrhage due to concomitant intracere-
bral haemorrhage, the local pressure effects of the Management
aneurysm itself (such as a third cranial nerve palsy Management of patients following rupture of a cer-
resulting from pressure from a posterior communi- ebral aneurysm is determined by three factors:
cating artery aneurysm) or cerebral vasospasm that • severity of the initial haemorrhage
follows subarachnoid haemorrhage. • rebleeding of the aneurysm
• cerebral vasospasm.
Clinical assessment About 30% of all patients suffering a subarachnoid
The major differential diagnosis of subarachnoid haemorrhage from a ruptured aneurysm either
haemorrhage is meningitis, although a minor undergo apoplectic death or are deeply comatose as
Box 53.2 Position of cerebral aneurysm
Anterior circle of Willis

Anterior communicating artery
Middle cerebral artery: bifurcation or trifurcation
Internal carotid artery
Posterior communicating artery
Terminal bifurcation
Anterior choroidal artery
Ophthalmic artery
Intracavernous
Pericallosal artery
Posterior circulation (15%)

Terminal basilar artery: most common
Vertebrobasilar junction
Posterior inferior cerebellar artery
Fig. 53.12 Diffuse blood in the basal cisterns confirming Anterior inferior cerebellar artery
the diagnosis of subarachnoid haemorrhage. Superior anterior cerebellar artery
Superior inferior cerebellar artery
Posterior cerebral artery
(a)
Source: Kaye AH. Essential Neurosurgery, 3rd edn. Oxford:
Blackwell Publishing, 2005. Reproduced with permission of
John Wiley & Sons.
a result of the initial haemorrhage. Rebleeding

occurs in about 50% of patients within 6 weeks
and in 25% of patients within 2 weeks of the initial
haemorrhage. The only certain way to prevent the
aneurysm rebleeding is to occlude it from the circu-
lation. Cerebral vasospasm usually does not com-
mence until 72 hours after the initial haemorrhage.
It occurs in 50% of patients following subarach-
noid haemorrhage and in 25% it results in serious
neurological complications. Clinical vasospasm is
treated using hypertension and volume expansion,
and consequently the treatment is most effective if
(b) the aneurysm has been occluded.
Surgery or endovascular occlusion

Although in the past surgery has often been delayed
for fear that it might exacerbate cerebral vasos-
pasm, the current treatment of cerebral aneurysm is
immediate obliteration of the aneurysm by either
surgery or an endovascular technique. Active inter-
vention is usually not performed on patients who
are comatose or have features of decerebrate pos-
turing unless the CT scan shows a large intracere-
bral haematoma resulting from the ruptured
aneurysm that needs to be evacuated, or hydro-
cephalus as a cause of the poor neurological state.
Evacuation of intracerebral haematoma or drain-
age of the hydrocephalus should be performed
urgently, and the aneurysm occluded.
Fig. 53.13 (a) Cerebral aneurysm on angiogram. The surgical procedure involves a craniotomy
(b) Arteriovenous malformation. with occlusion of the neck of the aneurysm, usually
506 Neurosurgery
with a titanium clip. Endovascular techniques, Clinical presentation

using detachable coils, have been shown to have an Bacterial meningitis is usually an acute illness with
increasing role in the treatment of cerebral aneu- rapid progression of the clinical signs. The major
rysms, particularly for posterior fossa (basilar tip) presenting features are high fever and meningismus,
aneurysms. Most centres treating aneurysms utilise including headache, neck stiffness, photophobia
endovascular coiling in over 60% of cases. and vomiting. Although patients are usually alert at
the commencement of the illness, they will fre-
quently become drowsy and confused.
INTRACRANIAL INFECTION In infants, neonates, the elderly and the immuno-
compromised, the presentation of bacterial meningi-
Although infections involving the nervous system tis may be different. Neck stiffness and fever are often
may present in many ways and involve a large vari- absent and the presentation includes listlessness and
ety of pathogens, the most common infections irritability in the young and confusion or obtunda-
involving the neurosurgeon are acute bacterial tion in the elderly. A careful search must be made for
meningitis and cerebral abscess. a skin rash. Meningococcal infection frequently man-
ifests a coexisting petechial rash, which occurs less
Meningitis frequently in other bacterial or viral infections.
In some patients the original source of the infec-
Bacterial meningitis is a serious life‐threatening
tion, for example sinusitis, bacterial endocarditis,
infection that requires urgent treatment with the
otitis media or mastoiditis, may be evident and
appropriate antibiotic. Most of the common organ-
many patients have evidence of pharyngitis – bacte-
isms that cause bacterial meningitis are related to
rial meningitis sometimes follows another respira-
the patient’s age and to the presence and nature of
tory tract infection.
any underlying predisposing disease. Table 53.4
The diagnosis is made by CSF examination
shows the common organisms causing bacterial
obtained by lumbar puncture, which should be per-
meningitis related to age.
formed immediately once the diagnosis is suspected.
The bacteria reach the meninges and CSF by
If the patient is drowsy, has other signs of raised
three main routes:
ICP or if there are focal neurological signs, an
• haematogenous spread from extracranial foci of
urgent CT scan must be performed prior to lumbar
infection
puncture to exclude an intracranial space‐occupy-
• retrograde spread via infected thrombi within
ing lesion.
emissary veins from infections adjacent to the
The CSF features in a lumbar puncture are:
CNS such as sinusitis, otitis or mastoiditis
• raised cell count, predominantly a polymorpho-
• direct spread into the subarachnoid space such as
nuclear leucocytosis
from osteomyelitis of the skull and infected para-
• protein level greater than 0.8 g/L
nasal sinuses.
• glucose level less than 2 mmol/L
• positive Gram stain in more than 70%.
Table 53.4 Common organisms causing primary Other tests that should be performed on the CSF
bacterial meningitis related to age. include examination for Cryptococcus neoformans
and for Mycobacterium tuberculosis. Other investi-
Age Organism gations should include blood cultures and radio-
Neonate (0–4 Group B streptococcus, Escherichia logical investigations to detect the source of the
weeks) coli infection (chest X‐ray, CT scan or skull X‐ray for
4–12 weeks Group B streptococcus, sinusitis).
Streptococcus pneumoniae, The differential diagnoses include:
Salmonella, Haemophilus • other types of meningitis (viral, fungal, carcino-
influenzae, Listeria monocytogenes matosis)
3 months to 5 Haemophilus influenzae, • subdural empyema (patients are drowsy, with focal
years Streptococcus pneumoniae, neurological signs, and usually have seizures)
Neisseria meningitidis
• subarachnoid haemorrhage
Over 5 years Streptococcus pneumoniae,
• viral encephalitis.
and adults Neisseria meningitidis
Source: Kaye AH. Essential Neurosurgery, 3rd edn. Treatment

Oxford: Blackwell Publishing, 2005. Reproduced with High‐dose intravenous antibiotic therapy should be
permission of John Wiley & Sons. commenced immediately, and the selection of the
antibiotic depends on the initial expectation of the In addition, intravenous dexamethasone may be
most likely organism involved, taking into account indicated but this must be discussed with an infec-
the age of the patient, source of infection, CSF tious disease specialist and/or neurosurgeon before
microbiology studies and the antibiotic that has commencement. Current evidence favours early
best penetration to CSF. treatment with dexamethasone in Haemophilus
There are many antibiotic regimens, but if bacte- meningitis in childhood and in adults with pneu-
rial meningitis is suspected empirical antibiotic mococcal meningitis and should be given before the
therapy must commence immediately as follows. first dose of antibiotics. However, antibiotic treat-
• Neonates (under 3 months): cefotaxime or ceftriax- ment must not be delayed if dexamethasone is
one plus benzylpenicillin or amoxicillin/ampicillin. unavailable.
• 3 months to 15 years: cefotaxime or ceftriaxone.
• 15 years to adults: cefotaxime/ceftriaxone plus
benzylpenicillin or amoxicillin. Complications of bacterial meningitis
• Add vancomycin if Gram‐positive streptococci Complications are more likely to occur if treatment
are seen in the CSF or if Streptococcus pneumo- is not commenced immediately. The major compli-
niae is suspected clinically (e.g. by the presence of cations are:
sinusitis or otitis) to cover the possibility of inter- • cerebral oedema
mediate and/or resistant S. pneumoniae. • seizures
When the organism has been identified, the most • communicating hydrocephalus, which may
appropriate antibiotic should be used, depending occur early in the disease or as a late manifestation
on sensitivities and the ability of the antibiotic to • subdural effusion, particularly in children, with
penetrate the CSF. most resolving spontaneously but some requiring
The usual specific antimicrobial therapy follow- drainage.
ing identification of the organism is as follows. Rarer complications include:
• Streptococcus pneumoniae or Neisseria menin- • subdural empyema, which usually requires
gitidis: benzylpenicillin (child: 60 mg/kg up to drainage
1.8–2.4 g i.v. 4‐hourly). If the organism is not sen- • brain abscess.
sitive to penicillin or the patient is allergic to peni-
cillin, use cefotaxime (child: 15 mg/kg 6‐hourly or
ceftriaxone 100 mg/kg daily). If a meningococcal
Brain abscess
rash is present or there are signs of septicaemia,
systemic antibiotic treatment must be instituted Cerebral abscess may result from:
immediately before diagnostic tests. About half • haematogenous spread from a known septic site
the patients with meningococcal meningitis have or occult focus
petechiae or purpura. Subclinical or clinical dis- • direct spread from an infected paranasal or mas-
seminated intravascular coagulation often accom- toid sinus
panies meningococcaemia and may progress to • trauma causing a penetrating wound.
haemorrhage, infarction of the adrenal glands, Metastatic brain abscesses arising from haematog-
renal cortical necrosis, pulmonary vascular enous dissemination of infection are frequently
thrombosis, shock and death. The antibiotic ther- multiple and develop at the junction of white and
apy must be accompanied by intensive medical grey matter. Most common sites of infection include
supportive therapy. If S. pneumoniae is resistant skin pustules, chronic pulmonary infection (bron-
to both penicillin and third‐generation cephalo- chiectasis), diverticulitis, osteomyelitis and bacte-
sporins (cefotaxime and ceftriaxone), then vanco- rial endocarditis. The site of origin of haematogenous
mycin is recommended. spread is unknown in approximately 25% of
• Haemophilus influenzae: amoxicillin/ampicillin if patients.
organism is susceptible. If the patient is allergic or Direct spread from paranasal sinuses, mastoid air
organism resistant, use cefotaxime or ceftriaxone. cells or the middle ear are the most common patho-
• Listeria: benzylpenicillin or amoxicillin/ampicil- genic mechanisms in many series. Infection from
lin or trimethoprim and sulfamethoxazole. the paranasal sinuses spread either into the frontal
• Hospital‐acquired meningitis: vancomycin plus or temporal lobe and the abscesses are usually sin-
ceftazidime or vancomycin plus meropenem. gle and located superficially. Frontal sinusitis may
The decision regarding the most appropriate cause an abscess in the frontal lobe. Middle ear
antibiotic must be made in conjunction with an infection may spread into the temporal lobe and
infectious disease consultant. uncommonly the cerebellum.
508 Neurosurgery
Table 53.5 Cerebral abscess: pathogenesis and

principal organisms.
History Site of Predominant organism

infection
Sinusitis: Frontal
Aerobic streptococci
frontal lobe Streptococcus milleri
Haemophilus species
Mastoiditis, Temporal Mixed flora
otitis lobe Aerobic and anaerobic
streptococci
Enterobacteria
Bacteroides fragilis
Haemophilus species
Haematogenous, Brain Aerobic streptococci
cryptogenic Anaerobic streptococci
Enterobacteria
Trauma Brain Staphylococcus aureus
Source: Kaye AH. Essential Neurosurgery, 3rd edn.

Oxford: Blackwell Publishing, 2005. Reproduced with
permission of John Wiley & Sons.
Fig. 53.14 Cerebral abscess: a ring‐enhancing mass.

Bacteriology Source: Kaye AH. Essential Neurosurgery, 3rd edn.
Table 53.5 details the pathogenesis and principal Oxford: Blackwell Publishing, 2005. Reproduced with
organisms in cerebral abscess. Streptococci are iso- permission of John Wiley & Sons.
lated from approximately 80% of brain abscesses.
The most common single species is the α‐haemo- be commenced as soon as the pus has been obtained.
lytic carboxyphilic Streptococcus milleri, whose The initial choice of antibiotic, before culture
major habitat is the alimentary tract including the results are available, will depend on the probable
mouth and dental plaque. Otogenic abscesses usu- cause of the brain abscess and the Gram stain. The
ally yield mixed flora, including Bacteroides, vari- therapy will be refined once the organism is known.
ous streptococci and members of the Anticonvulsant medication should be commenced
Enterobacteriaceae. Staphylococcus aureus is often as there is an incidence of seizures of 30–50%.
the pathogen in abscesses resulting from trauma. The abscess may need to be treated by either sin-
gle or repeat aspiration. Surgical excision of the
Presenting features abscess may be necessary if there is persistent reac-
• An intracranial mass (raised ICP, focal neurologi- cumulation of the pus, or if a fibrous capsule devel-
cal signs, epilepsy) ops that fails to collapse despite repeat aspirations.
• Systemic toxicity (fever and malaise in 60% of A cerebellar abscess requires excision.
cases)
• Clinical features of the underlying source of infec-
tion (sinusitis, bacterial endocarditis, diverticulitis) Further reading
Diagnosis Colli BC, Carlotti CG, Machado HR, Assirati JA.
CT and MRI (Figure 53.14) show a ring enhancing Intracranial bacterial infections. Neurosurg Q 1999;9:
mass often surrounded by considerable oedema. 258–84.
Dorsch NWC, King MT. A review of cerebral vasospasm
Management in aneurysmal subarachnoid haemorrhage. J Clin
Neurosci 1994;1:19–26.
The principles of treatment are:
International Subarachnoid Aneurysm Trial (ISAT)
• identify the bacterial organism
Collaborative Group. International Subarachnoid
• institute antibiotic therapy Aneurysm Trial (ISAT) of neurosurgical clipping vs
• drain or excise the abscess. endovascular coiling in 2143 patients with ruptured
A specimen of pus is essential for accurate identifi- intracranial aneurysms: a randomised trial. Lancet
cation of the organism. Antibiotic therapy should 2002;360:1267–73.
Kaye AH. Essential Neurosurgery, 3rd edn. Oxford: 3 Which of the following statements about brain
Blackwell Publishing, 2005. tumours in children is correct?
Kaye AH, Black PMcL. Operative Neurosurgery. a most commonly occur in the posterior fossa
Edinburgh: Churchill Livingstone, 1999. b can be cured with surgery
Kaye AH, Laws ER. Brain Tumors, 2nd edn. Edinburgh:
c never metastasise
Churchill Livingstone, 2001.
d invariably have an excellent prognosis
Stephanov S. Surgical treatment of brain abscess.
e most frequently present with epilepsy
Neurosurgery 1988;22:724–30.
Stupp R, Mason WP, van den Bent MJ et al. Radiotherapy
plus concomitant and adjuvant temozolomide for glio- 4 Which of the following statements about cerebral
blastoma multiforme. N Engl J Med aneurysms is correct?
2005;352:987–96. a usually occur on the peripheral intracranial vessels
Weir B. Unruptured intracranial aneurysms: a review. b can be definitively diagnosed by a CT scan
J Neurosurg 2002;96:3–42. c are the most common cause of subarachnoid
haemorrhage in adults
d are virtually always multiple
e usually present with focal seizures
MCQs
5 Which of the following statements about subarach-
noid haemorrhage is correct?
a is most commonly due to ruptured arteriovenous
malformation in adults
1 Which of the following statements is correct? b usually presents as an epileptic seizure as the
a meningioma is the most common malignant initial symptom
adult brain tumour c must be evacuated as an emergency
b brain tumours are rare in children d is characterised by the onset of a sudden severe
c high‐grade cerebral gliomas are invariably fatal headache
d metastatic cancer in the brain is uncommon e is frequently due to haemorrhage from a tumour
e oligodendroglioma is the most common type of
glioma 6 Which of the following statements about pituitary
tumours is correct?
2 Which of the following statements about cerebral a the tumour is always confined to the sella
gliomas in adults is correct? b adults frequently present with growth retardation
a do not infiltrate through the brain c prolactin‐secreting tumours are best treated with
b are best managed with chemotherapy surgery
c rarely cause raised intracranial pressure d ACTH‐secreting tumours cause Cushing’s disease
d are best visualised by MRI e posterior pituitary function is almost always
e most frequently occur in the cerebellum absent in patients presenting with large tumours
54 Nerve injuries, peripheral nerve
entrapments and spinal cord
compression
Andrew H. Kaye
Department of Surgery, University of Melbourne and Royal Melbourne Hospital, Melbourne, Victoria,
Australia
injuries which forms the basis for more refined

Introduction classifications. It is based on three main types of
nerve fibre injury and whether there is continuity
Peripheral nerves may be trapped, compressed or
of the nerve (Table 54.1).
injured at any position along their course, although
there are certain regions where they are especially
Neurotmesis
vulnerable. Injury to the nerve occurs when the
nerve is either relatively superficial and exposed, or Neurotmesis is the most severe injury. The nerve is
lying adjacent to bone so that the jagged fractured completely divided and complete distal Wallerian
ends of the bone may directly injure the nerve. degeneration occurs. There is complete loss of
Nerve entrapments occur particularly where the motor, sensory and autonomic function.
peripheral nerve passes through a tunnel formed by Although the term neurotmesis implies a cutting of
ligaments, bone and/or muscle. the nerve, the term is also used when the epineurium of
the nerve is still in continuity but the axons have been
destroyed and replaced by scar tissue to such a degree
Acute nerve injuries that spontaneous regeneration is impossible. If the
nerve has been completely divided, axonal regenera-
Peripheral nerve anatomy tion causes a neuroma to form in the proximal stump.
The axon projects from the cell body and is sur-

Axonotmesis
rounded by a basement membrane and myelin
sheath. The axon is covered by the endoneurium, the Axonotmesis is characterised by complete interrup-
innermost layer of connective tissue, and a number of tion of the axons and their myelin sheaths, but with
axons are grouped together in a bundle called a fasci- preservation of the epineurium and perineurium.
cle, which is invested by a further connective tissue Spontaneous regeneration will occur, with the
sheath called the perineurium. The peripheral nerve intact endoneurial sheaths guiding the regenerating
consists of a group of fascicles covered by the outer- fibres to their distal connections. Axonotmesis is
most layer of connective tissue, the epineurium. initially clinically indistinguishable from neurotme-
sis because there is complete and immediate loss of
motor, sensory and autonomic function distal to the
Classification of nerve injuries lesion with a similar picture on electromyogram
(EMG). Regeneration occurs at a rate of 1–2 mm
There is no single classification system that can per day so that the time of recovery will depend on
describe all the many variations of nerve injury. the distance between a lesion and the end organ, as
Most systems attempt to correlate the degree of well as on the age of the patient. The major types of
injury with symptoms, pathology and prognosis. injuries causing axonotmesis include compression,
Seddon in 1943 introduced a classification of nerve traction, missile and ischaemia.
511
512 Neurosurgery
Table 54.1 Classification of nerve injuries.
Neurotmesis Axonotmesis Neurapraxia
Pathological
Anatomical continuity May be lost Preserved Preserved
Essential damage Complete disorganisation, Nerve fibres Selective demyelination of larger
Schwann sheaths preserved interrupted fibres, no degeneration of axons
Clinical
Motor paralysis Complete Complete Complete
Muscle atrophy Progressive Progressive Very little
Sensory paralysis Complete Complete Usually much sparing
Autonomic paralysis Complete Complete Usually much sparing
Electrical phenomena
Reaction of Present Present Absent
degeneration
Nerve conduction Absent Absent Preserved
distal to the lesion
Motor‐unit action Absent Absent Absent
potentials
Fibrillation Present Present Occasionally detectable
Recovery
Surgical repair Essential Not necessary Not necessary
Rate of recovery 1–2 mm/day after repair 1–2 mm/day Rapid, days or weeks
March of recovery According to order of According to order No order
innervation of innervation
Quality Always imperfect Perfect Perfect
Source: adapted from Seddon H. Surgical Disorders of the Peripheral Nerves, 3rd edn. Oxford: Blackwell Publishing,
2005. Reproduced with permission of John Wiley & Sons.
Neurapraxia to a complex nerve injury in a patient with

multiple trauma.
Neurapraxia is the most mild form of injury and is
likened to a transient ‘concussion’ of the nerve,
where there is a temporary loss of function that is
Brachial plexus injury
reversible within hours to months of the injury
(with an average of 6–8 weeks). If there is initially a
The mechanisms of injury are the same as for any
complete loss of function, neurapraxia cannot be
peripheral nerve (see Box 54.1).
distinguished from the more serious type of injury
but will be recognised in retrospect when recovery
of function has occurred sooner than would be pos- Birth injuries
sible following Wallerian degeneration. Birth injuries include Erb’s palsy due to damage to
the upper trunk of the brachial plexus, Klumpke’s
paralysis due to damage to the lower trunk of the
Causes of peripheral nerve injury brachial plexus (C8 and T1; resulting from the arm
being held up while traction is applied to the body
The type of trauma will determine the nature of the during a breech delivery), and paralysis of the
injury to the nerve (Box 54.1). whole arm as a result of severe birth trauma.
Adolescents and adults
Management of nerve injuries
In adolescents and adults the most common cause is
The basis of management depends on a precise severe traction on the brachial plexus, resulting
assessment of the damage that has been done to most frequently from a motorbike or motor vehicle
the nerve (Box 54.2). The types of injuries vary accident. The trauma may result in damage to any
considerably, from an isolated single nerve lesion part of the plexus but severe traction may result in
54: Nerve injuries, peripheral nerve entrapments and spinal cord compression 513
Box 54.1 Types of trauma and the Box 54.2 General guidelines for
nature of nerve injury management of nerve injuries
• Lacerations cause neurotmesis, with complete or • Determination of the exact nerve involved by
partial division of the nerve. (i) the clinical deficit and (ii) the position of
• Missile injuries may cause the spectrum of nerve the injury.
injury from complete disruption of the nerve to a • Assessment of the type of nerve damaged by the
mild neurapraxia. mechanism of injury.
• Traction and stretch trauma may result in either • If a neurapraxia or axonotmesis is suspected on
complete disruption of the nerve or, if minor, a clinical grounds, there is no specific surgical
neurapraxia. This type of mechanism is responsible treatment for the nerve but physiotherapy should
particularly for brachial plexus injuries following commence as soon as possible to prevent stiffness
motorbike accidents, radial or peroneal nerve of the joints and contractures.
injuries. It is a common mechanism of nerve injuries • Immediate or early exploration of the nerve should
associated with skeletal fractures. be undertaken in the following circumstances:
• Fractures or fracture dislocation may cause nerve • When it is highly probable that the type of injury
injuries when the adjacent nerve is either (e.g. laceration) has caused the nerve to be severed.
compressed by the displaced bone fragments or, • If the nerve injury has been caused by a displaced
less commonly, severed by the jagged edge of fracture that needs reduction by open surgery, it is
the bone. appropriate to explore the nerve at that time.
• Compression ischaemia may produce a neurapraxia • Delayed exploration of the nerve will be indicated if
in mild cases or, if prolonged and severe, the clinical and EMG findings indicate failure of
axonotmesis or neurotmesis. It is the cause of the regeneration of the nerve beyond the time expected,
pressure palsies following improper application of a i.e. the injury has resulted in a neurotmesis rather
tourniquet or the ‘Saturday night palsy’, in which than an axonotmesis or neurapraxia.
the radial nerve has been compressed against the
humerus.
• Injection injury results from either direct trauma by be complete. If the injury is improving there is no
the needle or the toxic effect of the agent injected. indication for surgery and management includes
As would be expected, the sciatic and radial nerves intensive physiotherapy and mobilisation of the
are the most commonly affected. joints. There is no place for surgical repair of the
• Electrical and burn injuries are uncommon causes injured nerve itself if there is evidence of nerve root
of serious peripheral nerve damage. avulsion from the cord, but nerve and tendon trans-
fer procedures may considerably improve the func-
tional outcome.
tearing of the arachnoid and dura with nerve root
avulsion from the spinal cord.
Peripheral nerve entrapment
Management
The management involves determination of the Entrapment neuropathies occur particularly when
exact neurological injury, particularly the part of the nerves pass near joints. Less common forms of
brachial plexus involved (Figure 54.1). The presence entrapment neuropathies may lie at a distance from
of Horner’s syndrome is evidence there has been a joint. Box 54.3 lists the common and less frequent
avulsion of the nerve roots from the spinal cord. entrapment neuropathies.
Magnetic resonance imaging (MRI) may show
the pseudomeningocele characteristic of nerve root
Carpal tunnel syndrome
avulsion. Electrical studies provide useful baseline
data for future comparison. It is reasonable to
This is by far the most common nerve entrapment
obtain these studies 8 weeks after the injury.
and women are affected four times more frequently
There is debate concerning the indications for
than men.
surgical intervention for closed brachial plexus
injuries in adults. In general there is limited benefit
Anatomy
from early exploration of the plexus in closed inju-
ries, although some surgeons do advocate explora- The carpal tunnel is a fibro‐osseous tunnel on
tion approximately 4 months after the injury if the palmar surface of the wrist (Figure 54.2). The
clinical and electrical evidence shows the lesion to dorsal and lateral walls consist of the carpal bones,
514 Neurosurgery
Thoraclc outlet
Scalenus medius
Scalenus anterior
C5, C6
Brachial
plexus
C7
C8, T1
Subclavian
artery
2
Fig. 54.1 The brachial plexus passing through the cervicobrachial junction. Source: Kaye AH. Essential Neurosurgery,
3rd edn. Oxford: Blackwell Publishing, 2005. Reproduced with permission of John Wiley & Sons.
Aetiology
Box 54.3 Entrapment neuropathies (the
more common ones are shown in bold) The initial symptoms occur in women during preg-
nancy and in both sexes when they are performing
Median nerve unusual strenuous work with their hands, although
• Carpal tunnel syndrome the features of carpal tunnel syndrome may present
• Supracondylar entrapment
at any stage throughout the adult years. A number
• Cubital fossa entrapment
of systemic conditions are associated with, and may
• Anterior interosseus nerve entrapment
predispose to, carpal tunnel syndrome:
Ulnar nerve
• pregnancy and lactation
• Tardy ulnar palsy
• contraceptive pill
• Deep branch of ulnar nerve
Radial nerve (posterior interosseus nerve)
• rheumatoid arthritis
Suprascapular nerve • myxoedema
Meralgia paresthetica (lateral femoral cutaneous • acromegaly.
nerve of thigh) Any local condition around the wrist joint that
Sciatic nerve decreases the size of the carpal tunnel will also pre-
Tarsal tunnel syndrome dispose to carpal tunnel syndrome. These include a
Thoracic outlet syndrome ganglion, tenosynovitis, unreduced fractures or dis-
locations of the wrist or carpal bones, and any local
arthritis.
which form a crescentic trough. A tunnel is made by
the fibrous flexor retinaculum, which is attached to
Clinical features
the pisiform and hook of the hamate medially and
the tuberosity of the scaphoid and crest of the tra- The principal clinical features of carpal tunnel syn-
pezium laterally. The contents of the tunnel are the drome are pain, numbness and tingling.
median nerve and flexor tendons of the flexor digi- The pain, which may be described as burning or
torum superficialis, flexor digitorum profundus aching, is frequently felt throughout the whole
and flexor pollicis longus. hand and not just in the lateral three digits. There is
Flexor
Ulnar n. & a. Flexor retinaculum pollicis
Median n. longus
Extensor
pollicis
brevis
Pisiform
Trapezium
Triquetrum
Scaphoid Hamate Trapezium
Tendons of
flexor
digitorum
superficialis
and profundus Pisiform Scaphoid
Lunate
Capitate
Fig. 54.2 The carpal tunnel just distal to the wrist. Source: Kaye AH. Essential Neurosurgery, 3rd edn. Oxford:
Blackwell Publishing, 2005. Reproduced with permission of John Wiley & Sons.
often a diffuse radiation of the pain up the forearm intermittent or if there is a reversible underlying
to the elbow and occasionally into the upper arm. precipitating condition, such as pregnancy or oral
The symptoms are particularly worse at night, and contraceptive pill.
on awakening the patient has to shake the hand to
obtain any relief.
Numbness and tingling principally occur in the Ulnar nerve entrapment at the elbow
lateral three and a half fingers, in the distribution of
the median nerve, although the patient frequently Anatomy
complains of more diffuse sensory loss throughout
the fingers. This symptom is also worse at night and The ulnar nerve runs behind the medial epicondyle
with activity involving the hands. The patient of the humerus and enters the forearm through a
frequently complains that the hand feels ‘clumsy’, fibro‐osseous tunnel formed by the aponeurotic
but with no specific weakness. attachment of the two heads of flexor carpi ulnaris,
There are often only minimal signs of median which span from the medial epicondyle of the
nerve entrapment at the wrist. The Tinel sign humerus to the olecranon process of the ulnar form-
tingling in the median nerve‐innervated thumb,
( ing the cubital tunnel (Figure 54.3). During flexion
index and middle finger) may be elicited by tapping of the elbow the ligament tightens and the volume
over the median nerve but its absence has little of the cubital tunnel decreases, putting increasing
diagnostic value. pressure on the underlying nerve. Compression can
If the compression has been prolonged there may also be due to injuries in the region producing
be signs of median nerve dysfunction, including deformity of the elbow, although the features of
wasting of the thenar muscle, weakness of muscles ulnar nerve entrapment do not usually appear for
innervated by the distal median nerve, especially some years. This delay in the appearance of symp-
abductor pollicis brevis, and diminished sensation toms led to the term ‘tardy ulnar palsy’.
over the distribution of the median nerve in the
hand. The clinical diagnosis can be confirmed Aetiology
by EMG.
In most cases there is no particular predisposing
cause. In a minority there are underlying factors
Treatment
that predispose to nerve entrapment, including
Surgery involving division of the flexor retinaculum lengthy periods of bed rest from coma or major
is a simple and effective method of relieving the illness, and poor positioning of the upper limbs

compression and curing the symptoms. However, during long operations causing prolonged pressure
conservative treatment involving the use of a wrist on the nerve. Other causes include arthritis of the
splint and non‐steroidal anti‐inflammatory agents elbow, ganglion cysts of the elbow joint and direct
is appropriate if the symptoms are mild or trauma.
516 Neurosurgery
should avoid putting pressure on the nerve at the

elbow during reading, sitting or lying and should
Medial epicondyle
cease heavy work with the arms.
Surgery involves decompression of the nerve and
Radius is indicated if there are progressive symptoms or
Ulnar N.
signs and if there is any wasting or weakness.
Fascial
roof of Meralgia paresthetica
Ulna
cubital tunnel
Meralgia paresthetica results from entrapment of
the lateral cutaneous nerve of the thigh beneath the
Olecranon inguinal ligament, just medial to the anterior supe-
Flexor carpi uinaris
rior iliac spine. At this position the nerve passes
Fig. 54.3 The ulnar nerve passing behind the medial
between two roots of attachment of the inguinal
epicondyle of the humerus and through the cubital
ligament to the iliac bone and there is a sharp angu-
tunnel. Source: Kaye AH. Essential Neurosurgery, 3rd
edn. Oxford: Blackwell Publishing, 2005. Reproduced lation of the nerve as it passes from the iliac fossa
with permission of John Wiley & Sons. into the thigh.
Prolonged standing or walking and an obese pen-
dulous anterior abdominal wall accentuates the
Clinical features
downward pull on the inguinal ligament and may
The clinical features include paraesthesia and predispose to entrapment of the nerve. The syn-
numbness in the ring and little finger of the hand drome is most frequently seen in middle‐aged men
and the adjacent medial border of the hand, w asting who are overweight and in young army recruits
of the hypothenar eminence and interossei muscles, during strenuous training.
and weakness. The principal symptom is a painful dysaesthesia
In advanced cases, entrapment of the ulnar in the anterolateral aspect of the thigh, with the
nerve will lead to weakness of the muscles of the patient often describing the sensation as ‘burning’,
hypothenar eminence, the interossei, the medial two ‘pins and needles’ or ‘prickling’. The only neuro-
lumbricals, adductor pollicis, flexor digitorum pro- logical sign is diminished sensation over the antero-
fundus (ring and little finger) and flexor carpi ulnaris. lateral aspect of the thigh in the distribution of the
Paralysis of the small muscles of the hand causes lateral cutaneous nerve.
‘claw hand’, this posture being produced by the The symptoms may be only minor and the patient
unopposed action of their antagonists. As the may be satisfied with reassurance. The unpleasant
interossei cause flexion of the fingers at the metacar- features may resolve with conservative treatment,
pophalangeal joints and extension at the inter- including weight reduction in an obese patient.
phalangeal joints, when these muscles are paralysed Surgery may be necessary if the symptoms are
the opposite posture is maintained by the long debilitating and the procedure involves decompres-
flexors and extensors causing flexion at the inter- sion of the nerve; if that fails, occasionally division
phalangeal joints and hyperextension at the meta- of the nerve may be necessary.
carpophalangeal joints. This is most pronounced in
the ring and little fingers as the two radial lumbri-
cals, which are innervated by the median nerve, com- Spinal cord compression
pensate to some degree for the impaired action of the
interossei on the index and middle fingers. Froment’s Compression of the spinal cord is a common neuro-
sign is demonstrated by asking the patient to grasp a surgical problem and requires early diagnosis and
piece of cardboard between the index finger and urgent treatment if the disastrous consequences of
thumb against resistance. There will be flexion of the disabling paralysis and sphincter disturbance are to
interphalangeal joint of the thumb because the be avoided. Although there are a large range of pos-
median innervated flexor pollicis longus is used sible causes of spinal cord compression in clinical
rather than the weakened adductor pollicis. practice, the majority are due to the following.
• Extradural
Treatment
–– Trauma
Conservative treatment may be tried if the clinical –– Metastatic tumour
features are minor and not progressive. The patient –– Extradural abscess
• Intradural, extramedullary result in upper motor neurone weakness with little

–– Meningioma or no wasting, increased tone, increased deep ten-
–– Schwannoma don reflexes and positive Babinski response. As the
• Intramedullary cord becomes more severely compressed a complete
–– Glioma (astrocytoma and ependymoma) paraplegia will result. The compressing mass will
• Syrinx also cause weakness of the nerve root segment at
the involved level. In the cervical region this will
result in a lower motor neurone weakness of the
Presenting features
involved nerve roots in the upper limbs. In the lum-
bar region involvement of the conus medullaris
The two major presenting features that are the
may produce a mixture of lower motor neurone
hallmark of spinal cord compression are pain and
and upper motor neurone signs in the lower limbs.
neurological deficit. There is considerable variation
Cauda equina compression produces a lower motor
in the manner in which these two major features pre-
neurone pattern of weakness.
sent, and depend on the pathological basis, the site of
the compression and the speed of the compression.
Sensory disturbance
Pain A sensory level is the hallmark of spinal cord com-
Pain is a typical early feature of spinal cord compression. In the thoracic region the sensory level
pression and is especially common in extradural will be to all modalities of sensation over the body
compression due to metastatic cancer. Pain often or trunk, although there may be some sparing of
precedes any neurological disturbance, sometimes some modalities in the early stages of compression.
by many months. The pain is due to involvement of A useful guide is to remember that the T4 dermat-
local pain‐sensitive structures, such as the bone of ome lies at the level of the nipple, T7 at the xiphi-
the vertebral column. Involvement of a spinal nerve sternum and T10 at the umbilicus.
root will cause pain radiating in the affected region.
Thoracic cord compression with involvement of the Sphincter involvement
thoracic nerve root will often be associated with
pain radiating around the chest wall. This ‘girdle’ Sphincter disturbance often follows compression of
pain is an important feature associated with a lesion the spinal cord, with the first symptom being diffi-
which may cause spinal cord compression. In addi- culty in initiating micturition, which is followed by
tion, there is also a ‘central’ pain due to spinal cord urinary retention, often relatively painless.
compression, which is described as an unpleasant Constipation and faecal incontinence will subse-
diffuse dull ache with a ‘burning’ quality. quently occur. The clinical signs include an enlarged
Flexion or extension of the neck may cause ‘elec- palpable bladder, diminished perianal sensation and
tric shock’ or tingling sensations radiating down decreased anal tone.
the body to the extremities. This is called Lhermitte’s In summary the clinical features of spinal cord
sign, and is typically associated with cervical cord compression are:
involvement. It is an ominous sign of impending • pain, local and radicular
spinal cord compression. • progressive weakness of the limbs
• sensory disturbance, often with a sensory level
Neurological deficit • sphincter disturbance.
The neurological features of spinal cord compres-

sion consist of progressive weakness, sensory dis-
turbance and sphincter disturbance. Management
Motor impairment Spinal cord compression is a neurosurgical emergency.
The motor impairment will be manifest as a paraly- Investigation and treatment must be undertaken as a
sis, and the level of the weakness will depend on the matter of urgency once the diagnosis is suspected.
position of the cord compression. Thoracic cord The radiological studies undertaken to confirm
compression will result in a progressive paraparesis the diagnosis of spinal cord compression include:
of the lower limbs and if the cervical cord is • plain spinal X‐ray
involved the upper limbs will also be affected. • MRI (Figures 54.4 and 54.5)
Compression of the corticospinal pathways will • CT scan to show detail of bone involvement.
518 Neurosurgery
Fig. 54.4 MRI of thoracic fracture causing spinal cord compression.
Fig. 54.5 MRI of spinal metastases.

MRI is of considerable value in diagnosing the

cause and position of spinal cord compression and
is by far the best investigation, as it will clearly
show the pathological changes in the vertebral
body, spinal canal, spinal cord and paravertebral
region, thereby aiding with planning the treatment.
Plain X‐ray and CT scan will help show the focal
bony destruction.
Treatment Fig. 54.6 Spinal schwannoma at operation causing

spinal cord compression.
The standard treatment for spinal cord compres-
sion is urgent surgery, except in some cases of com- the intervertebral foramen to form a ‘dumb‐bell’
pression due to malignant tumour known to be tumour, which may rarely present as a mass in the
radiosensitive, in which treatment with high‐dose thorax, neck or posterior abdominal wall.
glucocorticosteroids and radiotherapy may be The presenting features are those of a slow‐
indicated. growing tumour causing cord compression. There
is frequently some degree of Brown–Séquard syn-
drome due to the lateral position of the tumour
(see section Incomplete lesions; Figure 54.6). The
Common causes of spinal cord treatment is surgical excision.
compression
Malignant spinal cord compression Spinal meningioma
By far the most common cause of spinal cord com- Spinal meningiomas are intradural and most
pression, this results from extradural compression frequently occur in the thoracic region (Figure 54.7).
by malignant tumours. The most common tumours They occur particularly in middle‐aged or elderly
involved are: patients and there is a marked female predomi-
• carcinoma of the lung nance. The tumour grows extremely slowly and
• carcinoma of the breast there is usually a long history of ill‐defined back
• carcinoma of the prostate pain, often nocturnal, and a slowly progressive
• carcinoma of the kidney paralysis prior to diagnosis.
• lymphoma
• myeloma. Intramedullary tumours
Surgical management for malignant spinal cord
Ependymoma (Figure 54.8) and astrocytoma of the
compression utilises either:
spinal cord are uncommon, with the presenting fea-
• decompressive laminectomy (posterior approach)
tures depending on the level of cord involvement.
• vertebrectomy and fusion (anterior approach).
Ependymomas not infrequently arise in the filum
Urgent radiotherapy, combined with high‐dose glu-
terminale and will cause features of cauda equina
cocorticosteroids, may be effective in controlling
compression. There is often a history of low back
the tumour causing spinal cord compression and is
and leg pain, progressive weakness in the legs (often
sometimes advisable if the patient has a known pri-
with radicular features), sensory loss over the sad-
mary tumour that is radiosensitive and if there is a
dle area and eventually sphincter disturbance.
partial incomplete neurological lesion that is only
It is usually possible to resect ependymomas, but
slowly progressive.
surgical resection of astrocytomas is not possible as
they spread diffusely through the spinal cord.
Schwannoma (neurofibroma)
Schwannomas are the most common of the intrathe-
Intervertebral disc prolapse
cal tumours and may occur at any position.
They arise invariably from the posterior nerve roots Intervertebral disc herniation is a common cause
and grow slowly to compress the adjacent neural of nerve root compression, but if the disc pro-
structures. Occasionally, the tumour extends through lapses directly posteriorly (centrally) it will cause
520 Neurosurgery
(a)
(b)
Fig. 54.8 T1‐weighted post‐contrast sagittal MRI of

lumbar ependymoma.
space, usually from an infective source elsewhere in

the body. It requires urgent treatment. The spinal
cord compression is due to both inflammatory
swelling and pus, and presenting features include
severe local spinal pain with rapidly progressive
neurological features of spinal cord compression.
There are frequently constitutional features of
infection such as high fever, sweating and tachycar-
dia. MRI is the preferred investigation and treat-
Fig. 54.7 T1‐weighted contrast‐enhanced MRI of ment consists of urgent surgery with appropriate
thoracic meningioma: (a) axial; (b) sagittal. antibiotic medication.
compression of the spinal cord in the cervical or Cervical myelopathy

thoracic region and of the cauda equina in the lum-
Cervical myelopathy results from cervical cord
bar region. Urgent surgery is essential to relieve the
compression due to a narrow cervical vertebral
compression.
canal. The constriction of the canal enclosing the
cervical cord is due to a combination of congenital
Spinal abscess
narrowing, and cervical spondylosis involving
Spinal abscess may be secondary to an infection in hypertrophy of the facet joints and osteophyte for-
the intervertebral disc or vertebral body (osteomy- mation, hypertrophy of the ligamenta flava and
elitis of the vertebra) or an infection in the epidural bulging of the cervical disc. The myelopathy results
from both direct pressure on the spinal cord and haematoma, interruption of the vascular supply
ischaemia of the cord due to compression and and/or traction.
obstruction of the small vessels within the cord or
to compression of the feeding radicular arteries Cervical spine
within the intervertebral foramen. Flexion and flexion–rotation injuries are the most
There is frequently a history of slowly progressive common type of injury to the cervical spine, with
disability, although it is not unusual for the neuro- the C5/6 level being the most common site. There is
logical disability to deteriorate rapidly, particularly often extensive posterior ligamentous damage and
following what might be even a minor or trivial these injuries are usually unstable. Compression
injury involving sudden movement of the neck. injuries also most frequently occur at the C5/6
Muscular weakness, manifest by clumsiness level. The wedge fracture injuries are often stable
involving the hands and fingers, impairment in fine‐ because the posterior bony elements and longitudi-
skilled movements and dragging or shuffling of the nal ligaments are often intact. However, those with
feet, is the most common initial symptom. Sensory a significant retropulsed fragment are likely to have
symptoms are frequent, and occur as diffuse numb- disruption of the associated ligaments and are con-
ness and paraesthesia in the hands and fingers. sidered unstable. When combined with a rotation
MRI will confirm the severity of the cord com- force in flexion, a ‘tear drop’ fracture may occur,
pression and show the exact pathological basis for with separation of a small anterior–inferior frag-
the compression. An additional benefit of MRI is ment from the vertebral body, and these should also
that it may show myelomalacia (high signal within be considered unstable.
the cord) indicating the severity of the compression Hyperextension injuries are most common in the
and a poorer prognosis following surgery. older age group and in patients with degenerative
Surgery is indicated for clinically progressive or spinal canal stenosis. The bone injury is often
moderate or severe myelopathy. The operation may not demonstrated and the major damage is to
involve either a posterior decompressive laminec- the
anterior longitudinal ligament secondary to
tomy or, if the compression is predominantly ante- hyperextension.
rior to the cord, an anterior approach with excision
of the compressive lesion involving the interverte- Thoracolumbar spine
bral disc and/or vertebral osteophytes followed by Flexion–rotation injuries most commonly occur at
fusion is preferred. the T12/L1 level and result in anterior dislocation
of T12 on the L1 vertebral body. Compression inju-
ries are common with the vertebral body being
Spinal injuries decreased in height. These injuries are usually stable
Trauma to the spinal column occurs at an incidence and neurological damage is uncommon. Open inju-
of approximately 2–5 per 100 000 population. ries may result from stab or gunshot wounds that
Adolescents and young adults are the most com- result in damage to the spinal cord.
monly affected, with most serious spinal cord inju-
ries being a consequence of road traffic accidents
Neurological impairment
and water sports (especially diving into shallow
water), skiing and horse riding accidents. There is a state of diminished excitability of the spinal
cord immediately after a severe spinal cord injury,
which is referred to as ‘spinal shock’. There is an are-
Mechanism of injury
flexic flaccid paralysis. The duration of spinal shock
Although severe disruption of the vertebral column varies, with minimal reflex activity appearing within a
usually causes serious neurological damage, it is not period of 3–4 days or being delayed up to some weeks.
always possible to correlate the degree of bone
damage with spinal cord injury. Minor vertebral Complete lesions
column disruption does not usually cause neuro- The most severe consequence of spinal trauma is a
logical deficit, but occasionally may be associated complete transverse myelopathy in which all neuro-
with severe neurological injury. The mechanism of logical function is absent below the level of the
the injury will determine the type of vertebral injury lesion, causing either a paraplegia or quadriplegia
and neurological damage. (depending on the level), impairment of autonomic
Trauma may damage the spinal cord by function including bowel or bladder function, and
direct compression by bone, ligament or disc, sensory loss.
522 Neurosurgery
Incomplete lesions Careful attention should be paid to body tempera-

There are numerous variations of neurological defi- ture as the spinal patient is poikilothermic and
cit manifest in incomplete lesions but with some will assume the temperature of the environment.
specific syndromes. A nasogastric tube should be passed to avoid prob-
• Anterior cervical cord syndrome: this is due to lems associated with vomiting due to gastric stasis
compression of the anterior aspect of the cord and paralytic ileus and a urinary catheter is neces-
resulting in damage to the corticospinal and sary. Prophylaxis for deep vein thrombosis and sub-
spinothalamic tracts, with motor paralysis below sequent pulmonary embolus should be commenced
the level of the lesion and loss of pain, tempera- as soon as possible.
ture and touch sensation but relative preservation Radiological investigations will include plain
of light touch, proprioception and position sense, X‐ray, CT and MRI.
which are carried by the posterior columns. High‐dose dexamethasone is usually adminis-
• Central cord syndrome: this is due to hyperexten- tered as soon as possible for patients with spinal
sion of the cervical spine with damage located cord compression but there is no conclusive proof
centrally causing the most severe injury to the of its effectiveness.
more centrally located cervical tracts, which sup-
ply the upper limbs. There is disproportionate Spinal reduction and stabilisation
weakness in the upper limbs compared with the Skeletal traction for restoration and/or mainte-
extremities. Sensory loss is usually minimal. nance of normal alignment of the spinal column is
• Brown–Séquard syndrome: from hemisection of an effective treatment, with a variety of cervical
the cord resulting in ipsilateral paralysis below traction devices available. The traction must be
the level of the lesion with loss of pain, tempera- commenced under X‐ray or fluoroscopic control
ture and touch on the opposite side. and great care should be taken to avoid distraction
at the fracture site, as traction on the underlying
cord will worsen the neurological injury. Reduction
Management of spinal injuries of facet dislocations may involve either manipula-
tion under fluoroscopic control with the patient
As little can be done to repair the damage caused by under general anaesthesia or may require open sur-
the initial injury, major efforts are directed towards gery. This management must only be undertaken in
prevention of further spinal cord injury and com- specialised neurosurgical or spinal injury depart-
plications resulting from the neurological damage. ments. In patients where the fracture/dislocation is
The general principles of management are: considered unstable a spinal fusion is usually per-
• prevention of further injury to the spinal cord formed, utilising either an anterior or posterior
• reduction and stabilisation of bony injuries approach. In cervical injuries this may be aug-
• prevention of complications resulting from spi- mented using halo immobilisation.
nal cord injury In the past most injuries of the thoracolumbar
• rehabilitation. spine were managed conservatively by postural
The initial first‐aid management of patients with reduction in bed, but now unstable injuries are
injuries to the spinal column and spinal cord require managed with surgical fixation.
the utmost caution in turning and lifting the patient. There has been considerable controversy over
The spine must be handled with great care to avoid surgical intervention with spinal cord injuries. The
inflicting additional damage. Sufficient help should damage to the spinal cord occurs principally at the
be available before moving the patient in order to time of the injury and there has been no evidence to
provide horizontal stability and longitudinal trac- show improved neurological function from acute
tion. Spinal flexion must be avoided. A temporary operative decompression of the spine. The follow-
collar should be applied if the injury is to the cervi- ing are the general indications for surgical
cal spine. Hypotension and hypoventilation imme- intervention.
diately follow an acute traumatic spinal cord injury • Progression of neurological deficit is an absolute
and this may not only be life‐threatening but may indication.
also increase the extent of neurological impairment. • Patients with a partial neurological injury who
Respiratory insufficiency may require oxygen ther- fail to improve, with radiological evidence of per-
apy and ventilatory assistance. Loss of sympathetic sisting compression of the spinal cord.
tone may result in peripheral vasodilatation with • An open injury from a gunshot or stab wound.
vascular pooling and hypotension. Treatment will • Stabilisation of the spine if there is significant
include the use of intravascular volume expanders, instability or if it has not been possible to reduce
α‐adrenergic stimulators and intravenous atropine. locked facets by closed reduction.
Further management b management of compression by a malignant

Following reduction and immobilisation of fractures, metastatic tumour is best undertaken utilising
the principles of continuing care involve avoidance of chemotherapy
potential complications in patients who are paraple- c the usual treatment for spinal cord compression
gic or quadriplegic and early rehabilitation, which due to malignant tumours is urgent surgery or
commences as soon as the injury has stabilised. radiotherapy
d spinal pain is a late feature of spinal cord
compression
Further reading e metastatic tumours are rarely a cause of spinal
cord compression
Kaye AH. Essential Neurosurgery, 3rd edn. Oxford:
Blackwell Publishing, 2005. 3 Which of the following statements about nerve
Kline DG, Judice DJ. Operative management of selected injuries is correct?
brachial plexus lesions. J Neurosurg 1983;58:631–49. a a neurapraxia almost never recovers
Pang D, Wessel HB. Thoracic outlet syndrome.
b neurotmesis is a mild form of injury, likely to be
Neurosurgery 1988;22:105–21.
transient
c Erb’s palsy is due to damage of the upper trunk
of the brachial plexus
MCQs d Horner’s syndrome in association with a brachial
plexus injury is indicative of an excellent
prognosis
e injury to the radial nerve in the upper arm causes
weakness of finger flexion
1 Which of the following statements about carpal
tunnel syndrome is correct? 4 Which of the following statements about peripheral
a most frequently occurs in men nerve entrapments is correct?
b is due to compression of the ulnar nerve at a the ulnar nerve is frequently trapped at the
the wrist elbow in front of the medial epicondyle
c usually causes severe weakness in the hand b carpal tunnel syndrome is due to entrapment of
d is especially associated with pregnancy and lactation the radial nerve at the wrist
e causes decreased sensation on the dorsum of the c meralgia paresthetica is due to entrapment of the
hand lateral cutaneous nerve of the thigh
d the principal symptom of meralgia paresthetica is
2 Which of the following statements about spinal weakness of the leg
cord compression is correct? e the early features of ulnar nerve entrapment at
a the most common cause is an intramedullary the elbow is numbness involving the thumb and
spinal cord tumour index finger
Section 13
Vascular Surgery
55 Disorders of the arterial system
Royal Prince Alfred Hospital, Sydney, New South Wales, Australia
little collateral present (as would occur in acute

Introduction occlusion), then ischaemia can be severe. With well‐
developed collaterals, arterial occlusion may even
Diseases of the arterial tree such as atherosclerosis
be asymptomatic.
affect all arterial beds and so a patient who presents
with an ischaemic limb is also susceptible to stroke
and myocardial infarction. Aneurysms
Epidemiology If you see an aneurysm in one place, look and feel for
Patients with peripheral arterial disease usually die it in another.
R. Qasabian, vascular surgeon
from coexistent coronary or cerebrovascular dis
An aneurysm is a greater than 50% dilatation of an
ease. Heart, stroke and vascular disease combined
artery’s diameter compared with the expected
caused 29% of all deaths in Australia in 2017, more
diameter of that artery. A true aneurysm is one in
than any other disease group. The prevalence of
which the dilated segment involves all three layers
diabetes has doubled over the last 20 years and
of the vessel wall. They may be morphologically
now affects 8% of the adult population.
distinguished as either saccular or fusiform.
A false aneurysm or pseudoaneurysm is when
Atherosclerosis
there is a collection of blood outside the vessel
In 90% of adults with peripheral arterial disease, lumen but remaining in continuity with the circula
the cause is atherosclerosis. The other 10% tion. It is not actually an aneurysm at all, but rather
comprise less common causes, including periph a defect in the artery wall, with the surrounding tis
eral thromboembolism, aneurysmal disease, trauma, sues preventing exsanguination. They are most
fibromuscular disease and rare inflammatory commonly due to vessel trauma, especially iatro
conditions. genic, but can also be due to anastomotic disrup
The pathogenesis of atherosclerosis is complex tion, infection of a vessel, or contained rupture of a
and can begin in the second decade of life, with pre‐existing true aneurysm.
implications for the timing of preventive measures. The clinical consequences of aneurysm formation
It may take many years for atherosclerotic plaques are as follows.
to enlarge sufficiently to narrow an artery. Peripheral • Rupture: the most feared complication, most
vascular disease may therefore remain asymptomatic likely to occur in the thoracic and abdominal
for many years. aorta and iliac vessels, and in visceral aneurysms.
The earliest detectable pathological feature of • Thrombosis: popliteal aneurysms form lami
atherosclerosis is the fatty streak, which later nated thrombus that can embolise and cause dis
evolves into the fibrous plaque. More complex tal ischaemia. Thrombus accumulation within
lesions occur with intra‐plaque haemorrhage, calci aneurysms can also lead to complete occlusion.
fication or disruption of the overlying fibrous cap. • Local compression: any aneurysm can cause local
Once the diameter of an artery starts to reduce, mass effect, impinging on veins and causing venous
collateral circulation develops to compensate. The hypertension or deep vein thrombosis, compres
clinical outcome of arterial occlusion depends on sion of nerves causing pain, sensory and motor
the adequacy of the arterial collateral. If there is loss, and occasionally erosion of adjacent bone.
527
528 Vascular Surgery
A patient with an abdominal aortic aneurysm is the presentation can be dramatic, with hypoten
likely to have other aneurysms involving the iliac sion and abdominal pain radiating through to the
arteries in 40% and popliteal arteries in 15%. back and syncope or presyncope. More usually,
Popliteal artery aneurysms are the most common an abdominal aortic aneurysm is an unexpected
peripheral aneurysms and account for 80% of all finding, either on astute routine physical examina
peripheral aneurysms; 50% of these are bilateral. tion or on incidental ultrasound or CT scanning.
Conversely, aortic aneurysms are present in about 40%
of patients with bilateral popliteal aneurysms.
Evaluation and treatment
Epidemiology Evaluation of a patient with a suspected aortic
aneurysm must begin with a thorough history to
The prevalence of abdominal aortic aneurysm
ensure they are not symptomatic and to ascertain
increases with age, from 5% in men aged 65–69
risk factors and comorbidities, followed by a clini
years to 11% in men aged 80–83 years and is higher
cal examination in which the abdomen and lower
in Caucasian males who smoke and have hyperten
and upper limb pulses are palpated. Whilst a plain
sion. The mortality from a ruptured abdominal aor
film X‐ray may delineate the calcium lining of an
tic aneurysm is over 75%, with most patients dying
aneurysm, ultrasound is the initial imaging modal
before they can reach hospital. Even with surgery
ity of choice for confirming a suspected abdominal
there is a 50% mortality rate. Every effort must
aortic or popliteal aneurysm. Ultrasound is also the
therefore be made to identify and treat abdominal
mainstay of surveillance of known aneurysms that
aortic aneurysm before rupture occurs.
are not in the chest.
Once an aneurysm reaches a diameter greater
Contrast‐enhanced CT angiography (CTA) offers
than 5 cm, the risk of rupture increases exponen
detailed information with regard to the anatomy of
tially with further expansion: at a diameter of 5–6
the aneurysmal segment and the access vessels, and
cm the annual risk of rupture is 5%, at 6–7 cm
is routinely performed prior to surgical repair of an
15%, and at over 7 cm approaches 40% (Table 55.1).
aortic aneurysm. It is also important in the detec
Aetiology tion of aneurysmal disease in the thorax, which is
difficult to demonstrate on ultrasound due to the
The aetiology of abdominal aortic aneurysms is presence of the ribs.
multifactorial, with matrix metalloproteinases in Asymptomatic aortic aneurysms should be
the media of the vessel, localised haemodynamic treated when the rupture risk is higher than the
stress and genetic predisposition all contributing. accepted surgical mortality of 5%, which occurs
There is a 15% familial association in first‐order at a diameter of 5–5.5 cm. Aneurysms can be
siblings and an association with genetic disorders treated by open surgery or endovascular means
such as Marfan or Ehlers–Danlos syndromes. and the type of operation depends on anatomical
considerations such as access and complexity,
on patient age, medical comorbidities, and the
Most abdominal aortic aneurysms are asympto preference and skills of the surgeon and the

matic unless rupture is impending, in which case equipment available.
Table 55.1 Demonstration of the exponential increase in rupture risk with increasing diameter of abdominal aortic
aneurysm (AAA).
AAA diameter (cm) Risk of rupture per year (%) Surveillance and surgery
<3 Negligible Ultrasound surveillance

3–3.9 0.4
4–4.9 1.1
5–5.9 3.3 Consider repair: open or endovascular
6–6.9 9.4
7–7.9 24
Source: Cronewett JL, Johnston KW (eds). Rutherford’s Vascular Surgery, 8th edn. Philadelphia: Elsevier Saunders,
2014. Reproduced with permission of Elsevier.
55: Disorders of the arterial system 529
Endoluminal repair of aneurysms (see also

Table 55.2 Types of endoleak.
Chapter 58)
The endovascular method of treating an abdominal Type Description
aortic aneurysm involves the radiologically guided Ia Periprosthetic at proximal attachment
insertion of an aortic stent‐graft (a covered stent) Ib Periprosthetic at distal attachment
through the common femoral artery via a catheter, II Back‐bleeding lumbars or inferior
avoiding the morbid open abdominal incision and mesenteric artery
the physiological stress of clamping arteries and III Graft component separation
thereby interrupting blood flow. IV Graft damage or porosity
Not all patients are suitable for treatment by the V Aneurysm sac enlarging in absence of
endoluminal method. In order to anchor the aortic demonstrable endoleak
endograft, sufficient normal aorta (>2.5 cm) is
Source: White GH, May J, Waugh RC, Chaufour X, Yu
needed below the renal arteries to securely fix the
W. Type III and type IV endoleak: toward a complete
device in place. Secure fixation may be impossible definition of blood flow in the sac after endoluminal
if this segment of aorta is too dilated. The femoral AAA repair. J Endovasc Surg 1998;5:305–9.
and iliac vessels may be occluded, narrow, calcified Reproduced with permission of SAGE Publications.
and/or tortuous, preventing access with the stent‐
graft. Some of these anatomical limitations may be repaired endovascularly is crucial. Device failure
overcome with further technical advances in endo may occur due to migration, occlusion (usually of
graft design and delivery systems such as bespoke an iliac limb) or endoleak (flow of blood into, and
fenestrated and branched stent‐grafts custom‐ pressurisation of, the aneurysm sac; Table 55.2).
made for individual patients. The same concept Serious complications of both open and endovas
can be extended to treat other peripheral aneu cular aneurysm repair include renal dysfunction,
rysms, for example in the thoracic aorta or pop paraplegia, ischaemic colitis and prosthetic graft
liteal artery. infection. Aorto‐enteric fistulas are very rare but
occur more commonly following open repair.
Open surgical repair of aneurysms Ruptured aneurysms or more extensive aneu
The open method of treating an abdominal aortic rysms involving the thoracoabdominal aorta have
aneurysm has been used for more than 50 years, been generally regarded as not suitable for treat
and late graft failure and rupture is rare. Conven ment by the endoluminal method, although more
tional repair of an abdominal aortic aneurysm and more centres are embracing endovascular
involves a laparotomy, clamping of the aorta and approaches as a treatment option for these complex
sewing in a prosthetic arterial graft to replace the pathologies.
aneurysmal aorta. This can be done in a straight or
bifurcated configuration.
In other settings, the aneurysm can be ligated and Chronic limb ischaemia
circulation maintained by a bypass procedure. This
is the commonest form of treatment for popliteal Chronic limb ischaemia is the commonest clinical
aneurysms. problem occurring in patients with peripheral vas
cular disease (Box 55.1).
Complications
Randomised trials have confirmed a short‐term
Claudication
advantage with endovascular repair, with a lower
perioperative mortality of 1.2% compared with Patients may present with intermittent claudica
4.6% for open repair. General complications, par tion, a characteristic muscle pain induced by exer
ticularly cardiorespiratory, are more common with cise, relieved by rest and recurring on walking the
open repair, but there is a higher incidence of local same distance again. Similar pain occurs less
vascular or implant‐related complications after commonly on a neurogenic basis from spinal cord
endovascular repair. or nerve root compression but can be distin
It is not yet known if the immediate advantage of guished from arterial claudication by physical
endovascular repair will be sustained in the longer examination and exercise testing. Referred pain
term because of late problems that can develop. For from arthritic joints can also mimic intermittent
this reason, ongoing surveillance of the aneurysm claudication.
the artery itself. The aorta and femoral pulses

Box 55.1 Patterns of disease affecting
should be palpated in every routine physical exami
the lower limb
nation. The femoral pulse is generally easy to feel
Superficial femoral artery (approximately 60%) and therefore a good site to check cardiac rate and
The most common site for atherosclerotic occlusion rhythm. The degree of arterial calcification can be
or stenosis is at the lower end of the superficial estimated by the rigidity of the pulse. Palpation of
femoral artery (adductor hiatus) where it passes the popliteal artery is more difficult. Whenever the
through the hiatus in the adductor magnus muscle popliteal pulse is prominent and easy to feel, a pop
into the popliteal fossa. liteal aneurysm should be suspected. The dorsalis
Aorto‐iliac disease (approximately 30%)
pedis and posterior tibial pulses must also be
Common patterns include disease of the lower aorta palpated.
involving the common iliac arteries and disease of the
external iliac artery extending into the common
femoral and profunda femoris arteries. Severe aorto‐ Investigations
iliac disease can result in Leriche syndrome involving
As atherosclerosis is a generalised disease, inves
buttock and thigh claudication with impotence and
tigations should be carried out to assess risk fac
the absence of femoral pulses.
tors and the involvement of other arterial beds,
Combined disease (approximately 10%) thinking particularly of the coronary and carotid
These patients have significant disease of both arteries.
systems. Other recognised patterns include disease of
the common femoral or profunda femoris artery and Measurement of ankle pressure
disease of the tibial arteries associated with diabetes.
The ankle–brachial index (ABI) can be derived by
dividing the highest ankle systolic pressure by the
arm systolic blood pressure. This measurement
The risk of limb loss is low, with a less than 1% adds a degree of objectivity to the detection and
chance of amputation in 5 years. A mortality of 30% grading of any arterial occlusive disease present.
at 5 years can be expected from associated medical The ABI has the following characteristics.
comorbidities, with coronary events the usual cause • Normal range: 0.95–1.2
of death. The outlook is considerably worse in clau • Intermittent claudication: 0.9–0.4
dicants with diabetes who continue to smoke. • Rest pain: 0.4–0.15
• Gangrene: less than 0.15
Patients with diabetes or chronic renal failure may
Critical limb ischaemia
have highly calcified incompressible arteries,
A patient is said to have critical limb ischaemia especially in the lower limbs, resulting in falsely
when they have rest pain for more than 2 weeks or elevated ABI determination.
tissue loss (ulceration or gangrene) secondary to
objectively proven arterial occlusive disease. Rest Duplex ultrasound imaging
pain is described as a burning sensation felt in the
Ultrasound can also be used to image blood ves
toes, made worse by elevation of the leg and relieved
sels, with the anatomical display of the artery
by placing the foot in a dependent position, thus
using B‐mode (or brightness‐mode) imaging com
allowing gravity to improve the delivery of blood
bined with spectral waveform analysis using the
flow to the peripheral tissues.
Doppler equation to calculate blood velocity. This
Without restoration of adequate blood supply in
is the simplest and most cost‐effective way to con
a patient with critical limb ischaemia, the chance of
firm the diagnosis and anatomical location of sus
amputation is about 30% within 3 months. A mor
pected peripheral arterial disease but the
tality rate of 10% per year can be expected, with
acquisition of a good‐quality study is highly oper
the higher mortality reflecting the more severe, gen
ator dependent.
eralised disease in such patients.
Angiography
Clinical evaluation
Angiography is regarded as the diagnostic gold
Evaluation of a patient’s pulses can reveal valuable standard. Angiography can be CT, MRI or catheter‐
information about the level of an arterial occlusion based. The complication rate is low, and is related
or thrombosis, and the size and characteristics of to arterial injury or adverse reaction to the contrast
agent used. Ultrasound has replaced angiography Depending on the procedure and patient, this may
for many applications because these risks are be done under a local anaesthetic. Balloon angio
avoided. Catheter‐based angiography has the added plasty enlarges the lumen by a controlled dissec
advantage of being therapeutic as well as diagnostic tion. The risk of serious complications is about 2%.
and is now more selectively used on an ‘intention‐ In the iliac arteries an initial success rate of about
to‐treat’ basis after duplex imaging. 90% is well maintained over a period of 5 years. In
the superficial femoral artery the results are less
satisfactory. Metallic stents may be deployed to
Management (Figure 55.1) maintain the lumen after angioplasty, improving
durability of arterial dilatation but adding to the
Atherosclerosis is the underlying cause of most
cost of intervention. Many of the local complica
peripheral vascular disease. All patients should be
tions of balloon angioplasty can be controlled by
advised to modify their risk factors for atheroscle
stent placement. The use of paclitaxel‐coated bal
rosis, and therefore all patients with peripheral
loon angioplasty is used in recurrent disease to
vascular disease should be encouraged to cease
minimise the risk of scarring and luminal narrow
smoking. They should be taking an antiplatelet
ing. Furthermore, technologies such as directional
agent such as aspirin and a cholesterol‐lowering
atherectomy, which aim to remove the culprit
and plaque‐stabilising agent such as a statin. Their
plaque, are also in early stages of use. The benefit of
blood pressure should be well controlled with
using drug‐eluting stents in the lower limb is still
antihypertensive agents and any diabetes tightly
not known and is the subject of randomised con
controlled.
trolled trials.
The type and timing of operative intervention for
chronic limb ischaemia is dependent naturally on
the degree of ischaemia, its effect on the patient and
Operative management
the complexity of the culprit lesions.
Arteries may be cleared by endarterectomy, i.e. sur
gically removing atherosclerotic plaque from the
Claudication intima and part of the media of the artery wall.
Historically speaking, patients suffering from clau Longer occlusions may be bypassed surgically, by
dication have been offered elective operative inter anastomosing a conduit to carry blood around an
vention only when it is short distance and is occluded arterial segment, even down to the tibial
significantly affecting quality of life or ability to arteries in the foot. A prosthetic graft may be
work. With the advent of percutaneous procedures, needed if autogenous vein, the preferred graft mate
which carry a lower risk than open surgery, there rial, is unavailable.
has been a paradigm shift towards offering claudi Femoropopliteal bypass has an operative mortal
cants these reasonably safe procedures to improve ity of 1–2% and a 5‐year patency of 50–70%, with
their quality of life. the best results achieved when autogenous vein can
be used as graft material. Aortofemoral bypass has
an operative mortality of 2–5% and a 5‐year
Critical limb ischaemia patency of 80%.
Patients with critical limb ischaemia (tissue loss, Open operations are being performed with
rest pain) are treated more urgently and aggres decreasing frequency because of the comparable
sively for limb salvage. This may include open sur results and lower morbidity of endovascular
gery (endarterectomy, bypass) or percutaneous methods. A patient may initially receive percuta
balloon angioplasty with or without stenting, or a neous treatment, with open options reserved for
combination. failure of percutaneous treatment or for young
In general terms, the more extensive the disease patients who have a longer life expectancy or for
and the more distal the disease within the arteries, those anatomically not suitable for percutaneous
the more difficult the treatment and the poorer the approaches.
outcome.
Surveillance
Endovascular procedures (see also Chapter 58)
Whether the patient has been treated by endovascu
Arterial stenoses or occlusion may be dilated or lar means or bypass surgery, regular surveillance
stented by minimally invasive catheter technology. is required to detect and correct late structural
History and physical examination

Ankle–brachial pressure index
Treadmill exercise
Confirm peripheral arterial disease

with intermittent claudication If ankle–brachial pressure index and
treadmill exercise normal, consider
Assess cardiovascular + Assess disability neurogenic basis for claudication
risk factors symptom severity
Initial evaluation:
• Haemoglobin
• Serum creatinine
• Smoking history
• Lipid profile
• Hypertention
• Diabetes
Mild symptoms: Moderate symptoms: Severe symptoms:
not disabled disabled disabled
Special investigation
• Hypercoagulability
• Homocysteine level Encourage supervised walking exercise program
• Other Consider pharmacotherapy
Continue
• Modify risk factors

• Antiplatelet therapy Successful Unsuccessful
outcome outcome
Locate lesion with:

• segmental limb
pressures
• duplex scanning
• angiography
Continue
non-invasive
measures
Endovascular or
surgical therapy
Fig. 55.1 Suggested management algorithm for intermittent claudication. Source: modified from Dormandy JA,
Rutherford RB. Management of peripheral arterial disease (PAD). J Vasc Surg 2000;31:S1–S296. Reproduced with
The diabetic foot: sepsis, arterial inflow

problems. Re‐stenosis is usually due to neointimal
and risk factors
hyperplasia (scarring), which occurs most fre
quently in the first 18 months after intervention Patients with long‐standing diabetes mellitus are
and can be detected by ABI measurement and predisposed to foot complications on the basis of
ultrasound scanning. arterial occlusive disease, neuropathy and infection.
Coexistent arterial disease, with calcification of the blood supply. Plain X‐ray of the foot may reveal
tibial arteries, is most likely in diabetics who smoke. any underlying orthopaedic abnormality such as
Diabetic neuropathy may affect motor, sensory bony changes associated with Charcot foot,
and autonomic nerves. Sensory neuropathy results in metatarsophalangeal dislocation or evidence of
loss of pain sensation. Motor neuropathy results osteomyelitis.
in paralysis and atrophy of the small muscles of the
foot. This produces clawing of the toes and distur
Management
bance of the foot architecture, with neuropathic
ulceration forming under the metatarsal heads, the Prevention is a major goal by careful control of the
maximum area of load bearing. Autonomic neu diabetes, and foot care to removing callus that can
ropathy results in dry skin (due to sweat gland precede ulceration. Surgery plays an important role,
dysfunction) and subsequent cracking of the skin, requiring interdisciplinary cooperation. Vascular
allowing a portal for infection. It also plays an surgeons are involved in improving lower extremity
important role in bone resorption associated with blood supply and orthopaedic surgeons in correct
Charcot foot deformities. ing local bone or soft tissue complications of
The key to managing the diabetic foot is to con diabetes to improve foot architecture and function
trol sepsis, optimise arterial inflow, ‘offload’ the and aid with offloading of the foot. The outlook is
neuropathic foot and manage risk factors. worst for patients with diabetic foot ulceration
due to peripheral arterial disease who continue to
Sepsis smoke.
Control infection with antibiotics or debridement
of infected tissue:
• if patient is haemodynamically stable and not
persistently febrile, antibiotics are usually enough Acute limb ischaemia
to control sepsis
• if unstable, patient should have emergency Acute arterial ischaemia can be caused by trauma
debridement/amputation for source control. (see section Vascular trauma) or non‐traumatic
conditions, notably arterial embolism or thrombo
Arterial inflow sis of a pre‐existing diseased arterial segment.
If there is significant tissue loss and suspected Unless blood flow is restored within hours, irrevers
arterial occlusive disease, then improve the arterial ible tissue damage will occur, leading to possible
flow in the foot ideally prior to amputation or amputation. The acuity of onset means that collat
debridement. erals have not had time to develop to compensate
for the ischaemia.
Offloading
Podiatrists play an important role in ensuring the Pathophysiology
diabetic foot is adequately offloaded with suitable
footwear to aid in the healing of pressure ulcers and The common causes of non‐traumatic acute limb
to minimise their risk of recurrence. ischaemia are embolus, thrombosis or graft occlu
sion following prior surgery. The most common site
of origin of an embolus is the heart, due to atrial
Risk factors
fibrillation or after myocardial infarction. Arterial
There should be medium‐ to long‐term control of
thrombosis can be precipitated by pre‐existing arte
blood glucose levels to limit microvascular disease
rial disease, resulting in sudden occlusion at the site
and continuation of antiplatelet drugs and statins.
of an atheromatous arterial stenosis.
Clinical presentation Evaluation

The foot lesion may be the presenting feature Features such as rapid onset of ischaemia, presence
of maturity‐onset non‐insulin‐dependent diabetes of atrial fibrillation or recent myocardial infarction,
mellitus. The patient may present with a ‘punched‐ or absence of a history of claudication are more
out’ ulcer or an area of localised gangrene, or common in patients with embolus. The ABI will
acutely with a major infection in the foot. indicate the severity of the ischaemia. In almost all
Assessment is directed at determining the extent cases, angiography (either CTA or catheter‐based
of local tissue damage and the adequacy of the angiography) is necessary to define the site and
extent of obstruction. In these patients, the ischaemic ischaemia causing tissue loss, vasodilator therapy
lower limb is characterised by: or occasionally endoscopic surgical sympathectomy
• pain is indicated to dilate the digital arteries and improve
• pulselessness cutaneous circulation.
• pallor
• perishingly cold
• paraesthesia
• paralysis. Vascular trauma
Treatment Vascular injury may be blunt or penetrating. Most

arterial injury in Australia is due to blunt trauma
The survival of the limb is threatened if there is loss
sustained in motor vehicle accidents, but there is an
of sensation and muscle tenderness or weakness.
increasing incidence of penetrating trauma related
The aim is to restore arterial inflow by thrombo
to urban violence.
lytic therapy to dissolve the occluding thrombus
(which is successful in 30% of cases), open
thrombectomy or embolectomy, or bypass. The Patterns of arterial injury
mortality remains on the order of 10% and the rate
of amputation about 20%. Arterial transection
This will present with haemorrhage and evidence of
distal ischaemia. The severity of the ischaemia
Upper extremity depends on the collateral circulation. With com
plete transection, arterial spasm and contraction
Upper extremity ischaemia occurs far less com occurs so that bleeding may spontaneously stop as
monly than lower extremity ischaemia and is usu the distal end of the artery thromboses. With partial
ally due to non‐atherosclerotic causes. Embolus, transection, arterial contraction cannot occur so
from atrial fibrillation or in the context of hyperco bleeding can be profuse while the distal pulses
agulable states (e.g. malignancy, thrombophilias, remain present.
polycythaemia), can lodge in the axillary or subcla
vian arteries. These require urgent thrombectomy. Arteriovenous fistula
If a penetrating injury involves the adjacent artery
Thoracic outlet syndrome and vein, a fistula between the two may develop,
The subclavian artery and vein and T1 nerve root with shunting of blood from artery to vein. External
pass over the first rib to enter the arm. These struc bleeding may therefore be minimal.
tures can be compressed in the presence of cervical
ribs or with the hypertrophic musculature that fol Closed injury/intimal dissection
lows hard work or in athletes.
This type of injury is most commonly encountered
The clinical presentation will vary, depending on
with blunt injury and is dangerous because there
whether the artery, vein or nerve is predominantly
may be no external haemorrhage and therefore the
compressed. In selected patients, removal of the
possibility of arterial injury overlooked. The artery
first rib, usually by a transaxillary approach, will
wall usually remains intact but may weaken, pro
relieve arterial, venous or neural compression.
ducing a false aneurysm classically seen with trau
matic dissection of the thoracic aorta.
Vasospastic disorders Certain orthopaedic injuries, such as supracon
Raynaud’s syndrome describes the changes which dylar fracture of the humerus or dislocation of the
result from intermittent vasospasm of the arterioles knee, are associated with concomitant arterial
in the hands or feet that occurs after exposure to injury.
cold. There is a classic sequence of colour change,
from pallor to cyanosis to redness as the arterioles
first spasm then slowly recover. This can be second
ary to an underlying connective tissue disorder such Vascular injury should be suspected when there is
as scleroderma or rheumatoid arthritis. pulsatile bleeding, signs of distal ischaemia, an
Management is directed towards treating the expanding haematoma, or a thrill or bruit overlying
underlying condition but with severe digital a site of suspected arterial injury.
Diagnosis Mohiuddin SM, Mooss AN, Hunter CB. Intensive

smoking cessation intervention reduces mortality in high‐
Regular clinical review with a high index of suspi risk smokers with cardiovascular disease. Chest 2007;
cion is essential in detecting arterial injury. Prompt 131:446–52.
assessment in an operating theatre, ideally equipped Norgren L, Hiatt WR, Dormandy JA et al. Inter‐society
for intraoperative angiography, is required for arte consensus for the management of peripheral arterial
rial injury associated with ongoing haemorrhage or disease (TASC II). Eur J Vasc Endovasc Surg 2007;
acute ischaemia. Less obvious arterial injury will 33(Suppl 1):S1–S75.
usually be detected with measurement of the ABI, Perler BA, Sidawy AN (eds) Rutherford’s Vascular Surgery
and Endovascular Therapy, 9th edn. Philadelphia:
duplex scanning and diagnostic angiography.
Elsevier, 2018.
Arterial spasm should not be assumed as an expla
nation for limb ischaemia after injury unless inti
mal disruption has been excluded by angiography,
MCQs
ultrasound or surgical exploration.
Treatment correct answers can be found in the Answers section
Arterial inflow must be restored within 4–6 hours at the end of the book.
of acute injury to prevent permanent muscle dam 1 Which of the following statements about a pulsatile
age and limb loss. mass in the abdomen is correct?
The technique of arterial repair depends on the a it must be an aortic aneurysm
pathology of the injury. In some cases of lacerated b an ultrasound would be the best initial investigation
wounds direct repair can be performed. If a seg c no imaging is needed if the mass is not tender
ment of artery has been damaged, an interposition d immediate surgery is indicated
graft may be necessary to bridge the defect. Covered e immediate angiography is indicated
stents are also used in selected cases.
Reperfusion syndrome can occur when blood 2 Which of the following suggest that acute arterial
supply is restored to muscle damaged by ischaemia, ischaemia is due to embolus in a 70‐year‐old
so that the breakdown products from ischaemic woman?
muscle necrosis are washed into the general circula a she is in atrial fibrillation
tion. Systemic features of reperfusion syndrome b her symptoms developed slowly over a month
include hyperkalaemia and myoglobinuria that can c she has had long‐standing intermittent claudication
cause sudden death, adult respiratory distress syn d she smokes
drome and cardiac or renal failure. e she is an insulin‐dependent diabetic
If muscle swelling is anticipated following resto
ration of blood flow, a fasciotomy will relieve high 3 Which of the following statements about arterial
intra‐compartmental pressure. trauma is correct?
a all arterial injury is associated with pulsatile
bleeding
b the commonest cause in Australia is penetrating
Further reading
injury
Adam DJ, Beard JD, Cleveland T. Bypass versus angioplasty c the distal pulses will be absent
in severe ischaemia of the leg (BASIL): multicentre, ran d there is no relationship to major joint dislocations
domised controlled trial. Lancet 2005;366:1925–34. e bleeding is more likely with partial than with
Australian Bureau of Statistics. Australia’s leading causes complete arterial transection
of death, 2017. Australian Bureau of Statistics 3303.0
Causes of Death, Australia, 2017. 4 Which of the following statements about diabetic
Greenhalgh RM, Brown LC, Powell JT. Endovascular ver foot complications is correct?
sus open repair of abdominal aortic aneurysm. N Engl
a the neuropathy is only sensory
J Med 2010;362:1863–71.
b there is no relation to ongoing smoking
Hirsch AT, Haskal ZJ, Hertzer NR et al. ACC/AHA 2005
practice guidelines for the management of patients with c the metatarsophalangeal joints do not dislocate
peripheral arterial disease (lower extremity, renal, mes d the prognosis is worse with arterial disease and
enteric, and abdominal aortic): executive summary. ongoing smoking
Circulation 2006;113:e463–e654. e there is no place for surgical management
56 Extracranial vascular disease
Royal Prince Alfred Hospital, Sydney, New South Wales, Australia
Introduction Pathogenesis (Box 56.2)
The four major arteries that supply the brain are the Haemorrhagic stroke can be readily differentiated
vertebral arteries, which originate from the subcla- from ischaemic stroke by computed tomography
vian arteries to form the basilar artery and supply (CT) or magnetic resonance imaging (MRI) and
the posterior cerebral circulation, and the internal will not be considered further.
carotid arteries, which arise from the carotid bifur- Atherosclerosis affecting the extracranial circu-
cation in the neck and lead onto the middle cerebral lation most commonly occurs at the carotid bifur-
arteries, the most important branches in the ante- cation, particularly at the origin of the internal
rior cerebral circulation. The circle of Willis pro- carotid artery, where there is a region of turbulent
vides potential communication between the anterior flow as the common carotid artery divides into the
and posterior cerebral circulations but may be inad- high‐resistance external carotid artery and low‐
equate to fully compensate for an occluded internal resistance internal carotid artery.
carotid artery in about 20% of individuals. Disease There are two main theories of how disease at
in these vessels may be due to atheromatous and the carotid bifurcation may cause TIAs and stroke.
non‐atheromatous causes and may be asympto- • Embolic theory: embolisation of atherosclerotic
matic or symptomatic, presenting as strokes or tran- material or thrombus can arise from the carotid
sient ischaemic attacks (TIAs). bifurcation. This is more likely to occur with
The term ‘stroke’ refers to an acute loss of focal complicated atherosclerotic plaques forming a
cerebral function with symptoms that last more tight (>70%) stenosis.
than 24 hours. Neurological symptoms or signs that • Haemodynamic theory: blood flow to the brain
last less than 24 hours are called TIAs. Stroke is the may be reduced by a tight stenosis or occlusion of
third most common cause of death worldwide and the carotid arteries. The effect of such lesions will
is the principal cause of neurological deficit. About depend on the extent of the intracranial collateral
40 000 Australians have a stroke each year, one‐ circulation. This is the mechanism of stroke after
third of which are fatal while another third are left profound hypotension from any cause.
with significant neurological deficit. Predominantly
middle‐aged males are affected but the incidence of
stroke increases exponentially with age, with 50% Box 56.2 Pathogenesis of stroke
of all strokes occurring in patients over 75 years of
Ischaemia (85%)
age. The risk factors for stroke are listed in Box 56.1. • Atherosclerosis of large arteries and atherothrom-
boembolism (65%): internal carotid artery origin is
the most common site of atherosclerosis
Box 56.1 Risk factors for stroke • Cardiac embolism (15%): atrial fibrillation,
myocardial infarction
Hypertension
• Small vessel occlusions: usually related to hyperten-
Tobacco smoking
sion causing lacunar infarcts (5%)
Heavy alcohol consumption
Hypercholesterolaemia Haemorrhage (15%)
Obesity • Intracerebral haemorrhage (intraparenchymal)
Diabetes (11%)
Sedentary lifestyle • Subarachnoid haemorrhage (4%)
537
These theories are not mutually exclusive, as the If the left subclavian artery or more rarely the
likelihood of embolisation from carotid plaque and innominate artery is stenosed or occluded, then the
occlusion of the internal carotid artery increases vertebral artery becomes an important collateral
with the degree of stenosis. pathway to sustain blood flow to the arm. When
the arm is exercised, vertebral arterial flow reverses
resulting in cerebral hypoperfusion. This is usually
Clinical presentation asymptomatic unless there is coexistent internal
carotid stenosis.
Cerebrovascular disease may be asymptomatic,
found incidentally on clinical examination and
imaging, or symptomatic (TIAs, stroke). The neuro- Non‐atheromatous carotid disease
logical symptoms will depend on whether the cul- Carotid aneurysm
prit lesion is within the internal carotid arteries A rare condition. Patients most commonly present
(anterior circulation) or vertebral arteries (poste- with pulsatile mass, dissection or embolisation.
rior circulation) or is due to global hypoperfusion.
Carotid dissection
This is associated with head or neck pain and cranial
Asymptomatic
nerve palsy, and presents as traumatic, iatrogenic or
This is often detected by the presence of a bruit, spontaneous. Anticoagulation and antihypertensives
which may lead to duplex ultrasound investigation. are the mainstay of treatment.
The presence or loudness of a bruit has no correla-
tion with the degree of arterial stenosis. Only 20% Carotid body tumour
of bruits are associated with carotid disease, the Carotid body tumours are rare and originate from
remainder being caused by valvular and coronary the preganglionic chemoreceptor cells of the carotid
artery disease. body. They are highly vascular and therefore should
not be biopsied. They present as a mass in the neck
and often mimic other neck lumps; 5% are locally
Symptomatic malignant, 5% systemically malignant and 5%
TIAs and stroke caused by carotid disease classi- bilateral. Surgical excision is the treatment of choice.
cally cause:
• ipsilateral retinal ischaemia manifesting as amau- Carotid arteritis
rosis fugax (fleeting blindness described as ‘a cur- Giant cell arteritis is a systemic granulomatous
tain coming down over the eye’) inflammatory condition affecting the medium and
• focal contralateral upper, with or without lower, large arteries in elderly patients. It mostly affects the
limb sensory and/or motor loss aortic arch and the extracranial carotid arteries.
• dysphasia with speech disturbance, which is Takayasu’s arteritis is a non‐specific arteritis of
common particularly when the dominant hemi- unknown aetiology that can manifest as arterial
sphere is affected (usually the left hemisphere in a occlusions, stenoses or aneurysms. There is a female
right‐handed individual). preponderance and it can affect the entire aorta and
its branches. Cerebrovascular involvement in the
form of carotid or brachiocephalic disease is com-
Symptomatic vertebrobasilar disease
mon. Arteritides are usually treated with steroids
When the vertebrobasilar system is involved, the and other immune‐modulating medications.
symptoms are less specific but may affect both sides
of the body, with bilateral visual disturbance. Fibromuscular dysplasia
Symptoms such as ataxia, imbalance, unsteadiness Fibromuscular dysplasia (FMD) is a non‐athero-
and vertigo can also be caused by middle ear disor- sclerotic, non‐inflammatory vascular disease that
ders or bradycardia causing the patient to collapse primarily involves long unbranched segments of
(Stokes–Adams attacks). medium‐sized and small arteries and is character-
ised by segmental irregularity of small and medium‐
sized muscular arteries, most commonly renal and
Subclavian steal
carotid (although mesenteric, subclavian and iliac
Another mechanism of haemodynamic cerebral arteries can be involved). This can give a character-
hypoperfusion occurs on basis of ‘subclavian steal’. istic ‘string of pearls’ appearance on angiography.
56: Extracranial vascular disease 539
There are several types, although medial fibropla-

sia accounts for 70–95%. Females are more com-
monly affected than males, typically aged 30–50
years old.
The aetiology is unknown but theories include
the following.
• Humoral: hormones, pregnancy
• Mechanical stresses: ptosis of right kidney,
increased severity with right‐sided disease
• Blood vessel wall ischaemia
• Genetic:
◦◦ High incidence in some families and in Caucasians
Fig. 56.1 Carotid duplex scan showing turbulent flow at
◦◦ Autosomal dominant inheritance pattern
the origin of the internal carotid artery with a peak
◦◦ HLA‐DRw6 association with FMD
systolic velocity of 571.5 cm/s and an end‐diastolic
• Smoking velocity of 198.5 cm/s indicating more than 80% stenosis
• Vasculitis of the artery.
• Infective: rubella
In general terms, FMD responds very well to bal-
loon angioplasty alone, but the indications for treat- show the morphology of the carotid bifurcation
ment in the carotid arteries is not well defined, and and accurately identify the degree of stenosis pre-
is usually limited to those with symptomatic or pro- sent (Figure 56.1).
gressive disease. Carotid angiography, considered the diagnostic
gold standard, is now used very selectively and par-
ticularly if the ultrasound findings are uncertain or
if the major aortic arch branches need to be imaged
Investigations
in planning carotid stenting (Figure 56.2).
With the advent of CT and carotid duplex scanning
it has become easier to define those patients who
Treatment
are likely to have hemispheric neurological symp-
toms on the potentially correctible basis of throm-
Best medical management (Box 56.3) is indicated for
boembolic phenomena arising from the carotid
all patients and comprises a single/dual antiplatelet,
bifurcation.
statin, antihypertensive and cessation of smoking.
General medical evaluation includes blood pres-
sure measurement to detect hypertension and
Symptomatic carotid disease
electrocardiography to assess any cardiac rhythm
disturbance like atrial fibrillation or evidence of Symptomatic carotid stenosis requires prompt
coexistent coronary artery disease. Haematological treatment, with the most benefit obtained for sten-
disorders such as polycythaemia, leukaemia or coag- oses of greater than 70% and when surgery is per-
ulopathies can cause stroke and should be sought. formed within 2 weeks of symptom onset. This is
Similarly, renal function and lipid and glucose levels based on the North American Symptomatic Carotid
are measured to exclude renal failure, hyperlipidae- Endarterectomy Trial (NASCET) which showed
mia and diabetes, respectively. that the risk of stroke in symptomatic patients with
CT or MRI will identify intracranial blood if a greater than 70% stenosis of the relevant internal
haemorrhagic stroke has occurred and will demon- carotid artery could be reduced at 2 years from
strate cerebral infarction or space‐occupying lesions 26% to 9% with carotid endarterectomy, provided
such as a brain tumour. Although sophisticated that the surgery is done with an acceptably low
three‐dimensional reconstruction of the extracra- morbidity and mortality. A recent audit of carotid
nial vasculature can be done with both MRI and surgery in New South Wales confirmed that in an
CT, these are usually not the first‐line investigations Australian setting, carotid endarterectomy is being
to assess the carotid arteries. performed with less than 2–3% combined stroke/
Duplex ultrasound is used in most centres as the death rate, in keeping with NASCET recommenda-
initial diagnostic test to evaluate the carotid arteries tions. Box 56.4 is a summary of the findings of the
and as the definitive investigation by many vascular NASCET and another randomised controlled trial
surgeons in planning carotid endarterectomy. the European Carotid Surgery Trial (ECST) that
Duplex ultrasound is operator dependent but can guide surgical practice.
Box 56.3 Management algorithm
Asymptomatic bruit
• Check for coexistent coronary artery disease
• Carotid duplex scan: >70% internal carotid
stenosis, consider carotid endarterectomy
Symptomatic
TIAs
• Carotid duplex scan shows >60% internal carotid
stenosis
◦◦ If patient fit perform carotid endarterectomy
◦◦ If patient unfit consider carotid stenting
Evolving stroke
• Non‐contrast CT scan/MRI
• Intracranial haemorrhage
• Ischaemic stroke
◦◦ Heparinise
◦◦ Investigate for cardiac embolic source
ECG
Cardiac echocardiography
◦◦ Investigate for extracranial arterial disease
Carotid duplex scan
MRI
CT angiography
Box 56.4 Benefit of carotid endartectomy

in the treatment of symptomatic carotid
stenosis
Fig. 56.2 Carotid angiogram showing more than 80% Complete No benefit from carotid
stenosis at the origin of the internal carotid artery. occlusion endarterectomy
70–99% Offer carotid endarterectomy
within 2 weeks
Asymptomatic carotid disease <50% Best medical therapy only
In the Australian setting, surgery is generally only
offered for severe (>80%) asymptomatic carotid in treatment of asymptomatic carotid stenosis, with
stenosis. Best medical management with antiplate- the majority of Australian surgeons offering surgery
let drugs and statins is the treatment of choice for for stenoses of greater than 80%, some selectively for
stenoses of less than 70% or in patients who have stenoses of greater than 60%, and some only best
a very high surgical risk or limited life expectancy medical management for all degrees of asympto-
(<5 years). The Asymptomatic Carotid Atherosclerosis matic stenosis.
Study (ACAS) suggested a modest benefit of carotid
endarterectomy versus best medical therapy in
Carotid endarterectomy
patients with carotid stenosis of greater than 70%.
The number needed to treat to prevent a stroke at The aim of this surgery is to remove the culprit ath-
5 years was 20, which is significantly higher than erosclerotic plaque and thus reduce the risk of
that for high‐grade symptomatic stenosis. Surgery thromboembolisation to the brain. The patient may
reduced the absolute risk by 6% and relative risk receive general or local anaesthetic depending on
by 60% at 5 years. Although there was therapeutic suitability and surgical preference. The skin incision
benefit at 1 year, the benefit was greater at 5 years. may be transverse or longitudinal anterior to the bor-
The benefit appeared greater for men than women. der of the sternocleidomastoid. Traversing through
This in turn accounts for the considerable variability the platysma and deep fascia, the surgeon identifies
Fig. 56.3 After the carotid arteries are (a) (b) (c)
clamped, the plaque (a) is removed
(b) and the arteriotomy closed either
primarily or with a patch (c).
and preserves the marginal mandibular branch of the anaesthetic can be avoided as can the neck incision
facial nerve. The common facial vein is a useful and risk of cranial nerve injury.
marker of the site of the carotid bifurcation which is Patients who have symptomatic carotid stenosis
carefully exposed, taking extreme care not to over‐ but with contraindications to surgery may be suit-
handle the diseased carotid. One careless flick or able for CAS. CAS is preferable when carotid
retraction prior to distal clamping could cause the lesions are anatomically unfavourable in cases of
culprit plaque to thromboembolise and the patient to re‐stenosis, high cervical or intrathoracic lesions or
have a significant stroke. The hypoglossal and vagus post radiation. The American Stroke association
nerves are also identified and preserved. Heparin also recommends CAS over carotid endarterectomy
5000 units is administered and the carotid arteries in patients at increased risk of surgery.
clamped so that the artery can be opened to endar- There have been concerns about a higher risk of
terectomise the atherosclerotic plaque (Figure 56.3). periprocedural cerebral embolisation and stroke and
There is a plane between the diseased portion of the late recurrent stenosis. The risk of periprocedural
carotid artery and the outer media so that a smooth stroke has been reduced with cerebral protection
surface can be restored to the artery. devices, designed to catch embolic material before it
Transcranial Doppler and/or sensory and motor can pass into the brain.
evoked potentials may be used to monitor for Controlled clinical trials should resolve the rela-
changes in middle cerebral artery velocities or brain tive merits of carotid stenting and endarterectomy.
function, respectively, after internal carotid artery Until that time, carotid endarterectomy is the estab-
clamping; if significant changes are found, the sur- lished intervention for high‐risk patients with high‐
geon may use a shunt to maintain cerebral perfu- grade symptomatic internal carotid stenosis.
sion whilst clamping. This is particularly important Angioplasty and stenting is usually indicated for
if the patient has significant contralateral carotid treating subclavian artery stenosis or occlusion
disease or posterior circulation disease. Most units causing subclavian steal. Carotid angioplasty has
in Australia are selective shunters. After the surgeon for some time been the therapy of choice for symp-
is confident that all atherosclerotic material has tomatic FMD, a relatively rare condition occurring
been removed, the lumen of the artery is flushed in fewer than 3% of patients with symptomatic
with heparinised saline and the artery closed. Many carotid arterial disease. Stenting is rarely needed in
surgeons close the artery with a patch made of vein, this setting.
Dacron or polyurethane to ensure a widely patent
lumen and to reduce the incidence of carotid re‐ste-
Perioperative management
nosis due to neointimal hyperplasia after surgery.
A drain is placed in the wound and the platysma Close monitoring is essential after any form of cer-
and skin are closed. ebrovascular intervention to observe for neurological
deficit, guide blood pressure control and decrease
the risk of adverse cardiovascular events. Patients
Carotid stenting
are usually kept on their regular antiplatelet ther-
Carotid artery stenting (CAS) is a more recent tech- apy soon after surgery to decrease the risk of
nical advance and remains a controversial aspect of thrombosis at the endarterectomy site.
carotid therapy. There has been continuing improve- Re‐stenosis is more common after stenting.
ment in the reported results of balloon dilatation Postoperative surveillance using ultrasound is com-
and stenting for atherosclerotic carotid arterial dis- monly done to monitor the operated or stented
ease. The proposed benefit of CAS is that an carotid artery.
Procedural complications Walker MD, Marler JR, Goldstein M. Endarterectomy for

asymptomatic carotid artery stenosis. JAMA 1995;
There is a 2–3% risk of ipsilateral stroke after carotid 273:1421–8.
endarterectomy (higher after CAS) related to emboli-
sation from the carotid during the manipulation of
intervention or to the interruption of cerebral blood MCQs
flow. Labile blood pressure is common and hyperten-
sion is related to the risk of postoperative intracer- Select the single correct answer to each question. The
ebral haemorrhage. Coexistent coronary artery disease correct answers can be found in the Answers section
is an important cause of postoperative myocardial at the end of the book.
infarction and death.
1 Which of the following statements about the
Carotid endarterectomy can be complicated
anatomy of extracranial arterial disease is incorrect?
postoperatively by the following.
a the left subclavian artery arises directly from the
• Cranial nerve injuries: can include the hypoglos-
aortic arch
sal and recurrent laryngeal nerves. Sensory loss in
b the vertebral artery is a branch of the subclavian
the distribution of the greater auricular nerve
artery
and the transverse cervical nerve of the cervical
c the vertebral arteries form the basilar artery
plexus is commonly observed.
d there is no communication between the anterior
• Neck haematoma: if severe can obstruct respiration,
and posterior cerebral circulations
requiring prompt return to the operating theatre.
e there is a low‐resistance flow pattern in the
internal carotid artery
Future developments
2 An 80‐year‐old woman presents with transient
There is an increased focus on preventing stroke by right hemiparesis lasting 15 minutes and resolving
risk factor modification and by identification of completely. She is otherwise healthy and independ-
subgroups at high risk of stroke who will benefit ent. Her carotid duplex scan shows >80% stenosis
from prophylactic intervention. Furthermore, the of her left internal carotid artery. Despite aspirin
concept of plaque morphology as an alternative to therapy, she has a further episode. Which of the
degree of stenosis in predicting stroke risk and indi- following statements is true?
cation for surgery is an evolving area that may a she is best managed on warfarin therapy
change future practice. b left carotid endarterectomy is indicated
c carotid stenting is a preferred option to surgery
d she is facing a cumulative 5% stroke risk within
Further reading the next 3 years
e lowering her blood cholesterol level will reduce
Ahn SH, Prince EA, Dubel GJ. Carotid artery stenting: her immediate risk of stroke
review of technique and update of recent literature.
Semin Intervent Radiol 2013;30:282–7. 3 Which of the following statements about the
Cronewett JL, Johnston KW (eds) Rutherford’s Vascular pathology of extracranial arterial disease is correct?
Surgery, 8th edn. Philadelphia: Elsevier Saunders, a atherosclerosis is the commonest cause of
2014.
internal carotid stenosis
Ferguson GG, Eliasziw M, Barr HW et al. The North
b recurrent stenosis occurs in more than 50% of
American Symptomatic Carotid Endarterectomy Trial:
surgical results in 1415 patients. Stroke 1999;30: patients after carotid endarterectomy
1751–8. c carotid body tumours arise from the vertebral
Halliday A, Mansfield A, Marro J et al. Prevention of arteries
disabling and fatal strokes by successful carotid endar- d fibromuscular disease is commonest in young men
terectomy in patients without recent neurological symp- e Takayasu’s disease is commonly known as
toms: randomised controlled trial. Lancet 2004;363: ‘pulsing disease’
1491–502.
Mughal MM, Khan MK, DeMarco JK, Majid A, Shamoun
4 Which of the following statements about carotid
F, Abela GS. Symptomatic and asymptomatic carotid
artery plaque. Expert Rev Cardiovasc Ther 2011;9:
endarterectomy is correct?
1315–30. a it is associated with a high (>5%) risk of
Robicsek F, Roush TS, Cook JW, Reames MK. From perioperative stroke
Hippocrates to Palmaz‐Schatz, the history of carotid b closure with a patch decreases the risk of
surgery. Eur J Vasc Endovasc Surg 2004;27:389–97. recurrent stenosis
c there is a plane between the atheromatous b the bruit may be arising from the aortic valve
plaque and the intima c a carotid angiogram in indicated
d it is the procedure of choice for fibromuscular d there is no relationship between angina and a
disease carotid bruit
e it precludes the use of a carotid stent for e the left internal carotid artery must be occluded
recurrent stenosis
5 A 65‐year‐old man presents with angina, and a left

neck bruit is heard. Which of the following
statements is correct?
a the first priority is investigation of the bruit
57 Venous and lymphatic diseases
of the limbs
Hani Saeed1 and Michael J. Grigg2
1,2
Eastern Health, Melbourne, Victoria, Australia
2
Monash University, Melbourne, Victoria, Australia
incompetence since failure to deal with these will

Varicose veins result in recurrence of the varicose veins.
The short saphenous system begins behind the
Varicose veins are a common condition, occurring
lateral malleolus of the ankle and runs along the
in 20% of adults. The characteristics of varicose
lateral and then the posterior aspect of the calf to
veins are that they are
penetrate the deep fascia in the upper calf. It termi-
• visible
nates in the popliteal fossa by joining the popliteal
• dilated
vein in the vicinity of the knee crease. The exact
• elongated
level of the junction is variable and may be either a
• tortuous.
few centimetres above or below the knee crease.
Varicose veins result from incompetent valves in the
venous system.
Deep veins
Anatomy of the venous system The deep veins run as venae comitantes of the major
arteries in the foot and calf, where they receive tribu-
The veins of the lower limb can be classified into taries from the muscles of the calf, including the
three groups: superficial, deep and perforating. venous sinusoids in the calf muscles. The venous
sinusoids within the calf muscles are important as
Superficial veins part of the venous pump mechanism. They are a fre-
quent site of origin for venous thrombosis. The deep
The superficial veins are collected in two major sys- system also receives the perforating veins from the
tems. These are the tributaries and main trunks of superficial system. At about the level of the knee joint
the long and short saphenous veins. a single popliteal vein is formed in most cases. This
The long saphenous system begins on the dorsum runs proximally in company with the main artery to
of the foot and runs anterior to the medial malleolus, become the femoral vein and then the external iliac
along the medial aspect of the calf and thigh and vein as it passes beneath the inguinal ligament.
ends at the saphenofemoral junction, where it joins
the common femoral vein. This junction is 2–3 cm
Perforating veins
below and lateral to the pubic tubercle. A major trib-
utary, the posterior arch vein, joins the long saphen- The perforating veins join the superficial and deep
ous vein just below the knee. This drains blood from systems. They contain valves which direct blood
much of the medial side of the calf and communi- flow from the superficial to the deep system.
cates with the deep venous plexus of the calf by way Perforating veins are variable in number and posi-
of several perforating veins, so named because they tion, but usual sites are the medial side of the lower
‘perforate’ the deep fascia. In the thigh, there are third of the calf between the posterior arch vein and
large medial and lateral tributaries and thigh per- the posterior tibial veins and at about the junction
forating veins. A number of tributaries join the of the middle and lower thirds of the thigh between
long saphenous vein close to its termination. These the long saphenous vein and the femoral vein. Other
are important in the surgery for saphenofemoral perforating veins join the anterior tibial veins, the
545
peroneal veins and the superficial veins. The incon- Symptoms

stancy of these veins makes precise localisation dif-
Symptoms result from fluid congestion of gravitation-
ficult and is an important reason for the development
ally dependent superficial tissues due to inadequate
of recurrent varicose veins following treatment.
venous return and increased venous pressure. Patients
may complain of tiredness and aching of the lower
legs at the end of the day. This is relieved by rest and
Physiology
elevation of the legs. They may develop mild ankle
swelling, particularly in warmer weather but signifi-
The superficial veins collect blood from the superfi-
cant lower limb oedema is not a characteristic of vari-
cial tissues. During the relaxation phase of the calf
cose veins. Leg pain is a common complaint and the
muscle cycle, the pressure in the superficial veins is
presence of varicose veins may be coincidental.
greater than the pressure in the deep veins and thus
blood flows from superficial to deep. Each contrac-
tion of the calf muscles results in high pressure
(approximately 250 mmHg) being generated in the Complications
calf compartments. This empties the veins in the mus-
Thrombophlebitis
cles and transmits a pulse of blood proximally.
Retrograde flow, or reflux, due to gravity is pre- Thrombosis in a segment of varicose vein is com-
vented by valves. If the valves in the veins directing mon. The patient presents with signs of inflamma-
venous return proximally or the perforating veins are tion spreading from a hard lump, which is the
incompetent the venous return from the leg is less effi- thrombosed vein. The redness, pain and heat falsely
cient. This results in higher pressures in the superficial suggest the presence of infection. The condition
system and progressive dilatation occurs, causing usually resolves over a period of days provided the
more valves to become incompetent. This is accompa- thrombosis does not extend into the deep venous
nied by elongation of the superficial veins, which system, when pulmonary embolus becomes a risk.
results in tortuosity. The high pressure in the superfi- Hence thrombus extending from the long saphen-
cial veins, particularly in the most gravitationally ous vein into the common femoral vein can be very
dependent part of the leg around the ankle, may be dangerous. The thrombus often extends 15 cm or
sufficient to impair the nutrition of the subcutaneous more proximal to the clinical signs of inflamma-
tissue and dermis and contribute to ulcer formation. tion, and a duplex scan will readily demonstrate the
Varicose veins are a disorder of the superficial and true level of the clot. Urgent treatment, usually by
perforating veins. In most cases the disorder is way of full anticoagulation, needs to be considered
inborn, although the mode of inheritance is uncer- for thrombophlebitis extending above the level of
tain. Varicose veins often first appear in young the knee joint. If there is a contraindication to anti-
adults. Females are affected more commonly and coagulation, urgent saphenofemoral ligation can be
the veins are more prominent during pregnancy undertaken.
due to the combined effects of the muscle‐relaxing
effects of hormonal (especially progesterone) Haemorrhage
changes and the pressure effects of the pregnant
The subcutaneous varices of the lower calf and
uterus, which also acts as an arteriovenous fistula in
around the ankle may rupture through the skin
the pelvis. Partial regression occurs following deliv-
causing profuse bleeding. This bleeding will con-
ery but there is progression of the varicosities with
tinue unabated whilst the limb remains dependent,
succeeding pregnancies. Tributaries of the internal
even to the point of exsanguination. The patient
iliac vein and even the ovarian vein may be involved,
should lie down immediately and elevate the limb.
producing posterior thigh and vulval varices (pelvic
Pressure should be applied directly over the bleed-
venous insufficiency).
ing point. This pressure can be reinforced by a firm
bandage. A tourniquet should not be used as a rise
Clinical presentation in venous pressure can be produced and may actu-
ally worsen the bleeding.
Patients with varicose veins most commonly pre-
sent for cosmetic reasons. Some patients present Ulceration
with tiny veins – telangiectasia or venous flares. Prior to the advent of duplex scanning, which ena-
Others present with large veins that may have been bles non‐invasive evaluation of the venous system,
present for 10– 20 years or longer. it was mistakenly believed that superficial varicose
57: Venous and lymphatic diseases of the limbs 547
veins rarely caused venous ulceration. It is now collaterals which have formed in response to
realised that severe long‐standing varicose veins are deep venous obstruction.
a common cause of leg ulcers. Before the develop- • Ulcers sited proximal to the mid‐calf level are
ment of frank ulceration, secondary venous tissue unlikely to have a venous aetiology and are more
changes occur, including pigmentation due to hae- likely to be neoplastic.
mosiderin deposition, lipodermatosclerosis and With the availability of ultrasound examination,
atrophie blanche. eponymously named tourniquet tests are now of
historical interest only.
Other complications
Rare presentations occur in children and are associ-
Investigations
ated with major congenital abnormalities of the
venous system, often associated with arteriovenous
Duplex ultrasound
malformations.
Duplex ultrasound incorporates both B‐mode
ultrasound (image) and Doppler ultrasound (blood
flow). It is used to identify sites of valvular incom-
petence and to determine the presence of deep
Examination venous incompetence and the presence of venous
thrombosis.
The purpose of the examination is to determine
(i) the distribution of the varicose veins, (ii) if Venography
there are secondary venous tissue changes, and
(iii) if lower limb pulses are present (this is par- Venography is an obsolete investigation for these
ticularly important if compressive stockings are patients and should be avoided because of the poor
to recommended). risk‐to‐benefit ratio.
The patterns of disease are:
• long saphenous incompetence
• short saphenous incompetence Treatment
• incompetence of thigh or calf communicating
veins There are few serious sequelae of untreated vari-
• combinations of the above. cose veins (see earlier section Complications) so
The patient is initially examined standing, which treatment is not essential, except in those patients
makes the veins more obvious. The size and distri- with pre‐ulcerative secondary venous tissue changes
bution of varicose veins are examined. If the veins in the lower calf or with complications (see section
are predominantly medial and if they involve the Symptoms).
thigh, it is likely that the long saphenous vein is
involved. If they are posterior and lateral in the calf,
Elastic stockings
it is likely that the short saphenous vein is involved.
It should be remembered that there are many com- Elastic stockings will not cure varicose veins but
munications between the two systems so that, for will provide relief from symptoms of swelling and
example, incompetence in the long saphenous sys- tiredness in the legs and prevent complications.
tem may fill varices on the posterior and lateral They are particularly helpful for the pregnant
aspects of the calf. An incompetent vein will trans- patient with varices. A range of stockings are avail-
mit a cough impulse. able: low‐, medium‐ and high‐grade compression
The examiner should also be aware of findings and below‐ and above‐knee lengths. For patients
which signify that the patient does not have a with varicose veins, a below knee‐stocking of mod-
‘straightforward’ varicose vein problem, such as in erate compression (grade 2, 20–30 mmHg pressure)
the following circumstances. will suffice. If there is doubt that the veins are the
• Varices of the medial aspect of the upper thigh cause of the symptoms in a particular patient, relief
may indicate pelvic venous insufficiency. of symptoms while wearing stockings supports the
• The presence of significant leg oedema is unlikely diagnosis of varicose veins and, conversely, failure
to be due to varicose veins alone. of stockings to relieve symptoms suggests that other
• Prominent superficial veins extending above the causes should be sought. Graduated compression
level of the inguinal ligament in the suprapubic stockings should be prescribed with caution for
area suggest that these veins are dilated patients in whom pedal pulses are not palpable.
Injection–compression therapy Stripping

Injection therapy should not be considered while Stripping of the long saphenous vein from the groin
there are major uncontrolled sites of deep to super- to the knee removes a large dilated vein which, if
ficial incompetence. When these sites have been left, may be the site of thrombophlebitis or recur-
controlled, injections may be used to control small rence. A varicose long saphenous vein is not useful
veins that may remain. An important part of injec- for later coronary or leg artery bypass. Stripping
tion therapy is compression, which keeps together the long saphenous vein between the ankle and the
the surfaces irritated by the sclerosant. This facili- knee should not be performed since it is unneces-
tates fibrous organisation and inhibits recanalisa- sary and may result in troublesome neuritis of the
tion of the vein. Recently, techniques have been saphenous nerve.
introduced for injecting very small cutaneous veins.
These often cause cosmetic disability because they
Multiple extractions
are prominent blue or red lines in the skin that are
hard to disguise. Most of the obvious varicosities are removed
through multiple small incisions. The veins are then
grasped either by small artery forceps or specially
Operation designed hooks. As much as possible of the dilated
vein is removed. The next incision is made 2–4 cm
Operation is an appropriate method of control for
away and the process repeated until all the major
major sites of incompetence. The aims of operation
varices have been removed.
are to obliterate the major sites of deep to superfi-
cial incompetence and to remove the larger varicose
veins. The presence of varicose veins predisposes to Ligation of incompetent perforating veins
the development of postoperative deep vein throm-
bosis so appropriate prophylaxis should be This usually involves an incision over the perforat-
undertaken. ing vein as it passes through the deep fascia.
Preoperative duplex scan provides accurate locali-
sation. The vein is ligated and divided beneath the
Saphenofemoral ligation deep fascia. Ligation of perforating veins is usually
Saphenofemoral ligation is the procedure per- reserved for patients undergoing operation for
formed most commonly. The saphenofemoral junc- recurrent veins or those who have significant sec-
tion is exposed through a skin crease incision about ondary venous tissue changes or ulceration. It is not
3 cm long placed below and lateral to the pubic a cosmetic procedure.
tubercle and 1 cm above the groin crease. The long
saphenous vein and its tributaries are dissected. All
tributaries are ligated and divided. Once the junc- Postoperative care
tion between the long saphenous and femoral veins The leg is firmly bandaged to promote haemostasis
has been clearly identified, the long saphenous vein from the extraction sites. Early and continued
is divided and ligated flush with the femoral vein. mobility is encouraged to reduce the risk of deep
The femoral vein is explored for 1 cm proximal and vein thrombosis. Patients having bilateral opera-
distal to the junction to ensure that there are no tions or operation for major recurrences usually
more tributaries entering the vein. Any that are stay in hospital overnight. The outer bandages are
found are ligated and divided. removed 24–48 hours after operation and elastic
stockings are applied. These are worn for about
Saphenopopliteal ligation 2 weeks while there is a tendency for the leg to
swell.
Saphenopopliteal ligation is carried out in a man-
ner analogous to saphenofemoral ligation. The dis-
section may be difficult because of the fat in the Prognosis and results of surgery
popliteal fossa and is greatly facilitated by precise
knowledge from duplex ultrasound scanning of the The result of surgery that has been carefully
exact level of the saphenopopliteal junction. Care is planned and carried out should be good. With well‐
necessary to avoid inadvertent injury to the sural performed surgery the recurrence rate is 15–20%
nerve which runs with the short saphenous vein. at 5 years. Injection therapy may be used to
obliterate telangiectatic vessels that it is not possi-

ble to remove surgically.
Lymphoedema
Lymphoedema is the consequence of abnormal

Complications amounts of fluid and protein in the interstitial
spaces of the skin and subcutaneous tissues, par-
Deep venous thrombosis is uncommon if prophy-
ticularly with respect to the limbs. The high protein
laxis is employed. Wound infections can occur in
content of the fluid distinguishes this type of swell-
relation to skin crease incisions but respond well
ing, or brawny oedema, from that seen occurring as
to antibiotics as no prostheses are implanted.
a result of the filtration oedema of heart and kidney
Recurrence is perhaps the most important issue
failure, venous obstruction and hypoproteinaemia
for patients and this can occur for four reasons:
(pitting oedema).
(i) there was unrecognised pre‐existing valvular
incompetence at a site other than where opera-
tion was performed; (ii) operation was not ade- Incidence
quate where a major tributary has been missed;
(iii) remote (from operative site) valvular incom- This is an unusual cause of limb swelling. There are
petence has developed subsequent to operation; two principal types:
and (iv) neovascularisation has occurred (the • a congenital abnormality of the lymphatic chan-
development of multiple tiny channels between nels (primary lymphoedema)
the deep and superficial systems through scar tis- • secondary lymphatic obstruction resulting from
sue at the site of ligation). infection, trauma (including surgery and radio-
therapy), secondary metastatic tumours and, occa-
sionally, primary tumours such as lymphoma.
Other techniques of venous ablation
Radiofrequency ablation
Physiology
The radiofrequency catheter delivers radiofre-
quency energy to achieve heat‐induced venous The brain and the spinal cord are the only body tis-
spasm and collagen shrinkage. Under ultrasound sues that do not have significant lymphatic vessels.
guidance, a sheath is introduced into the vein at an For all other structures, lymphatic vessels function
appropriate point near the knee crease using a to collect lymph – tissue fluid including protein that
Seldinger technique. The radiofrequency applicator leaks from the capillary bed – and convey this to
is passed through the sheath and into the great the regional lymph nodes, to the major lymphatic
saphenous vein under ultrasound control. The tip is trunks and ultimately into the thoracic duct, which
usually positioned approximately 2 cm below the terminates by joining the junction of the subclavian
saphenofemoral junction. The radiofrequency abla- and internal jugular vein in the left side of the neck.
tion catheter is then withdrawn at a controlled rate The lymphatic capillaries are thin‐walled
and treatment stopped once the catheter has entered endothelial tubes, the endothelium being supported
the sheath. on collagen with occasional smooth muscle cells.
The onward progression of the lymph in these chan-
nels is maintained by the presence of valves and the
Endovenous laser therapy
compression applied by neighbouring structures,
Endovenous laser therapy releases thermal energy such as the contraction of muscles and the varying
both to the blood and to the venous wall, causing pressures and movements of the gut in the abdomi-
localised tissue damage. Tumescence fluid (0.9% nal cavity. The onward flow is also enhanced by the
saline with local anaesthetic) is injected into the changes in intrathoracic pressure generated by res-
saphenous compartment to reduce risk of skin piration. The composition of the lymph will vary
burn. A laser sheath is inserted in a similar way to with the drainage site; for example, in the intestine
radiofrequency ablation and a laser fibre is inserted it will contain chylomicrons. In all cases there is a
into the sheath. A laser generator is used to provide high concentration of albumin. The lymph flow in
laser energy as the catheter is pulled back at a con- the thoracic duct varies from 1 to 4 L per day and
trolled rate. the proportions of its final composition will
Both these techniques can be performed under depend on the relative flow from the various sites
local anaesthesia and on an outpatient basis. of the body and the food intake at the time.
Pathogenesis and pathology Clinical presentation
The pathogenesis of lymphoedema is invariably a Primary lymphoedema

consequence of inadequate lymphatic flow, either
Primary or idiopathic lymphoedema can manifest
because the lymph vessels are congenitally abnor-
clinically at various ages. Congenital lymphoedema
mal or deficient or because of obstruction to the
is apparent at, or within a few weeks of, birth, often
vessels or the draining lymph nodes. Less frequently,
in association with some other congenital
temporary lymphoedema can occur in a limb on
abnormality.
account of muscle inactivity, as occurs with pro-
Lymphoedema praecox refers to lymphoedema
longed sitting, but resolves swiftly with muscle
not present at birth but which appears before the
activity.
age of 35 years. It usually affects adolescent women.
Lymphoedema tarda becomes evident after the
Primary lymphoedema age of 35 years. This group of patients, usually
females, may have unilateral or bilateral limb swell-
Primary or idiopathic lymphoedema refers to swell-
ing which can affect the upper or lower limbs.
ing due to intrinsic abnormalities of the lymphatic
There may be a temporal relationship with a minor
vessels. This can be a familial abnormality and is
injury or surgery on the limb that precedes the
often bilateral and symmetrical. The lymphatic ves-
onset of the swelling. Initially the swelling is soft
sels are aplastic in 15% and hypoplastic in 65% of
and pitting but with time the tissues become more
patients, being fewer and smaller in calibre than is
indurated and fibrous. This change is hastened and
normal. They may be varicose, dilated and incom-
accentuated by attacks of cellulitis.
petent in 20% due to fibrosis in the draining lymph
Lymphoedema tends to affect the foot and the
nodes. In this group with an intrinsic abnormality
toes. In the later stages, the skin becomes thickened
present at birth, lymph may reflux into the skin,
and hyperkeratotic with wart‐like excrescences. In
leak through the skin (especially between the toes),
the severe and chronic stage, the limb has a tree
into the peritoneum as chyloperitoneum, into the
trunk‐like appearance and can be distinguished from
thorax as chylothorax and into the urine as
venous oedema by the absence of prominent pig-
chyluria.
mentation and the chronic venous ulceration com-
monly seen in severe venous insufficiency oedema.
Acquired lymphoedema
Secondary lymphoedema
Acquired lymphoedema often affects only one limb,
except when the obstructing lesion is due to an The swelling of secondary lymphoedema develops
infective agent such as the filarial nematode more rapidly, often in an older age group and may
Wuchereria bancrofti. This is a mosquito‐borne be associated with dragging discomfort. This form
parasite of tropical regions. The other infective of lymphoedema is frequently secondary to an
agents that cause secondary lymphoedema are lym- obstructing lesion; thus there may be changes at the
phogranuloma inguinale, tuberculosis and recur- site of obstruction such as scarring, swelling and
rent non‐specific infection. local erythema. As with primary lymphoedema,
Tumour‐induced secondary lymphoedema is these patients are prone to episodes of cellulitis and
most commonly associated with metastatic tumour lymphangitis.
of the breast, causing upper limb lymphoedema,
and pelvic tumours of the cervix, ovary and uterus
in the female and of the prostate in males, giving Investigation
rise to lower limb lymphoedema.
Iatrogenic or trauma‐induced lymphoedema It is important to distinguish lymphoedema involv-
occurs most frequently as a result of block dissec- ing the lower limbs from venous oedema (deep
tions of either the axilla or groin, or in association venous incompetence or obstruction). The clinical
with radiation of the same region. presentation, history and examination will usually
The pathological complications of lymphoedema suggest either of these conditions but each can be
include recurrent infection such as cellulitis and readily excluded by the use of duplex scanning of
chronic thickening of the skin with hyperkeratosis. the lower limb venous system. If the scan does not
In the very long term, lymphangiosarcoma may demonstrate venous obstruction or deep venous
develop (see Chapter 45). valvular incompetence, the swelling is more likely
to be lymphatic in origin. It is important to ensure Patients with lymphoedema are predisposed to cel-
that the iliac venous system has been sonographi- lulitis and spreading lymphangitis. The problem is
cally interrogated before a venous cause is excluded. that infection will further damage the lymphatic sys-
Oedema associated with generalised problems, tem. Patients should be warned to avoid trauma and
such as hypoproteinaemia, nephrotic syndrome or to seek early and aggressive management of skin sep-
cardiac failure, will be excluded on clinical exami- sis. Streptococci are the most common organisms
nation, biochemical tests (e.g. liver function tests, causing cellulitis. Early treatment with systemically
serum protein levels, urea, creatinine and electro- administered penicillin is indicated if any form of skin
lytes) and examination of the urine for protein. sepsis develops. The most common portal of entry is
Specific investigations for lymphoedema are not via associated interdigital fungal infection with tinea
usually employed as they rarely impact on manage- pedis. If a patient has recurrent attacks of cellulitis,
ment, but include lymphoscintigraphy. Radioactive long‐term prophylaxis with pencillin 250 mg twice
labelled colloids can be injected into the interdigi- daily is appropriate. For those allergic to penicillin,
tal spaces and should appear within 30 minutes in erythromycin may be given as treatment for acute
the regional nodes if the lymphatic vessels are nor- infections. Any interdigital fungal infection should be
mal. Reduced uptake implies hypoplastic or oblit- treated regularly with an antifungal powder; if there
erated lymphatic vessels. In obstructive secondary is an established infection, oral griseofulvin can be
lymphoedema, the radionuclide uptake in the taken. If the infection fails to respond to standard
regional nodes is often normal. It may be slow in treatment, alternative antibiotics can be considered.
the more proximal nodes, indicating an obstruc- Limb swelling is best managed with graded com-
tion at that level. pression stockings. The patient should sleep with
Computed tomography of the regional node the foot of the bed elevated on the equivalent of
area will allow an assessment of nodal enlarge- two house bricks and graded compression stock-
ment if these are obstructive; in primary lymphoe- ings fitted before the patient gets out of bed. The
dema the number and size of nodes may be stockings may range from 30 to 50 mmHg in their
diminished. Lymphangiography is now seldom compression depending on the tolerance of the
used because it may accentuate the obliterative patient. For those with whole limb swelling, the
process of primary lymphoedema and give rise to pantyhose or thigh stocking should be used. Similar
infection or an inflammatory process that may stockings can be used for those with arm oedema.
relate to the contrast medium used. It provides Intermittent pneumatic compression may help to
information about the type and site of lymphatic reduce limb swelling. The pneumatic compression
obstruction and valvular incompetence in the is applied as a multi‐cell unit arranged concentri-
lymph vessels in particular cases. cally. The multi‐cell unit inflates successively from
Hence the diagnosis of lymphoedema, particu- peripheral to proximal and thus has a ‘milking’
larly primary lymphoedema, tends to be a diagnosis action that drives fluid from the periphery to the
of exclusion. The major aim when investigating a centre. The use of compression stockings and the
patient with lymphoedema is to determine whether intermittent use of external pneumatic compression
or not underlying pathology exists. The extent and devices will achieve very satisfactory limb size con-
severity of lymphoedema should be determined and trol in the majority of patients.
recorded as baseline information to gauge subse- Surgical treatment is rarely performed, being
quent treatment. The minimum is precise measure- reserved for the few patients who cannot have their
ments of limb circumference with reference to swelling controlled by compression, have repeated
defined bony points, for example 2 cm above the bouts of sepsis or in whom skin changes and the
medial malleolus. persisting swelling might suggest there is a risk of a
neoplasm. Surgery may either involve excision of
subcutaneous tissue (Charles operation) or
Treatment attempts at lymphatic bypass, the latter being still
experimental.
The treatment of lymphoedema is essentially conserv-
ative. Conservative treatment aims to preserve the
quality of the skin, prevent lymphangitis and reduce Prognosis and results of treatment
limb size. Skin quality can be maintained by careful
avoidance of trauma and regularly applying a water‐ The majority of patients can control their leg swell-
based skin lotion. Non‐skin‐drying soaps should be ing with compression stockings during the day and
used to minimise the loss of oil from the skin. nocturnal elevation. The ability to achieve this goal
is largely dependent on the determination and com- 2 Which of the following statements about patients
pliance of the patient. This can be facilitated by put- with varicose veins is incorrect?
ting the patient in touch with the local lymphoedema a they experience calf pain after walking 200 m
society (see Further reading). that is relieved by resting for 5 minutes
b present with a superficial ulcer on the ankle
c experience aching discomfort in the calf after
Further reading prolonged standing
d present with superficial thrombophlebitis
Australasian Lymphology Association, www.lymphoedema.
e show spontaneous bleeding from a varix
org.au
Davies D, Rogers M. Morphology of lymphatic malfor-
mations: a pictorial review. Australas J Dermatol 3 Which of the following statements is correct?
2000;41:1–5. a venography is an accurate method for
Fitridge RA, Thompson MM (eds) The Mechanisms of investigating varicose veins
Vascular Disease: A Reference Book for Vascular b duplex scanning has little to add to the
Specialists. Adelaide: University of Adelaide Press, preoperative investigation of varicose veins
2011:497–510. c the most frequent cause of recurrent varicose
Gloviczki P. Principles of surgical treatment of chronic veins is neovascularisation
lymphoedema. Int Angiol 1999;18:42–6. d due to frequent and serious late complications,
Merchant RF, Pichot O. Long‐term outcomes of end-
all patients with varicose veins should be advised
ovenous radiofrequency obliteration of saphenous
to have surgery
reflux as a treatment for superficial venous insuffi-
e patients with varicose veins and who have
ciency. J Vasc Surg 2005;42:502–9.
Moore WS (ed.) Vascular and Endovascular Surgery: A haemosiderin deposits and liposclerosis at the
Comprehensive Review, 8th edn. Philadelphia: Elsevier ankle should be treated
Saunders, 2013, chapter 51.
Rabe E, Schliephake D, Otto J, Breu FX, Pannier F. 4 Which of the following statements about the
Sclerotherapy of telangiectases and reticular veins: a management of patients with varicose veins is
double‐blind, randomized, comparative clinical trial of incorrect?
polidocanol, sodium tetradecyl sulphate and isotonic a below‐knee elastic stockings may be
saline (EASI study). Phlebology 2010;25:124–31. definitive treatment in the patient in whom
Sidawy AN, Perler BA (eds) Rutherford’s Vascular Surgery
surgery is contraindicated because of
and Endovascular Therapy, 9th edn. Philadelphia:
comorbidities
Elsevier, 2018.
Szuba A, Rockson SG. Lymphoedema: classification, diag- b injection with a sclerosing agent followed by
nosis and therapy. Vasc Med 1998;3:145–56. elastic compression for 4–6 weeks can be
beneficial
c using a below‐knee elastic stocking may
MCQs help decide if calf symptoms are due to
varices
Select the single correct answer to each question. The d surgical trials have demonstrated that it is not
correct answers can be found in the Answers section necessary to remove the long saphenous vein in
at the end of the book. the thigh
e incompetent perforating veins should be
1 Which of the following statements about varicose
subfascially ligated if there are secondary skin
veins is incorrect?
changes
a varicose veins are dilated, tortuous and visible
when the patient is standing
5 Primary lymphoedema:
b valvular incompetence is an integral component
a should be differentiated from oedema due to
of the pathogenesis of varicose veins
varicose veins with a duplex scan
c the principal superficial venous systems of the
b should be investigated with lymphoscintigraphy
lower limbs are the long and the short saphenous
before deciding on treatment
systems
c is due to an underlying malignancy
d the principal route of venous drainage from the
d is cured by diuretic therapy
lower limb is via the superficial venous system
e the response to therapy can be monitored by
e the principal driver of venous drainage from the
serial measurement of limb circumference
legs in the erect position is the calf pump
58 Endovascular therapies
Timothy Buckenham
Monash University and Department of Imaging, Monash Health, Melbourne, Victoria, Australia
equipped with a high‐quality angiographic imaging

Introduction system (hybrid theatre) (Figure 58.1). The angio-
graphic equipment has a number of features
The management of vascular disease has made a
that facilitate endovascular procedures, including a
steady movement toward minimally invasive thera-
C‐arm that may be floor or ceiling mounted and
pies over the last 20 years. These minimally invasive
allows the X‐ray tube and the detector to rotate
techniques when applied to arteries are called
around the patient to facilitate multiplanar imag-
endovascular or endoluminal, meaning the therapy
ing. The table is made of carbon to ensure radiolu-
is delivered through the lumen of the artery.
cency and it floats, meaning the operator can easily
This change in practice has been driven by the
raise or lower the table or move it side to side or
rapid development of new technologies and the
end to end by depressing a table‐side control.
increasing sophistication of multiplanar imaging,
Essential to the procedure is the ability to subtract
facilitating accurate planning and deployment of
out background so that only the detailed image
endoluminal devices. Most endovascular proce-
provided by the contrast media is visible; this is
dures require the use of ionising radiation (X‐rays)
called digital subtraction angiography. Another
and contrast media (ionic or gaseous) and therefore
important feature is the ability to superimpose live
have risks as well as benefits for the patient, but
fluoroscopic imaging on a stored image (called a
overall endovascular procedures are attractive for
‘road map’) and, on some equipment, to superim-
their low morbidity and mortality and rapid recov-
pose CT or MRI images to help complex inter-
ery of the patient. High‐resolution imaging, par-
ventions. Radiation protection for both the patient
ticularly modalities not utilising ionising radiation
and the operator is important. Therefore, equip-
such as ultrasound and magnetic resonance imag-
ment characteristics include virtual collimation,
ing (MRI), has improved the efficacy of endovascu-
lead shields and a low‐dose mode, and operators
lar repair by allowing the detection of treatment
wear lead gowns, lead glasses and increasingly
failure or facilitating intervention to prevent
commonly lead helmets.
treatment failure. This is particularly important in
endovascular repair of arteries as secondary inter-
vention is much more common than in traditional
Ultrasound
open surgery and durability is often dependent on
these secondary interventions Ultrasound located within the angiographic suite
allows rapid and safe access to a range of arteries,
usually the femoral although other commonly used
Equipment requirements for access sites include the brachial, radial and pedal
endovascular therapy arteries. With the common use of closure devices to
facilitate haemostasis, ultrasound has an important
Angiography suite role in selecting the optimal access site. Many endo-
vascular procedures require large‐access catheters
Imaging
up to 24F and ultrasound can help assess the opti-
The majority of endovascular interventions are mal point of puncture. Ultrasound can also be used
carried out in an angiography suite (also known as to assess the intraoperative outcome of an endovas-
a catheter laboratory) or an operating theatre cular procedure in superficial arteries and conduits
553
Fig. 58.1 Angiography suite: note the ceiling‐mounted C‐arm configuration (vertical arrow) with ultrasound machine
to assist with vessel access (horizontal arrow). The operator is wearing a lead apron and lead glasses and is standing
behind a lead window to maximise radiation protection (double arrow).
Endoluminal devices microspherules with a wide range of diameters,

the diameter being matched to the diameter of the
It is beyond the scope of this chapter to detail the
target arteries.
huge range of devices available for endovascular
procedures but they can be divided into a number
Devices for reopening diseased arteries
of groups.
Angioplasty balloons are the most important tool
for revascularising stenotic and occluded arteries.
Devices used for arterial occlusion
They are delivered into the body over a guidewire
Arteries may be occluded with a range of materials and inflated when traversing the diseased segment.
called embolic agents. These are delivered through Angioplasty balloons come in a wide range of
the lumen of an arterial catheter into the target diameters and lengths that the operator matches to
arterial lumen. Embolic agents maybe solid, par- the arterial segment being treated. The balloons are
ticulate or liquid. A common example of a solid inflated to a predetermined pressure using an infla-
embolic agent is a metallic coil made of stainless tion manometer. Some balloons have a drug coating
steel or tungsten. These coils are linear when mixed with an excipient that allows controlled
loaded into the lumen of the delivery catheter but transfer of the drug (usually paclitaxel) to the wall
on entering the arterial lumen assume a predeter- of the artery to reduce re‐stenosis by inhibiting
mined coil shape that occludes the target artery. An smooth muscle proliferation.
example of a liquid embolic agent is cyanoacrylate, Arterial stents (Figure 58.2) are designed to act
which is not radiopaque but when mixed with con- as a scaffold that hold the treated arteries open and
trast media can be seen and injected into target are used to improve patency or manage an injury to
arteries with great accuracy, where it sets as a glue the artery such as a dissection or a rupture; some of
cast that occludes the vessel. Particulate embolic these stents are drug‐eluting. Stents come in two
material usually takes the form of polyvinylalcohol basic designs.
58: Endovascular therapies 555
Fig. 58.2 A flexible self‐expanding stent.
• Self‐expanding stents: these are often made of

Nitinol and have a thermal memory, re‐forming to
Fig. 58.3 Bifurcated endograft for exclusion of an
a particular size when released by the delivery cath- abdominal aortic aneurysm. Note the uncovered
eter and warmed by the blood. These stents tend to suprarenal fixating tines (vertical arrow) and the V‐
be more flexible that balloon‐expandable stents. shaped metallic exoskeleton (horizontal arrow). The
• Balloon‐expandable stents: these are commonly proximal covered segment of the aortic graft provides
made of stainless steel and are deployed by inflat- the infrarenal sealing zone (star).
ing an angioplasty balloon on which the stent is
loaded. Once the stent achieves the diameter
has been deployed from, is then extended with an
determined by the delivery balloon, the balloon is
endograft into the common iliac artery giving an
removed and the stent remains in position
aorto bi‐iliac configuration (Figure 58.3). Some of
expanding the arterial lumen. Balloon‐expanda-
these grafts have tines or similar that cross the renal
ble stents are usually shorter and more rigid than
arteries and fix in the suprarenal aorta, while others
self‐expanding stents and are used mainly above
are deployed entirely inferior to the renal arteries.
the inguinal ligament where the need for flexibil-
Most require ballooning to ensure graft apposition,
ity is less significant.
with the sealing zones below the renal arteries and
Endografts or covered stents have a covering made
in the common iliac arteries and at the junctions of
of PTFE or Dacron and may be mounted on a bal-
the components.
loon‐expandable or self‐expanding stent platform.
These stents are primarily used to exclude aneu-
rysms but are used for revascularisation particu- Endovascular procedures: the basics
larly in the suprainguinal circulation, but they
require much larger delivery catheters and therefore Seldinger technique
much larger percutaneous access site punctures.
This technique underpins all percutaneous arterial
access and was described by the Swedish radiolo-
Devices for excluding aneurysms
gist Sven Seldinger in 1953 (Figure 58.4). Its mod-
There are many endoluminal devices that are ern iteration involves introduction of a soft
designed to exclude aneurysms, particularly abdom- guidewire into the arterial lumen through the barrel
inal and thoracic aortic aneurysms. They all have a of a hollow bevelled needle. The needle tip is placed
fabric covering (usually PTFE or woven polyester) in the lumen of the access artery percutaneously,
attached to a metal endoskeleton or exoskeleton usually under ultrasound guidance. Once the guide-
and are deployed through a sheath (Figure 58.3). wire is successfully deployed in the arterial lumen, a
Most consist of multiple components: a body with a suitably sized access sheath can be advanced over
long and a short limb. After infrarenal deployment the guidewire into the access artery. After passing
of the graft body, the short limb is extended with an the sheath, the guidewire is withdrawn. Other
endograft into the contralateral common iliac artery. devices such as catheters, balloons and stents can
The longer graft limb, ipsilateral to the side the body then be introduced through the access sheath.
(1) (2)
(3) (4)
(5)
Fig. 58.4 Seldinger technique. (1) The artery is punctured with a hollow needle; (2) a flexible guidewire is introduced
through the needle; (3) the needle is withdrawn, leaving the guidewire in the artery; (4) the arterial catheter is
introduced over the guidewire; (5) the guidewire is removed and the catheter remains in the vessel.
Selective arterial catheterisation Access artery closure

Pre‐shaped catheters, with names such as Cobra On completion of an endovascular procedure,
and Sidewinder, allow access to all major arteries access site haemostasis needs to be achieved. If a
in the body, and are used in conjunction with guide- small access sheath such as 5F or 6F has been used,
wires of varying stiffness and lubricity. In small manual compression for 10 minutes is usually ade-
arteries (<4 mm), microcatheters may be used. quate and safe. If larger access sheaths have been
These are placed inside the lumen of the shaped used, for example over 20F in thoracic endovascular
catheter and pass over a very fine guidewire lying aneurysm repair (TEVAR) and endovascular aneu-
centrally in the lumen. rysm repair (EVAR), multiple suture closure devices
may be used. These devices deploy an endoluminal
Arteriography needle that is deflected by a cup and recaptured by
Opacification of the lumen of the access artery, of the device, allowing the suture to be tightened and
an arterial segment for revascularisation or closing the access site. There are multiple other per-
exclusion or of target arteries for embolisation cutaneous closure devices that use alternative tech-
requires the injection of contrast media through a nologies, such as collagen plugs and Nitinol clips.
catheter and the rapid acquisition of digitally
subtracted images. Pre‐shaped or selective cathe-
ters have a single end hole, but if larger volumes Endovascular management of arterial
of contrast are required in order to opacify the aneurysm disease
aorta a multi‐holed pigtail catheter is used.
Contrast media can be positive or negative. Aortic aneurysmal disease
Iodinated contrast is positive as it attenuates the
Indications
X‐ray beam, but is associated with allergy and
renal dysfunction. Carbon dioxide is a negative The indications for EVAR of abdominal aortic aneu-
contrast and displaces blood and reduces attenu- rysm are similar to those for open surgery, i.e. diam-
ation of the X‐ray beam. Carbon dioxide is non‐ eter of 55 mm, rapid expansion on serial imaging, or
allergenic and non‐nephrotoxic but may be are symptomatic. CT scanning will determine the
uncomfortable for the patient. diameter and suitability for EVAR. These parameters
include adequate infrarenal aortic neck (undiseased endoleak is when systemically pressurised arterial
non‐dilated parallel segment of aorta), adequate‐ blood enters the aneurysm sac external to the endo-
sized iliac arteries for access and common iliac arter- graft. This may occur around the sealing zones (type 1)
ies that are suitable for distal sealing. or more commonly via retrograde flow from lum-
The indications for TEVAR of thoracic aortic bar or visceral branch arteries such as the inferior
aneurysms are again similar to those for surgery, i.e. mesenteric artery (type 2). Other sources of
diameter of 60 mm, rapid expansion on serial imag- endoleak are from the junctional zones (type 3) or
ing, or symptomatic. through the fabric (type 4). Sac expansion second-
ary to a type 2 endoleak or the presence of a type 1
Procedure and outcomes or 3 leak merits treatment to prevent aortic rupture.
Other complications are access site and access
Aortic aneurysmal disease is characterised by struc-
artery trauma and kidney injury from contrast
tural dysfunction of the aortic wall, with gradual
media.
expansion that can progress to rupture. This com-
monly occurs in the abdominal aorta and less fre-
quently in the thoracic aorta. The aim of aortic Current status of EVAR and TEVAR
aneurysm repair is to prevent aneurysm rupture Endoluminal repair is currently the preferred
and aneurysm‐related death by excluding the aneu- treatment modality for thoracic aortic aneurysms
rysm from the aortic circulation. There are two distal to the left subclavian artery and infrarenal
options for the treatment of aneurysms: traditional abdominal aortic aneurysms because of low mor-
open surgery and endovascular repair. Open surgi- bidity and mortality and inpatient stay of 24–48
cal repair has higher risks of morbidity and mortal- hours. Similar endoluminal techniques are also
ity compared with the minimally invasive often applied in the treatment of other aortic pathology
percutaneous EVAR. EVAR has a 30‐day mortality such as acute type B dissection, aortic trauma,
of around 2% compared with 4% for open surgical mycotic aneurysms, fistulas and penetrating ather-
repair, but interestingly all‐cause mortality is equal omatous ulcers.
at 5 years and the periprocedural survival advan-
tage is not sustained. Patients undergoing EVAR
have a significant re‐intervention rate of around
30% within 5 years, mainly to correct endoleaks, Endovascular management of peripheral
and the very long term durability is still uncertain. vascular disease
Despite advancing technology not all aortic
aneurysms can be repaired with EVAR. In abdomi- Chronic limb ischaemia
nal aneurysms, this is usually related to an unfa-
vourable sealing zone in the infrarenal abdominal Lower limb arterial disease may result in ischaemia
aorta, which can be overcome with more complex which develops over time and may present as non‐
EVAR procedures that involve apertures or fenes- limb‐threatening claudication or as chronic critical
trations to maintain visceral artery patency, the limb ischaemia (CCLI), which results in rest pain
sealing zone in these cases being the suprarenal and tissue loss. The classification usually used for
aorta. In TEVAR, similar limitations apply. In tho- determining the severity of chronic limb ischaemia is
racic aortic aneurysm disease most endoluminal the Rutherford system (Table 58.1). Thus Rutherford
repair is performed distal to the left subclavian grade I patients (claudicants) may be managed con-
artery but the proximal landing zone (the segment servatively and have a low lifetime risk of amputa-
of aorta just distal to the left subclavian artery) may tion. Patients with grades II and II CCLI require
be inadequate, requiring more proximal aortic revascularisation using endovascular or open surgical
landing with graft fenestrations for the carotid and procedures. Given that atherosclerosis is a systemic
subclavian arteries. Similar re‐intervention rates to disease, patients with CCLI are likely to have
EVAR are seen in TEVAR but a greater proportion coexistent coronary and carotid
disease, making
of these secondary interventions are with open minimally invasive techniques attractive due to their
surgery rather than minimally invasive techniques low morbidity and mortality.
which are predominant in EVAR.
Which arterial lesions are amenable to
endovascular therapy?
Limitations and complications
The Trans‐Atlantic Inter‐Society Consensus Document
The Achilles heel of both EVAR and TEVAR is the on Management of Peripheral Arterial Disease
high incidence of endoleaks (Figure 58.5). An (TASC II) has divided the lower limb arterial
Classification of endoleak
Ia
lllb
llla
llb lla
lb lc
Type Ia: Proximal fixation site

Type Ib: Distal fixation site
Type Ic: IIiac occluder
Type IIa: Inferior mesenteric artery
Type IIb: Lumber artery
Type IIIa: Dysfunction
Type IIIb: Fabric tear
Type lV: Fabric porosity
Fig. 58.5 Endoleak classification.
Table 58.1 Rutherford classification for chronic limb ischaemia.
Grade Category Clinical description Objective criteria
0 0 Asymptomatic: no haemodynamically Normal treadmill or reactive hyperaemia test

significant occlusive disease
1 Mild claudication Completes treadmill exercise; AP after
exercise >50 mmHg but at least 20 mmHg
lower than resting value
I 2 Moderate claudication Between categories 1 and 3
3 Severe claudication Cannot complete standard treadmill exercise,
and AP after exercise <50 mmHg
II 4 Ischaemic rest pain Resting AP <40 mmHg, flat or barely pulsatile
ankle or metatarsal PVR; TP <30 mmHg
III 5 Minor tissue loss: non‐healing ulcer, Resting AP <60 mmHg, ankle or metatarsal
focal gangrene with diffuse pedal PVR flat or barely pulsatile; TP <40 mmHg
ischaemia
6 Major tissue loss: extending above Same as category 5
TM level, functional foot no longer
salvageable
AP, ankle pressure; PVR, pulse volume recording; TM, transmetatarsal; TP, toe pressure.
tree into components with recommendations as to distal disease, surgical bypass with autologous
the appropriateness of endovascular treatment. venous conduits have an important role
In summary, most iliac disease is amenable to
percutaneous repair, including complex occlusive
Acute limb ischaemia
disease involving the aorta and iliac arteries. New
Acute limb ischaemia (ALI) usually results from
technology has allowed safer and more effective
in situ thrombosis of an atheromatous artery with
treatment of complex suprainguinal disease. An
acute clot or occlusion from an embolus that may
example of this is covered endovascular repair of
originate in the heart or a more local source such as
the aortic bifurcation (CERAB), where two covered
a popliteal artery aneurysm. ALI has a separate clas-
iliac stents are introduced into an aortic stent creat-
sification to CCLI (Table 58.2). Rutherford grade IIa
ing an endovascular version of an aorto bi‐iliac
and IIb patients may benefit from catheter‐directed
graft (Figure 58.6).
therapy in the acute phase, primarily aspiration
Lesions below the inguinal ligament in patients
thromboembolectomy or catheter‐directed throm-
with CCLI are treated with an angioplasty first if
bolysis. Both these techniques require a catheter to
the lesion is judged amenable to angioplasty and
traverse the acutely occluded arterial segment and
stenting. With long‐segment occlusions and very
the clot is removed through the lumen of the catheter
(a) (b)
Fig. 58.6 (a) Complex aortic stenotic disease (broad horizontal arrow) and iliac bifurcation disease with an occluded
right common iliac artery (not seen). Note the extensive collateral circulation (vertical arrow). (b) Arteriogram after
percutaneous revascularisation using an aortic stent and bilateral iliac stents (arrows), the CERAB technique, in a
patient with intermittent claudication.
Table 58.2 Rutherford classification for acute limb ischaemia.
Findings Doppler signal
Category Description/prognosis Sensory loss Muscle weakness Arterial Venous
I Viable Not immediately None None Audible Audible

threatened
II Threatened
a Marginally Salvageable if Minimal (toes) None Inaudible Audible
promptly treated or none
b Immediately Salvageable with More than toes, Mild, moderate Inaudible Audible
immediate associated rest
revascularisation pain
III Irreversible Major tissue loss or Profound, Profound, Inaudible Inaudible
permanent nerve anaesthetic paralysis
damage inevitable
manually or by mechanical suction or it is laced with (Figure 58.7). Not all bleeding arteries are treated
a lytic agent such as urokinase (which is infused with embolisation and if end‐organ ischaemia is
across the occluded segment though a catheter with a potential problem, the bleeding site may be
multiple small side holes). The therapeutic manage- excluded with a covered stent.
ment of ALI often needs careful thought as time
frames to achieve revascularisation are crucial and
the ischaemic limb may require other interventions
Other applications of endovascular
such as fasciotomy. Given these constraints, endo-
therapy
vascular techniques play a secondary role to surgical
embolectomy, thrombectomy and bypass.
Endovascular therapy is widely used in the venous
circulation to treat conditions such as May–
Thurner syndrome (compression of the left
Endovascular treatment of haemorrhage
common iliac vein by the right common iliac

artery), acute lower limb deep venous thrombosis
Endovascular techniques have an important role in
and Paget–Schroetter disease (effort thrombosis of
the management of acute haemorrhage, particu-
the subclavian and axillary veins). Other applica-
larly bleeding from the colon usually presenting as
tions include the endovascular management of
haematochezia or in the management of traumatic
failing dialysis fistulas and central venous obstruc-
injury complicated by bleeding. Multidetector CT
tion from all causes. Chemoembolisation has an
is capable of identifying the source of bleeding in
important role in the treatment of tumours, par-
many cases, allowing rapid and focused closure of
ticularly in the liver, and the management of stroke
the bleeding point with embolisation. The principle
and subarachnoid haemorrhage has been revolu-
of embolisation requires the operator to isolate the
tionised by endovascular techniques that can
bleeding segment by embolising both proximal and
remove intracerebral clot and treat leaking cere-
distal to the site of bleeding (‘closing the front and
bral aneurysms.
back doors’). As previously discussed, delivery of
embolic material such as coils or glue causes rapid
artery closure. In non‐traumatic haemorrhage it is
important to recognise that embolisation is not Conclusion
treating the underlying lesion and further investi-
gation is important. In the colon this may be diver- Endovascular management of vascular disease is an
ticular disease or a neoplasm and colonography or attractive minimally invasive treatment option that
colonoscopy is required. In some cases lesions is rapidly increasing in scope as technology provides
that are associated with a high risk of bleeding are more devices and the miniaturisation and improve-
prophylactically embolised, for example pancreatic ment of current devices. However, the best approach
pseudoaneurysms and psuedoaneurysms associ- for each patient is a knowledgeable discussion of
ated with tumours such as angiomyolipomas medical, surgical and endovascular options.
(a) (b) (c)
Fig. 58.7 Catheter arteriogram of a highly vascular renal carcinoma of the right kidney (a) shows a selective
catheterisation (red arrow)and arteriography of the right renal artery demonstrating abnormal tumour circulation in a
renal carcinoma (black arrows), (b) shows a balloon occluding catheter placed proximal to the tumour prior to
embolization (open arrow), (c) shows an arteriogram after the injection of liquid embolic agent (red arrow) into the
tumour circulation. Untreated arteries are indicated by black arrow.
a ngioplasty in a 70‐year‐old woman with short‐

Further reading distance bilateral intermittent claudication?
a the femoral artery lesion is a 90% stenosis over a
Conte SM, Vale PR. Peripheral vascular disease. Heart
length of 1 cm
Lung Circ 2018;27:427–32.
England A, McWilliams R. Endovascular aortic aneurysm b the ipsilateral common femoral artery is severely
repair (EVAR). Ulster Med J 2013;82:3–10. diseased with calcified plaque
Robertson L, Paraskevas KI, Stewart M. Angioplasty and c obesity
stenting for peripheral arterial disease of the lower d prior ipsilateral groin surgery
limbs: an overview of Cochrane Reviews. Cochrane e a >10 cm heavily calcified femoral arterial occlusion
Database Syst Rev 2017;(2):CD 012542.
3 Which of the following statements about
percutaneous arterial embolisation is incorrect?
MCQs a solid organ arterial injury associated with
bleeding demonstrated on a CT angiogram
Select the single correct answer to each question. The may be suitable
correct answers can be found in the Answers section b a common indication is haematochezia
at the end of the book. c complete arterial transection of the femoral or
1 Which of the following statements about elective popliteal arteries is an indication
endovascular repair (EVAR) of an abdominal aortic d embolic agents maybe solid, liquid or particulate
aneurysm is correct? e embolisation of lumbar arteries may be required
a only infrarenal aortic aneurysms can be to treat a type 2 endoleak
repaired
b preoperative imaging with ultrasound is 4 Which of the following statements about thoracic
sufficient aortic endovascular repair (TEVAR) is incorrect?
c 30‐day operative mortality is lower with EVAR a coarctation is an indication
than open surgical repair b acute complicated type B dissection is an
d type 2 endoleaks are the least common type of indication
endoleak after EVAR c an extra anatomical graft from the carotid to
e requires open surgical access to the femoral subclavian artery may be required to allow
arteries coverage of the origin of the left subclavian artery
d complications include spinal cord ischaemia
2 Which of the following is not a relative e aneurysmal disease of the descending thoracic
contraindication to percutaneous balloon aorta is unsuitable for TEVAR
Section 14
Urology
59 Benign urological conditions
Anthony J. Costello1, Daniel M. Costello2 and
Fairleigh Reeves1
1
2
St. Vincent’s Hospital, Melbourne, Victoria, Australia
Prostate
Anatomy of the urinary tract
The prostate is a fibromuscular gland (plum‐sized in
Kidneys the male after 50 years, walnut‐sized in the postpu
bertal male) that lies beneath the bladder and above
The kidneys lie in the retroperitoneum at the level
the urogenital diaphragm. The prostatic urethra
of T12 to L3 with the right slightly lower than left
traverses the prostate and receives the prostatic and
due to the bulk of the liver. The renal hilum faces
ejaculatory ducts, the latter being formed by the
medially and contains the renal vein, renal artery
seminal vesicles and vas deferens. The prostate ana
and ureter, in that order from anterior to posterior.
tomically is described by surfaces, lobes and zones.
Blood supply is from the aorta via single renal
Its base abuts the bladder neck, and apex opens into
arteries, although up to 30% of people have acces
the membranous urethra which is surrounded by
sory arteries. The renal vein, single on both sides,
the horseshoe‐shaped striated muscle of the external
drains to the inferior vena cava. The left renal vein
urethral sphincter. Its inferolateral surfaces are cra
crosses anterior to the aorta.
dled by levator ani and its posterior surface lies in
front of the rectum and is palpable on digital rectal
Ureters
examination. The prostate has left and right lobes
The ureters are approximately 25 cm long and and a median lobe at the bladder neck. Zonal anat
travel behind the peritoneum into the pelvis omy comprises a peripheral zone, where prostate
before swinging forward and medially at the level cancer usually begins, a transition zone (the site of
of the ischial spine to enter the bladder. The benign prostatic hyperplasia, which can obstruct
ureter narrows at the pelviureteric junction, at its urinary outflow), and a ‘central zone’ surrounding
crossing of the pelvic brim and at its oblique the urethra. There is also an anterior fibromuscular
entrance into the bladder wall (vesicoureteric zone that can be difficult to target with traditional
junction). The ureteric blood supply is derived transrectal ultrasound biopsy technique. Blood sup
from multiple vessels as it descends from abdo ply is predominantly from the inferior vesical artery
men to pelvis. with variable additional supply. Venous drainage is
through the vesico‐prostatic plexus to the internal
Bladder iliac veins. Lymph drainage is to internal and exter
nal iliac, obturator, presacral and para‐aortic nodes.
The bladder lies within the pelvis, with a
distended volume of 400–500 mL. The ureteric
orifices and bladder neck form the triangular
Stones
area known as the trigone at the bladder base.
Bladder arterial supply derives from branches of
Aetiology
the internal iliac artery with named superior and
inferior vesical arteries. Venous drainage is by the Calcium‐based stones account for the vast majority
internal iliac veins. Lymphatics run with the of all renal calculi (80–85%). These are usually due
blood vessels. to elevated urinary calcium, uric acid or oxalate or
565
566 Urology
decreased urinary citrate (an inhibitor of stone for but this is not diagnostic as it may be absent and
mation). Conditions which lead to hypercalcaemia can also be seen in other conditions.
such as hyperparathyroidism may be causative. If someone presents with renal colic, coexisting
However, in many patients an underlying metabolic urinary infection must also be excluded as the pres
defect cannot be identified. ence of an infected obstructed kidney is a surgical
Infection stones (struvite stones) account for emergency and mandates urgent drainage of the
1–5% of all stones. These stones can grow rapidly infected system.
and commonly present as a staghorn calculus.
They contain magnesium, ammonium and phos
Investigation
phate. Urea‐splitting organisms (such as Proteus,
Pseudomonas and Klebsiella) produce urease, The majority (90%) of all renal calculi are radio
which catalyses the conversion of urea into ammo paque and can therefore be visualised on plain
nia and carbon dioxide, resulting in alkalinisation X‐ray (Figure 59.1). For initial diagnosis, however,
of the urine and providing an environment condu CT of the kidneys, ureters and bladder (non‐contrast;
cive to this type of stone formation. Figure 59.1b) is the imaging modality of choice as
Less than 5% of all stones are uric acid based. not only will it identify calculi, but also provides
Risk factors for uric acid stones include diabetes, helpful information with regard to their anatomical
gout, myeloproliferative disease, rapid weight location as well as any associated hydronephrosis
loss, chemotherapy treatment, haemolytic anae indicating obstruction. CT intravenous pyelogra
mia and chronic diarrhoea. These stones are phy (contrast study including delayed phase) can be
characteristically radiolucent on X‐ray and can used to delineate the urinary system to differentiate
be dissolved with urinary alkalinisation to a pH phleboliths or other external calcification from
above 6.5. ureteric calculi. If CT is contraindicated (preg
Cysteine stones are uncommon (only 1–2% of all nancy), ultrasound may reveal hydronephrosis and
stones). They occur due to a genetic metabolic can sometimes demonstrate renal calculi, although
defect leading to increased urinary cysteine. These ultrasound has a low sensitivity for detecting ureteric
patients begin forming stones at a young age and calculi.
have a high recurrence rate, and therefore need Patients with renal calculi should have initial met
close observation and medical management for the abolic screening with serum urea, creatinine and
prevention of stones. electrolytes including calcium, magnesium, phos
Aetiology of renal calculi is often multifactorial. phate and uric acid. Urine should also be sent for
Dehydration certainly increases the risk of uro microscopy and culture and pH evaluation.
lithiasis, with a higher incidence of stones being More formal metabolic testing is indicated in
seen in hot dry climates. Individual patients may patients with recurrent calculi or other risk fac
also have underlying structural (any condition tors, and a 24‐hour urine collection (particularly
that leads to urine stasis) or metabolic (as high for recurrent stone formers) should be evaluated
lighted above) disorders that increase their risk of for pH, volume, calcium, oxalate, citrate and uric
stone formation. acid; this may reveal an underlying metabolic
abnormality that can be targeted to prevent future
episodes.
Non‐obstructing intrarenal calculi rarely cause any
Management
symptoms and are often detected incidentally on
imaging done for other reasons. In contrast, renal Many ureteric calculi can be managed conserva
colic, perhaps more accurately considered ureteric tively. The smaller the stone and the more distal,
colic, results in severe pain that has a sudden onset the more likely it will pass spontaneously.
and a typical ‘loin to groin’ distribution. An acute Approximately 70% of stones less than 5 mm in
abdomen must be excluded. Those with renal colic size will pass. Acute renal colic pain is best man
characteristically shift in bed constantly struggling aged by non‐steroidal anti‐inflammatory drugs
to get comfortable, in stark contrast to the patient rather than opioids. Medical expulsion therapy
with peritonitis who will be lying very still. Clinical with alpha‐blockers such as tamsulosin is often
examination in renal colic tends to be rather unre prescribed to improve rate of spontaneous stone
markable. Patients may have renal angle tenderness passage, although the evidence regarding efficacy is
but have a soft abdomen with no signs of perito unclear. In patients who elect for conservative
nism. A urinalysis often demonstrates haematuria, management, follow‐up imaging to ensure stone
59: Benign urological conditions 567
(a) (b)
Fig. 59.1 X‐ray of kidneys, ureters and bladder (a) and non‐contrast abdominal CT (b) showing bilateral staghorn
calculi.
passage is important as symptoms may resolve Large intrarenal calcluli (including staghorns) are
despite persistence of an obstructing calculus due best managed with percutaneous nephrolithotomy.
to autoregulation of renal blood flow. Patients Smaller ureteric or renal calculi may be managed
who fail conservative management after 4–6 weeks with ureteroscopy/pyeloscopy and stone frag
warrant surgical intervention to prevent renal mentation (usually with laser) or extraction, or
impairment. Indications for intervention include extracorporeal shockwave lithotripsy (ESWL). As
infection, obstruction in a solitary kidney, bilateral highlighted earlier, some stones may be amenable
obstruction and uncontrolled pain. to dissolution therapy.
In the setting of an infected obstructed kidney, All stone formers should be given general dietary
resuscitation, antibiotics and urgent drainage of advice to increase oral fluid intake, decrease sodium
the collecting system should be undertaken. and meat intake, and have a moderate calcium
Decompression can be achieved either by cysto intake (as risk of stone formation can increase with
scopic insertion of a ureteric stent or radiological calcium intake that is either too low or too high).
insertion of a nephrostomy tube. Once the sepsis If a metabolic defect is isolated, treatment should
has been adequately treated, definitive stone treat be targeted at correction of this.
ment is undertaken on an elective basis.
Non‐obstructing intrarenal stones do not always
Haematuria
require treatment depending on size and associated
symptoms. The risk of a symptomatic episode for
small non‐obstructing renal calculi is 10–25% per
year. However, all staghorn calculi should be treated Haematuria may originate anywhere along the
as they may lead to progressive renal damage and urinary tract. Differential diagnoses of haematu
infection if left. Indications for treating smaller ria include benign (trauma, infection, calculi,
intrarenal stones include infection, symptoms (pain/ iatrogenic, intrinsic renal disease, benign prostatic
haematuria), patient preference, stones larger than hypertrophy, inflammation, stricture) and malig
5 mm, high‐risk stone formers and social circum nant causes.
stances that would make seeking future medical Haematuria may be macroscopic (visible) or
attention difficult should an emergency arise. microscopic (evident on testing but not visible). The
Definitive stone treatment depends on the size, distinction is important as the risk of malignancy
location and composition (if known) of the stone. is significantly higher if the haematuria is visible
568 Urology
(approximately 20% in visible haematuria com may also have poor bladder emptying. In the long
pared to 5% for microscopic haematuria). Associated term, the bladder may become overworked, mani
symptoms and timing of macroscopic haematuria festing either with urgency and frequency from det
can assist in determining the source of haematuria. rusor overactivity, or with inadequate contractions
For example, initial haematuria is suggestive of leading to retention or overflow incontinence.
anterior urethral pathology compared with terminal
haematuria from the posterior urethra, whereas
Investigation
blood throughout the urinary stream suggests the
pathology is coming from the bladder or higher. When assessing patients with lower urinary tract
symptoms it is important to establish if their
Investigation symptoms are prostatic in origin or if there may
be other underlying pathology or contributing
Radiological investigation for haematuria is best
factors. A thorough history should be taken and
done using CT intravenous pyelography. This has
examination, including of the prostate per rectum,
the best sensitivity and specificity for identifying
and urinalysis performed in all. A bladder diary is a
upper tract causes for haematuria, but generally
valuable tool to gain insights into patients voiding
radiological imaging provides inadequate evaluation
patterns and likely aetiology.
of the bladder. Therefore, a cystoscopy is also required
A urinary tract ultrasound is not essential for
to complete investigation of the lower urinary tract.
investigation of all cases of lower urinary tract
Urine cytology may also be performed.
symptoms but can be helpful in triaging patients, by
identifying complications of BPH (e.g. presence of
Management
hydronephrosis or bladder calculi). Also, although
Management of haematuria should be directed at prostate size does not correlate with patient symp
underlying pathology. Acutely, any coagulopathy toms, this information can be useful in guiding
should be corrected, and anticoagulants should be appropriate BPH treatment selection.
withheld. If the patient has a stable haemoglobin A poor voiding flow rate supports a diagnosis of
and is voiding well, haematuria may be investigated BOO. However, in complex cases where it is unclear
as an outpatient. If there is evidence of urinary if poor flow is due to obstruction or detrusor fail
retention due to clot, then a urinary catheter is ure, formal urodynamic testing will confirm high
required for bladder washout. In some cases, if this detrusor pressure in the setting of BOO.
fails to resolve the haematuria, a patient may need For men with a life expectancy of 10 years of
emergency endoscopic evaluation to evacuate more, testing for prostate‐specific antigen (PSA)
remaining clots in the bladder and coagulate active should be considered because a diagnosis of pros
bleeding or resect tumour if present. tate cancer may change treatment choices.
Management
Lower urinary tract symptoms The decision to treat BPH largely comes down to
the degree of inconvenience the patient experiences.
Benign prostatic hyperplasia If a man is not bothered by his lower urinary tract
symptoms, it is reasonable to defer treatment in
Presentation
most cases as not all patients with BPH will have
Benign prostatic hyperplasia (BPH) is commonly progression of their symptoms. For most men with
seen in older men, affecting more than 80% of men BPH, medical management will be first line. Alpha‐
in their eighties. As men age, there is a normal blockers and 5α‐reductase inhibitors are the main
increase in the amount of prostatic stroma and stay of pharmacological management, either alone
smooth muscle tone, which may ultimately result in or in combination.
bladder outlet obstruction (BOO). In contrast to Alpha‐blockers act by relaxing the smooth muscle
prostate cancer, which tends to occur in the periph of the bladder neck and prostate, with symptom
eral zone of the prostate (and therefore rarely pre improvement noted within a few days of initiation
sents with local symptoms), BPH occurs in the of treatment. They are generally well tolerated
periurethral transition zone and therefore readily with relatively few side effects (retrograde ejacula
affects voiding. BPH can result in a range of symp tion, dizziness and postural hypotension). Hypo
toms including weak and/or intermittent stream, tension is now seen less frequently, as selective
hesitancy, terminal dribbling and nocturia. Patients alpha‐blockers (such as tamsulosin) target only the
α1A receptor subtype (localised to the bladder, enucleate the adenomatous tissue, leaving behind
prostate, vas deferens and seminal vesicles), sparing the prostatic capsule. The threshold to elect for open
the α1B receptors (located in blood vessels) which surgery will vary from surgeon to surgeon, although
caused troublesome hypotension with previous a prostate volume of in excess of 100–150 cm3
generation non‐selective drugs. would be considered too large for TURP by many.
The 5α‐reductase inhibitors (e.g. finasteride or As technology and surgical expertise advance, lasers
dutasteride) block the conversion of testosterone to are being used to tackle glands that were previously
dihydrotestosterone, which results in reduction of considered too large for endoscopic intervention.
prostate volume over time. This ultimately leads to Lasers can be used to either vaporise BPH tissue
improvement of urinary flow as well as reduction in (GreenLight photoselective vaporisation of the
risk of urinary retention and need for surgery. prostate, usually utilised in small to moderate‐sized
However, due to the mechanism of action noticeable glands) or enucleate the prostate (holmium laser
symptom improvement is generally only achieved enucleation of the prostate, which achieves a similar
after 6–9 months of treatment. Logically, consider outcome to open prostatectomy in large glands with
ing their effect relates to reduction of prostate vol reduced blood loss). One of the drawbacks of laser
ume, these drugs tend to work best in larger glands therapies is a higher rate of irritative voiding symp
(>40 mL). When prescribing 5α‐reductase inhibitors, toms postoperatively.
patients need to be counselled about the possible
side effects, which include erectile dysfunction, Urethral stricture
decreased libido, decreased ejaculate volume and
A stricture is an abnormal narrowing, and in the
gynaecomastia as these can cause significant dis
urethra this obstructs the usual passage of urine,
tress. It is also import to note that 5α‐reductase
leading to a weak flow. Some patients may also
treatment is associated with a decrease un PSA of
describe spraying or a double urinary stream as
approximately 50% after treatment for 9–12
well as frequency, dysuria or haematuria.
months. This must be kept in mind when considering
Acquired urethral strictures are common in men
a patient’s PSA results. Because of their difference in
and are usually due to previous infection (histori
mechanism of action and onset of symptom relief,
cally most commonly gonococcal urethritis) or
alpha‐blockers and 5α‐reductase inhibitors can be
trauma, such as catheterisation, surgical instrumen
effectively combined if required.
tation or external trauma such as a straddle injury
An absolute indication for surgical relief of
or pelvic fracture. A retrograde urethrogram
obstruction is the presence of hydronephrosis and
(Figure 59.2) is important in evaluating these
renal impairment due to high‐pressure retention
(obstructive uropathy). Other indications for surgical
intervention include voiding symptoms refractory to
medical therapy, recurrent urinary retention, infec
tions, gross haematuria or bladder calculi.
Transurethral resection of the prostate (TURP) is
considered the gold standard for surgical manage
ment of BPH. It involves endoscopic resection of
the prostate using a cutting diathermy loop to shave
away chips of prostate to leave a wide‐open prostatic
fossa. Potential complications include bleeding,
infection, retrograde ejaculation, stricture, and tran
surethral resection syndrome (collection of symp
toms/signs including hyponatraemia, hypervolaemia,
hypertension, nausea, vomiting, visual disturbance
and altered conscious state due to excess absorption
of hypotonic irrigation fluid).
Although TURP still remains a mainstay in many
urology practices, other surgical options also exist.
In small prostates where there is simply a tight blad
der neck, the bladder neck may be incised endoscop
ically without formally resecting any tissue. Very
large prostates may be more safely and effectively Fig. 59.2 Retrograde urethrogram showing urethral
treated with an open simple prostatectomy to stricture.
570 Urology
patients as it will demonstrate the extent and location Upper tract infection
of any stricture and can help guide management.
Upper tract infection most often occurs in the
Urethral dilatation or urethrotomy (endoscopic
setting of ascending Gram‐negative infection but
incision of stricture) will usually relieve any symp
may also arise from haematogenous spread (often
toms, but in many cases the stricture will recur.
Gram positive). A spectrum of disease can be seen:
Urethroplasty involves formal repair of the stric
progression of pyelonephritis can lead to renal or
ture and has a higher chance of long‐term success.
perinephric abscess. If a patient with presumed
For short strictures, excision of the stricture with
pyelonephritis fails to respond to appropriate
end‐to‐end anastomosis may be used, but longer
antibiotics, an abscess should be excluded. Upper
strictures require grafting of the affected area
tract infection can also occur in the setting of
(usually with buccal mucosa). Alternatively,
stone disease (see section Stones).
patients can keep the urethral lumen patent with
intermittent self‐catheterisation.
Prostatitis
Nocturia The prostate can be a source of infection and
Nocturia is defined as waking once or more at night inflammation. Four different categories of prostatitis
to void. Although it is commonly related to BPH in are recognised: (i) acute bacterial prostatitis, (ii)
men, there are many other causes that must be con chronic bacterial prostatitis, (iii) chronic pelvic pain
sidered. These causes can be grouped into three and (iv) asymptomatic inflammatory prostatitis.
broad categories: (i) polyuria (voided volume >2800 Acute bacterial prostatitis is most commonly
mL per 24 hours); (ii) nocturnal polyuria (amount due to Escherichia coli infection. Patients present
voided overnight is more than one‐third the daily with systemic signs of infection (such as fever)
total volume, which may be due to behavioural along with pain and lower urinary tract symptoms.
issues or underlying medical disease); and (iii) bladder A total of 4–6 weeks of antibiotics are required.
capacity problems (including BOO, overactive Failure to respond to antibiotics should prompt
bladder, neurogenic bladder). Management needs to pelvic CT to exclude a prostatic abscess. In the set
be directed at the underlying cause. ting of urinary retention, a catheter (possibly a
suprapubic catheter) is required to allow bladder
drainage.
Urinary tract infections Chronic bacterial prostatitis describes lower‐
grade recurrent symptomatic infections, which tend
Urinary tract infection (UTI) is a common condi to affect older men. This may require prolonged
tion that a variety of clinicians will manage in their antibiotic therapy, and after initial treatment may
practice. The urologist’s role is to manage compli even need low‐dose suppressive therapy to prevent
cated cases and recurrent infection. UTIs most com recurrent infection. In these men it is also sensible
monly present with symptoms of infection of the to consider TURP to remove infected tissue and
bladder (cystitis), but may also involve other parts prevent recurrence.
of the urinary tract including epididymis, testis (see Chronic pelvic pain is a very important entity
section Epididymitis) and prostate (see section that is gaining increasing recognition. It is a com
Prostatitis) in men, and kidney in both sexes. plex and debilitating condition that is associated
Often empirical treatment will be commenced with pain and urinary, bowel, psychological and
based on a clinical diagnosis made in the presence sexual symptoms. Treatment requires a multidisci
of symptoms of UTI and pyuria, but definitive diag plinary approach, with the team often comprising a
nosis requires urine culture. Specimen for culture urologist, specialised pelvic floor physiotherapist,
should be a clean catch and midstream. In an era of psychologist and pain specialist.
increasing antibiotic resistance, culture results can
be valuable in directing therapy. Asymptomatic bacteriuria
Asymptomatic bacteriuria is commonly seen in
Recurrent UTI
clinical practice. Predisposing conditions include
Recurrent infection may be due to incomplete treat catheter use (permanent or intermittent), bowel
ment of a UTI (unresolved) or a truly recurrent UTI incorporated into the urinary system (e.g. ileal
where there is an intervening negative culture and conduit, bladder augmentation), diabetes and
re‐infection occurs either as a result of bacterial persis institutionalised elderly patients. Treatment of
tence within the urinary tract or from new infection. asymptomatic bacteriuria can lead to emergence of
resistant bacteria, so is not recommended in most continued from the skin of the anterior abdominal
situations. An exception is in pregnancy. Pregnant wall, and folds back on itself at its distal end over
women should be screened and treated, as asymp the glans, forming the foreskin (prepuce). Arterial
tomatic bacteriuria confers at least a 20‐ to 30‐fold supply is from branches of the internal pudendal
risk of progression to pyelonephritis in pregnancy, artery. Venous drainage is through a complex of
which is associated with preterm labour and low veins, culminating in superficial dorsal and deep
birthweight. dorsal veins, to the vesico‐prostatic plexus. The
deep dorsal vein carries the majority of the penile
venous return. Control of this vein by ligation is an
essential step in radical (cancer) prostatectomy. The
Penis
lymph drainage of the penile skin, the corporal
tissue and glans penis is to the superficial and deep
Anatomy (Figure 59.3)
inguinal nodes. The penis is richly supplied by
The penis facilitates urination and the process of pudendal nerves via the dorsal nerves, which follow
erection and ejaculation for sexual intercourse. the course of the dorsal arteries, and are especially
It has a root, body and glans and comprises three prevalent in the sensitive glans. The cavernous
cylinders of erectile tissue, the two corpora cavern nerves ramify in the erectile tissue, providing sym
osa dorsally and the corpus spongiosum ventrally. pathetic and parasympathetic supply to the erectile
The penile urethra travels within the corpus spon tissue. Neural control of erections is parasympa
giosum, which expands distally to form the glans thetic causing vasodilation, while sympathetic and
penis. The corpora are filled with sinusoidal tissue somatic nerves stimulate contraction and ejacula
that becomes engorged with blood during erection. tion. The neurovascular bundle runs alongside the
The penis is invested with penile skin which is prostate in a groove above the rectum. It contains
Superficial
v. & a.
Deep dorsal
a. & v.
Dorsal n.
Circumflex
vein Superficial
penile n.
Corpus
cavernosum Skin
Superficial fascia
Buck’s
fascia
Sinusoids
Tunica albuginea
Corporal
junction
Corpus spongiosum
Urethra
Fig.59.3 Anatomy of the penis.

572 Urology
sympathetic nerves from the hypogastric plexus cases are due to unregulated arterial blood flow
(T12–L1) and parasympathetics (S2–S4). and are often due to trauma. The diagnosis can be
confirmed with cavernosal blood gas and treatment
Penile conditions is not an emergency as the penile tissue continues to
receive oxygenated blood.
Phimosis
Phimosis describes a tight foreskin that cannot be
retracted fully behind the glans. This can lead to Peyronie’s disease
overgrowth of smegma bacillus under the foreskin
Abnormal penile curvature is commonly due to
due to inability to cleanse the area and may be asso
Peyronie’s disease, in which plaques of fibrotic
ciated with voiding dysfunction with urine balloon
tissue develop in the tunica albuginea of the cor
ing behind the tight foreskin.
pora cavernosa that limits expansion, resulting in
Phimosis is physiological in the paediatric popu
curvature in the opposite direction during erec
lation, but beyond puberty the foreskin is retrac
tion. The cause is unknown but may relate to
tile in almost all men. In adults, phimosis may be
trauma. Peyronie’s disease is linked to Dupuytren’s
due to a pathological scarring process called lichen
contracture of the hands and Ledderhose disease
sclerosis (previously known as balanitis xerotica
of the feet.
obliterans).
Peyronie’s disease has an initial acute phase
Circumcision effectively treats phimosis.
which is often associated with pain. This usually
settles after 6–18 months as the condition stabilises
and the chronic phase begins. Once stable, surgical
Paraphimosis
correction can be undertaken if the curvature is
Paraphimosis describes an inability to replace the interfering with intercourse.
retracted foreskin over the glans. It is often associ
ated with significant oedema and pain and may
result in tissue necrosis if not corrected. One of the Scrotum and testes (see also Chapter 79)
common causes in hospital is failure to replace the
foreskin after inserting a urinary catheter. Anatomy
Compression and manual reduction is successful
Scrotum
in most cases. If this fails then a dorsal slit to release
the constricting band is needed. Many patients The scrotum is a bag‐like structure which hangs
will require an elective circumcision to prevent below the penis and contains the male reproductive
recurrence. units, the testes, and associated structures. The
scrotum is divided into spaces by a fibromuscular
septum in the form of the median raphe and is cov
Priapism ered by hair‐bearing skin, thrown up into multiple
rugae. Under the skin lies the dartos muscle layer.
Priapism is defined as a persistent erection (lasting
Arterial supply is from the external pudendal arter
greater than 4 hours) unrelated to, or lasting
ies anteriorly and the perineal arteries posteriorly.
beyond, sexual stimulation. There are two distinct
The venous drainage of the scrotum is via external
types of priapism.
pudendal veins to the great saphenous vein. Scrotal
The most common is ischaemic priapism, also
skin receives multiple sources of innervation,
known as low flow or venous occlusive. This is a
including the ilioinguinal nerve anteriorly and
urological emergency as the penis is engorged with
branches of the pudendal nerve posteriorly.
deoxygenated blood, which can lead to penile
necrosis and long‐term erectile dysfunction if not
treated. Emergency drainage of the blood from the
Testes
corpora cavernosa is required. Risk factors for
ischaemic priapism include injectable medications The adult testes are paired ovoid‐shaped reproduc
for the treatment of erectile dysfunction and sickle tive glands of approximately 30 mL in volume.
cell disease or other hypercoagulable states as well They produce sperm and the hormone testosterone.
as certain medications. The testes descend in utero just before birth from
The less common, non‐ischaemic priapism (also an intra‐abdominal position. They take coverings
known as arterial, high flow or non‐occlusive) from the abdominal wall layers as they pass
accounts for less than 5% of all priapism. These through the inguinal canal. In some cases, they fail
to descend before birth. The undescended (cryp felt as a more generalised abdominal pain due to
torchid) testis is more prone to malignancy. The the sensory fibre mediation by T10 dorsal root
external oblique muscle continues as the external ganglions.
spermatic fascia, and the internal oblique muscle
continues as the cremasteric muscle. The internal Scrotal pain and masses
spermatic fascia is a continuation of the transversa
Testicular torsion
lis fascia and the tunica vaginalis is a continuation
of the peritoneal layer. These layers constitute the Torsion is a surgical emergency. It involves rotation
spermatic cord, which also contains the vas deferens, of the testis and spermatic cord that compromises
testicular artery and vein, nerves and lymphatics the blood supply to the testis, leading to ischaemia
and adipose tissue. The testes themselves are sur and ultimately necrosis if not corrected urgently.
rounded by tunica vaginalis, which has two layers, It tends to occur in males 12–18 years of age or
a visceral and a parietal layer. This is a potential newborns but may occur at any age. Risk factors
space that can normally contain 2–3 mL of fluid. for torsion include undescended testis and ‘bell
This space can be the origin of a fluid sac called a clapper’ deformity where the tunica vaginalis
hydrocele. The tiny appendix testis is attached to inserts high on the spermatic cord, allowing the
the superior surface of the tunica vaginalis. Deep to testis to rotate freely.
the tunica vaginalis lies the extremely tough tunica Patients present with sudden‐onset, severe,
albuginea, the dense fibrous capsule of the testes. unilateral testicular pain and swelling. On exami
The seminiferous tubules leading from the lobules nation the testis is extremely tender and often
of the testes coalesce and enter the rete testis, which high‐riding due to cremasteric spasm.
passes into the epididymis. This combines to Clinical suspicion of torsion mandates urgent
become a single vas deferens, travelling upward in surgical exploration. Although Doppler ultra
the spermatic cord. sonography may show lack of testicular blood
The testis draws its own blood supply with it flow, theatre should not be delayed for imaging as
from the abdomen, and thus the testicular artery the time this takes may result in death of the
which travels in the spermatic cord originates from testicle. In addition, there is a risk of a false‐nega
the aorta. Further arterial supply to the testis comes tive result. The best chance for testicular survival
from the artery to the vas, and a large area of anas is if the torsion is corrected within 6 hours of
tomosis occurs at the epididymis between these symptom onset. After the testis has been untwisted,
arteries and the cremasteric artery, allowing for a both testes are fixed to the scrotum to prevent
rich supply to the testis. recurrence.
The testis is drained by many veins that anasto Torsion of testicular appendices is an important
mose extensively forming the pampiniform plexus. differential diagnosis in acute scrotal pain.
These veins join forming two to three branches in
the inguinal canal and ultimately a single gonadal Hydrocele
(testicular) vein, which drains into the inferior vena
A hydrocele is a collection of fluid within the
cava on the right and the renal vein on the left
tunica vaginalis. It often obscures palpation of the
(related to varicocele formation).
underlying testis and is readily transilluminable.
The delineation of scrotal lymph drainage from
Although it is usually painless, it can become
that of the testes is of vital importance in the surgical
quite large. If bothersome, it can be treated.
treatment of testis cancer. The skin of the scrotum is
While aspiration may provide relief, fluid fre
drained by the superficial inguinal lymph nodes of
quently reaccumulates. Therefore, surgical hydro
the ipsilateral side. The testis drains via the sper
celectomy is preferable.
matic cord to the para‐aortic nodes on the same
Hydroceles may represent primary pathology or
side. This implies that scrotal integrity should not
occur in response to another process (such as tumour,
be breached when performing an orchidectomy for
trauma or infection). Ultrasound (Figure 59.4) is
testis cancer, as this will ensure that two areas of
essential to exclude underlying pathology prior to
lymphatic drainage are now involved.
treatment.
The testes are supplied by sympathetic nerves
from the renal and aortic plexuses, as well as by
Spermatocele/epididymal cyst
contributions from the pelvic plexuses accompany
ing the vas deferens. The testes have a rich sensory These fluid collections usually occur in relation to
innervation, and thus even minor trauma can be the head of the epididymis. They often present as a
followed by severe pain in the testes, which is often painless palpable lump or are noted incidentally on
574 Urology
Fig. 59.4 Testicular ultrasound showing hydrocele.
imaging for another reason. Many patients are culture. Scrotal ultrasound typically demonstrates
asymptomatic and generally require no treatment. an enlarged epididymis with increased blood flow.
If they are large and uncomfortable, they may be In men younger than 35 years old, epididymitis is
excised surgically. usually due to a sexually transmitted infection, whereas
in older men or young children it is most often due to a
Varicocele urinary pathogen (such as E. coli). Treatment involves
bed rest, scrotal support, analgesia and empirical anti
A varicocele is a group of dilated veins of the pam
biotics directed at the most likely causative organism
piniform plexus. They occur more commonly on
until culture results are available to direct therapy.
the left and usually develop slowly over time.
Although often asymptomatic, a varicocele may
cause a dull ache that increases with standing and Further reading
worsens over the course of the day. Discomfort is
typically relieved with lying down. In some, but American Urological Association Guidelines, http://www.
not all, cases it may be associated with impaired auanet.org/guidelines
fertility or atrophy of the affected testicle. European Association of Urology Non‐Oncology
Scrotal examination classically reveals a ‘bag of Guidelines, https://uroweb.org/individual‐guidelines/
worms’ that is more readily appreciated when examin non‐oncology‐guidelines/
Wieder JA. Pocket Guide to Urology, 5th edn. J. Wieder
ing the patient standing and with Valsalva manoeuvre.
Medical, 2014.
If symptomatic or associated with infertility, it
may be treated with surgical ligation or radiological
embolisation of the gonadal vein. MCQs
Epididymitis Select the single correct answer to each question. The
Epididymitis or epididymo‐orchitis can also present
with significant scrotal pain and enlargement. In con
trast to torsion, symptoms usually have a gradual 1 A 14‐year‐old boy presents to the emergency
onset. There may also be other associated lower department with 2 hours of left testicular pain.
urinary tract symptoms of infection such as dysuria Which of the following statements is incorrect?
or frequency. Urinalysis will often be suggestive of a history of undescended testis is associated with a
infection and urine should be sent for microscopy and higher risk of torsion
b pain may be due to appendix testis torsion d if her urinalysis shows no haematuria, it is
c an ultrasound should be done to check testicular unlikely that she has a stone
blood flow as the pain may be due to testicular e if there are signs of infection, the stone can be
torsion managed conservatively if the patient is given
d the best chance for testicular survival is if torsion antibiotics
is corrected within 6 hours of symptom onset
e the patient should be taken to theatre immedi- 4 A 75‐year‐old man describes poor urinary flow and
ately if there is a clinical suspicion of torsion nocturia. Which of the following statements about
his condition is correct?
2 Which of the following statements about haematu- a obstructive symptoms in this age group are most
ria is correct? often due to stricture
a blood throughout the urinary stream suggests b nocturnal polyuria may be the cause of his
that bleeding is coming from the urethra nocturia (defined as the production of more than
b if it resolves it does not need further investigation one‐quarter of 24‐hour urine output between
c the risk of malignancy is the same if haematuria midnight and 8 a.m.)
is detected on microscopy or is visible c even if he is not bothered by his symptoms he
(macroscopic) should have treatment
d if the CT intravenous pyelogram is normal, a d BPH occurs in the periurethral transition zone of
cystoscopy does not need to be performed the prostate
e it always needs investigation as it may be due to e a bladder diary is only necessary if the patient is
malignancy a poor historian
3 A 54‐year‐old woman presents to the emergency 5 Which of the following statements about UTIs is
department with acute flank pain. You suspect she incorrect?
has renal colic from a ureteric stone. What is the a urinary stasis is a risk factor for infection
correct response? b asymptomatic bacteriuria should always be
a X‐ray of the kidneys, ureters and bladder is the treated to avoid development of clinical infection
investigation of choice c definitive diagnosis requires urine culture
b patients with renal stones should be encouraged d presence of sepsis in the setting of an obstructing
to decrease calcium intake to prevent future ureteric calculus is a surgical emergency
stone episodes as most stones contain calcium e empirical antibiotics for epididymo‐orchitis in a
c non‐steroidal anti‐inflammatory drugs are more sexually active 30‐year‐old man should treat
effective than opioids for controlling renal colic sexually transmitted infections
pain
60 Genitourinary oncology
Homayoun Zargar and Anthony J. Costello
University of Melbourne and Department of Urology, Royal Melbourne Hospital, Melbourne,
Victoria, Australia
cystoprostatectomy for bladder cancer (40–60% of

Prostate cancer bladder specimens).
In cases of locally advanced disease, patients can
Prostate cancer (PC) is the most commonly diag-
present with difficulty urinating, urinary retention
nosed cancer and the second most common cause
or haematuria. Metastatic disease can present with
of cancer death in men in Australia. In Australia,
bony pain, pathological fractures or spinal cord
the lifetime prevalence of PC is one in six. Most
compression due to metastatic deposits in the
men with PC die of other causes and only 3% of men
thoracic/lumbar spine.
with PC will die of their disease.
Aetiology and pathology Investigations

The prevalence of PC increases with age and devel- Prostate‐specific antigen
opment of PC before age of 40 is rare. Men with a
Prostate‐specific antigen (PSA) is a serine protease
family history of PC in a first‐degree relative have a
produced by the prostate. It is a physiologically
higher risk of developing PC. This risk further
important enzyme for the process of semen lique-
increases if more than one first‐degree relative has
faction. Raised PSA levels are observed in 90% of
had PC. History of breast or ovarian cancer in a
men with PC, although elevated PSA levels are not
first‐degree relative also increases the lifetime risk
specific to PC. Any process affecting the prostate,
of developing PC in the same manner. Mutations in
including benign enlargement, prostatitis, urinary
the tumour suppressor genes BRCA1 and BRCA2,
tract infection and urological instrumentation, can
involved with DNA repair mechanisms, have been
cause a rise in PSA levels.
identified in men with a strong family history of
PSA as a screening tool for detection of PC has
PC. The lifetime prevalence of PC is higher in
become a controversial topic in recent years.
African‐American men.
Screening leads to earlier cancer detection and
Adenocarcinoma is the most common type of PC
improvement in survival in men with clinically sig-
and the majority cancers arise from the peripheral
nificant PC but at the same time can lead to over‐
zone of the prostate. PC is a heterogeneous disease
diagnosis, psychological stress and over‐treatment
and often multifocal on diagnosis. PC generally
of men with non‐significant PC.
progresses slowly but this also is influenced by the
Patient with minimum 10 years’ life expectancy
stage and grade of the cancer.
should be counselled about the risks, benefits and
limitations of PC screening prior to PSA testing.
PSA screening should accompany digital rectal
The majority of PC patients are asymptomatic on examination. PSA screening should start from the
diagnosis. PC can also be diagnosed incidentally in age of 40 and the screening interval should be
prostatic tissue resected in men undergoing tran- guided by the initial PSA level. If initial PSA is less
surethral resection of the prostate (TURP) for than 1 ng/mL, the next assessment can be made at
benign prostatic enlargement (10% of TURP proce- age 45. PSA screening should be performed annu-
dures) or in the prostate of patients treated with ally after the age of 50.
577
578 Urology
Prostate imaging Table 60.1 The 2010 TNM (tumour, node, metastasis)
Transrectal ultrasound imaging of the prostate staging of prostate cancer.
allows assessment of the size and shape of the T Primary tumour
prostate but cannot accurately identify PC. Tx Primary tumour cannot be assessed
Multiparametric magnetic resonance imaging T0 No evidence of primary tumour
(MRI) uses various sequences and can identify PC T1 Clinically tumour not palpable or visible
in 80–90% of the cases. This can aid in targeting by imaging
the abnormal areas during prostate biopsy. Prostate T1a Tumour incidental histological finding in
biopsy and histological assessment of the samples is 5% or less of tissue resected
T1b Tumour incidental histological finding in
the only method for the identification of PC.
more than 5% of tissue resected
Prostate biopsy can be performed via the transrec-
T1c Tumour identified by needle biopsy, e.g.
tal or transperineal route. due to elevated prostate‐specific antigen
(PSA) level
Staging T2 Tumour confined within the prostate
T2a Tumour involves half of one lobe or less
PC spreads locally to periprostatic tissues, via lym-
T2b Tumour involves more than half of one
phatics to pelvic and retroperitoneal lymph nodes lobe, but not both lobes
and via vascular spread to bones and viscera. TNM T2c Tumour involves both lobes
staging is outlined in Table 60.1. T3 Tumour extends through the prostatic
capsule
T3a Extracapsular extension (unilateral or
Grading bilateral) including microscopic bladder
The Gleason grading system is based on the archi- neck involvement
tectural pattern of the prostate glands under low‐ T3b Tumour invades seminal vesicle(s)
T4 Tumour is fixed or invades adjacent
magnification light microscopy. The two most
structures other than seminal vesicles:
abundant tumour patterns are graded from 1 to 5.
external sphincter, rectum, levator muscles,
The Gleason score is reported as the most common and/or pelvic walls
grade plus the second most common grade, fol-
N Regional lymph nodes
lowed by the sum (e.g. 3 + 4 = 7). Higher‐grade
Nx Regional lymph nodes cannot be assessed
tumours are associated with higher risks of recur- N0 No regional lymph node metastasis
rence, metastasis and death from PC. The newer N1 Regional lymph node metastasis
International Society of Urological Pathology
M Distant metastasis
(ISUP) grading system aims at simplifying PC Mx Distant metastasis cannot be assessed
grading and reporting. The relationship between M0 No distant metastasis
Gleason score and ISUP grading system is as M1 Distant metastasis
follows. M1a Non‐regional lymph node(s)
• ISUP Group 1, equivalent to Gleason score ≤6 M1b Bone(s)
(3 + 3 and below) M1c Other site(s)
• ISUP Group 2, equivalent to Gleason score
3 + 4 = 7
• ISUP Group 3, equivalent to Gleason score
4 + 3 = 7
• ISUP Group 4, equivalent to Gleason score 8
(4 + 4, 3 + 5 or 5 + 3)
• ISUP Group 5, equivalent to Gleason scores 9
and 10
Table 60.2 Risk groups for prostate cancer.
D’Amico
Risk groups
risk group Criteria
Based on pre‐biopsy PSA, clinical T stage (cT stage)
Low PSA <10 and Gleason score ≤6 and
and grading of the tumour, patients can be stratified
cT1 or cT2a
into low‐, intermediate‐ and high‐risk groups Intermediate PSA 10–20 or Gleason score 7 or
(D’Amico risk groups; Table 60.2). The risk groups cT1 or cT2b or cT2c
have prognostic implications and guide in tailoring High PSA >20 or Gleason score >7 or cT3
treatment for PC patients.
60: Genitourinary oncology 579
Treatment (this may vary depending on the grade of PC).

Urinary control is initially compromised after radi-
Treatment for patient with PC is influenced by
cal prostatectomy but over time this function recov-
many factors, including patient factors (age, comor-
ers for most men. Certain technical manoeuvres
bidities, personal preferences, presence of urinary
during surgery have been associated with earlier
symptoms), disease factors (stage and grade of PC)
continence recovery. Pelvic floor muscle exercises
as well as access to healthcare (e.g. proximity to a
implemented by a specialist pelvic physiotherapist
hospital or radiation centre). For patients with
have been shown to improve continence rate in
localised PC, treatment options include active sur-
men undergoing radical prostatectomy. The conti-
veillance, watchful waiting, surgery or radiation.
nence continues to improve for the first year post
surgery. The rate of persistent urinary incontinence
Active surveillance versus watchful waiting after surgery is around 7–15%.
Depending on the risk, surgery can be modified
Low‐risk PC typically progresses slowly and has a to include sparing of neurovascular bundles respon-
low potential for metastasis. Treatment of PC sible for male erectile function. With high‐risk dis-
regardless of modality utilised is associated with ease, where the risk of extraprostatic spread is high,
some degree of decline in quality of life with regard wide local excision of neurovascular bundles are
to urinary control and sexual function. The concept performed and this leads to erectile dysfunction.
of active surveillance is to closely monitor the men Both urinary incontinence and erectile dysfunc-
with low‐grade (and typically small‐volume) PC tion occurring after radical prostatectomy can
and as long as the disease remains stable (estab- be addressed by future surgeries with successful
lished by regular examination, PSA test, MRI and outcomes.
regular interval biopsies) definitive treatment can
be avoided. If during the course of surveillance the
disease progresses (changes in stage or grade), the Radiotherapy
patient still remains a good candidate for definitive
therapy. The other curative treatment option for PC is radi-
Watchful waiting follows a similar pattern but is otherapy. Radiation can be delivered via external
considered in patients with comorbidities who are beam radiotherapy (typically, daily treatment over
not candidates for definitive therapies. The patients period of 6 weeks) or in selected patients radioac-
are followed up, but only treated symptomatically. tive seeds can be planted within the prostate gland
If the patients develop systemic disease, then they (brachytherapy). A combination of the two
are offered hormonal therapy (not curative) in treatments can also be delivered. The rate of erec-
order to minimise the complications of PC. The tile dysfunction and incontinence after radiother-
majority of men on watchful waiting do not require apy is similar to surgery but these often occur
any treatment in their lifetime and die with but not later. Depending on PC risk, radiotherapy needs
due to their PC. to be accompanied by up to 2 years of androgen
deprivation therapy. Some of the side effects
of radiotherapy, such as bladder and bowel toxic-
Surgery (radical prostatectomy) ity (bowel/bladder frequency that can be accompa-
nied by recurrent bleeding) or urethral stricture,
Radical prostatectomy is the surgical removal of
are rare but are often difficult to treat and can
the entire prostate and seminal vesicles. Depending
be permanent.
on the risk of spread to the lymph nodes, it can be
accompanied by pelvic lymph node dissection. The
surgery can be performed via an open, laparo-
Ablative therapies
scopic or robotic‐assisted approach. If performed
by an expert surgeon there is no difference in the This approach should not be considered as a
outcomes of surgery performed by different mainstream treatment and remains experimental.
modalities. Robotic‐assisted surgery allows this Ablative energy (cryotherapy, high‐intensity focal
complex surgery to be performed in a minimally ultrasound, laser or irreversible electroporation)
invasive fashion, with reduction in pain, blood is applied to part or all of the prostate gland with
loss, transfusion rate, hospital stay and postopera- the aim of killing cancer cells without damaging
tive complications. the neurovascular bundles or urinary continence
Surgery provides over 90% 10‐year disease‐free mechanism. Whole‐gland treatment has a similar
survival in patients with organ‐confined disease side‐effect profile to radiation, and focal ablation
580 Urology
has a significant rate of disease recurrence as PC Aetiology and pathology

is often multifocal and ablating only part of the
Cigarette smoking is the most common cause for
prostate does not treat cancer elsewhere in the
bladder cancer. Occupational exposure to aniline
gland.
dyes and petroleum products has also been associ-
ated with an increased rate of bladder cancer,
Systemic therapy seen in those working in the textile, dye, leather
and petroleum industries. Other known risk factors
Androgen deprivation therapy (ADT) has long been
include iatrogenic exposure (radiation, cyclophos-
used to suppress PC in patients with locally
phamide, and phenacetin – no longer used)
advanced or metastatic disease. ADT does not
and chronic inflammatory conditions including
improve survival but minimises complications
Schistosoma haematobium infection (bladder SCC).
associated with metastatic disease such as bony
Bladder cancer is more common in men than
fractures or spinal cord compression. ADT achieves
women.
chemical castration and as PC cells rely on testos-
terone to grow, ADT suppresses their growth
initially. Both surgical (bilateral orchiectomy) and Clinical presentation
medical castration can achieve this goal. Medical
castration can be achieved by the means of luteinising The most common presentation is painless haema-
hormone‐releasing hormone analogues, gonadotropin‐ turia. Haematuria can be gross (visible) or micro-
releasing hormone antagonists, antiandrogens or in scopic. Haematuria is a serious symptom and
combination. should never be dismissed and always requires full
ADT causes andropause, which leads to hot investigation.
flushes, adverse lipid profile, diabetes, cardiovascu- Some patients can present with frequency and
lar disease, weight gain, loss of muscle mass, gynae- urgency or a history of recurrent bladder infections.
comastia, anaemia, osteoporosis, depression and Patients with UTUC can present with symptoms
decline in cognition. Men on ADT should be well similar to renal colic (clot colic) or with symptoms
counselled about these side effects. Close monitor- due to ureteric obstruction.
ing of cardiovascular risk factors and addressing
them, physical activity, weight‐bearing exercises,
Investigations
calcium and vitamin D supplements, and psycho-
logical counselling can counteract some of the In patients presenting with haematuria or those
adverse effects of ADT. suspected to have bladder cancer, after history and
Some men with PC will develop castrate‐resistant risk assessment urological evaluation of the bladder
prostate cancer after a period of ADT. These men with cystoscopy is essential. For the assessment of
can be treated with chemotherapy and/or novel the upper tracts, CT intravenous pyelography is the
antiandrogen agents such as abiraterone acetate or gold standard. It visualises the urothelial linings of
enzalutamide. Such agents are increasing used at the kidneys and ureters. It will not detect small
earlier stages of the systemic disease with or with- bladder lesions. Ultrasound can visualise the kid-
out ADT with very encouraging results. neys but cannot assess the ureters adequately. For
patients with contrast allergy or renal impairment,
magnetic resonance urography is an alternative.
Urine cytology has poor sensitivity for low‐grade
Urothelial cancer tumours but is often positive in patients with high‐
grade cancers and should be considered as part of
The epithelial lining of the urinary tract, from renal the work‐up. The 2010 TNM staging system for
collecting tubes to urinary meatus, is termed urothe- bladder cancer is shown in Table 60.3.
lium. Urothelial cancer (UC), previously known as
transitional cell cancer, can arise from urothelium Treatment
anywhere within the urinary tract. UC of the blad-
Treatment of UC is governed by the grade, stage
der is the most common followed by UC in the
and location of the tumour.
renal pelvis and the ureters, also termed upper tract
urothelial cancer (UTUC). UC is the most common
Upper tract urothelial cancer
form of bladder cancer. Other, less common types
of bladder cancer include squamous cell carcinoma The gold standard treatment for UTUC is nephro-
(SCC) and adenocarcinoma. ureterectomy, which involves removal of the entire
Table 60.3 The 2010 TNM (tumour, node, metastasis) tumour (low grade vs. high grade) is also assessed.
staging of bladder cancer. High‐grade tumours are more likely to recur or
progress (to higher stages). Instillation of chemo-
T Primary tumour therapeutic agents (mitomycin C as well as others)
Tx Primary tumour cannot be assessed
in the bladder after TURBT has been associated
T0 No evidence of primary tumour
with reduction in the rate of tumour recurrence.
Ta Non‐invasive papillary tumour
Tis Carcinoma in situ (CIS): always high grade
For those patients with high risk of disease recur-
T1 Tumour invades lamina propria rence or progression (CIS, T1 or high‐grade Ta
(subepithelial connective tissue) disease), intravesical instillation of bacillus

T2 Tumour invades muscularis propria Calmette–Guérin (BCG) can reduce the risk of
(bladder muscle) disease recurrence and progression. BCG treatment
T3 Tumour invades perivesical tissue is not without risks and can cause local symptoms
T3a Microscopically such as frequency and urgency and rarely can lead
T3b Macroscopically to systemic mycobacterial infection.
T4 Tumour invades prostate, seminal vesicles, When the disease is muscle invasive, TURBT is no
uterus, vagina or pelvic/abdominal wall
longer a curative option. The treatment of choice in
N Regional lymph nodes such instances is radical cystectomy. This is often
Nx Lymph node metastasis cannot be assessed preceded by a course of systemic chemotherapy
N0 No distant metastasis
(neoadjuvant chemotherapy) with cisplatin‐based
N1 Single regional lymph node metastasis
agents and this approach has shown to improve
N2 Multiple regional lymph node metastasis
N3 Lymph node metastasis to common iliac patient survival. Radical cystectomy includes
and beyond removal of prostate in men and removal of uterus
and upper vagina in women. After radical cystec-
M0 No distant metastasis tomy the urinary stream needs to be diverted. The
M1 Distant metastasis diversion can be incontinent (ileal conduit) or conti-
nent (catheterisable urinary reservoir, neobladder).
Bladder‐sparing therapy, employing a combina-
tion of TURBT and chemoradiotherapy in patients
kidney and ipsilateral ureter and a cuff of the blad- whom due to comorbidities cannot undergo sur-
der around the concerned ureter. This can be gery, is an alternative. The risk of disease recurrence
achieved via an open, laparoscopic or robotic after this approach remains high.
approach. In a select few cases when the tumour is Metastatic bladder cancer has a very poor prog-
small and low grade, ablation of the tumour with nosis. Palliative chemotherapy and recently immu-
laser can be attempted but such patients require notherapy can reduce the symptoms and modestly
intense follow‐up and are likely to require retreat- improve patient survival.
ment as UC is often a recurrent problem. Patients
with UTUC also require periodic cystoscopy for the
assessment of the bladder as this is a common site Renal cell carcinoma
of recurrence.
With the global increase in the use of cross‐sec-
tional imaging, the majority of renal masses are
Bladder cancer
identified incidentally. The term ‘small renal mass’
Nearly two‐thirds of bladder cancers on presenta- (SRM) applies to renal lesions of less than 4 cm.
tion are limited to the superficial layer of the blad- Around 20–30% of SRMs are benign but the
der, not involving the muscularis propria of the available imaging techniques cannot differentiate
bladder. These tumours are termed ‘non‐muscle between benign and malignant lesions. Renal
invasive bladder cancer’ and are generally resected biopsy is increasingly used to help further identify
by transurethral resection of bladder tumour these lesions. The biopsy can differentiate benign
(TURBT). During this procedure, an instrument from malignant tumours in the majority of cases
mounted on a cystoscope is passed via the urethral but is not always 100% accurate and is highly
meatus into the bladder and the bladder tumour is dependent on the quality of the biopsy specimen
resected or ablated using an energy source (electric- taken. For example, it can be difficult to differentiate
ity or laser). The resected specimen is removed and an oncocytoma (benign) from a chromophobe‐type
assessed for grade and stage. The staging of bladder renal cell carcinoma (malignant). The treatment options
cancer is outlined in Table 60.3. The grade of the for a SRM include surveillance, extirpative therapy
582 Urology
(partial or radical nephrectomy) or ablation (using Staging

various energy sources including cryotherapy, rad-
The local staging for RCCs is outlined in Table 60.4.
iofrequency ablation or microwave).
Chest imaging (X‐ray or CT) is mandatory at the
A renal mass can be solid or cystic. Cystic lesions
time of diagnosis. Further imaging such as bone
are classified according to the Bosniak classifica-
scan or CT of the head is recommended when there
tion (I–IV) that stratifies the lesions based on their
are symptoms suspicious for metastatic disease.
radiological appearance and risk of malignancy.
Solid lesions can be benign (angiomyolipoma,
Treatment
oncocytoma) or malignant (renal cell cancer, Wilms’
tumour or metastatic disease). Surveillance
SRMs can be treated in many ways. For a small
Aetiology and pathology lesion (<3 cm) even when malignant the tendency for
spread beyond the kidney remains low. The risk
Renal cell carcinoma (RCC) is the most common
of malignancy for an SRM is 70–80% and the risk of
type of primary renal cancer. The risk of RCC is
spread over a period of 3 years is around 1%. Given
higher in patients with a history of smoking, obe-
this, in a patient with coexisting comorbidities sur-
sity and hypertension. Patients with certain genetic
veillance of an SRM with or without biopsy offers a
predispositions and hereditary syndromes are at
safe strategy, as such patients often live the rest of
increased risk for developing RCC. These include
their lives without any need for further therapy.
von Hippel–Lindau syndrome (clear cell RCC),
Birt–Hogg–Dubé syndrome (clear cell, chromo-
phobe and oncocytoma) and tuberous sclerosis Ablation techniques
(RCC and angiomyolipoma). RCC is often clear cell
Ablation therapies using various energy sources
type but can also be papillary, chromophobe
delivered laparoscopically or percutaneously are
or unclassified variety. These subtypes are based
on histological assessment and have prognostic
implications.
Table 60.4 The 2010 TNM (tumour, node, metastasis)
staging of renal cancer.
T Primary tumour
The triad of abdominal pain, haematuria and flank Tx Primary tumour cannot be assessed
mass is the tell‐tale sign of late RCC presentation T0 No evidence of primary tumour
and is seldom seen these days. Increasingly RCCs are T1 Tumour 7 cm or less confined to the kidney
diagnosed incidentally (see description of SRM). In T1a Tumour 4 cm or less confined to the kidney
T1b Tumour 4–7 cm confined to the kidney
men, development of left‐sided varicocele due to
T2 Tumour >7 cm confined to the kidney
obstruction of the gonadal vein can be seen with
T2a Tumour >7 cm but ≤10 cm confined to the
RCCs. Around 20–30% of patients with RCC kidney
develop paraneoplastic syndromes due to circulating T2b Tumour >10 cm confined to the kidney
cytokines and hormones produced by the tumour T3 Tumour extends to major veins or perinephric
cells. Paraneoplastic syndromes include toxic effects fat but confined to Gerota’s fascia
such as fever, cachexia, anaemia, deranged liver func- T3a Tumour extends to renal vein or
tion test (Stauffer’s syndrome) and high erythrocyte perinephric fat
sedimentation rate; and endocrine effects such as T3b Tumour extends to the vena cava below the
polycythaemia (erythropoietin production), hyper- diaphragm
tension (renin production) and hypercalcaemia (par- T3c Tumour extends to the vena cava above the
diaphragm or the wall of the vena cava
athyroid hormone‐like substances).
T4 Tumour invades beyond Gerota’s fascia
(including extension into the ipsilateral
Investigations adrenal gland)
N Regional lymph nodes
An abdominal CT scan with and without contrast
Nx Lymph node metastasis cannot be assessed
is the investigation of choice for the assessment N0 No distant metastasis
of renal masses. The presence of post‐contrast N1 Regional lymph node metastasis
enhancement (surrogate for tumour vascularity) is
often seen with RCCs. The presence of fat within M0 No distant metastasis
the lesion points toward angiomyolipoma (benign M1 Distant metastasis
tumour).
minimally invasive and offer 80–90% success rate Clinical presentation

depending on tumour location and energy source
A palpable painless lump is the most common pres-
used. In cases of recurrences (10–15%), further
entation but up to 10% of patients present with
ablation can be attempted. These therapies have
pain. Metastatic disease can present with back pain
minimal impact on renal function and are ideal for
or abdominal pain in cases with extensive bulky
patients where surgery is not suitable.
retroperitoneal disease.
Surgery
Investigations
Surgery is the gold standard for the treatment of
Clinical examination should include careful inspec-
renal malignancies. For certain tumours, depending
tion of both testes including assessment of size.
on size, location, kidney function and presence of
Assessment of the lymph nodes, breasts (gynaeco-
the contralateral kidney, surgical removal of the
mastia is seen in some cases), abdomen (retroperi-
tumour with sparing of the rest of the kidney (par-
toneal mass) and neurological system is essential.
tial nephrectomy or nephron‐sparing surgery) is rec-
Scrotal ultrasound can identify and characterise
ommended. The remaining nephrons within the
testicular lesions. Tumour markers, such as alpha‐
operated kidney can continue to perform their func-
fetoprotein, human chorionic gonadotropin and
tion and the risk of renal impairment is mitigated.
lactate dehydrogenase, are part of staging. Once the
Partial nephrectomy can be done in an open fashion
diagnosis is confirmed, CT of chest and abdomen is
or laparoscopically. Robotic platforms allow this
required for complete staging.
complex surgery to be performed in a minimally
invasive fashion and with minimal complications.
Treatment
For larger tumours, radical nephrectomy is recom-
mended (open or laparoscopic). The prognosis of Radical orchiectomy removes the primary tumour
the patient is determined by the stage of the disease and provides local staging information. The surgery
as well as histological characteristic of the tumour. is performed via the inguinal approach (rather than
Larger tumours carry a worse prognosis. Up to 25% scrotal) in order to keep the lymphatic drainage of
of patients with kidney tumours have metastatic dis- the testes unaltered. Testes lymphatics drain into
ease or develop it within the first year of diagnosis. the retroperitoneum, but in patients with scrotal
After surgical removal of the kidney, in addition to surgery this drainage path can be altered and hence
oncological follow‐up renal function needs to be lymphatic spread can occur in an unpredictable
closely monitored. Such patients need to see their GPs fashion. Depending on the staging and characteris-
a few times per year and any modifiable factors con- tics of the tumour (size, lymphovascular invasion),
tributing to renal impairment (hypertension, diabe- surveillance or chemotherapy might be required.
tes, smoking) should to be identified and mitigated. The retroperitoneum is the most common site of
testicular metastasis. In cases where a retroperito-
neal mass after chemotherapy persists, retroperito-
neal lymph node dissection is performed to remove
Testicular cancer all the residual testicular tumours.
The majority of testicular tumours are germ cell

tumours (90–95%) with stromal tumours such as Penile cancer
Leydig cell and Sertoli cell tumours being the
minority. Germ cell tumours are divided into semi- Penile cancer is a rare cancer and SCC accounts for
noma or non‐seminoma. Non‐seminoma tumours more than 95% of the cases.
can have embryonal, yolk sac, choriocarcinoma or
teratoma elements. Aetiology and pathology
Human papillomavirus (HPV), smoking, poor
hygiene (particularly if uncircumcised) and chronic
Aetiology and pathology inflammation are associated with SCC of the penis.
Undescended testis or cryptorchidism is a risk fac-
tor for the development of testicular cancer. Other Clinical presentation
conditions, such as HIV infection, chromosomal An ulcerative painless penile lesion is a common
abnormalities, infertility and family and personal presentation. The lesion can become fungating and
history of testicular cancer, also increase the risk of can be associated with inguinal lymphadenopathy. If
testicular cancer. phimosis is present the lesion might not be visible.
584 Urology
Investigations b prostate cancer is always associated with

elevated PSA
Biopsy of the lesion, ideally excisional biopsy, can
c some patients with prostate cancer have a
confirm the diagnosis. MRI can provide further
normal serum PSA reading
details about the depth of the lesion. Inguinal lymph
d MRI detects more than 95% of prostate cancers
nodes are the most common sites of metastasis and
should be imaged and/or biopsied depending on the
2 Which one of the following findings leads to the
clinical situation. Chest imaging as well as cross‐
diagnosis of high‐risk prostate cancer?
sectional abdominal/pelvic imaging in patients with
a PSA >15
nodal disease are mandatory.
b Gleason score of 4 + 3 on biopsy
c palpable nodule on digital rectal examination
Treatment d ISUP grade 4 prostate cancer
Excision of the lesion with a surgical margin is the
goal of treatment. For low‐grade small tumours, 3 Which of the following statements about bladder
depending on the location, penile‐sparing surgery cancer is correct?
can be offered. For larger high‐grade lesions, partial a the majority of bladder cancers at diagnosis do
or total penectomy plus inguinal lymph node dis- not involve the muscle layer
section is recommended. b haematuria is the most common mode of
presentation of bladder cancer
c haematuria always requires investigation
Further reading d all of the above
European Association of Urology Guidelines, https:// 4 Which of the following is a risk factor for the
uroweb.org/guidelines/ development of bladder cancer?
McAninch JW, Lue TF (eds) Smith and Tanagho’s General a smoking
Urology, 18th edn. New York: McGraw‐Hill, 2013.
b occupational exposure
Wein AJ, Kavoussi LR, Partin AW, Peters CA (eds)
c radiation
Campbell‐Walsh Urology, 11th edn. Philadelphia:
Elsevier, 2016. d all of the above
Wieder JA. Pocket Guide to Urology, 5th edn, 2014.
Available at http://www.pocketguidetourology.com/ 5 Which one of the following is not a serum marker
for testicular cancer?
a β‐human chorionic gonadotropin
MCQs b alpha‐fetoprotein
c alkaline phosphatase
Select the single correct answer to each question. The d lactate dehydrogenase
1 Which of the following statements about prostate
cancer is correct?
a prostate cancer is always visible on transrectal
ultrasound imaging
Section 15
Cardiothoracic Surgery
61 Principles and practice
of cardiac surgery
James Tatoulis1 and Julian A. Smith2
1
2
Department of Surgery, Monash University and Department of Cardiothoracic Surgery, Monash
Health, Melbourne, Victoria, Australia
problems are time‐related, becoming noticeable

Introduction after 2 hours of CPB.
Hypothermia (30–34°C) is used to help protect
Cardiac surgery is a modern surgical specialty. The
vital organ function against brief periods of possible
development of the heart–lung machine in 1953
hypotension. Haemodilution (haematocrit 21–25%)
provided total circulatory support and oxygenation
is used to help reduce blood product use, reduce red
while intracardiac procedures were performed on
cell loss during surgery, and improve small vessel
the empty, and preferably still (asystolic), heart.
blood flow in hypothermic conditions. For complex
Other milestones were the successful introduction
surgery of thoracic aortic arch aneurysm, CPB is used
of cardiac valve replacement in 1960, and coronary
to cool the patient to 18°C (profound hypothermia),
artery bypass graft (CABG) surgery in 1968.
blood is drained into the CPB reservoir, and the cir
In addition, complex and lethal conditions such
culation arrested for up to 60 minutes, allowing
as acute dissection of the thoracic aorta, cardiac
excellent and rapid asanguineous access to major
wall and valve rupture after myocardial infarction,
vessels, yet maintaining cerebral and renal protection.
and infective endocarditis can be dealt with and
At the completion of the vascular procedure the
mechanical cardiac assist devices and transplanta
patient is rewarmed to 37°C over 30–40 minutes.
tion for the failing heart have become routine
Deep hypothermic circulatory arrest techniques
techniques.
are also used to facilitate surgery on or within the
inferior vena cava, especially in venous extensions
of renal neoplasms into the renal vein and inferior
Cardiopulmonary bypass: heart–lung
vena cava, where precise safe clearance of these
machine
endovascular extensions is required.
CPB is not always necessary. CABG can be per
Cardiopulmonary bypass (CPB) revolutionised
formed without using the heart–lung machine and
cardiac surgery, allowing precise intracardiac repair
indeed is the preferred technique for some surgeons
while vital organ perfusion, oxygenation and func
either routinely or when the aorta is ‘hostile’,
tion were maintained. The essential components
when any manipulation of the aorta may result in
of the CPB circuit are described in Box 61.1.
an embolic stroke, and in ‘closed’ cardiac surgery
The duration of CPB for most operations is
(see later section).
between 1 and 2 hours. Complex operations may
require 3–4 hours of CPB and occasionally several
days or weeks (see section Circulatory support). Myocardial protection
Major shortcomings are blood cell destruction
(roller pump) leading to haemoglobinuria and In some conditions it is possible to perform an
thrombocytopenia, coagulation factor consumption excellent cardiac operation using CPB but with the
and systemic inflammatory response (due to con heart normally perfused and beating, for example
tact with silastic tubing), as well as neurological, closure of an atrial septal defect (ASD). However,
pulmonary, renal and hepatic dysfunction. All these precise coronary artery anastomoses and complex
587
588 Cardiothoracic Surgery
Box 61.1 Cardiopulmonary bypass Box 61.2 Cardiac surgery without CPB
circuit
PDA closure
Venous Drains blood from right atrium or Coarctation of aorta repair
cannula(s) both venae cavae Mitral valvotomy (for mitral stenosis)
Suckers Return shed blood from operative Pericardiectomy
field to the reservoir Coronary bypass (selected cases)
Reservoir Drainage sump for venous and
shed blood to be collected, and
then oxygenated
from the heart, such as closure of patent ductus
Oxygenator Venous blood oxygenated across
arteriosus (PDA), or where disruption of cardiac
a membrane
function is transient and can be well tolerated
Heat exchanger Cools and rewarms blood (and
(mitral valvotomy).
thereby the patient)
With the evolution and refinement of imaging
Roller or Performs function of left
centripetal pump ventricle, flow rates of 4–6 L/min
and technology, many ‘closed’ and some ‘open’
Arterial cannula Returns oxygenated blood to the (CPB‐requiring) operations have been replaced by
distal ascending thoracic aorta or endovascular or percutaneous transcatheter tech
other major artery niques, for example dilatation of aortic coarctation,
PDA closure, atrial and ventricular septal defects
and, more recently, aortic, pulmonary and mitral
valvular procedures are best performed in a still valve replacements and mitral valve repair (see later).
flaccid heart. Operations commonly performed without CPB
Ideally, this state is achieved by clamping the distal are listed in Box 61.2. The vast majority (>90%)
ascending thoracic aorta and infusing ‘cardioplegia of cardiac operations worldwide are performed
solution’ (oxygenated blood with additional potas using CPB.
sium, magnesium, lidocaine and amino acid substrates)
at 10–20°C in order to arrest the heart, reduce its
metabolic requirements and provide appropriate
Coronary artery surgery
substrates, thus protecting the heart while being
operated upon and being deprived of its normal
Coronary atherosclerosis is a major disease process
coronary blood flow. There are many formulas of
in western countries and is rapidly increasing in
cardioplegic solutions, and methods of administra
incidence in developing countries. Coronary angiog
tion, although the principles remain the same.
raphy (by retrograde cannulation of the coronary
Cardioplegia is also frequently administered ret
ostia via the femoral or radial artery under local
rogradely via the coronary sinus (the main venous
anaesthetic) was introduced in 1962. Coronary
drainage of the myocardium) using specially
bypass surgery became established in 1968 and
designed cannulas, in addition to antegrade admin
coronary angioplasty in 1978.
istration. This technique is particularly useful for
protecting the myocardium downstream from very
Pathology
stenotic or occluded coronary arteries or when
the heart is positioned such that it is difficult or Atherosclerotic stenotic lesions develop proximally
inefficient to easily administer further antegrade at the origins of main coronary branches or at
cardioplegia (aortic valve incompetence). major branching points. The coronary vessels are
The usual cardiac arrest times are 45–90 minutes, usually free of disease distally. A stenosis of more
although up to 180 minutes is possible with preser than 50% diameter loss is considered significant.
vation of cardiac function. Sinus rhythm is usually Atheromatous plaques may disrupt, occlude or
restored within 1–2 minutes of re‐establishing suffer from intraplaque haemorrhage, causing
coronary blood flow. acute spasm, occlusion or thrombosis. Gradual
progressive chronic stenosis causes angina. Acute
spasm results in ischaemic chest pain at rest, and
Closed cardiac surgery thrombotic occlusion results in acute myocardial
infarction.
Many procedures do not require CPB. The early Risk factors for coronary artery disease include
operations were performed with the heart beating. family history, male gender, diabetes, hypertension,
Such operations are possible where they are remote smoking, hypercholesterolaemia and obesity.
61: Principles and practice of cardiac surgery 589
Symptoms the stenotic lesion (FFR <0.80) is considered sig

nificant and allows an objective evidence‐based
Angina pectoris on exertion is the most common
and targeted strategy towards revascularisation,
symptom. Ischaemic chest pain occurring sponta
which in turn results in better short‐ and long‐
neously at rest (unstable angina) also occurs and
term outcomes.
is associated with spasm in the vicinity of the
The SYNTAX score, developed for a randomised
stenotic plaque and/or transient coronary artery
trial of coronary stenting versus CABG, allows
occlusion. Myocardial infarction occurs with pro
scoring of the ‘severity and complexity’ of coronary
longed or permanent coronary occlusion resulting
lesions and choice of appropriate revascularisation
in severe chest pain lasting several hours. Diabetic
strategy: angioplasty and stenting for discrete short
patients may not experience chest pain because of
lesions in one or two arteries; CABG for complex
neuropathy.
or bifurcation lesions in multiple coronary
Between 10 and 15% of patients, especially
branches.
women, may experience atypical symptoms such
as back pain and epigastric, throat or jaw discom
Medical management
fort. Myocardial infarction must not be confused
with the symptoms of acute aortic dissection, Low‐dose aspirin, nitrates (sublingual, spray or
which presents as sudden and dramatic severe topical), beta‐blockers (metoprolol, atenolol),
interscapular pain, as opposed to the progressive calcium antagonists (nifedipine, amlodipine) and
crescendo of myocardial infarction. cholesterol‐lowering agents (statins) are used.
Investigations Indications for intervention

• Chest X‐ray may indicate cardiomegaly or left • Uncontrolled symptoms: where symptoms persist
ventricular aneurysm as a result of prior myocar despite appropriate medical therapy or where
dial infarction. medication cannot be tolerated.
• Electrocardiogram (ECG) may show ST‐segment • Prognosis: patients with severe stenoses in the
elevation or depression with acute chest pain, or left main coronary artery, proximally in a large
‘Q’ waves due to old myocardial infarction. left anterior descending artery, or when all the
• Stress test (treadmill or bicycle with ECG moni main coronary arteries (left anterior descending,
toring), where positive, will result in chest pain, circumflex and right coronary artery) have severe
ST‐segment depression and a fall in blood stenoses, revascularisation has been clearly
pressure. shown to provide major long‐term prognostic
• Thallium, sestamibi and positron emission benefit.
tomography (PET) scans may indicate areas of
hypoperfusion, ischaemia, viability and reversi Percutaneous coronary intervention: coronary
bility of left ventricular function. angioplasty and stenting
• Computed tomography (CT) is useful for screen
Discrete stenotic plaques in one or two arteries may
ing, especially in young patients presenting with
be treated by percutaneous transluminal coronary
chest pain. If negative, this excludes coronary
angioplasty (PTCA) to dilate the plaque to its nor
artery disease (99% specificity). Conversely, a
mal lumen size (2–2.5 mm), with the plaque held
high calcium score indicates a high chance of
open by placement of a stent. Advances include
coronary artery disease. Currently, coronary
drug‐eluting stents, which inhibit proliferation of
angiography is then required as the definitive
neointima and have reduced in‐stent re‐stenosis
investigation to outline the number, location and
rates to 1–5% at 1 year.
severity of the stenotic lesions, and the size and
quality of the vessels beyond.
Coronary artery bypass graft surgery
• Intravascular (coronary) ultrasound details the
extent, severity and nature of coronary artery Multiple severe coronary artery stenoses associated
plaques, especially useful when evaluation on with chronic uncontrolled angina, or unstable
coronary angiography is uncertain. angina, are best treated surgically. CABG comprises
• Fractional flow reserve (FFR) is measured by an 60% of all adult cardiac operations. There are
intracoronary pressure wire at the time of angi many variations of surgical techniques but the
ography and provides a physiological assessment general principles are as follows.
of the degree of ischaemia distal to the stenotic Sternotomy is performed. The left internal thoracic
lesion. A pressure drop of more than 20% across artery (LITA) is harvested and is usually anastomosed
The patient spends 24–48 hours in the intensive

care unit, where blood pressure, right atrial pres
sure, pulmonary artery pressure, left atrial pressure,
and cardiac and urine outputs are measured and
interventions performed as appropriate.
The patient is mobilised on the first or second
LITA postoperative day, and aspirin, a statin, and beta‐
blocker and calcium antagonists are recommenced.
Most patients are discharged from hospital 5–7 days
postoperatively. Recovery is rapid, with most
returning to ‘office work’ in 4–6 weeks and to full
RA activity within 3 months.
RITA Results of CABG surgery

The operative mortality is 1% (although higher in
re‐operations or where left ventricular function is
LAD poor). The main morbidity relates to perioperative
stroke (1%), myocardial infarction (1%), sternal
and mediastinal infections (1%) and haemorrhage
(2%) (see section Complications of cardiac surgery).
Graft patency is best for the left ITA and worst for
the saphenous vein (Table 61.1).
RCA CxOM Long‐term freedom from recurrent angina
pectoris is 85% at 5 years and 70% at 10 years
Fig. 61.1 Typical coronary artery revascularisation of the
(recurrence rate of approximately 3% per annum).
anterior, lateral and inferior walls of the heart. LITA, RITA,
Long‐term survival is excellent: 90–95% at 5
left and right internal thoracic artery; RA, radial artery;
LAD, left anterior descending artery; RCA, right coronary
years and 80–85% at 10 years. Survival is signifi
artery; CxOM, circumflex (obtuse) marginal artery. cantly influenced by age at surgery (current mean
age 68 years), presence of diabetes, degree of left
ventricular dysfunction, and control of risk factors
to the left anterior descending artery (LAD), which after surgery. The presence of one or more ITA
is considered to be the most important artery. grafts enhances survival and long‐term freedom
In younger patients (<70 years), the right internal from angina. A patent LITA to the LAD appears
thoracic artery (RITA) is harvested and anastomosed to be the most important prognostic component
to the second most important affected coronary of myocardial revascularisation (Figure 61.2).
vessel. Other coronary vessels are grafted using either Multiple large longitudinal studies (beyond 10
the radial artery (Figure 61.1) or saphenous vein. years) have shown that the use of multiple arterial
CPB is used, and the heart is arrested and pro grafts (including radial artery grafts) is associated
tected with cardioplegia while performing the distal with identical perioperative results but with supe
anastomoses. The proximal graft anastomoses may rior long‐term survival and fewer cardiac events
be performed to the ascending thoracic aorta while and re‐operations compared with when the
the heart is arrested or using a specially designed majority of bypass grafts are with saphenous vein.
clamp. Alternatively, the proximal inflow may be
from the subclavian artery or via the construction
of pedicled grafts off the internal thoracic artery Table 61.1 Coronary bypass graft patency.
(ITA). A typical operation takes 3–4 hours, including
cardiac arrest for 30–60 minutes and bypass times Conduit 5 years 10 years 20 years
of 60–90 minutes, depending on the number of
bypasses performed (average of three to four). The Left internal 96% 95% 90%
thoracic artery
pericardium is usually loosely closed to protect the
Right internal 93% 90% 80–90%
right ventricle in future re‐sternotomy, drain tubes thoracic artery
placed behind the sternum and into the pleural Radial artery 90% 85–90% 80–90%
cavities if they have been entered, and the sternum Saphenous vein 75% 50% 25–30%
re‐wired so that it is extremely stable.
(a) (b) (c)
Fig. 61.2 Postoperative angiography of (a) the left internal thoracic artery sequentially to the diagonal and left anterior
descending coronary arteries; (b) an aortocoronary radial artery to the posterior descending coronary artery; and (c) a
radial artery placed sequentially to the first and second circumflex marginal arteries.
In general, for every 100 patients undergoing to the extensive myocardial damage and to the
CABG, 10 more ‘multi‐arterial’ patients will be precarious preoperative state of the patients.
alive at 10 years (80% vs. 70%).
Coronary surgery confers prognostic benefits Off‐pump coronary surgery
(over medical management and percutaneous
coronary intervention) to patients with stenosis of Devices and techniques have been developed that
the left main coronary artery, those with high‐ allow excellent stabilisation of the coronary arter
grade proximal LAD stenoses, those with triple ies, making it possible to perform precise coronary
vessel coronary disease (LAD, right and circumflex anastomoses, especially to the LAD and diagonal
coronary arteries), where there is left ventricular arteries (anterolateral aspects of the heart), while
dysfunction, and in diabetics. These groups account the heart is beating and maintaining circulation.
for approximately 85% of patients undergoing Similarly, the circumflex and right coronary arteries
coronary surgery. may be grafted.
Potential advantages are avoidance of CPB and
manipulation of the aorta (by cannulas and clamps),
Surgery for complications of myocardial
which may be an important factor in older patients
infarction
or where the aorta is atheromatous or calcified,
Complications of coronary artery disease, espe thereby reducing the possibility of bleeding or
cially myocardial infarction, may require treatment stroke. There are also potential economic gains
in conjunction with CABG surgery. Myocardial through avoidance of CPB, with savings on con
infarction involving the left ventricular wall, sumables and personnel and potential to reduce
including papillary muscles of the mitral valve, in intensive care and hospital stays, although this has
combination with left ventricular dilatation may not been proved thus far.
result in severe ischaemic mitral regurgitation. This However, there are also potential disadvantages,
would need correction by mitral valve repair or with greater operative technical difficulty, possible
replacement (operative mortality approximately coronary artery damage, and episodes of hypoten
10%). Left ventricular aneurysms, particularly in sion with excessive displacement and manipulation
relation to occlusion of the LAD, may require exci of the heart. The role of off‐pump coronary artery
sion and repair (operative mortality 3%). bypass is still being debated. Randomised con
Extensive infarction may result in left ventricular trolled trials have not shown perioperative differ
free wall rupture into the pericardium (tamponade) ences, nor differences in cognitive function.
or rupture of the interventricular septum (acute However, there appears to be reduced graft patency,
cardiogenic shock). These complications, treated earlier return of angina, a greater need for re‐inter
conservatively, are almost universally fatal. Surgical vention and compromised long‐term survival.
repair using appropriate techniques (patches and Conversely, it may be associated with better short‐
biological glues) is essential, although operative term results in high‐risk patients with poor left ven
mortality is high (25%), relating predominantly tricular function and ‘hostile’ atheromatous aortas.
New concepts in CABG surgery

Endoscopic harvesting techniques for saphenous
vein and radial arteries minimise incisions, discom
fort and infection. ‘Hybrid’ procedures are those
where the LAD is bypassed with the LITA via a
small left thoracotomy and other stenoses are
addressed by stents, either at the same time in a
‘hybrid’ operating room (with angiographic and
CT facilities) or as sequential procedures (LITA–
LAD first). These may be used in older higher‐risk
patients to minimise surgical trauma and facilitate
recovery.
The application of robotic techniques in CABG
surgery is still in its infancy.
Cardiac valve surgery

Fig. 61.3 Severe calcific aortic stenosis with associated
The initial valve operations were performed on the aortic valve insufficiency secondary to the rigidity and
distortion of the aortic valve leaflets.
beating heart (closed mitral valvotomy). The first
successful aortic and mitral valve replacements
were performed in 1960. Valve pathology is still a pulmonary hypertension. Myxomatous degenera
significant factor in clinical cardiac disease. A high tion affecting the aortic valve results in progressive
incidence of rheumatic valve disease persists in aortic regurgitation.
developing countries (India, China, Indonesia, The chronic effects of rheumatic fever are c ardiac
South America) and also in Australia’s Northern valve leaflet thickening and retraction. In the aortic
Territory. In western countries the most common valve this results in a combined lesion of aortic
valve problems are due to degenerative processes stenosis and regurgitation. In the mitral valve, ste
and ageing, which have increased in incidence, nosis is the predominant effect of leaflet thickening,
while rheumatic pathology has declined. fusion at commissures and shortening of chordae
tendineae. Regurgitation occurs with severe leaflet
Pathology fibrosis, retraction and failure of leaflet coaptation.
The two most common valve pathologies in western Symptoms

countries are calcific aortic stenosis and degen
erative myxomatous mitral regurgitation. Aortic The key symptom is dyspnoea, although this occurs
stenosis results from dystrophic calcification of a late in the course of valve disease as each of the
bicuspid aortic valve (including calcification as valve pathologies is generally well tolerated because
part of the degenerative ageing process) and is more of left ventricular reserve and the initial compliance
commonly seen in older patients (a result of of the left atrium. Dyspnoea requires immediate
improved living standards and longevity). There is investigation and aggressive intervention because it
progressive narrowing of the aortic valve orifice indicates exhaustion of the cardiac compensatory
with resultant left ventricular hypertrophy and left mechanism and a poor prognosis and rapid demise
ventricular failure in advanced cases. Aortic valve for the patient if left untreated.
distortion may also result in aortic regurgitation Angina and syncope may be additional symp
with additional deleterious effects (Figure 61.3). toms in aortic stenosis due to pressure loss across
Myxomatous degeneration predominantly affects an extremely stenotic aortic valve and resultant
the mitral valve (collagen and elastin abnormalities, poor coronary and cerebral perfusion.
and increased mucopolysaccharide deposition). It Cerebral emboli or endocarditis may occur if the
results in annulus dilatation, chordae tendineae valve lesions are complicated by valvular or left
elongation, leaflet redundancy and prolapse and, in atrial thrombus, infections or vegetations.
extreme cases, chordal rupture and mitral leaflet
Investigations
flail, resulting in massive mitral regurgitation.
Sequelae are left ventricular and left atrial dilata Chest X‐ray may show cardiomegaly, calcification
tion, left heart failure, atrial fibrillation (AF) and in the aortic or mitral valves, and pulmonary
Aortic valve surgery

A mean gradient of more than 40 mmHg in aortic
stenosis or a left ventricular end‐diastolic diameter
of more than 60 mm in aortic regurgitation are
indications for surgery. The mean age for aortic
valve replacement (AVR) is 69 years. Sternotomy
and CPB are required. The aorta is opened trans
versely 2–3 cm above the aortic valve. Occasionally
the valve can be repaired. The valve is excised, all
calcium removed from the annulus and an aortic
valve prosthesis is placed using non‐absorbable
sutures. The aortotomy is then closed, and air is
Fig. 61.4 Transoesophageal echocardiogram to evaluate evacuated from the heart prior to re‐establishment
the aortic valve (centre of image). LA, left atrium of circulation through the heart. Carbon dioxide in
posteriorly; LV, left ventricle; Ao, ascending thoracic the operative field (heavier and more soluble than
aorta. Dots represent 1‐cm markings. oxygen and nitrogen) is used to minimise potential
air embolism. The ascending aorta is usually
congestion. ECG may show left ventricular hyper occluded for 60 minutes, CPB time is 80 minutes
trophy, a wide bifid P wave in severe mitral stenosis, and total operative time approximately 3 hours.
or AF. Where the predominant pathology is aortic valve
Echocardiography is the key investigation in regurgitation, and the leaflets are nearly normal, it
valvular heart disease. Accurate measurements can is possible to repair such valves by plicating pro
be made of the cardiac chambers, pulmonary artery lapsed leaflets or enhancing leaflet coaptation by
pressure and the valvular orifices. Calcification, tailoring the aortic annulus and the aortic root
degree of stenosis or regurgitation, leaflet excur (David, Yacoub, Lansaac procedures), which pre
sion, flow, valve area, gradient and annular size serves the natural leaflets and avoids long‐term
can be precisely measured and compared with warfarin. These procedures are complex but are
prior or future measurements. Transthoracic appropriate for young patients with aortic valve
echocardiography is an excellent screening tool. incompetence.
Transoesophageal echocardiography (TOE) gives
greater anatomical detail of valves and their Mitral valve surgery
pathologies and is particularly useful in planning
Rheumatic mitral stenosis may be treated by percu
for and predicting surgical outcomes and in the
taneous balloon valvuloplasty. The procedure is
intraoperative setting (Figure 61.4).
carried out by catheterisation of the femoral vein,
Coronary angiography is performed in patients
passing superiorly into the right atrium, across the
older than 40 years to screen for coexistent coro
interatrial septum into the left atrium and eventu
nary artery disease, with 30% of patients undergo
ally dilatation of the mitral valve.
ing cardiac valve surgery requiring concomitant
Alternatively, and now rarely used, closed mitral
CABG surgery.
valvotomy via a left thoracotomy and trans‐left
atrial or trans‐left ventricular dilatation of the
Medical management
mitral valve is performed. These procedures are
Where patients are asymptomatic, and echocardi performed under TOE guidance and are best when
ography shows normal function and cardiac the valve leaflets are pliable and there is no valve
chamber size and normal pulmonary artery pres calcification nor thrombus in the left atrium.
sures, conservative management is indicated. Valve leaflet thickening, calcification, fused
Peripheral vasodilating medications such as cal chordae and left atrial thrombus are all indica
cium antagonists (nifedipine, amlodipine) or angi tions for open operation (via sternotomy and
otensin‐converting enzyme (ACE) inhibitors CPB), which may include commissurotomy to free
(perindopril, ramipril, etc.) are useful in aortic the fused commissures between the anterior and
regurgitation and mitral regurgitation for reduc posterior mitral leaflets, debridement of calcifica
ing the afterload for left ventricular ejection. tion, and fenestration or resection of portions of
Diuretics (frusemide) are required for pulmonary thickened chordae. A severely distorted valve,
congestion. Warfarin anticoagulation and digoxin especially if additionally regurgitant, will require
may be required if there is AF. replacement.
Myxomatous degenerative mitral valve regurgi primarily a leaflet problem, severe mitral valve
tation is due to elongated and ruptured chordae, regurgitation that leads to pulmonary hypotension,
leading to prolapse and flail of the mitral valve leaf heart failure and dyspnoea may be addressed by a
lets, usually in combination with mitral annular restrictive mitral rigid annuloplasty ring to enforce
dilatation. If the gross changes are localised to a the leaflet coaptation, or via mitral valve replace
specific part of the valve (e.g. central scallop of ment (as the left ventricular muscle pathology can
the posterior leaflet), mitral valve repair is possi not be addressed).
ble. If the changes are widespread with multiple
areas of prolapse, flail and lack of leaflet coapta Cardiac valve prosthesis
tion, repair is more complex and challenging and
There are two categories of valve prosthesis
then valve replacement may be indicated, especially
available for implantation: mechanical and tissue
in older patients (tissue valve).
(Figure 61.5).
Mitral valve repair is performed via a sternotomy,
Mechanical valves are made of pyrolytic carbon
CPB and direct left atriotomy. Many techniques are
with a Dacron sewing cuff, are low profile and
used and include quadrangular resection of the flail
inert, and commonly have two semicircular leaflets
or prolapsed segment, annulus and leaflet repair,
(St Jude, ATS/ Medtronic). Mechanical valves always
and placement of an annuloplasty ring to reinforce
require warfarin anticoagulation maintaining
the annulus repair and correct annular dilatation
and valve geometry. Leaflet prolapse can also be
corrected by replacing elongated or ruptured chordae
(Gore‐Tex neochordae). Retention of the native mitral
valve avoids the need for warfarin anticoagulation
in the long term (if the patient is in sinus rhythm)
and maintains the geometry and function of the left
ventricle.
Mitral valve replacement is performed if the
valvular pathology is too extensive. However, as
much of the subvalvular mechanism (including
leaflet tissue, chordae and papillary muscles) is
retained to maintain left ventricular geometry and
function, hence resulting in a low operative mortality
and improved long‐term left ventricular function
and patient survival. Low profile mechanical
valves are used in patients aged less than 70 years
(see following section). Warfarin anticoagulation
is always required when a mechanical valve pros
thesis has been placed.
Many patients with mitral valve pathology have
AF. This is addressed by closure of the left atrial
appendage (where thrombi and potential emboli
may occur) and incorporating by a Maze procedure
to isolate the pulmonary veins where AF originates,
disrupt macro re‐entry circuits and create an ante
grade pathway for atrial conduction to the atrio
ventricular node. This is usually performed with a
set of ‘cryolesions’ and adds approximately 20–30
minutes to the procedure. It has a 50–80% success
rate in converting AF to sinus rhythm in the longer
term and is more likely to be successful if the
atrium is not too dilated, and the AF has been more
recent (<5 years).
Extensive or recurrent myocardial infarction may
lead to left ventricular and mitral annular dilata Fig. 61.5 Prosthetic cardiac valves: (top) pericardial
tion, and failure of the mitral leaflets to meet and xenograft tissue valve; (bottom) bileaflet mechanical
coapt results in mitral regurgitation. Although not (pyrolytic carbon) mechanical valve.
warfarin, which can be teratogenic, but recognising

Table 61.2 Cardiac valve prosthesis.
that further surgery will be required.
Valve type Advantages Disadvantages Unfortunately, all tissue valves are subject to
wear and tear and gradual degeneration. Inevitably,
Mechanical Durable Warfarin if any type of bioprosthesis is used in patients
anticoagulation younger than 60, there is a very high probability
Higher bleeding and
that re‐operation will be required, although this is
thromboembolic rates
uncommon within 10 years.
Tissue No anticoagulation 15‐year durability
Better (Ca2+, dehiscence),
haemodynamics re‐operation
(stentless valves) Recent developments in cardiac valve surgery
Small incisions
international normalised ratio (INR) values between Short (5 cm) upper sternal and right parasternal
2.5 and 3.5. incisions have been used for aortic valve surgery,
Tissue valves (bioprostheses) are derived from and right submammary and short lower sternal
humans (human cadaver aortic valve allograft), incisions for mitral, atrial septum and tricuspid
pulmonary valve autografts (discussed later) or valve surgery. These approaches are facilitated by
xenografts (specially treated porcine or bovine video telescope assistance, especially designed
valves). Additionally, tissue valves may be mounted long‐shafted instruments and peripheral (femoral
on a stent for ease of implantation, or may be vessel) cannulation for CPB. Left submammary
stentless to enhance haemodynamics, allowing a incisions may be used for isolated coronary bypass
larger valve into any anatomical situation. The to the LAD.
advantages and disadvantages of each type of valve Advantages include cosmesis, less bleeding and
are indicated in Table 61.2. fewer wound infections. Disadvantages include a
In the mitral position, mechanical valves are used substantial learning curve, longer CPB times, less
in patients younger than 70 years or if the patient is certain myocardial protection, potential retrograde
to be on long‐term warfarin (AF). Xenograft tissue emboli where there is aortic atheroma, and limb
valves may be used in older patients, which allow vascular problems as femoral vessel cannulation
lesser degrees of warfarin anticoagulation. has been complicated by aortic dissection, leg
However, xenografts fail rapidly in young patients ischaemia and venous thrombosis. Limited expo
(<60 years). sure may compromise safety and lengthen the
In the aortic position, there are a number of duration of the procedure. Overall the results in
choices determined by age and patient lifestyle. In experienced centres are similar to those by estab
patients older than 70 years, a xenograft tissue lished techniques.
valve is generally used. Only low‐dose aspirin is
required long term if the patient is in sinus rhythm.
Sutureless rapid deployment aortic tissue valves
In patients younger than 70, generally a mechani
cal valve together with warfarin anticoagulation is These can be efficiently implanted once the diseased
used. A human cadaver allograft is used if warfarin valve has been excised. Advantages include shorter
is to be avoided (e.g. patient lives in a remote area, operative times, especially when multiple cardiac
patient participates in contact sports) or when there procedures are required. Such valves predominantly
is endocarditis affecting the aortic valve annulus. depend on expansion of the stents or scaffolds they
However, allografts are relatively difficult to pro are mounted upon. Disadvantages include higher
cure and are in short supply. degrees of heart block and occasional paravalvular
Some younger patients (15–50 years) have a pul leaks. Implantation techniques are particularly
monary autograft (Ross) procedure in which the suited to aortic valve replacement via small incision
diseased aortic valve is replaced with the patient’s access.
own pulmonary valve, which in turn is replaced
with a human cadaver pulmonary valve allograft.
Other developments
This is an extensive procedure, but well tolerated in
young patients. Anticoagulation is avoided. • Robotic techniques are also used for mitral and
However, long‐term results beyond 15 years are not atrial septum surgery. The results are similar but
established. Women of childbearing age requiring there is a substantial learning curve and greater
mitral replacement have tissue valves to avoid expense which have limited their application.
• Percutaneous transcatheter aortic valve implan Tricuspid valve annuloplasty to correct tricuspid
tation and mitral procedures are now also widely annulus size and shape to normal is performed at
practised. the time of aortic or mitral surgery. Organic tricus
• Tissue aortic valves on nitinol stents can be pid valve stenosis or regurgitation due to rheumatic
crimped onto a catheter and implanted into the disease is rare and is managed following the princi
aortic valve position via the femoral artery, ples of mitral valve surgery.
axillary artery or ascending thoracic aorta, or
antegradely by the left ventricular apex. Once in Results
position the old diseased (stenotic) aortic valve
leaflets are pushed laterally into the capacious Operative mortality varies from 1% (AVR, mitral
sinuses of Valsalva, and the new aortic valve is valve repair) to 3% (mitral valve replacement).
aligned and expanded into position. Operative mortality for combined CABG and valve
• Mitral valve clips (MitraClip) or mitral valve surgery is 3–5%, and for re‐operation is 5–8%. Long‐
prostheses can be introduced percutaneously via term results are excellent. Survival following mitral
the femoral vein across the interatrial septum valve repair or AVR is 90% at 5 years, and 80% at 10
and used to enhance coaptation between the two years. Survival following mitral valve replacement is a
mitral leaflets (MitraClip) or replace the mitral little less than this due to late referral and excision of
valve. the subvalvar apparatus in the previous era.
These techniques are highly reproducible and have
been very successful in older, inoperable or high‐ Morbidity of valve replacement surgery
risk patients, with procedural mortalities of less
Unfortunately, each valve prosthesis has a group of
than 5%, rapid recovery and promising early results
long‐term problems associated with its use:
out to 5 years.
• anticoagulant‐related haemorrhage, which may
be extremely serious (cerebral, gastrointestinal)
Postoperative management
• thromboembolism from small thrombi that form
Perioperative prophylactic antibiotics are given to around the annulus or within the prosthetic valve
protect against endocarditis (prior to anaesthesia, • endocarditis from an infection on the valve
and for 48 hours postoperatively) and meticulous prosthesis
care taken to avoid any sepsis. Warfarin anticoagula • perivalvular leaks, or structural deterioration of
tion (if appropriate) is commenced 24 hours postop tissue valve which, when severe enough, would
eratively, and a therapeutic INR of 2.5–3.5 achieved require re‐operation.
by day 7. Warfarin is continued indefinitely (except Each of these complications occurs with an annual
in mitral repair or where aortic tissue valves have incidence of approximately 0.5–1.0%, and hence
been used). Diuretics and ACE inhibitors are usually the potential for a patient to be totally free from
required for several weeks or months. General post any one of these complications over the course of
operative management and progress is similar to 10 years is only of the order of 70%.
that of patients undergoing coronary artery surgery.
Other valve conditions Congenital cardiac surgery

Severe infective endocarditis affecting either the aortic
Cardiac anomalies occur in 8 per 1000 live births.
or mitral valve is usually caused by Staphylococcus
The range of anomalies is extensive. Only the com
aureus and results in fever, aortic and/or mitral regur
mon ones are discussed here. Congenital cardiac
gitation, and eventual renal and hepatic dysfunction.
abnormalities are best corrected as early as possible
It is best managed aggressively with appropriate
after birth (preferably in the first 3 months). Some,
antibiotic loading and early surgery to eradicate the
such as a large persistent PDA, which creates a huge
infection and either replace or repair (uncommon but
shunt from the aorta to the pulmonary artery, or
sometimes possible) the affected valve.
severe coarctation of the aorta, which places a large
Tricuspid valve surgery is uncommon. Tricuspid
afterload on the left ventricle, need urgent correc
regurgitation may be the end product of chronic
tion at birth.
aortic or mitral valve disease, left heart failure and
pulmonary hypertension. The mechanism is that
Patent ductus arteriosus
of right ventricular and tricuspid valve annular
dilatation and loss of central leaflet coaptation. PDA allows blood flow from the pulmonary artery
The leaflets and chordae are otherwise normal. trunk to the aorta when the lungs and pulmonary
circulation are not functioning in utero. The PDA be single or multiple and placed either just below
usually closes at birth. A persistent small PDA is the tricuspid valve and the origin of the great ves
vulnerable to endocarditis. A persistent large PDA sels, or more inferiorly in the body of the muscular
allows shunting of blood from the aorta back into septum. Most commonly, VSDs occur in isolation
the pulmonary circulation, overloading it as well as but may also be present as part of a more complex
the right heart, eventually leading to pulmonary cardiac anomaly (e.g. tetralogy of Fallot). Small
hypertension and right heart failure. Closure of the VSDs, particularly in the central muscle septum,
PDA is essential and this can be achieved either by may close spontaneously with cardiac growth. Larger
percutaneous catheter closure or by direct suture VSDs associated with pulmonary‐to‐systemic flow
ligation or division and oversewing via a small left ratios of more than 1.5 : 1 are repaired to avoid
thoracotomy. endocarditis, and also the sequelae of pulmonary
and right heart overload (see preceding section).
Coarctation of the aorta Surgical closure is by using CPB, and by direct
suture or patch. Percutaneous closure is also possi
The most common site is just distal to the left
ble. The main specific complication is heart block
subclavian artery, with the lumen of the aorta often
as the conducting bundle passes near the inferior
narrowed to 1–2 mm. Left untreated, upper body
rim of the VSD, and care is taken not to damage the
hypertension, left ventricular hypertrophy and left
conducting bundle with sutures at VSD closure.
ventricular failure develop. Correction is by either
percutaneous retrograde (from the femoral artery)
catheter balloon dilatation or surgical resection and Other congenital abnormalities
repair via a small left thoracotomy.
Other congenital abnormalities that may be surgically
corrected with excellent long‐term results include
Atrial septal defect pulmonary valve stenosis, tetralogy of Fallot,
transposition of the great vessels and endocardial
Atrial septal defect is the most common congenital
cushion defects (atrioventricular canal). However,
cardiac defect and occurs as a result of developmen
there are numerous rarer, more complex conditions
tal failure of the interatrial septum and can be high
(e.g. hypoplastic left heart syndrome, single ventri
(sinus venosus), mid (ostium secundum) or low
cle, tricuspid atresia) where surgery is also possible,
(ostium primum) defects. A significant ASD is more
but often multiple procedures are required, with
than 1 cm in diameter and if left uncorrected results
suboptimal results. (The reader is directed to texts
in a persistent left atrium to right atrium shunt,
of paediatric cardiology and cardiac surgery.)
eventually leading to right heart overload, right
atrial and ventricular enlargement, AF and pulmo
nary hypertension. Life expectancy may be reduced
by 10–30 years (depending on the size of the ASD Surgery of the thoracic aorta
and shunt).
Echocardiography gives excellent depiction of Aneurysms of the thoracic aorta, especially the
the anatomical location, size of the ASD and flow transverse arch, are challenging. The most common
through it, as well as the size of the cardiac cham pathologies are atheromatous or myxomatous
bers and pressure in the right ventricle and pulmo degeneration of the aortic wall media, leading to
nary artery. aneurysmal dilatation and eventual rupture or
ASD closure is indicated if pulmonary circula dissection. Marfan’s syndrome (autosomal dominant
tory flow is more than 1.5 times the systemic circu inheritance) is one entity that is part of the spec
latory flow. Surgical repair is readily performed trum of myxomatous degeneration of connective
(using CPB) by either direct suture or a patch of tissues. Hypertension and atherosclerosis are now
autologous pericardium, and has an extremely low better controlled in the population and are less
mortality (1 in 400). Percutaneous ASD closure common contributing factors to thoracic aneurysms.
via the femoral vein with a catheter‐mounted baf Dilatation of the thoracic aorta to a diameter of
fle‐type device is applicable where the ASD is well more than 5 cm is associated with a marked increase
circumscribed with a defined circumferential rim. in the possibility of rupture or dissection and so
elective repair/replacement is advised (Figure 61.6).
The patients are usually asymptomatic. The aneu
Ventricular septal defect
rysm is often noted on routine chest X‐ray. Rupture
Ventricular septal defect (VSD) occur when ven or dissection is associated with dramatic, sudden,
tricular septal development is incomplete and may severe chest and interscapular pain, possibly collapse,
glues are used to bind and stiffen the fragile myx

omatous layers of the aorta at the site of anasto
moses and repair. This complex surgery is usually
facilitated by use of deep hypothermia (18°C) and
total circulatory arrest (see section Cardiopulmonary
bypass: heart–lung machine). Major morbidity
may result from these urgent difficult operations
and includes postoperative haemorrhage, stroke
and renal dysfunction. The operative mortality is
between 10 and 30%, depending on the preopera
tive clinical state, organ or limb malperfusion prior
to surgery and age.
Vigilant long‐term follow‐up with control of
hypertension, and serial CT scans or echocardio
grams, are required because other parts of the
aorta (descending thoracic or abdominal) may
dilate over time.
Pacemaker and dysrhythmia surgery
Degenerative fibrosis associated with age can affect

the cardiac conduction mechanism to produce
heart block. The heart rate may fall to 30 beats/min
(ventricular escape rhythm) and result in dizziness
Fig. 61.6 Large aneurysm of the ascending thoracic or syncope. This is a common clinical problem in
aorta that preferentially affects the aortic root and the older patients. Occasionally, heart block may result
proximal ascending thoracic aorta. from trauma to the conducting bundle at cardiac
surgery or from some antiarrhythmic medications
hypotension (due to blood loss into the mediastinum, (verapamil, sotolol).
pleural cavity or pericardium) and unequal pulses Treatment is relatively simple and achieved by
(due to dissection around the origins of the large implantation of a pacing lead into the right ventri
artery). The ECG is usually normal. cle via the cephalic or subclavian vein below the
CT and TOE are the most important diagnostic clavicle and implantation of a lithium‐powered,
tests and should be performed urgently. They will low‐profile pacemaker generator, all performed
show the size and location of the aneurysm, any under local anaesthesia. The pacing rate is adjusted
dissection flaps, the site of the aortic wall tear, to 70–80 beats/min as required by telemetry. An
extent of dissection, and the function of the aortic atrial lead can also be inserted to allow sequential
valve, which may partly dehisce from the outer atrial–ventricular pacing, which is more efficient.
aortic wall and become regurgitant. The pacemaker may be programmed to allow
Elective repair is indicated when the aneurysm is spontaneous increase of pacing rates according to
more than 5 cm in diameter. This will involve patient activity.
replacement of the aneurysm with a Dacron tube Programmed sequential biventricular pacing may
graft, but may also require AVR, re‐implantation of be beneficial in patients with left ventricular dilata
the coronary artery ostia or even replacement of the tion, severe dysfunction and cardiac failure.
transverse arch with re‐implantation of the great Rapid atrial arrhythmias (AF, atrial flutter,
vessels. Results of elective surgery are excellent, junctional tachycardia) that remain uncontrolled
with operative mortality generally less than 3%. on medication (digoxin, sotolol, amiodarone)
If rupture or dissection has occurred, emergency and which are significantly symptomatic can be
surgery is indicated. Over 50% of patients die before treated either surgically or, more commonly, by
reaching hospital. The systolic blood pressure should percutaneous catheter radiofrequency ablation.
be kept at approximately 90 mmHg en route to Life‐threatening rapid ventricular arrhythmias
surgery (nitroprusside, glyceryl trinitrate, beta‐ (ventricular tachycardia, ventricular fibrilla
blockers). Similar operative techniques are used, tion), which may occur in cardiomyopathies,
preserving the aortic valve if possible. Biological chronic ischaemia and hypertrophic obstructive
cardiomyopathy for example, may also be treated Potential problems include leg ischaemia, systemic
by implantable cardioverter defibrillators with infection and mechanical blood cell destruction
minimal operative mortality and morbidity, and leading to anaemia and thrombocytopenia.
excellent long‐term results.
Ventricular assist devices
Ventricular assist devices provide additional (and
Circulatory support
superior) mechanical support when inotropes
and IABP are insufficient. Typically, cannulas are
Circulatory support may be required to allow time
placed on the inlet side (left atrium or apex of the
for cardiac recovery after a temporary but reversi
left ventricle) and into the outlet side (aorta) with
ble insult, or permanently.
a mechanical device in between, effectively per
forming the work of the left ventricle. (A similar
Afterload‐reducing agents
circuit can be constructed for the right side of the
Nitroprusside and glyceryl trinitrate infusions heart.) Numerous devices are available (Thoratec,
allow rapid peripheral, arterial and venous dilata Novacor, Heartmate, Abio‐Med) with varying
tion, and reduction of cardiac preload and after characteristics relating to size, implantability,
load. Calcium antagonists (nifedipine, amlodipine) portability, ease of use and expense. Ventricular
and ACE inhibitors (perindopril, ramipril) are oral assist devices may be in situ from 3 to more than
medications that also cause peripheral vasodilata 300 days.
tion and reduce cardiac afterload, allowing myo Ventricular assist devices may allow myocardial
cardial (left ventricular) contraction and ejection of recovery over weeks or months or be used to
stroke volume against a lower systemic vascular optimise the patient’s clinical state as a bridge to
resistance. transplantation. Total artificial hearts can also be
implanted as a bridge to transplantation or
Inotropic agents potentially (in the USA) as ‘destination therapy’.
Inotropic agents are usually given as infusions for The devices are compromised by thromboembo
short‐term use (hours or days). They include dopa lism (or bleeding), infection and mechanical failures.
mine, dobutamine, adrenaline, isoprenaline, mil However, they do allow a reasonable quality of
rinone, levosimendan and calcium. All have varying ambulant life in the interim. The ‘drives’ are
properties and effects, but the underlying mechanism external, about the size of a large handbag, and
is an enhanced inotropic effect on the myocardium. allow excellent patient mobility.
Milrinone is a potent vasodilator (and inotrope),
particularly useful in pulmonary hypotension. Addi Extracorporeal membrane oxygenation
tionally, intravenous or oral prostacyclin (iloprost), Where temporary (days to weeks) but major support
bosentan, glyceryl trinitrate, sildenafil and inhaled of either (or both) the circulation and oxygenation is
nitric oxide are effective in severe pulmonary hyper required (where oxygenation cannot be maintained
tension or where the right ventricle is failing. with mechanical ventilation, 100% oxygen and
maximum positive end‐expiratory pressure), extra
Intra‐aortic balloon pump corporeal membrane oxygenation (ECMO) can be
Intra‐aortic balloon pump (IABP) is indicated used. ECMO is identical to regular CPB but with
when hypotension and poor cardiac output persist special cannulas and circuit modifications for long‐
despite appropriate inotropic support. A catheter term use. The management is extremely demanding
with a 30 or 40 mL balloon is introduced into the as the patient requires anticoagulation and constant
descending thoracic aorta, usually percutaneously supervision.
by the femoral artery. The balloon inflates (helium) Respiratory indications include pneumonia,
and deflates in sequence with the ECG. It inflates influenza and asthma, where the cause is poten
in diastole, suddenly increasing diastolic pressure, tially reversible, and in the meantime the patient
mean blood pressure and organ perfusion, espe cannot be kept alive via mechanical ventilation
cially coronary blood flow and myocardial perfu with 100% oxygen.
sion. The balloon rapidly deflates just prior to Cardiac indications include support after cardiac
cardiac systole, dramatically reducing the afterload operations, after massive myocardial infarctions
on the left ventricle. The usual duration of IABP and drug overdoses (e.g. tricyclic antidepressants),
support is between 1 and 5 days but use up to 21 and for acute cardiomyopathies in conditions
days has been reported. where heart function is deemed recoverable and the
patient is relatively young (<70 years). ECMO use 5–10%), age being a marker for multiple associ
is now expanding into witnessed cardiac arrests ated comorbidities.
with ongoing cardiopulmonary resuscitation, pro
viding it can be instituted within 60 minutes.
Stroke
The incidence of major neurological events in the
Cardiac transplantation perioperative period is 1–2%. Causes include
primary cerebrovascular disease in older patients,
The first human cardiac transplant was performed atheroembolism from the ascending thoracic aorta,
in 1967 by Dr Christiaan Barnard in South Africa. hypoperfusion during CPB, and air or particulate
This was preceded by extensive laboratory work by embolism during valve surgery. Fortunately, there is
Dr Norman Shumway and colleagues at Stanford usually a significant recovery. Subtle neuropsycho
University, USA. The initial results were suboptimal logical dysfunction can also occur, with abnormalities
because of difficulties with rejection and fulminat lasting up to 6 months.
ing infections.
Ciclosporin, which was introduced in 1980, dra Sternal and mediastinal infection
matically reduced the severity of the rejection and
infection episodes to manageable levels, promoting Sternal and mediastinal infection is a devastating
renewed interest. Other advances included superior complication, with an incidence of 1–2%. Risk factors
donor heart preservation, better tissue typing, myo include diabetes, obesity, bilateral ITA grafting,
cardial biopsy surveillance and more efficient anti‐ prolonged preoperative hospitalisation and multiple
rejection regimens. instrumentations/procedures. Prophylactic antibiotics
Indications for cardiac transplantation include are used in all cardiac surgery. Protection against
permanent severe heart damage and failure from mediastinitis is afforded by closure of the thymus
myocarditis, cardiomyopathy and multiple myocar and pericardium behind the sternum. Bacteria
dial infarctions. Donor hearts are usually procured commonly involved include Staphylococcus aureus
following brain death from motor vehicle or cere (including meticillin‐resistant S. aureus).
bral trauma. Recipients are usually less than 65 years Clinical features include fever, increased sternal
of age with no other significant coexisting medical discomfort, redness and movement of a previously
or psychological problems. stable sternum. Early diagnosis is essential, as
The surgery is straightforward: reconnection of established mediastinitis has a mortality of 30%.
the atria, pulmonary artery trunk and ascending Treatment depends on the extent of pathology,
thoracic aorta after removal of the failing heart. from intravenous antibiotics, to local debridement
The challenges are in logistics, personnel and post and sternal rewiring, to extensive debridement and
operative management. use of omental and myocutaneous flaps.
The results of cardiac transplantation are very
good, with an operative mortality of 2–3%, 1‐year Postoperative haemorrhage
survival of 90% and 5‐year survival of 80%.
Approximately 100 cardiac transplants are per Postoperative haemorrhage occurs with an inci
formed in Australia each year and almost 3000 are dence of 2–5%. Specific causes include bleeding
performed annually worldwide; however, numbers from suture lines, branches of grafts and the ITA
are limited by donor shortages. In response to bed. However, in the majority no specific bleeding
this, much development is centred on implantable point is found but re‐operation is useful to remove
artificial hearts. retained blood and clots from the pericardium,
mediastinum and pleural cavities, and establish
haemostasis in the oozing areas. Aspirin and other
more potent antiplatelet drugs (clopidogrel, ticagre
Complications of cardiac surgery
lor) or newer anticoagulants (dabigatran, rivaroxa
ban) within 5 days of cardiac surgery may be
Operative mortality
contributing factors.
Most cardiac operations have an operative mor Numerous other complications may also develop,
tality of approximately 1% (including the first including AF, pulmonary atelectasis, pneumonia,
30 days post operation). Mortality rates are pleural and pericardial effusions, pneumothorax
increased in re‐operations (5%), multiple proce and fluid retention. These are all readily treatable
dures (5%) and with increasing age (>80 years, and reversible.
Cohn LM, Adams DH (eds) Cardiac Surgery in the Adult,

Box 61.3 Percutaneous cardiac 5th edn. New York: McGraw‐Hill Education, 2018.
procedures Fuster V, Harrington RA, Narula J, Eapen ZJ (eds) Hurst’s The
Heart, 14th edn. New York: McGraw‐Hill Education, 2017.
Balloon angioplasty and coronary stents Sellke FW, del Nido PJ, Swanson SJ (eds) Sabiston and
Closure of ASD, VSD, PDA, paravalvular leaks Spencer’s Surgery of the Chest, 9th edn. Philadelphia:
Balloon valvotomy for mitral, aortic and pulmonary Elsevier, 2017.
valve stenosis
Balloon dilatation of coarctation
Mitral valve repair (MitraClip)
MCQs
Valve implantation: aortic, mitral, pulmonary
Thoracic aorta stent grafts
Radiofrequency ablation for atrial fibrillation
Left atrial appendage closure
Septal muscle ablation for hypertrophic cardiomyopathy
1 The coronary artery bypass conduit with the
highest patency after 5 and 10 years is:
a left internal thoracic artery
b right internal thoracic artery
The future of cardiac surgery
c left radial artery
d right radial artery
Over the past 10 years there has been much interest
e left or right long saphenous vein
in less (minimally) invasive surgery, reducing trauma,
improving cosmesis and, where possible, avoiding
the potentially deleterious effects of CPB. Earlier
results of coronary artery bypass grafting is correct?
return to work and activity, especially for younger
a an operative mortality of over 10% is common
patients is usual. These techniques are based on
b patients with poor left ventricular function have
smaller incisions, peripheral cannulation for CPB
a higher operative mortality
or off‐pump surgery. These have been discussed
c older patients have less postoperative morbidity
within the relevant topic areas.
d diabetes has no influence on postoperative
Advances in imaging with CT, echocardiography
morbidity
and MRI with three‐dimensional reconstruction,
e the use of an internal mammary artery improves
and ingenious developments in technology and
survival but does not provide long‐term freedom
instrumentation have enabled an ever‐increasing
from angina
number of potentially definitive cardiac treatments
and procedures to be accomplished by percutaneous
3 Which of the following statements about cardiac
catheter‐based platforms under local anaesthesia.
valve prostheses is correct?
This list will continue to expand (Box 61.3).
a mechanical valves require no long‐term
The number of cardiac operations performed
anticoagulation
worldwide per annum continues to increase.
b tissue valves are highly durable
Interventional cardiology techniques such as angio
c mechanical valves have lower bleeding and
plasty have changed the spectrum of ‘open’ cardiac
thromboembolic rates
surgery to more complex and redo operations, and
d tissue valves are generally preferred in the mitral
the mean age of patients is older.
position
Robotics for cardiac surgery is being developed
e structural failure is extremely rare in mechanical
and promises to assist minimally invasive tech
valves
niques, while substantial endeavour continues in
improving prosthetic cardiac valve and artificial
4 The complications of cardiac valve replacement
heart technology.
surgery include:
a anticoagulant (warfarin)‐related haemorrhage
Further reading b cerebral thromboembolism
c prosthetic valve endocarditis
Buxton BF, Frazier OH, Westaby S (eds) Ischaemic Heart d structural deterioration of tissue valves after
Disease: Surgical Management. Mosby International, 10–15 years
1999. e all of the above
62 Common topics in thoracic
surgery
Julian A. Smith
Department of Surgery, Monash University and Department of Cardiothoracic Surgery,
Monash Health, Melbourne, Victoria, Australia
Introduction Non‐invasive diagnostic investigations
Thoracic surgical topics discussed in this chapter Chest X‐ray

are related to disorders of the chest wall, pleural
All patients with a suspected thoracic problem
space, lungs and mediastinum. Other conditions
should have an erect posteroanterior and lateral
frequently managed by general thoracic surgeons
chest X‐ray. This will help define the location and
include diseases of the oesophagus and chest
extent of the problem.
trauma. Both of these topics are presented in
Chapters 14, 15 and 48.
Pulmonary function testing and arterial
blood gases
Pulmonary function tests (PFTs) help to define the
Presentation of thoracic disorders degree of respiratory impairment on presentation,
the amount of functional reserve, and hence the
Symptoms ability of the patient to tolerate lung surgery and, at
Common thoracic symptoms include cough, chest follow‐up, the response to therapy. There are two
pain, shortness of breath (on exertion or at rest), major types of PFT:
excessive or abnormal sputum production, haem- • those that assess the movement of air in and out
optysis, wheeze or stridor. Many conditions (espe- of the lungs (e.g. forced expiratory volume in 1
cially neoplasms) are asymptomatic and are first second, forced vital capacity, peak flow, total
detected on chest X‐ray. lung capacity, residual volume)
• those that measure the ability to transfer gas
across the alveolar–capillary membrane (e.g.
Examination findings tests of carbon monoxide diffusing capacity).
When considering surgical therapy for a given
On examination, the patient may appear quite
patient, it may be evident that the patient has insuf-
normal or severely short of breath (e.g. from a
ficient ventilatory capacity to withstand a chest
spontaneous pneumothorax). Clues to intratho-
wall incision or a major pulmonary resection, and
racic problems may be found in the other parts of
alternative therapies will need to be offered.
the body, such as clubbing of the fingernails,
Arterial blood gas analysis is an important inves-
peripheral cyanosis and lymphadenopathy. The
tigation in patients with acute and chronic thoracic
jugular venous pressure may be elevated (e.g. from
conditions. Parameters measured include Pao2,
neoplastic superior vena caval obstruction or ten-
Paco2, pH, bicarbonate level and arterial oxygen
sion pneumothorax) and the trachea may be devi-
saturation.
ated from the midline. Signs found in the chest in
some common thoracic conditions are shown in
Computed tomography
Table 62.1. Again, in some conditions, the find-
ings on examining the chest can be completely High‐resolution images of the chest wall, pleural
normal. space, lungs and mediastinum are provided in
603
Table 62.1 Physical signs in thoracic disease.
Chest wall Mediastinum and Tactile/vocal Percussion Breath sounds

movement trachea fremitus note
Large pleural Reduced on Shift to opposite Absent Stony dull Absent. May be
effusion affected side side bronchial above
fluid level
Large Reduced on Shift to opposite Decreased Increased Decreased
pneumothorax affected side side
Massive lung Reduced on Shift to affected Absent Dull Decreased
collapse affected side side
Pneumonic Reduced on Central Increased Dull Bronchial
consolidation affected side
Advanced Reduced on Central Decreased Increased Decreased
emphysema both sides
(‘barrel chest’)
cross‐section. Tissue density is quantified and a therapeutic rigid bronchoscopy is required to con-
fairly accurate map of pathological lesions through- trol massive haemoptysis, remove aspirated foreign
out the chest is obtained. Serial computed tomogra- bodies, or clear retained inspissated sputum leading
phy (CT) is helpful in following up suspicious to postoperative lung or lobar collapse.
lesions. Percutaneous needle biopsy of pulmonary
or pleural lesions is frequently performed under CT Endobronchial ultrasound‐guided biopsy
guidance. The upper abdomen should also be
Endobronchial ultrasound images are obtained by
scanned in patients with known or suspected pul-
passing an endoscope fitted with an ultrasound
monary malignancy to assess the liver and adrenal
processor into the patient’s airway. Biopsy speci-
glands, which are common sites for secondary
mens from mediastinal masses, lung lesions or
deposits. Magnetic resonance imaging (MRI) is also
nearby lymph nodes may be obtained by passing a
used in centres where it is available.
needle through the wall of the airway under ultra-
sound guidance. This has proven to be a valuable
Positron emission tomography
method for staging the mediastinum in patients
Positron emission tomography (PET), performed in with lung cancer and has avoided the need for the
isolation or in combination with CT (PET/CT), is a more invasive procedure mediastinoscopy (see next
nuclear medicine imaging modality that uses section) in many instances.
fluorodeoxyglucose as a tracer to assess the meta-
bolic activity of lung lesions and possible metasta- Mediastinoscopy
ses in lymph nodes or elsewhere.
The mediastinoscope is a lighted cylindrical instru-
ment used to biopsy paratracheal and subcarinal
lymph nodes, most commonly in the work‐up to
Invasive and operative investigations
stage a patient with known or suspected lung can-
cer. This investigation usually precedes any major
Bronchoscopy
pulmonary resection for lung cancer. It is also used
Diagnostic bronchoscopy, using a flexible or rigid in the investigation of mediastinal masses. The
instrument, provides direct visualisation of airway instrument is introduced via a transverse supraster-
lesions for biopsy. Lesions of the lung parenchyma nal incision and passed caudally in a plane deep to
or lymph nodes in the subcarinal space may be the pretracheal fascia. The mediastinoscope passes
biopsied using a transbronchial technique. Most close to the superior vena cava (to its right), the
commonly, diagnostic bronchoscopy is performed innominate artery and arch of aorta (in front) and
by respiratory physicians using the flexible bron- the recurrent laryngeal nerves (to the left and right
choscope and a combination of topical anaesthesia posterolaterally). Care should be taken to avoid
and intravenous sedation. More difficult and poten- biopsying vascular structures such as the superior
tially complicated situations are handled by tho- vena cava, azygos vein and pulmonary artery.
racic surgeons in the operating room. Occasionally, Access is obtained to the upper middle and
62: Common topics in thoracic surgery 605
posterior mediastinum except for the subaortic Thoracotomy

area below the aortic arch, which is best approached
Rarely, a diagnostic thoracotomy is required when
via an anterior mediastinotomy.
less invasive procedures are inappropriate or have
failed to provide a diagnosis. Access is obtained to
Anterior mediastinotomy the mediastinal lymph node groups, the great ves-
Anterior mediastinotomy is a left parasternal inter- sels, oesophagus, lung and pericardium for tissue
costal incision employed to access tissue from the sampling. Frozen section analysis usually provides
anterior mediastinum (e.g. thymic lesions). A short an immediate diagnosis and this result will deter-
horizontal or vertical incision may be made either mine what further intraoperative measures, if any,
in the second or third intercostal space or by resect- are required.
ing a costal cartilage. A left anterior mediastinot-
omy allows excellent access to the subaortic lymph
nodes, the primary site of spread for tumours in the Basic thoracic surgical techniques
left upper lobe.
Pleural aspiration
Pleural aspiration and biopsy Pleural aspiration may be used in diagnosis, as the
primary treatment of a pleural collection or as a
When a pleural effusion is present (Figure 62.1),
preliminary measure prior to the insertion of a chest
pleural fluid may be aspirated (thoracocentesis)
tube for the drainage of a pleural effusion. The pres-
using a needle and syringe. Cytological, microbio-
ence of fluid should be confirmed on physical exam-
logical and biochemical analyses may provide a
ination and chest X‐ray (see Figure 62.1) prior to
clue as to the cause of the pleural effusion. Pleural
commencement. With the patient in a comfortable
biopsy can be performed at the same time using an
position sitting up, the chest is widely prepared and
Abram’s needle.
the puncture site chosen. Local anaesthetic is infil-
trated liberally down to the pleura. The aspiration
Percutaneous biopsy needle is inserted at the upper edge of the rib and up
Many chest wall, pleural, pulmonary or mediastinal to 1 L can safely be removed at a given sitting. Upon
masses can be biopsied under CT control. This completion, the needle is removed and a small
allows a tissue diagnosis to be made prior to any dressing applied. A chest X‐ray is then performed to
surgical intervention. It must be noted that a nega- exclude a pneumothorax.
tive biopsy result does not exclude malignancy.
Chest tube insertion and management
Video‐assisted thoracoscopic surgery Common indications for chest tube insertion include
spontaneous pneumothorax, tension pneumotho-
Thoracoscopy, the thoracic equivalent of laparos- rax, a large pleural effusion or empyema and post‐
copy, uses cameras, telescopes and television moni- traumatic haemothorax. Chest tubes are placed
tors to inspect the pleural space, lung and routinely at the completion of intrathoracic
mediastinum. Biopsy material may be taken from
lesions in all these areas. The most common appli-
cation is for lung and pleural biopsy. Three ports
made by 2‐cm incisions in the chest wall are used in
the hemithorax, one for the telescope with the cam-
era and light source and two for the instruments.
Some therapeutic procedures, especially the man-
agement of recurrent spontaneous pneumothorax,
recurrent pleural effusions and thoracodorsal sym-
pathectomy, are routinely carried out using video‐
assisted thoracoscopy (VATS) techniques. More
recently, minor and major resections of lung tissue
such as a lobectomy have been performed in this
way. VATS techniques have resulted in patients
experiencing less postoperative pain, having a
shorter in‐hospital stay and returning to a normal Fig. 62.1 Chest X‐ray showing a large left‐sided pleural
life and/or work sooner. effusion.
operations. In all situations, it is mandatory that an

Box 62.1 Indications for tracheostomy
experienced operator insert the tube, because a
badly performed placement is extremely dangerous. • Respiratory tract obstruction
The usual site for insertion is the fourth or fifth • Tracheobronchial toilet/retained secretions
intercostal space in the mid‐axillary line, but for the • Prolonged mechanical ventilation
drainage of specific air, fluid or blood collections, the • Elimination of respiratory dead space
appropriate location on the chest wall should be cho- • Radical laryngeal surgery
sen. The patient should be in a comfortable and
relaxed position, and adequate local analgesia is
essential. Following antiseptic skin preparation and anaesthesia. Alternative settings include the inten-
infiltration of local anaesthetic into the skin, muscle sive care unit (percutaneous tracheostomy) or the
layers and pleura, a skin incision is made over the bedside (minitracheostomy). Via a midline lower
middle of the chosen intercostal space. The incision is cervical incision, a stoma is created at the level of
deepened using blunt dissection (with artery forceps) the second and third tracheal rings through which a
down to and through the pleural layer. Final dissec- cuffed tracheostomy tube is placed. The lower air-
tion into the pleural space is made with a finger, and way is suctioned with a fine catheter and, after the
the point of entry can be widened by opening the tube is secured in position and the cuff inflated,
artery forceps widely in two directions at 90° to each ventilation can commence.
other. If a tension pneumothorax is present, this
manoeuvre will result in a rush of air and immediate Complications
relief for the patient. The chest drain is inserted
through the chest wall and firmly retained in position The complications of tracheostomy are listed in
with strong non‐absorbable sutures. The drain tube Box 62.2.
is then connected to an underwater drainage system.
In almost all situations the drain should be connected
to wall suction, usually high flow and low pressure Thoracotomy
(e.g. 20 cmH2O). A chest X‐ray must always be per- Posterolateral thoracotomy
formed following chest tube insertion to confirm
tube position and to exclude a large pneumothorax. Posterolateral thoracotomy is the standard approach
A chest drain should be removed only when all for major pulmonary resections. The incision is
air leak and fluid drainage has ceased. The lung located below the inferior angle of the scapula, the
should be fully expanded on chest X‐ray. A chest latissimus dorsi is divided and the pleural space is
tube must never be ‘clamped’ prior to removal. The entered along the superior surface of the fifth or
patient is asked to breathe in maximally while the sixth rib.
tube is briskly removed and an occlusive dressing
placed over the wound. Lateral thoracotomy
Lateral thoracotomy is used when only limited
Tracheostomy access is required, such as in the operative treatment
of recurrent pneumothorax. The incision is made
Tracheostomy is the making of a surgical opening between the anterior and posterior axillary lines.
in the trachea. Recent modifications have included
percutaneous tracheostomy and minitracheostomy.
Box 62.2 Complications of tracheostomy
Indications
Operative
The common indications for tracheostomy are • Haemorrhage
listed in Box 62.1. The benefits of a tracheostomy • Pneumothorax
are that it overcomes respiratory tract obstruction, • Tube malposition
allows control of secretions, reduces respiratory Postoperative
dead space and allows mechanical ventilation other • Tube obstruction or dislodgement
than via an endotracheal tube. • Haemorrhage
• Tracheal stenosis
Method • Dysphagia
• Tracheo‐oesophageal fistula
An elective surgical tracheostomy is performed
• Tracheo‐innominate fistula
in the operating room usually under general
Anterior thoracotomy Secondary chest wall tumours

Anterior thoracotomy is commonly used for open Involvement of the ribs and sternum by secondary
lung biopsy. An incision is made beneath the male tumours far exceeds that by primary bone tumours.
nipple or female breast. There is a low incidence of Direct extension to the chest wall may occur in
post‐thoracotomy neuralgia using this approach. breast or lung carcinomas. Chest wall mestatases
are often multiple and commonly originate in the
Median sternotomy lung, prostate, kidney, thyroid, stomach, uterus or
Median sternotomy or ‘sternal split’ gives excellent colon. Tumours with multiple chest wall secondary
access to the anterior mediastinum, pericardium, deposits usually have a very poor prognosis.
heart and great vessels. Anterior mediastinal
tumours (e.g. thymomas) and apices of each lung (in Chest wall infections
lung volume reduction operations) can be removed
via this approach. De novo infections of the chest wall are extremely
rare, and currently infection is most associated with
a recent sternotomy or thoracotomy wound. Risk
Common thoracic disorders factors for postoperative wound infection include
diabetes and morbid obesity. Abscesses can occur
Chest wall within the soft tissue planes and very rarely an
empyema thoracis can ‘point’ through the chest
A classification of common chest wall conditions is wall (empyema necessitans).
given in Box 62.3. Chest injuries are presented in
Chapter 48. Soft tissue tumours and primary bone
tumours will not be discussed further (see Chapters
45 and 51). Pleural effusion
The pleural space is a potential cavity that normally
Pectus excavatum contains negligible amounts of fluid due to equilib-
In pectus excavatum or ‘funnel chest’, there is a vari- rium between its production and absorption. The
able amount of depression of the sternum, lower accumulation of fluid within this space may be a
costal cartilages and ribs. Frequently asymmetric, manifestation of local or systemic disease.
the deformity may displace the heart into the left
chest. Heart and respiratory function are seldom Classification and aetiology
impaired. Surgery, when indicated, is entirely cos-
metic to correct the deformity. There are two types of pleural effusion: a transu-
date or exudate. The common causes of each are
given in Box 62.4.
Pectus carinatum
In pectus carinatum or ‘pigeon chest’, the opposite
Pathophysiology
deformity exists, where the sternum protrudes for-
ward like the keel of a boat. Again, surgical correc- A transudate (specific gravity <1.016 and protein
tion is possible if the deformity is cosmetically content <3 g/dL) results from the altered production
unacceptable. or absorption of pleural fluid. There is elevated sys-
temic or pulmonary capillary pressures, lowered
Box 62.3 Classification of chest wall
conditions
Box 62.4 Causes of pleural effusion
• Congenital anomalies: pectus excavatum, pectus
Transudates
carinatum
• Congestive heart failure
• Chest injuries
• Cirrhosis
• Soft tissue tumours: lipomas, neurofibromas,
• Nephrotic syndrome
fibrosarcomas, liposarcomas
• Hypoalbuminaemia
• Primary bone tumours: chondromas, fibrous
dysplasia, osteosarcomas, Ewing’s tumour, myeloma Exudate
• Secondary chest wall tumours • Infective (post‐pneumonic)
• Chest wall infections • Malignancy
• Thoracic outlet syndrome • Chylothorax
plasma oncotic pressure or lowered intrapleural pres-

Box 62.5 Investigations of pleural
sure. There is no disorder of the pleural surfaces. An
effusion
exudate (specific gravity >1.016 and protein content
>3 g/dL) is found in the presence of diseased pleural • Chest X‐ray
surfaces or lymphatics where there is increased capil- • CT scan of chest
lary permeability or lymphatic obstruction. • Diagnostic pleural aspiration
• Pleural biopsy (needle, video‐assisted thoracoscopy
or thoracotomy)
Surgical pathology
• Bronchoscopy
Pneumonia of any cause may be complicated by the
formation of a pleural effusion. Should pus form
within the pleural space, the collection is known as or non‐diagnostic. Should the effusion prove to be
an empyema thoracis. Currently, the most common the result of a malignant process, it is important to
cause of a post‐pneumonic pleural effusion and adequately stage the disease prior to the commence-
empyema is bacterial infection. ment of therapy.
Malignant pleural effusions can result from sec-
ondary pleural deposits, extension of the primary Management
(lung) tumour to the pleural surface or lymphatic
Therapy should be directed to any underlying cause
obstruction. Metastatic lung or breast carcinoma is
such as pneumonia (antibiotics), congestive heart
the most common cause of malignant pleural effu-
failure (diuretics) or malignancy (chemotherapy or
sions, but other common primary sites include the
radiotherapy).
ovary, colon and kidney. There are frequently asso-
The prognosis in patients with a malignant pleu-
ciated pulmonary metastases, but in some instances
ral effusion is poor; an average survival of 6 months
the intrathoracic metastatic lesion may be confined
follows diagnosis. Treatment of the effusion is there-
to the pleural space. The effusions are often blood‐
fore, at best, palliative. Closed chest tube drainage
stained (serosanguineous), with positive cytology in
will provide short‐term symptomatic relief, but the
up to 70% and a positive pleural biopsy in 80% of
effusion usually re‐accumulates on tube removal. An
malignant effusions.
attempt should be made to obliterate the pleural
Chylothorax refers to the accumulation of
space (pleurodesis) to prevent the effusion re‐accu-
chyle within the pleural space due to disruption of
mulating. This may be achieved by introducing a
the thoracic duct. Very rarely a congenital anom-
sclerosing agent (e.g. talc) into the pleural space via
aly of the thoracic duct and seldom from tumour
a chest tube or at operation (VATS or thoracotomy)
involvement, chylothorax is usually the result of
following drainage of the effusion.
surgical trauma to the duct somewhere along its
Chylothorax usually responds to non‐operative
course.
therapy: chest tube drainage of the collection and
measures to reduce chyle flow (no‐fat diet, paren-
Clinical features teral nutrition). Should the effusion persist or
re‐accumulate, operative intervention (thoracic
Common symptoms of a pleural effusion include
duct ligation and/or pleurodesis) is indicated.
pleuritic chest pain, shortness of breath, cough and
Empyema is managed in its early stages with
haemoptysis (malignant effusion). The physical
dependent chest tube drainage. The pleural space
signs of a large pleural effusion are shown in
may be irrigated with antiseptic solution. In chronic
Table 62.1.
cases, a thick fibrous wall or cortex forms around the
pus‐filled pleural space. Treatment options include
Investigations prolonged closed‐chest tube drainage, open chest
tube drainage after resection of a segment of rib and
Investigations are listed in Box 62.5. Chest X‐ray open surgical decortication to remove the entire
(see Figure 62.1) will determine the extent of the abscess wall. This releases the restricted chest wall
effusion and may demonstrate underlying lung dis- and diaphragm and allows the lung to re‐expand.
ease. CT will also reveal significant intrathoracic
disease. Diagnostic pleural aspiration will reveal
the type of effusion based on appearance and cyto-
Pneumothorax
logical, microbiological and biochemical analyses.
Pleural biopsy should be performed utilising VATS Pneumothorax refers to the presence of air within
if the diagnostic pleural aspiration is unsuccessful the pleural space. The air usually originates from
against the chest wall, thereby sealing the site of

Box 62.6 Types of pneumothorax
the air leak. Once the tube stops bubbling it can be
• Primary spontaneous pneumothorax removed.
• Secondary spontaneous pneumothorax
• Tension pneumothorax Secondary spontaneous pneumothorax
• Traumatic pneumothorax
Secondary spontaneous pneumothorax occurs in
the presence of significant underlying lung or pleu-
the lung itself, but it may come from outside (after ral disorders, such as primary or secondary malig-
penetrating trauma) or from the oesophagus (after nancy, chronic airway disease (especially bullous
endoscopic perforation). The common types of emphysema) and pulmonary infections (bronchiec-
pneumothorax are listed in Box 62.6. Traumatic tasis and lung abscess). The clinical features reflect
pneumothorax is discussed in the chapter on chest the underlying disorder, and the presentation and
injuries (see Chapter 48). initial management of the pneumothorax is as dis-
cussed in the preceding section.
Primary spontaneous pneumothorax

Tension pneumothorax
Primary spontaneous pneumothorax is the most
A tension pneumothorax is present when the site
common type of pneumothorax and usually
of air leak in the lung acts as a one‐way valve
results from the rupture of a tiny bleb or bulla at
such that air enters the pleural space during inspi-
the lung apex. Occurring in tall, thin, young adults
ration and coughing but its escape is prevented
of either sex, it presents with acute chest pain and
during expiration, thus raising the pressure within
shortness of breath. Physical findings are given in
the pleural space. Such pressure or tension com-
Table 62.1. Chest X‐ray reveals an absence of
presses the lung and shifts the mediastinum
peripheral lung markings and often a poorly
towards the other side. This compresses the nor-
defined line marking the border between lung and
mal lung and may also kink and distort the supe-
air (Figure 62.2). The lung may be completely col-
rior vena cava. The diagnosis should be suspected
lapsed at the hilum.
when signs of a large pneumothorax are associ-
If the pneumothorax is small, it may need no
ated with mediastinal shift and an elevated jugu-
therapy other than observation and a repeat chest
lar venous pressure. This constitutes a medical
X‐ray to confirm lung re‐expansion or it may be
emergency. A large‐bore needle should be inserted
aspirated with a needle. If the pneumothorax is
to the affected side and if the diagnosis is correct
large or under tension (discussed later) or if there
will be met by the hiss of escaping air and relief of
is an associated pleural effusion, a formal chest
the immediate problem. A formal chest tube
tube should be inserted. As air is evacuated from
should then be inserted.
the pleural space, the lung expands and presses
Recurrent spontaneous pneumothorax
Approximately 30% of primary spontaneous pneu-
mothoraces will recur and after a second episode
this figure rises to 70%. If the same side has been
affected twice or more, and especially if tension has
occurred, a definitive procedure should be consid-
ered. Approaches via VATS or a limited thoracot-
omy include stapling of apical bullae to prevent
further air leakage, and pleurodesis (either abrasive
or chemical) or pleurectomy, which allows the vis-
ceral pleura to adhere to the parietal pleura or the
bare chest wall.
Carcinoma of the lung
Fig. 62.2 Chest X‐ray showing a large right‐sided
spontaneous pneumothorax. Arrows show the collapsed Carcinoma of the lung is the most common cause of
lung edge. cancer deaths in males and the second most common
cause of cancer deaths after breast cancer in females. Tending to be peripheral in location, their behaviour
Usually occurring in patients older than 50, the over- is based on the most prominent cell type.
all incidence in both sexes continues to rise. Small‐cell carcinomas make up about 10% of
malignant lung tumours. Mostly centrally located,
they are the most malignant and carry the worst
Aetiology
prognosis. The cells are small, round or oval in
Cigarette smoking is the single most common pre- appearance (‘oat cell’). Ectopic formation of adren-
disposing factor. Environmental or occupational ocorticotropic hormone (ACTH) or antidiuretic
exposure to asbestos, arsenic, nickel, chromium hormone (ADH) may occur. Lymphatic and pleural
and hydrocarbons also play a role. The highest geo- invasion is common. Extrathoracic involvement at
graphical incidence is in parts of Scotland, suggest- presentation is seen in 70% of tumours.
ing a possible genetic influence.
Clinical features
Surgical pathology
Approximately 10–20% of lung cancers are asymp-
The pathological types of lung carcinoma are listed tomatic and present as a chance finding on routine
in Box 62.7. chest X‐ray. Symptoms may be thoracic or
Squamous cell carcinoma accounts for about extrathoracic.
35% of all lung carcinomas. Most often centrally Thoracic symptoms include cough, haemoptysis,
located, these tumours arise from metaplasia of the shortness of breath, chest pain (pleuritic or retroster-
normal bronchial mucosa. Varying degrees of dif- nal), hoarseness of voice (involvement of recurrent
ferentiation are seen depending on the presence of laryngeal nerve), arm pain and weakness (Pancoast’s
keratin, epithelial pearls, prickle cells, basal palli- syndrome; apical tumour involving brachial plexus).
sading, cell size and mitotic activity. Extrathoracic symptoms include those of metasta-
Adenocarcinoma represents about 45% of lung ses (e.g. bone, central nervous system, liver, adrenals)
carcinomas. More often found in women and and those of non‐metastatic paraneoplastic syn-
located peripherally in the lung, the histopathology dromes. These include the production of ectopic
reveals acinar or papillary glandular elements. The ACTH, ADH and parathyroid hormone. Wrist and
tumour may form in long‐standing scars (e.g. post‐ ankle pain due to hypertrophic osteoarthropathy
tuberculosis) and spreads via the bloodstream. and a variety of myopathies are also found.
Alveolar cell carcinoma is a highly differentiated Physical findings include hypertrophic pulmo-
form of adenocarcinoma. Tall columnar epithelial nary osteoarthropathy, fingernail clubbing, supra-
cells proliferate and spread along the alveolar walls. clavicular and cervical lymphadenopathy, signs of
The tumour may be solitary, multinodular or dif- brachial plexus involvement, Horner’s syndrome
fuse (pneumonic). It may be indistinguishable from (ptosis, miosis, anhidrosis, enophthalmos from
metastatic adenocarcinoma to the lung. involvement of the cervical sympathetic ganglia),
Large cell carcinoma comprises another 15% of elevated jugular venous pressure and facial oedema
malignant lung tumours. Peripherally located, there (superior vena caval obstruction). In the chest there
is abundant cell cytoplasm with a cellular pattern may be signs of a pleural effusion or lung collapse
that is predominantly anaplastic. (see Table 62.1).
Adenosquamous carcinoma is the most common
of the mixed non‐small‐cell types of lung carcinoma.
Investigations
Investigations are listed in Box 62.8 and will pro-
vide a tissue diagnosis and aid in determining the
Box 62.7 Pathological types of lung
extent of intrathoracic disease. Figure 62.3 shows
carcinoma
typical findings on chest X‐ray and CT scan. If met-
Non‐small‐cell lung cancer astatic disease is suspected in sites such as bone or
• Squamous cell carcinoma the brain, additional scans of these areas should be
• Adenocarcinoma included so as to accurately stage the disease and
• Large‐cell carcinoma avoid unnecessary surgical intervention. PET scan-
• Mixed (adenosquamous) ning is important in the evaluation of regional
lymph nodes and also distant metastases. The radio-
Small‐cell carcinoma
active tracer fluorodeoxyglucose detects differences
Staging of lung cancer

Box 62.8 Investigations for lung
carcinoma Staging of non‐small‐cell lung cancer is clinical and
based on descriptors for the size and location of the
• Chest X‐ray primary tumour (T), the spread to lymph nodes
• Sputum cytology within the thorax (N) and to the presence or absence
• CT scan of chest and upper abdomen of distant metastases (M). TNM subsets are grouped
• PET scan
together into stages 0 through IV and these stages
• Needle biopsy under CT control
provide information about prognosis, allow a com-
• Bronchoscopy and biopsy
parison of outcomes from different clinical series
• Mediastinoscopy or anterior mediastinotomy
and also guide therapy.
• Video‐assisted thoracoscopic biopsy
(a)
Carcinoma of the bronchus presenting as a solitary
pulmonary nodule (‘coin lesion’) in the lung periph-
ery should be differentiated from:
• secondary tumours
• benign lung tumours (bronchial adenoma)
• non‐specific granuloma
• tuberculous granuloma.
Management
Unfortunately, two‐thirds of patients are incurable
at presentation owing to spread evidenced by one
or more of the following:
• distant metastases
(b) • a malignant pleural effusion
• involved cervical lymph nodes
• superior vena caval obstruction
• recurrent laryngeal nerve palsy.
If the patient has an otherwise resectable tumour
and adequate respiratory reserve, surgical resection
offers the only hope of long‐term survival.
Surgical treatment consists of a thoracotomy with
removal of the entire lung or lobe along with
regional lymph nodes and contiguous structures.
Where possible, lobectomy is the procedure of
choice. Pneumonectomy is used if the tumour
involves the main bronchus, extends across a fissure
or is located such that wide excision is required.
Survival following ‘curative’ resection is approxi-
Fig. 62.3 (a) Chest X‐ray showing a right hilar lung mately 30% at 5 years and 15% at 10 years. The
cancer with collapse and consolidation of the right best results are found in squamous cell carcinoma
upper lobe. (b) CT scan showing the right hilar lung followed by large‐cell carcinoma and adenocarci-
cancer.
noma. There are very few survivors of small‐cell car-
cinoma beyond 2 years.
in metabolism between normal and malignant tis- Radiotherapy may be ‘curative’ in patients with
sue. Metastatic disease has been found in up to 15% early‐stage disease unfit for surgical resection.
of lung cancers thought to have resectable disease. However, the usual role for radiotherapy is in
The number of these investigations required by a the palliation of pain from bone secondaries,
given patient is determined by the ease with which a superior vena caval obstruction or haemoptysis.

tissue diagnosis and accurate staging is reached. Combinations of radiotherapy and platinum‐based
chemotherapy provide the best palliation for Solitary pulmonary nodule

patients with good performance status and non‐
A solitary pulmonary nodule is a single well‐defined
resectable disease.
opacity up to 3 cm in diameter seen radiologically.
Multi‐agent chemotherapy is indicated for small‐
Frequently asymptomatic and found on chest X‐ray
cell carcinoma. There is a small survival benefit
screening (Figure 62.4), there are numerous possi-
from palliative combination chemotherapy in non‐
ble causes (Box 62.9) but malignant lesions must be
small‐cell lung cancer. Trials are currently under-
excluded. Those less than 1 cm in diameter carry a
way to determine whether there is a role for
low chance of being malignant and can be observed.
induction chemotherapy in patients with locally
Where possible, increases in size should be deter-
advanced non‐small‐cell lung cancer. Responders, if
mined by sequential imaging and such occurrence
down‐staged, can be offered surgical resection with
mandates non‐surgical biopsy or surgical resection.
a view to long‐term survival. This management
However, stable lesions over a 2‐year period
strategy remains controversial and should currently
may also be observed. Investigative modalities
only be offered in the context of a properly con-
(Figure 62.4) are similar to those used for patients
ducted randomised clinical trial.
(a) (c)
(b)
Fig. 62.4 (a) Chest X‐ray, (b) CT scan and (c) PET scan appearance of a solitary pulmonary nodule.
Box 62.9 Causes of a solitary pulmonary Box 62.10 Classification of primary

nodule mediastinal tumours
Benign Anterosuperior masses

• Infectious granuloma (tuberculosis, atypical • Germ cell tumours
mycobacteria, histoplasmosis, coccidioidomycosis) • Thymoma
• Hamartoma • Lymphadenopathy
• Arteriovenous malformation • Retrosternal thyroid
• Aneurysm of the aortic arch
Malignant
• Lung carcinoma Middle mediastinal masses
• Solitary metastasis (from breast, colon, kidney) • Lymphadenopathy
• Malignant carcinoid tumour • Mediastinal cysts
• Extranodal lymphoma • Aneurysm of ascending aorta
Posterior mediastinal masses

• Neurogenic tumours (benign and malignant)
• Peripheral intercostal nerves: neurofibroma,
with suspected lung carcinoma. A negative needle
neurilemmoma
biopsy does not exclude a malignant cause and so a
• Sympathetic ganglia: ganglioneuroma,
surgical biopsy/excision may be required regardless
neuroblastoma
of the needle biopsy finding.
• Paraganglia: phaeochromocytoma, paraganglioma
• Oesophageal: duplication, tumours, diverticulae
Mediastinal tumours • Hiatus hernia
• Bronchogenic cyst
The mediastinum is a midline space between the
pleural cavities. It is divided into the superior, ante-
rior, middle and posterior compartments.
Mediastinal tumours may be primary or secondary malignant and this feature is more frequent in chil-
in origin. Secondary neoplasms most often result dren. All nerve types may be affected (Box 62.10).
from lymphatic spread to mediastinal lymph nodes. Germ cell tumours are the most common ante-
Common primary sites are lung, oesophagus, lar- rior mediastinal tumours and are more common in
ynx, thyroid and stomach. A classification of pri- the young. Types include teratoma, seminoma and
mary mediastinal tumours is given in Box 62.10. non‐seminomatous. Tumour markers may be ele-
vated in non‐seminomatous types and can be used
to monitor the response to therapy.
Mediastinal lymphoma is usually associated with
Approximately half are asymptomatic and have no widespread disease and is seldom the only site
abnormal findings on examination. They are dis- (5%). The majority (90%) are either lymphoblastic
covered by chance on a plain chest X‐ray. Lesions in (Hodgkin’s) or diffuse large cell (non‐Hodgkin’s) in
the young and those with symptoms are more likely type.
to be malignant. Thymoma is more common in adults than chil-
Thoracic symptoms result from compression of dren. About 30% of patients have myasthenia gravis
adjacent structures and include pain (back or chest), and about 15% of patients with myasthenia gravis
shortness of breath, cough or dysphagia. Systemic develop thymoma. The differentiation between
symptoms may be fever, malaise, weight loss and benign (encapsulated) and malignant (invasive)
night sweats. Local findings include cervical lym- thymoma can be difficult.
phadenopathy, facial and/or arm swelling and tra-
cheal shift. General findings may include testicular
Investigations
masses, hepatosplenomegaly and muscle weakness.
Investigations are summarised in Box 62.11. In some
instances, the combination of clinical features and
Surgical pathology
findings on imaging allow a precise diagnosis.
Neurogenic tumours are the most common medias- A patient with myasthenia gravis and an anterior medi-
tinal tumours and are found almost exclusively astinal mass will most likely have a thymoma. The site
in the posterior mediastinum. About 10% are of the lesion will determine the type of biopsy required.
Box 62.11 Investigation of mediastinal Further reading

tumours
Kaiser LR, Jamieson GG, Thompson SK (eds) Operative
Imaging Thoracic Surgery, 6th edn. Boca Raton, FL: CRC Press,
• Chest X‐ray 2018.
• CT scan with contrast LoCicero J, Feins R, Colson YL, Rocco G (eds) Shields’
• MRI (neurogenic or vascular) General Thoracic Surgery, 8th edn, Vols 1 and 2.
• Angiography (vascular) Philadelphia: Wolters Kluwer, 2019.
• Barium swallow (posterior mediastinum)
• Radionuclide (thyroid or parathyroid; gallium for
lymphoma) MCQs
Biochemistry Select the single correct answer to each question. The
• Lactate dehydrogenase (elevated in lymphomas, correct answers can be found in the Answers section
seminomas) at the end of the book.
• β‐Human chorionic gonadotrophin (may be
1 Which of the following clinical signs is not present
elevated in seminomas)
• Alpha‐fetoprotein (non‐seminomatous germ cell
in a patient with a tension pneumothorax?
tumours) a tachypnoea
b hypotension
Tissue diagnosis c elevated jugular venous pressure
• Fine‐needle aspiration biopsy d tracheal deviation towards the side of the
• Mediastinoscopy pneumothorax
• Video‐assisted thoracoscopy
e hyperresonant percussion note on the side of the
• Thoracotomy
pneumothorax
2 Immediate insertion of a chest tube may be

Box 62.12 Management of common
life‐saving in which of the following conditions?
mediastinal tumours
a carcinoma of the lung
• Asymptomatic cysts b pulmonary embolism
–– Pericardial: aspirate c tension pneumothorax
–– Bronchogenic: observe d pleural effusion
• Symptomatic cysts: surgical resection e lung abscess
• Neurogenic tumours
–– Benign, asymptomatic: may observe 3 Which of the following pathological types of
–– Symptomatic: surgical resection carcinoma of the lung has the worst prognosis?
–– Malignant: surgical resection a small‐cell carcinoma
• Thymoma b large‐cell carcinoma
–– Benign: surgical resection c adenocarcinoma
–– Malignant: surgical resection and chemotherapy d squamous cell carcinoma
• Lymphoma: chemotherapy, radiotherapy (rarely e adenosquamous cell carcinoma
surgical resection)
• Germ cell tumours: chemotherapy, radiotherapy,
4 The greatest chance of long‐term survival in a
surgical resection
patient with a localised carcinoma of the lung is
provided by:
Management a chemotherapy
b radiotherapy
Options in management include simple observation c combined chemotherapy and radiotherapy
and follow‐up, aspiration, surgical resection, radio- d surgical excision
therapy, chemotherapy and combinations of surgical e immunotherapy
resection, radiotherapy and chemotherapy. A sum-
mary of the approach to management of the common
primary mediastinal tumours is given in Box 62.12.
Section 16
Problem Solving
63 Chronic constipation
Kurvi Patwala1 and Peter De Cruz2
1
Austin Health, Melbourne, Victoria, Australia
2
Inflammatory Bowel Disease Service, Austin Health, and
contents of the small intestine empty into the

Introduction large intestine, distension of the colon activates
the myenteric plexus leading to three patterns of
Constipation is a common presenting symptom.
motility:
The Rome IV consensus approach to the diagnosis
• Retrograde peristalsis, which occurs mainly in
of functional constipation requires the following.
the right colon
1 Must include two or more of the following:
• Segmentation, which results in minimal transit
a Straining during more than 25% of defecations
over the colon and occurs mainly in the left colon
b Lumpy or hard stools for more than 25% of
• Mass movement, which results in propelling con-
defecations
tents over long distances but occurs only a few
c Sensation of incomplete evacuation for more
times daily.
than 25% of defecations
Motility is likely controlled by a pacemaker in the
d Manual manoeuvres to facilitate more than
transverse colon, which also acts as the main region
25% of defecations (e.g. digital evacuation,
of storage. Colonic motility is under enteric nerv-
support of the pelvic floor)
ous and endocrine control. It can be significantly
e Fewer than three spontaneous bowel motions
affected by physical activity, dietary fibre and emo-
per week
tional states.
2 Loose stools are rarely present without the use of
Colonic motility causes the bowel contents to be
laxatives
retained and mixed to facilitate absorption. It takes
3 Insufficient criteria for irritable bowel syndrome.
3–4 days for the meal residue to finally be evacu-
A more practical approach defines constipation as
ated in the stools. The frequency of bowel move-
a syndrome related to bowel symptoms such as
ments in most normal humans ranges from three
difficult or infrequent passage of stool, hardness
per week to three per day and about 70% of stool
of stool or a feeling of incomplete evacuation that
consistency is water. Consequently, inadequate
may occur secondary to an underlying disorder or
water intake may result in harder stools that are
in isolation. Although constipation is a symptom
difficult to evacuate.
and not a disease, it affects 6–30% of the popula-
The rectum is usually empty until faeces arrives
tion and, if associated with abdominal pain, results
periodically from the colon. Distension of the rectal
in poorer overall health and function. Management
or pelvic muscle walls causes an urge to defecate.
involves diagnosing the underlying cause and tai-
Initially, this can be suppressed by voluntary con-
loring therapy towards improving quality of life
traction of the anal sphincters and pelvic floor mus-
(Figure 63.1).
cles. Further arrival of faeces will eventually make
defecation unavoidable. At defecation, expulsion
is aided by raised intra‐abdominal pressure and
Physiology colonic contraction. The pelvic floor muscles and
the anal sphincters relax so the faeces can be dis-
A solid meal passes from the mouth to the caecum charged through the anus. Subsequently, the pelvic
in 4 hours and residue from this meal reaches the floor muscles and the anal sphincters resume their
rectosigmoid junction by 24 hours. When luminal tone in order to maintain bowel continence.
617
History
Including length of symptoms,
manoeuvres, bristol stool chart scale,
red flags, impact on quality of life
Examination
Including abdominal examination, per
rectal examination, general examination
Consider appropriate investigations
Blood tests Imaging Colonoscopy

FBE, UEC, CMP, AXR To rule out
iron studies, barium swallow carcinoma
glucose, TFTs
Treat underlying disorders

if no underlying pathology, treat
symptoms
Non-phamacological management
Encourage exercise, healthy dietary
intake and good bowel habits
Phamacological management
Fibre supplementation
Laxatives
Bulking agents,
stimulants, stool
softeners, osmotic
laxatives
Physiological studies
Prucalopride
Sitzmark’s test, anorectal
Consider if no effect with
manometry, defecating
laxatives
proctography
Biofeedback aided therapy

Consider for patients with defecatory
disorders
Surgical options
Consider if no response to above and
significant impact on quality of life
Colectomy
sacral nerve stimulation
antegrade colonic enema
STARR procedure
Fig. 63.1 Management algorithm for constipation. AXR, abdominal X‐ray; CMP, calcium, magnesium, phosphate; FBE,
full blood examination; TFTs, thyroid function tests; UEC, urea, electrolytes and creatinine.
63: Chronic constipation 619
malaise) and impact on quality of life determined

Risk factors by use of laxatives, complications and interference
with their sense of well‐being. Lastly, it is important
Box 63.1 outlines the common risk factors asso-
to elicit a thorough past medical history focusing
ciated with the development of constipation.
on conditions associated with constipation, as
Prevalence rates of constipation are higher in
outlined in Box 63.3.
women, ethnic populations and elderly populations
living in residential aged care facilities. Furthermore,
Examination
elderly patients are more likely to be prescribed
therapy for comorbidities that contribute to consti- Abdominal examination may be unremarkable or
pation. Common medications with constipation as reveal distension secondary to a colon full of faeces.
an adverse effect are listed in Box 63.2. A perianal and rectal examination must be per-
formed assessing for faecal soiling on perianal skin,
haemorrhoids, anal fissure, rectocele, puborectalis
Aetiology tenderness and stool in the rectal vault. It is also
important to assess anal resting tone and tone on
A systematic approach incorporating history, straining.
examination and investigations is required to delin- Although the physical examination will concen-
eate underlying aetiology and ongoing manage- trate on the abdomen and anorectum, careful sys-
ment of constipation. A classification of the more temic examination is also important to exclude
common causes of constipation is given in Box 63.3. systemic causes of constipation.
Investigations
Evaluation
Simple blood test investigations such as full blood
count, renal function studies, electrolyte levels, iron
History
studies, glucose and thyroid function tests should
Clinical assessment must begin with a detailed his- be considered to assess for complications or under-
tory that elicits the patient’s symptoms of constipa- lying causes of constipation. Evidence of anaemia,
tion. In particular, questions must be asked about particularly microcytic iron deficiency anaemia,
the timing of onset, manoeuvres used to defecate should prompt further investigation to rule out a
and stool consistency based on a rating scale such malignancy. Deranged electrolytes or endocrino-
as the Bristol Stool Scale. Self‐reported stool fre- logical abnormalities may suggest an underlying
quency is a subjective measure and is often underes- aetiology for constipation. A colonoscopy or
timated. Consequently, utilising a bowel diary may double‐contrast barium enema is often needed to
be of value. Furthermore, red flags such as sudden exclude dangerous organic pathology such as a
change in bowel habits, per rectal blood loss, weight neoplasm. In chronic constipation, a barium enema
loss or a family history of colon cancer must be may be preferable because the colon can be dilated
addressed and investigated appropriately to rule and tortuous, especially with megacolon making
out a sinister cause. The patient should be ques- colonoscopic intubation difficult.
tioned about associated symptoms such as abdominal
bloating, non‐gastrointestinal symptoms (fatigue,
Physiological testing
Physiological testing is based on colonic physiology
Box 63.1 Risk factors associated and is performed in patients with chronic constipa-
with the development of constipation tion that is refractory to fibre supplementation or
laxative use. It can also be utilised when clinical
• Female suspicion of disordered defecation is high.
• Low socioeconomic status
• Lower parental education rates
• Less physical activity Slow transit constipation
• Living in a residential aged care facility This refers to colonic motor dysfunction, which
• Medications (see Box 63.2)
may be due to a marked reduction in interstitial
• Depression
cells of Cajal and colonic intrinsic cells. Slow transit
• Physical and sexual abuse
constipation can be determined using a Sitzmark
• Stressful life events
test, which involves ingestion of a capsule
620 Problem Solving
Box 63.2 Medications associated Box 63.3 Aetiology of constipation

with constipation
Dietary
5‐HT3 antagonists: ondansetron Poor fibre intake
Analgesics Poor fluid intake
Opioids: morphine
Physiological
NSAIDs: ibuprofen
Slow transit constipation
Anticholinergic agents
Intestinal pseudo‐obstruction (Ogilvie’s syndrome)
Tricyclic antidepressants: amitriptyline >
nortriptyline Mechanical obstruction
Antiparkinsonian therapy: benztropine Colon cancer
Antipsychotics: chlorpromazine External compression from malignant lesion
Antispasmodics: dicyclomine Strictures
Antihistamines: diphenhydramine Diverticular
Anticonvulsants: carbamazepine Post‐ischaemic
Antihypertensives Post‐surgical abnormalities
Calcium channel blockers: verapamil, nifedipine Megacolon
Diuretics: frusemide Perianal: rectocele, anal fissure
Centrally acting: clonidine
Neuromuscular disease
Antiarrhythmics: amiodarone
Cerebral: cerebrovascular accidents, Parkinsonism,
β2 antagonists: atenolol
tumours
Bile acid sequestrants: colestyramine, colestipol
Spinal: cauda equina tumour, multiple sclerosis,
Cation‐containing agents
paraplegia
Aluminium
Peripheral: Hirschsprung’s disease, autonomic
Calcium
neuropathy, Chagas’ disease
Bismuth
Myopathies: amyloidosis, scleroderma
Iron supplements
Lithium Functional
Chemotherapy agents Irritable bowel syndrome
Vinca alkaloids: vincristine Immobility: degenerative joint disease
Alkylating agents: cyclophosphamide Pregnancy
Endocrine: pamidronate, alendronic acid Psychiatric and psychological causes: depression,
Other antidepressants: monoamine oxidase inhibitors confusion, cognitive impairment
Other antipsychotics: clozapine, haloperidol,
Endocrine and electrolyte disturbance
risperidone
Diabetes mellitus
Other antiparkinsonian drugs: dopamine agonists
Hypothyroidism
Other antispasmodics: mebeverine, peppermint oil
Hyperparathyroidism
Sympathomimetics: adrenaline, terbutaline
Hypercalcaemia
Miscellaneous: barium sulphate, oral contraceptive
Hypokalaemia
pill, polystyrene resins
Hypomagnesaemia
Other
Uraemia
Scleroderma
containing 20–50 radiopaque markers followed
Heavy metal poisoning
by either serial abdominal X‐rays until all mark-
ers are defecated or a single abdominal X‐ray on
day 5. The presence of more than 20% retained
Defecatory disorders
markers at day 5 is consistent with delayed transit
constipation. Intraluminal assessments with manom- These are defined by impaired rectal evacuation
etry and barostat can be used, although these are with normal or delayed colonic transit. This may be
imperfect surrogate markers for normal and caused by inadequate propulsive rectal forces or
abnormal colonic motor function. Colonic transit increased resistance to evacuation secondary to
testing is not recommended in early assessment as anismus (high resting anal pressure) or dyssynergia
it does not exclude the presence of defecatory (incomplete relaxation or paradoxical contraction
disorders and further anorectal testing is often of the pelvic floor or external anal sphincters).
required. Defecating proctography can be performed by
Table 63.1 Laxatives used in the management of constipation.
Class Mechanism of action Examples
Bulking agents Absorption of water in colon to increase faecal bulk Ispaghula husk
Methylcellulose
Sterculia
Stimulant Increase intestinal motility through stimulation of Bisacodyl
laxatives colonic nerve endings Senna
Sodium picosulphate
Stool softeners Soften stool by assisting water to mix with faeces Docusate
and lubricate stool to allow easier passage Liquid paraffin
Osmotic Increase colonic water absorption through osmosis Lactulose
laxatives and have local irritant effects to increase motility Fleet phosphosoda
Magnesium sulphate
filling the rectum with radiological contrast and are significantly effective in reducing symptomatic
allowing the patient to attempt defecation on a constipation. However, patients should be coun-
radiolucent toilet seat. The progress of the contrast selled on their delayed effect, taking several weeks
is assessed by fluoroscopy. Another option is the to reduce symptoms. A number of laxative options
rectal balloon expulsion test, which monitors the exist with varying pharmacological properties.
patient’s ability to evacuate a water‐filled balloon. Examples of each laxative option with the corre-
Requiring up to 5 minutes is considered normal. sponding mechanism of action are described in
Anorectal manometry assesses the integrity of the Table 63.1. No evidence is currently available
intrinsic innervation of the rectum and anus by that indicates which laxative or laxative regimen is
inflating a rectal balloon and assessing for a tran- superior.
sient drop in anal pressures. A clinically absent rec- Treatment with prucalopride, a 5‐HT4 agonist, is
tosphincteric reflex is suggestive of Hirschsprung’s appropriate for use in patients with chronic consti-
disease. pation unresponsive to laxatives and works by
While these tests are useful in the diagnosis of increasing colonic transit time. It can result in clini-
defecatory disorders, they are often difficult to cally significant improvements in the number of
interpret given the difficulty patients face in per- spontaneous bowel movements and reduction in
forming these tests in a clinical and public environ- severity of symptoms. There is a rapid onset of
ment. Therefore, an environment as private as action and improvement is maintained for at least
possible is advised. 12 weeks.
For patients with defecatory disorders, biofeed-
back‐aided pelvic floor retraining plays a role.
Management Using visual and auditory feedback recorded by
manometry or electromyographic sensors, patients
The management of constipation is directed can learn to relax pelvic floor muscles and increase
towards the underlying aetiology. If the primary abdominal pressure during defecation. Biofeedback
pathology is not amenable to treatment or no pathol- therapy is safe and evidence suggests that 55–82%
ogy is identified, management is symptomatic. of patients maintain symptom improvement.
Non‐pharmacological approaches suggest improv- However, the expertise to perform this is not yet
ing dietary practices and encouraging exercise. widely available.
There is limited evidence for probiotic use or Surgical intervention plays a role when non‐sur-
increasing fluid intake unless the patient is mark- gical measures fail and symptoms significantly
edly dehydrated. Other simple behavioural prac- impact the patient’s quality of life. For patients with
tices such as developing a regular bowel routine documented slow transit constipation not respond-
and responding to the urge for defecation should be ing to conservative therapy, a colectomy and ileo-
encouraged. rectal anastomosis can be performed. Although this
Over‐the‐counter therapy including fibre supple- treats primary symptoms, it is unlikely to improve
ments and laxatives, enemas or suppositories form abdominal pain and bloating. Other options for
the bulk of outpatient constipation management. slow transit constipation or constipation refractory
Soluble dietary fibre supplements, up to 30 g/day, to laxative use include sacral nerve stimulation and
622 Problem Solving
antegrade colonic enemas, which have limited Saha L. Irritable bowel syndrome: pathogenesis, diagno-
exposure in adults. Response to sacral nerve stimu- sis, treatment and evidence‐based medicine. World J
lation is variable and many patients have signifi- Gastroenterol 2014;20:6759–73.
cant loss of efficacy after some time. Alterations in
the pulse width or frequency of stimulation appear
to have no significant effect on the improvement of MCQs
symptoms in patients with constipation. For
patients with defecatory disorders secondary to rec-
tal intussusception or rectocele, a stapled transanal
rectal resection (STARR) procedure can be consid-
ered. The STARR procedure involves stapling 1 A 22‐year‐old female has had constipation for 4
excess rectal mucosa with the aim of alleviating weeks since starting medical school. She occasion-
symptoms. However, long‐term outcomes of ally has mild cramping abdominal pain. She has no
patients are questionable and rates of complica- other symptoms and no family history of colorectal
tions, such as pelvic sepsis, fistula formation and cancer. Which of the following is the most
bowel perforation, are relatively high. appropriate management?
a encouraging oral dietary fibre and fluids
b colonoscopy and anorectal physiology tests
Irritable bowel syndrome c anorectal biofeedback therapy
d right hemicolectomy
Irritable bowel syndrome classically presents with e teaching self‐digital extraction of faeces from
abdominal discomfort that is relieved by defecation rectum
or is associated with a change in stool frequency or
appearance in the absence of organic pathology. It 2 An 88‐year‐old male with multiple comorbidities
can be divided into diarrhoea‐predominant or con- including Parkinson’s disease, hypothyroidism and
stipation‐predominant subtypes. Management is depression represents with a several‐year history of
directed towards symptomatic relief of pain and ongoing constipation. A colonoscopy performed a
bowel frequency, with counselling to avoid stress or year ago was normal with no evidence of obstruc-
precipitating factors, dietary advice and pharma- tion, malignancy or stricturing. Which of the
cotherapy. More severely affected patients may following is the most likely cause?
require formal psychological management. The a psychological
majority of patients will be satisfied with reassur- b colon cancer
ance that dangerous diseases like colorectal cancer c medication adverse effects
have been excluded. d immobility
e poor fibre and fluid intake
Other causes 3 A 51‐year‐old male presents with a 1‐year history

of worsening constipation, abdominal cramps and
Specific conditions like rectal intussusception, sig- weight loss. Blood test investigations reveal a
moidocele, Hirchsprung’s disease (especially short‐ microcytic iron deficiency anaemia. There is no
segment disease in adults) and Chagas’ disease are family history of colon cancer. The most appropri-
relatively rare and discussed further in standard ate next step is:
textbooks on colorectal surgery. a anorectal physiology tests
b colonoscopy
c barium swallow
Further reading d use a combination of laxatives and enemas
e right hemicolectomy
Bharucha AE, Pemberton JH, Locke GR. American
Gastroenterological Association technical review on
4 A 43‐year‐old mother of two children complains of
constipation. Gastroenterology 2013;144:218–38.
difficulty in initiating rectal evacuation. She feels
Lehur PA, Stuto A, Fantoli M et al. ODS II Study Group.
Outcomes of stapled transanal rectal resection vs. bio- there is a lump in the perineum which requires
feedback for the treatment of outlet obstruction associ- vaginal reduction prior to effective evacuation.
ated with rectal intussusception and rectocele: a Which of the following is the most appropriate
multicentre, randomised, controlled trial. Dis Colon management?
Rectum 2008;51:1611–18. a transit marker studies
b defecating proctogram of the following is the most appropriate

c anorectal biofeedback management?
d teach good hygienic practices a regular use of St. Mark’s anal dilator prior to
e use rectal enemas to assist bowel movements defecation
b mandatory use of squatting posture at
5 After a previous hysterectomy, a 55‐year‐old defecation
mother of three children complains of constipation. c transit marker studies
Defecating proctogram showed a lack of relaxation d avoid laxatives but teach rectal washout instead
of the puborectalis paradoxus at defecation. Which e anorectal biofeedback therapy
64 Faecal incontinence
Andrew Bui
approximately A$66.7 billion, according to a study

Introduction by Deloitte Access Economic.
Faecal incontinence is defined as an involuntary

loss of liquid or solid stools. This symptom may be Pathophysiology
further divided into passive and urge incontinence.
Passive incontinence means that the patient is not The maintenance of normal faecal continence
aware of the passage of stools and is mainly due to depends on complex interactions between
impaired internal anal sphincter or anorectal sen various factors: an intact anorectal structure
sory dysfunction. Urge incontinence refers to the consisting of internal anal sphincter (IAS),

situation where the patient is aware of the signal to external anal sphincter (EAS) and puborectalis,
pass stools but is unable to prevent it from happen rectal reservoir and compliance, anorectal angle,
ing. It is due to dysfunction of contraction or neu stool consistency, intact sensory and motor
rological control of the external anal sphincters. neural pathways, and normal mental function
Patients often present with mixed symptoms of pas (Figure 64.1).
sive and urge incontinence. Another term in use is The sphincter muscle complex, which controls
anal incontinence, which refers to the loss of stools the exit of stools, is composed of the puborectalis
and flatus. and internal and external sphincter muscles.
The estimated prevalence of faecal incontinence The IAS is smooth muscle under involuntary con
from various studies is 2–18%, with a higher trol and mainly accounts for the resting anal tone.
prevalence of up to 25% among the older popula The puborectalis and EAS are striated muscle con
tion and people in institutional care. The large trolled by the pudendal nerve via the S2–S4 nerve
variation in the prevalence reported is attributed roots.
to the different definitions of faecal incontinence The arrival of stool or gas in the rectum leads to
used in various studies, sample size and popula distension and relaxation of the IAS and sampling
tion sampled. Additionally, there is under‐reporting of the contents by the richly innervated anal canal
as most people find it embarrassing and distress mucosa, which sends signals to the central nervous
ing to discuss even with healthcare providers. system (CNS) via the spinal cord for interpretation
A recent systematic review of the literature high of whether evacuation is acceptable. If it is socially
lighted the difficulties and the inaccuracy of the acceptable, the EAS is voluntarily relaxed for evac
prevalence studies of faecal incontinence and pro uation of rectal contents. If it is not, then the EAS is
vided an estimated prevalence rate of 1 in 8 com commanded to contract to close the anal canal and
munity adults. defer defecation.
Faecal incontinence is a distressing and socially Loss of continence therefore results from inter
isolating condition that leads to poor quality of ruption of this complex coordination between
life. It is also costly to the wider community: in neural and motor pathways, from impairment of
Australia in 2010, the estimated cost per person was the anorectum and sphincter complex, and from
A$14 023, with an overall cost to the community of change in stool consistency.
625
626 Problem Solving
Box 64.1 Causes of faecal incontinence
Incontinence with abnormal sphincters and rectum

• Sphincter defect: obstetric, previous anorectal
surgery, perineal trauma
• Neuropathic sphincters: lower motor neurone
lesions (e.g. stretch pudendal neuropathy, diabetes,
Levator demyelination), upper motor neurone lesions (e.g.
ani stroke, cerebral tumours, demyelination)
Anorectal
ring • Rectal prolapse and internal rectal mucosal
(puborectalis) intussusception
External
sphincter • Loss of rectal capacity or compliance from rectal
Internal surgery, irradiation or IBD
sphincter • Anorectal/pelvic cancer
• Congenital anorectal abnormalities
Dentate
line Incontinence with normal sphincters and rectum
• Faecal impaction
Fig. 64.1 Anal canal and rectum.
• Severe diarrhoea
• Dementia or mental retardation
Causes of faecal incontinence
Faecal incontinence is due to impairment of the

necessary to define the patient’s symptoms and
various factors involved in maintaining normal
expectations. It is important to differentiate true
continence. They may be classified into the follow
faecal incontinence as defined previously from
ing broad categories.
pseudo‐incontinence due to overflow of liquid
• Impaired anal sphincter: injuries during child
stools around faecal impaction in the rectum.
birth account for the majority in female patients;
Specific questions are outlined here.
impalement injuries from falls or motor vehicle
• Enquire about onset of symptoms, precipitating
accidents.
events, urge or passive incontinence, stool con
• Reduced rectal reservoir and sensation: proctitis
sistency, frequency of incontinence, severity and
from inflammatory bowel disease (IBD), radia
impact on daily living and quality of life.
tion, resection of rectal cancer (low and ultra‐low
• Ask about risk factors such as obstetric history,
anterior resection).
with regard to baby size, prolonged labour,
• Change in stool consistency and frequency: infec
forceps delivery and perineal tear.
tive diarrhoea or IBD.
• Other risks include anorectal surgery such as
• Impaired nerve function, pudendal neuropathy
haemorrhoidectomy, anal dilatation or sphincter
from stretch or chronic straining, diabetes.
otomy for fissure, and fistulotomy.
• Spinal cord injuries.
• Ask about other surgery such as spinal surgery
• Impaired mental function.
affecting pelvic nerves, cholecystectomy or other
The most common cause of faecal incontinence in
upper gastrointestinal tract surgery causing diar
females is obstetric injury, resulting from tearing of
rhea, colorectal surgery causing low anterior
the perineum and anal sphincter muscle, stretching of
resection syndrome.
the pudendal nerve and subsequent neuropathy. Sphincter
• Additional routine questions should enquire about
damage may be detected clinically in 10–13% of all
medications and other medical illnesses such as
vaginal deliveries and occult injury may be detected by
thyroid disease, diabetes or multiple sclerosis.
endoanal ultrasound in up to 80% of forceps deliver
ies. Other causes are shown in Box 64.1.
Continence scoring systems
These are used to quantify the severity of faecal
Diagnostic approach incontinence objectively for the purpose of moni
toring progress and for research. The commonly
History used incontinence score systems include the Wexner
Careful and sensitive history taking is key to deal incontinence score, Vaizey scale and Faecal
ing with patients with this embarrassing condi Incontinence Quality of Life Scale. The Wexner
tion. Direct and tactful questioning will also be incontinence score is probably the most widely
64: Faecal incontinence 627
Table 64.1 Wexner score.
Frequency
Type of incontinence Never Rarely Sometimes Usually Always
Solid 0 1 2 3 4
Liquid 0 1 2 3 4
Gas 0 1 2 3 4
Wears pad 0 1 2 3 4
Lifestyle alteration 0 1 2 3 4
Never, 0; rarely, <1/month; sometimes, <1/week, ≥1/month; usually, <1/day, ≥1/week; always, ≥1/day.
Totals: 0, perfect; 20, complete incontinence.
used and takes into account the frequency of incon Sigmoidoscopy is performed to inspect the anal
tinence to solid, liquid and gas, the use of pads and canal and rectal mucosa for internal prolapse,
effects on lifestyle (Table 64.1). proctitis, tubulovillous adenoma or tumour.
Further investigations
Examination Further investigations may be indicated, and these
Patients are usually examined in the left lateral include colonoscopy to rule out malignancy, colitis
position. It is also important to examine the patient or rectal tubulovillous adenoma. Specialised inves
in a comfortable and private setting to allay any tigation of faecal incontinence includes endoanal
anxiety. The perineum is inspected for faecal soil ultrasound, anorectal manometry, pudendal nerve
ing, perianal scars, gaping deformity of the anal latency time and defecating proctogram.
margin, skin tags or prolapsed rectal mucosa or
haemorrhoids on straining. Descent of the peri
Endoanal ultrasound
neum of more than 4 cm on straining indicates sig
nificant weakness of the pelvic floor. Digital Endoanal ultrasound uses a rigid ultrasound probe
examination is performed to assess the integrity of with a 360° rotating transducer that scans the anal
the anal sphincter, resting tone and voluntary con canal to produce a circular picture of the puborec
traction and any abnormal masses. talis and IAS and EAS (Figure 64.2). It is highly
(a) (b)
Fig. 64.2 Endoanal ultrasound: (a) mid‐anal canal; (b) external and internal sphincter defects. EAS, external
anal sphincter; IAS, internal anal sphincter; SD, sphincter defect; STP, superficial transverse perinei. Source: Clinical
Uses of Pelvic Ultrasound by Dr. Marianne Starch, BK Medical Publication BG 0460‐A/ March 2010.
628 Problem Solving
sensitive for detecting structural defects in the IAS

and EAS. The three‐dimensional modality improves
Treatment
the accuracy and provides further structural detail
Treatment of faecal incontinence is challenging and
of sphincter anatomy. It is the preferred modality
needs to be individualised according to the underly
for investigation of anal sphincters.
ing functional and structural defects, symptom
MRI is an alternative imaging technique, but is less
severity and effects on quality of life, as well as the
accurate in detecting defects of the sphincter muscles
patient’s wishes. The ideal management approach
compared with endoanal ultrasound. Furthermore,
to this complex condition is with a multidiscipli
MRI is costly and less readily available.
nary team of specialists comprising colorectal
Manometry surgeons, urogynaecologists, continence nurses, physio
therapists and dietitians. Conservative measures
This provides an objective measure of the pressure and surgical therapies are not mutually exclusive
within the anal canal. It involves the use of a bal and in fact they are often used to complement each
loon‐tipped catheter with pressure sensors inserted other to improve patient outcome.
into the anal canal to measure resting pressure and
squeeze pressure. Low resting pressure reflects
Conservative therapy
underlying IAS defect and low squeeze pressure
poor EAS contraction. The first‐line treatment measures are usually con
Rectal compliance or capacity is measured by the servative and can be summarised as follows.
response to inflation of the balloon at the tip of the • Diarrhoea can be treated with antidiarrhoeal
catheter. The balloon is progressively inflated to medications such as loperamide, while codeine
various volumes and the patient is asked to indicate phosphate helps to reduce stool frequency.
the sensation detected, as first sensation, urge sen Cholestyramine may be useful in patients who
sation and maximal tolerated volume. developed diarrhoea following cholecystectomy.
The rectoanal inhibitory reflex is measured by • Addition of bulking agents such as psyllium or
inflating the balloon rapidly and deflating it to see bran to the diet will improve consistency of liq
if there is relaxation of the IAS in response to bal uid stools. Often, formed solid stools are easier to
loon distension. Positive response is normal and be held back by a weakened sphincter.
indicates reflex. • Pre‐emptive measures to empty the rectum
using glycerine suppository or enema before
Pudendal nerve latency time venturing out of the house will reduce the risk
of faecal leakage and provide some confidence
The pudendal nerve latency time (PNLT) refers to
to individuals.
the time between stimulation of the pudendal
• Biofeedback therapy uses visual, auditory or ver
nerve and contraction of the EAS. This is meas
bal feedback techniques to assist patients in the
ured by the St. Mark’s electrode attached to the
training of the pelvic floor and sphincter muscles
gloved index finger and connected to a special
to improve their strength, sensation and coordi
nerve stimulator and recorder. Delay in PNLT
nation. It requires patients to be motivated and
indicates pudendal nerve neuropathy but it does
to have the ability to understand and follow
not appear to correlate fully with severity of
instructions. Additional supportive counselling
incontinence. Measurement of PNLT is operator
and practical advice regarding diet and skin care
dependent and has not been shown to correlate
help to improve the success of this treatment.
with severity of incontinence.
Non‐randomised studies have reported 64–89%
Defecating proctogram improvement in incontinence episodes.
• Anal plugs are disposable absorbent devices
This is a fluoroscopic study of the defecation pro which may be useful in patients with minor
cess after patients have been given an enema of incontinence or neurological impairment, such as
diluted barium. It provides information on the ano spinal injuries.
rectal angle, presence of enterocele, rectocele or
internal rectal intussusception and the extent of
Surgery
full‐thickness rectal prolapse. The concept of inter
nal rectal intussusception is new and has been pro The indications for surgery are failed conservative
posed by some colorectal surgeons to cause faecal therapy and when symptoms are sufficiently severe to
incontinence, particularly in the group of patients warrant it. The principle of surgery is, first do no
with idiopathic incontinence. harm. Although faecal incontinence is a debilitating
condition, it is not life‐threatening and therefore the a neo‐sphincter. The nearby muscles that have been
risks and benefits of surgery must be carefully consid used include gracilis, gluteus maximus, sartorius
ered for each individual patient. The operation can be and adductor longus. The transposed muscle can
broadly divided into the following groups: sphincter be used in an electro‐stimulated state or a non‐
repair, sphincter augmentation, sphincter replace stimulated state. Electro‐stimulated graciloplasty
ment, neuromodulation and stoma formation. has been the most widely used and studied opera
tion. It is a complex and expensive operation with a
success rate of up to 60% but high complication
Anterior anal sphincter repair
and re‐operation rates of over 50%.
This operation is used to repair the defect in the Other alternatives to muscle transposition are
EAS, which is usually situated in the anterior por artificial bowel sphincter and magnetic anal
tion of the sphincter complex. The EAS defect usu sphincter. The artificial bowel sphincter consists of
ally results from childbirth injury caused by tearing a fluid‐filled silicone elastomer cuff encircling the
of the anterior portion of the external sphincter anal canal, which is in turn connected to a pressure‐
muscle. The torn ends of the EAS are dissected from regulating balloon and a pump system placed in
the surrounding tissue and sutured in an overlap the labial or scrotal skin. Fluid is manually pumped
ping manner using absorbable suture such as 0 PDS. in and out of the cuff to close or open the anal
Successful restoration of continence can be achieved canal for defecation. This operation is less techni
in 60–80% of cases, but there is a tendency for dete cally demanding than graciloplasty, but the higher
rioration over a 5‐year period of time. complication rate of device erosion and infection
Post‐anal repair (Park’s operation) involves plica (20–45%) is a major concern. Nevertheless, it
tion of the posterior aspect of the EAS to restore remains a useful alternative in patients with defi
the acute anorectal angle. It is no longer a recom ciency of pelvic floor muscles due to congenital
mended treatment option for faecal incontinence. anomalies or trauma.
The magnetic anal sphincter is a novel device
consisting of a ring of titanium beads with internal
Sphincter augmentation by injectables magnetic cores. It is surgically placed around the
This is the procedure where bulking agents are EAS to close the anus, and during defecation the
injected into the defect in the anal sphincter com beads separate to open the anus for passage of
plex, usually in the IAS, to restore the normal con stool. This new device is currently undergoing
tour of the anal canal. Various biological or synthetic clinical trials and its role in faecal incontinence

materials have been trialled with varying success. treatment remains undetermined.
These materials include autologous fat, glutaralde
hyde cross‐linked collagen, Teflon, PTFE, PTQ,
Neuromodulation
NASHA (dextranomer in stabilised hyaluronic
acid), and new agents such as Solesta and Sphin Sacral nerve stimulation
Keeper™. The injection into the sphincter defect can This procedure (Figure 64.3) involves the place
be done under endoanal ultrasound guidance or ment of a thin electrode wire into the sacral fora
blindly into the IAS defects previously mapped by men to stimulate the sacral nerve, optimally the S3
endoanal ultrasound. nerve roots, by an implanted nerve stimulator gen
A non‐randomised study of the NASHA injection erator. The nerve stimulation results in contraction
for the Food and Drug Administration in the USA in of the anal sphincter and pelvic floor musculature
2011 reported that 52% of the patients had over to maintain continence.
50% reduction in incontinence episodes compared The exact mechanism of action remains unclear,
with 31% receiving sham injection. A Cochrane but it is thought to involve neuromodulation of the
review in 2013 of five randomised studies concluded sacral reflexes and parasympathetic nerves to
that long‐term outcome data was not available. alter rectal compliance, rectal sensitivity and anal
Injection therapy may have a role in treating canal resting tone. Recent brain MRI studies also
patients with mild passive incontinence. implicate higher centre involvement in this neuro
modulation process.
A unique and attractive feature of sacral nerve
Sphincter replacement operation
stimulation is that it is a reversible and minimally
This operation involves replacing the existing invasive procedure. There are two stages to the
sphincter with a nearby skeletal muscle, which is operation: the first is the testing phase and the
transposed to encircle the anal canal and acts as second, the implantation of the permanent nerve
630 Problem Solving
Fig. 64.3 Implantation of sacral nerve stimulation equipment consisting of a battery (IPG) and tined lead inserted into
S3 foramen alongside the S3 nerve root. Source: reproduced with permission of Medtronic plc.
stimulator, is performed if the patient achieves over A prospective non‐randomised multicentre study
50% reduction in incontinence episodes. conducted in 14 centres across the USA, Canada
The first stage procedure involves the insertion of and Australia reported a greater than 50% improve
a tined lead or a temporary wire electrode into the ment in 89% of patients and complete continence
S3 foramen to lie alongside the S3 nerve root. The in 36% at 5‐year follow‐up. However, a Cochrane
electrode is then connected to an external nerve review in 2015 of six trials assessing the effective
stimulator for a trial stimulation of 2 weeks. If the ness of sacral nerve stimulation concluded that the
patient experiences a greater than 50% reduction technique can improve continence in a proportion
in incontinence episodes, this is considered to be of people but longer‐term efficacy data are still
successful and the patient can proceed to the sec lacking.
ond stage. If the response is less than 50% improve Because of its reversibility, minimal invasiveness
ment in continence, then the electrode is simply and efficacy, sacral nerve stimulation has now
removed. The second stage involves insertion of a emerged as the treatment of choice for faecal incon
tined lead electrode and implantation of a perma tinence in suitable patients. However, the high cost
nent pulse generator (like a pacemaker) in the sub precludes it from wider use.
cutaneous pocket in the upper buttock region. Both
procedures can be performed under intravenous Posterior tibial nerve stimulation
sedation and local anaesthetic infiltration using This therapy involves stimulation of the posterior
X‐ray guidance, as day cases. tibial nerve at the ankle, either percutaneously via a
Some adverse effects of sacral nerve stimulation fine needle or transcutaneously for 30 minutes at a
include infection in approximately 5% of cases and time for 12 treatment sessions. The rationale is that
perineal pain from chronic stimulation. Longer‐ this produces retrograde stimulation of the S3 nerve
term effects on the nerve are unknown. Additionally, roots. The results are conflicting, with some studies
some older pulse generators may not be compatible showing some improvement in patients with mild
with MRI scanners and hence patients will not be faecal incontinence, but long‐term sustained improve
able to be investigated by MRI. ment has not been confirmed in large studies.
Radiofrequency (SECCA) therapy sphincter identification and preservation when

performing anorectal operations such as haemor
This therapy uses radiofrequency energy to create
rhoidectomy, sphincterotomy and fistulotomy.
thermal burns in the anal canal, causing fibrosis
within the internal sphincter muscle and thereby
tightening the anal canal to maintain continence.
Summary
The radiofrequency energy is delivered via a special
endoanal probe inserted into the anal canal under
Faecal incontinence is an embarrassing and debilitat
sedation and local anaesthetic. There are limited
ing symptom caused by a multitude of aetiological
long‐term data on its efficacy and hence its use is
factors affecting the anal sphincter muscle complex,
limited to a few major centres.
the pelvic floor musculature, pudendal nerve, rectal
capacity and compliance, stool consistency, spine
Stoma formation
and central nervous system. Treatments are directed
The formation of a diverting stoma, either a colos at the underlying structural or functional abnormali
tomy or ileostomy, is an effective treatment of fae ties and are tailored to individual needs.
cal incontinence. The faecal stream is diverted from Conservative therapies include dietary modifica
the anus to the anterior abdominal wall where a tion, medications, pelvic floor training and biofeed
small opening is created for the colon or ileum to back therapy. Surgical interventions, which attempt
exit as a conduit (stoma). The faecal content is col to restore anal sphincter anatomy and function,
lected in a sealed plastic bag, which is disposed of in include anal sphincter repair, post‐anal repair,
a controlled manner. sphincter augmentation, artificial bowel sphincter,
This surgical option is considered the last resort injection therapies, sacral nerve stimulation, poste
in the management of faecal incontinence and may rior tibial nerve stimulation and Secca therapy.
not be acceptable to some patients who have a Treatment outcomes in terms of reduction in incon
physical and psychological aversion to wearing a tinence and improvement in quality of life are highly
stoma bag. Furthermore, intestinal stomas are not variable between techniques and less than optimal.
without complications, such as leakage around the Sacral nerve stimulation has emerged as the least
appliance, parastomal hernia, prolapse of the invasive and most effective treatment for faecal
stoma, the odour and uncontrolled flatus. It is incontinence. However, a recent systematic review
therefore important to counsel patients carefully of surgical treatments for faecal incontinence con
and manage their expectations appropriately to cluded that high‐quality evidence is still lacking to
ensure a satisfactory outcome. assist proper clinical decision‐making and more rig
orous randomised studies are required.
It can be concluded that there is currently no single
cure for faecal incontinence and that this debilitating
Prevention condition should be managed as a chronic disease by
a combination of conservative, supportive and surgi
The old adage ‘prevention is better than cure’ cer cal measures through a multidisciplinary team.
tainly rings true in the management of faecal incon
tinence. Patients can reduce their risks of developing
faecal incontinence by maintaining a regular bowel Further reading
habit, avoiding constipation and straining at stools,
avoiding injury to the rectum by foreign bodies, Benezech A, Bouvie M, Vitton V. Faecal incontinence: cur
and practising pelvic floor exercises especially rent knowledge and perspectives. World J Gastrointest
postpartum. Pathophysiol 2016;7:59–71.
In obstetric practice, posterior midline episiot Brown SR, Wadhawan H, Nelson RL. Surgery for faecal
omy should be avoided and the posterolateral incontinence in adults. Cochrane Database Syst Rev
approach used, a prolonged second stage circum 2010;(9):CD001757.
Lehur PA, Wong MTC. Incontinence. In: Phillips RK,
vented, and caesarean section considered for large
Clark S (eds) Colorectal Surgery, 5th edn. Elsevier,
babies or at‐risk anal sphincters.
2014.
In general surgery, the practice of Lord’s proce Norton C, Whitehead WE, Bliss DZ, Harari D, Lang J.
dure has been abandoned as it involves forceful Conservative and pharmacological management of fae
anal dilatation for anal fissure or constipation, cal incontinence in adults. International Continence
causing internal sphincter injury and incontinence. Society. Available at https://www.ics.org/Publications/
Surgeons should be aware of the principle of ICI_4/files‐book/comite‐16.pdf
632 Problem Solving
Paquette IM, Varma MG, Kaiser AM, Steele SR, Rafferty c chronic constipation and excessive straining at
JF. The American Society of Colon and Rectal Surgeons’ defecation
Clinical Practice Guideline for the Treatment of Fecal d impalement trauma to the anus
Incontinence. Dis Colon Rectum 2015;58:623–36. e type 1 diabetes mellitus

MCQs pudendal nerve is incorrect?
a it arises from S2–S4 nerve roots of the
Select the single or multiple correct answers to each
sacral plexus
b it arises from L4–L5 nerve roots
c it carries sensory nerve supply to the perineal
1 Normal faecal continence is maintained by structures
a intact anal sphincters d it carries motor nerve supply to the perineum
b normal rectal reservoir and compliance e it becomes stretched during prolonged
c functioning pudendal nerve childbirth and may cause faecal incontinence
d normal stool consistency in later life
e all the above
4 Which of the following treatments for faecal
2 Which of the following causes of anal sphincter incontinence is incorrect?
injury is incorrect? a biofeedback therapy
a childbirth injury from prolonged labour, episiotomy b sacral nerve stimulation
and use of forceps to deliver the baby c injection of anal sphincter bulking agent
b anorectal surgery such as haemorrhoidectomy, d loperamide tablet
sphincterotomy or fistulotomy e subtotal colectomy
65 Rectal bleeding
Adele Burgess
should determine the presence of anal fissure, pro-

Chronic rectal bleeding lapsed haemorrhoids and most anal canal cancers.
During straining, look for prolapsing haemorrhoids
Rectal bleeding can be alarming for patients,
or rectal prolapse. Digital examination is used to
although most causes are benign. Bleeding may be
feel for an anal or rectal polyp or cancer. This may
overt and noticed by the patient or occult when the
not be possible in the presence of an acute anal
blood loss can only be detected by a faecal occult
fissure because of anal sphincter spasm and pain.
blood test or its consequences noted on blood tests
Proctoscopy can be used to visualise any anal
as iron deficiency or anaemia. Management of
canal lesion and haemorrhoids. On rigid sigmoi-
rectal bleeding involves exclusion of a colorectal
doscopy the level of the rectum visualised should be
neoplasm and finding the cause of the bleeding.
recorded together with the level of any abnormality
The classification and common causes of chronic
seen. The presence of blood clots or blood‐stained
rectal bleeding are given in Table 65.1.
faeces beyond the reach of the sigmoidoscope
indicate a more proximal pathological process.
History Fibre‐optic flexible sigmoidoscopy allows for an
A detailed history should be taken. The nature of easier examination of the rectum and a variable
the rectal bleeding must be determined (duration, length of the sigmoid and descending colon.
colour and amount of blood). Macroscopic bleed- In many specialist colorectal practices, this has
ing recognised by the patient usually arises from the replaced rigid sigmoidoscopy.
left side of the colon or rectum. Right‐sided colonic
bleeding usually presents with anaemia or iron Special investigations
deficiency but without overt bleeding. The presence
Colonoscopy is the test of choice in the majority of
of anal pain should be inquired about. This occurs
patients. Colonoscopy allows examination of the
with anal fissure, strangulated haemorrhoids and
large bowel and the distal part of the small bowel
some anorectal cancers. Prolapse occurs with
and provides both a visual diagnosis (e.g. ulcera-
second‐ and third‐degree haemorrhoids and with
tion, polyps) and therapeutic opportunity. Small
mucosal or full‐thickness rectal prolapse. Other
polyps can be removed, angiodysplasia can be con-
symptoms that may be seen are mixture of blood
trolled with argon plasma coagulation or cautery,
with stool, tenesmus, alteration in bowel habit,
and it grants the opportunity for biopsy and tattoo
abdominal pain or distension and weight loss.
marking of suspected colorectal cancer lesions.
A past and family history of colorectal neoplasm
Virtual colonoscopy, which uses two‐ and three‐
must be gained from the patient, as well as a past
dimensional imagery reconstructed from CT scans
history of colonic diseases such as inflammatory
(or less commonly MRI), is also possible. This is
bowel disease.
not standard, however, because it does not allow
for therapeutic manoeuvres nor visualisation of
Anorectal examination
lesions smaller than 5 mm. It also does not negate
Anorectal examination is essential in any patient the need for bowel preparation. It is usually
presenting with rectal bleeding. This should be reserved for patients in whom a colonoscopy was
undertaken on every patient after gaining consent unable to be completed or for those unable to have
and offering (or having) a chaperone. Inspection sedation.
633
634 Problem Solving
Table 65.1 Classification and common causes Box 65.1 Causes of massive rectal
of chronic rectal bleeding. bleeding
Classification Common causes • Diverticular disease

• Angiodysplasia/angioma
Anal outlet bleeding
• Ulcerated cancer
Bright blood per rectum, Haemorrhoids, anal
• Rare colonic causes (e.g. radiation colitis, inflam-
separate from the stool and fissure, rectal prolapse,
matory bowel disease, ischaemic colitis)
often present as a smear of angiodysplasia,
• Upper gastrointestinal lesions
bright blood on the toilet malignancy
paper
Bleeding associated with
in 24 hours. In these circumstances, the patient has
defecation
No change in bowel habits signs of shock on admission that demand urgent
No past or family history of management with transfusion. Massive rectal bleed-
colorectal neoplasm ing will cease spontaneously in 80% of cases.
A prior history of a bowel disorder such as
Suspicious bleeding
inflammatory bowel disease or haemorrhoids is
Dark blood or blood mixed Diverticular disease,
with stool inflammatory bowel ascertained. Use of anticoagulant therapy or non‐
Change in bowel habit or disease, proctitis, steroidal anti‐inflammatory drugs may contribute
passage of mucus anorectal cancer, to bleeding. Liver disorders with impaired coagu-
Tenesmus colorectal neoplasm lation are also noted. A rectal examination with
Past or family history of rigid proctosigmoidoscopy is performed to exclude
colorectal neoplasm bleeding haemorrhoids or rectal tumours.
Capsule endoscopy is an investigation to identify Localisation of the bleeding site

a bleeding source in the small bowel. and therapeutic intervention
Upper gastrointestinal endoscopy
Massive rectal bleeding In cases of severe rectal bleeding with shock, upper
gastrointestinal endoscopy should be performed as
The management of massive rectal bleeding soon as clinically feasible to exclude an upper
involves: gastrointestinal lesion, such as a bleeding peptic
• resuscitation and clinical evaluation ulcer, oesophageal varices or aorto‐enteric fistula.
• investigations to locate bleeding site Alternatively, a nasogastric tube is passed to exclude
• therapeutic intervention. blood in the stomach.
Resuscitation and initial assessment Colonoscopy
Resuscitation should be immediately initiated with Colonoscopy has been the first‐line investigation for
massive rectal bleeding while diagnostic tests are colonic bleeding. Emergency colonoscopy is difficult
performed. with active bleeding and requires a great deal of
experience. Colonoscopy is performed as soon as
Clinical evaluation feasible once the patient has been resuscitated. There
is debate around the use of full bowel preparation
A detailed history is important. The nature and
and colonic blood often works as a cathartic.
amount of bleeding give an indication of the cause
Colonoscopy is the first‐line choice of investigation
of the bleeding (Box 65.1). Massive colonic haem-
and management in post‐interventional bleeding.
orrhage is dark red or plum coloured and is to be
Once the bleeding site has been identified, treatment
differentiated from melaena, which is black.
may include coagulation and injection with vasocon-
Melaena almost invariably arises from the stomach
strictors or sclerosing agents or the use of metal clips.
or small bowel. A rapidly bleeding peptic ulcer may
occasionally present with bright red rectal bleeding.
CT angiography
The haemodynamic condition of the patient will
also reflect the severity of bleeding. Massive CT angiography is available in most hospitals and
bleeding indicates bleeding of more than 1500 mL has the advantage of being non‐invasive, readily
65: Rectal bleeding 635
available and requires no bowel preparation. In angiodysplasias or small bowel angiomas. In rare cir-
many centres this has now become the first line of cumstances if the site of bleeding remains unclear, a
investigation after resuscitation. A recent meta‐ subtotal abdominal colectomy is performed.
analysis of 672 patients reported sensitivity and
specificity rates of 85.2% and 92.1%, respectively. Review
If the diagnosis is unresolved despite a full investiga-
Capsule endoscopy tion, the patient is observed. If bleeding recurs, a full
investigation is repeated as in a new case of active
This involves the patient swallowing a small vide-
bleeding. Laparotomy and intraoperative enteros-
ocapsule (PillCam) which will capture digitised
copy may be necessary if these rebleeding episodes
images of the small bowel. The duration of test
are moderately severe.
is limited by the battery life of the videocapsule
(8 hours). This is best done in a patient who is
haemodynamically stable and who has had recur-
rent gastrointestinal bleeding of unknown origin Further reading
despite being previously investigated with upper
García‐Blázquez V, Vicente‐Bártulos A, Olavarria‐
gastrointestinal endoscopy, colonoscopy and CT
Delgado A, Plana MN, van der Winden D, Zamora J.
angiography. Accuracy of CT angiography in the diagnosis of acute
gastrointestinal bleeding: systematic review and meta‐
Radionuclide scan analysis. Eur Radiol 2013;23:1181–90.
Hewitson P, Glasziou PP, Irwig L, Towler B, Watson E.
If bleeding continues and the site of haemorrhage is Screening for colorectal cancer using the faecal occult
not located by colonoscopy, a radionuclide scan is blood test, Hemoccult. Cochrane Database Syst Rev
done using technetium‐99m sulphur colloid or 2007;(1):CD001216.
technetium‐99m‐labelled autologous red cells. One Hongsakul K, Pakdeejit S, Tanutit P. Outcome and predic-
advantage of this examination is its ability to detect tive factors of successful transarterial embolization for
the treatment of acute gastrointestinal hemorrhage.
bleeding rates as low as 0.05–0.1 mL. The accuracy
Acta Radiol 2014;55:186–94.
of these scans is variable, ranging from 40 to 90%.
Mesenteric angiogram MCQs

Selective angiogram of the inferior mesenteric, Select the single correct answer to each question. The
superior mesenteric and coeliac arteries is per- correct answers can be found in the Answers section
formed if bleeding continues and the rate is greater at the end of the book.
than 0.5 mL/min. Angiography is likely to be posi-
tive if there is active bleeding at the time of injection 1 Most patients presenting with massive rectal
of contrast. If the site of bleeding is identified, bleeding:
haemostasis with super‐selective intra‐arterial a will bleed to death unless they have surgery
embolisation can be considered. b usually are found to have colon cancer
c usually are found to have rectal cancer
d should be appropriately resuscitated
e should have an immediate colonoscopy
Surgery
If bleeding continues, laparoscopy or laparotomy is 2 A patient with chronic rectal bleeding:
performed. If the site of bleeding is not clearly a usually will be found to have a cancer
localised preoperatively or intraoperatively, b should always have an anorectal examination
intraoperative endoscopy can be performed. The c will have a history of inflammatory bowel disease
bowel is transilluminated during intraoperative d needs virtual CT as first‐line examination
enteroscopy in a darkened room to detect e requires immediate blood transfusion
66 Haematemesis and melaena
Wendy A. Brown
Monash University Department of Surgery, Alfred Health, Melbourne, Victoria, Australia
The list of causes of haematemesis and melaena is

Introduction long (Box 66.1). The common causes are:
• peptic ulcer (i.e. gastric or duodenal ulceration)
Definition • oesophageal varices
Haematemesis is the vomiting of blood, either • gastritis or duodenitis.
bright or altered blood (so‐called ‘coffee grounds’ The site of bleeding usually lies in the oesophagus,
vomitus) due to the action of acid on the blood. stomach or duodenum.
Melaena is the passage of black tarry stools. The
tarriness is characteristic and distinguishes mel- Oesophagus
aena from the passage of black stools due to
The most common cause of bleeding in the oesoph-
dietary agents, including the ingestion of iron.

agus is from oesophageal varices secondary to
Haematemesis occurs from a point that is usually
portal hypertension. Oesophageal varices are the
not distal to the duodenum but melaena may occur
cause of some 10–30% of major haematemesis
not only from a proximal bleeding site but rarely
episodes in most western countries. Less com-

from a small intestinal cause.
monly, oesophagitis secondary to gastro‐oesophageal
reflux is associated with haemorrhage. Oesophageal
Incidence cancer rarely presents with bleeding.
Haematemesis and melaena is a common and

Stomach
important symptom complex presenting either as
an acute catastrophic illness or more electively with Gastric ulcer is one of the most common causes of
prolonged minor bleeding. Patients with this condi- haematemesis and melaena. The ulcer may be in the
tion make major demands on hospital beds.
Box 66.1 Common causes of

Significance haematemesis and melaena
Patients with haematemesis and melaena require
Oesophageal
admission to hospital. The condition has a high
Reflux oesophagitis: other associated hiatus hernia
mortality and demands a systematic approach to Oesophageal varices (portal hypertension)
the initial resuscitation process, the diagnostic Oesophageal tumours
method and the therapeutic program. The overall Mallory–Weiss mucosal tear
management of this condition has been revolution-
ised by the introduction of new endoscopic tech- Gastric
niques to control bleeding. Gastric ulcer, usually benign
Haemorrhagic gastritis
Gastric varices
Gastric cancer
Causes of haematemesis Delafoy lesion
Duodenum
Swallowed blood from, for example, a bleeding site
Duodenal ulcer
in the post‐nasal space must be excluded as a cause
Duodenitis
for haematemesis.
637
638 Problem Solving
body or the antrum of the stomach. The pre‐pyloric findings but with mild tachycardia and postural
position is the most common. Gastric ulcer may drop in blood pressure is consistent with 10–20%
be the site of torrential haemorrhage because of the blood volume loss. This estimation of circulatory
invasion of a major vessel (e.g. the splenic artery). status gives an indication of the urgency of fluid
Gastritis is also a common cause of gastric replacement.
bleeding. The cause of bleeding must then be diagnosed.
The common use of non‐steroidal anti‐flamma- This is often not obvious. However, the presence of
tory drugs (NSAIDs) is associated with haematem- a previous history of peptic ulceration or evidence
esis and melaena due to gastric ulceration in many of hepatic cirrhosis may indicate a likely site of
elderly patients. Despite the use of cyclooxygenase blood loss.
(COX)‐2 inhibitor antiarthritic agents, ulceration
can still occur, particularly when these drugs are
prescribed in conjunction with aspirin. A Mallory–
Management of the patient
Weiss tear is a laceration of the gastro‐oesophageal
junction as a result of retching, with differential Optimal management of the patient with haemate-
intra‐abdominal and thoracic pressures leading mesis and melaena involves vigorous resuscitation
to the tear. Characteristically the haematemesis and early diagnosis.
appears after initial blood‐free vomit.
Gastric varices may be associated with portal
Resuscitation
hypertension and coexist with oesophageal varices.
Gastric cancer is not a common cause of haemate- Intravenous therapy is started with normal saline
mesis and melaena but a gastric ulcer may bleed and/or colloid (Haemaccel or 5% albumin solu-
and prove to be malignant on biopsy. tion). Blood is then taken for cross‐matching.
Depending on the clinical state of the patient,
urgent cross‐match can be performed and blood
Duodenum
given immediately. Rarely, O‐negative blood is
Duodenal ulcer is traditionally the most common required for a patient in extremis.
cause of haematemesis and melaena. The ulcer is Monitoring is essential to estimate the effective-
usually on the posterior wall of the duodenum and ness of blood replacement. Successful resuscitation
characteristically invades the gastroduodenal can be observed by noting improvement in the clin-
artery. Haemorrhage may be profuse but is usually ical state of the patient, return of blood pressure
self‐limited. and pulse rate towards normal, and the presence of
In western societies the number of patients pre- a satisfactory urine output.
senting with duodenal ulcers is decreasing.
However, there is an increasing number of patients
presenting with gastric ulceration, particularly Diagnosis
elderly patients on NSAIDs. Early endoscopy has been shown to be a safe and
effective way of making a diagnosis. Once the
patient’s clinical condition is stabilised, this proce-
dure is carried out either urgently if there is concern
Management about continuing bleeding, or on the next elective
endoscopy list if there is no indication for urgent
Initial assessment
intervention.
In most hospitals, patients with haematemesis and The patient is sedated with intravenous medica-
melaena are managed in a special unit and employ- tion and the gastroscope is passed. The oesophagus,
ing a clinical pathway or algorithm to systematise stomach and duodenum are carefully examined.
management (Figure 66.1). There may be some difficulty in this examination
The circulatory state of the patient is assessed. process with the presence of old blood, blood clot
The extent of blood loss can be estimated on the or fresh bleeding. Adequate suction and irrigation
basis of the patient’s clinical status. Apprehension, are required in order to define the bleeding point.
air hunger, cerebral changes, marked pallor, thready Rarely the bleeding point is not identifiable.
pulse and hypotension indicate significant blood Throughout this procedure the patient requires
loss (up to 50% of blood volume). Maintenance of adequate monitoring, and the airway must be
normal peripheral circulation without cerebral controlled and oxygen administered.
66: Haematemesis and melaena 639
Patient
admission
Assessment of
circulatory state
Shock No shock
BP<110
PR>110
Urgent
resusitation
Continued Condition
bleeding stabilises
Emergency Diagnosis by
endoscopy endoscopy
within 24 hours
Bleeding Bleeding
identified and overwhelming
treated and cannot be
endscopically controlled
endscopically
Ulcer Varices Other

Emergency
Surgery
Endoscopic Endoscopic Usually
haemostasis • Injection pursue
• Diathermy • Ligation of conservative
• Injection varices management
• Heater probe
If re-bleed Re-bleed
Consider Repeat
surgery endoscopic
procedure
Re-bleed
Consider
surgery
Fig. 66.1 Algorithm for management of haematemesis and melaena.
Therapy
varices, then immediate consultation with the surgi-
Usually a therapeutic procedure can be carried out cal team is mandatory and combined management
at the time of endoscopy. Injection of alcohol or is implemented.
adrenaline close to the bleeding point will usually There is an increasing role for radiological interven-
result in cessation of bleeding. If oesophageal tion. Angiogram and embolisation of bleeding vessels
varices are present, these may be injected or banded. may be useful, especially if the patient is too frail for
If it is evident that a major problem exists, such surgical intervention. Transjugular intrahepatic porto-
as a large gastric ulcer or persistent bleeding from a systemic shunt (TIPS) may be used to reduce portal
large duodenal ulcer, or bleeding from oesophageal pressures and improve bleeding from varices.
640 Problem Solving
Indications for surgical intervention the best results are obtained in dedicated units for
the management of this condition.
The indications for surgical intervention include
massive haemorrhage not responding to conserva-
tive means, patients requiring more than 6 units of
Further reading
blood, and elderly patients, particularly if a large
ulcer is present, because they tolerate blood loss Fujishiro M, Iguchi M, Kakushima N et al. Guidelines for
poorly. endoscopic management of non‐variceal upper gastro-
Where a second haemorrhage occurs in hospital intestinal bleeding. Dig Endosc 2016;28:363–78.
or there is concern about persistent ongoing bleed- Samuel R, Bilal M, Tayyem O, Guturu P. Evaluation and
ing, surgery is necessary. management of non‐variceal upper gastrointestinal
bleeding. Dis Mon 2018;64:333–43.
Shah AR, Jala V, Arshad H, Bilal M. Evaluation and
Results of treatment management of lower gastrointestinal bleeding. Dis

Most bleeding sites causing haematemesis and mel- Mon 2018;64:321–32.
aena stop bleeding spontaneously or with interven- Storace M, Martin JG, Shah J, Bercu Z. CTA as an adju-
vant tool for acute intra‐abdominal or gastrointestinal
tional endoscopy. The modern medical management
bleeding. Tech Vasc Interv Radiol 2017;20:248–57.
of peptic ulcers, including the eradication of
Tayyem O, Bilal M, Samuel R, Merwat SK. Evaluation
Helicobacter pylori, is so effective that surgery is to and management of variceal bleeding. Dis Mon
be avoided unless absolutely indicated to save life. 2018;64:312–20.
The results of treatment of bleeding from varices
due to portal hypertension will depend on the
degree of liver disease and the extent of the varices. MCQs
These patients usually require an intensive care unit
program of therapy. In the short term, injection or Select the single correct answer to each question. The
banding of varices is usually effective in stopping correct answers can be found in the Answers section
the bleeding. If bleeding persists, then the use of a at the end of the book.
Sengstaken–Blakemore tube or Linton balloon to
apply direct pressure to the cardia will usually
passage of black tarry stools is incorrect?
result in tamponade of the bleeding point and con-
a is usually an indication of bleeding from the
trol the haemorrhage. Occasionally emergency sur-
upper gastrointestinal tract
gery is required, with some form of direct ligation
b can be mimicked by the ingestion of iron medication
of varices or gastric disconnection in order to con-
c is commonly a symptom of a cancer of the colon
trol bleeding. Direct ligation of varices involves
d can be present without other symptoms
opening the stomach or oesophagus and directly
e is often but not universally associated with
suturing the varices. A gastric disconnection proce-
haematemesis
dure involves devascularising the stomach com-
pletely in order to interrupt the venous channels
2 Which of the following causes of haematemesis
supplying the varices.
and melaena is incorrect?
a oesophageal varices
b gastric ulceration
Prognosis c epistaxis with swallowed blood
d beetroot ingestion
The prognosis from this condition will depend on e gastritis
the underlying cause and the clinical state of the
patient. Overall, patients with haematemesis and 3 Which of the following statements about the patient
melaena have a high mortality and morbidity rate, who has suffered a gastrointestinal bleed is incorrect?
varying from 5 to 20% in most series. This is a pale and sweaty
because most patients with haematemesis and mel- b faint and has a bradycardia
aena are elderly, often with cardiac and pulmonary c faint and has a tachycardia
disease. These patients tolerate surgery poorly. d requires urgent resuscitation with normal saline
Thus, the balance between surgical intervention initially
and persisting with medical management in the face e appears quite well with normal supine blood
of continuing haemorrhage is often very fine and pressure
66: Haematemesis and melaena 641
4 Which of the following statements about diagnosis 5 Which of the following statements about haemate-
of the cause of the bleeding episode is incorrect? mesis and melaena is incorrect?
a is the most urgent requirement in patient a is a serious condition with a high mortality and
management morbidity rate
b may be suspected from a history of NSAID intake b now occurs in an older age group of patients
c can be made by early endoscopy of upper c has been eliminated with the advent of COX‐2
gastrointestinal tract inhibitor anti‐inflammatory drugs
d can often be combined with treatment at the d when associated with oesophageal varices may
initial endoscopy require repeated interventions for control
e surgical intervention is required for ongoing e is best managed in a dedicated specialist
blood loss treatment unit
67 Obstructive jaundice
Frederick Huynh1 and Val Usatoff 2
1
Alfred Health, Melbourne, Victoria, Australia
2
University of Melbourne and Western Health, Melbourne, Victoria, Australia
injury, while prior endoscopic retrograde cholangi-

Introduction opancreatography (ERCP) may be due to a recur-
rence of the original pathology, or a stricture/
Jaundice is a common medical presentation and
stenosis secondary to the sphincterotomy.
can be broadly classified into:
Choledocholithiasis is also less likely in a patient
• prehepatic
with an absent gallbladder.
• hepatic
On examination, once the bilirubin is more than
• posthepatic (obstructive) jaundice.
double the normal level, icterus should be evident
Common causes for each category are outlined
in the sclera. Skin scratch marks in response to pru-
in Box 67.1. This chapter addresses the assess-
ritus should be noted, as should signs of chronic
ment and management of obstructive jaundice
liver disease, such as petechiae/ecchymoses, spider
(Figure 67.1).
naevi and gynaecomastia. The patient’s general
nutritional status is gauged, as cachexia may repre-
sent an advanced cancer. Abdominal examination
consists of palpating for any abdominal masses and
The first step to evaluating a patient with jaundice
is a detailed history and physical examination. One
of the key objectives is to differentiate between
Box 67.1 Causes of jaundice
benign and malignant causes of obstructive
jaundice. Prehepatic
It should be assessed whether the jaundice is Increased haemolysis
associated with pain and, if present, an impression Hereditary red blood cell disorders
of its onset, character and pattern of radiation Acquired haemolytic disorders
should be elicited. Enquiries about associated Autoimmune haemolytic anaemia
symptoms such as nausea, pale stools and dark
Hepatic/hepatocellular
urine should be made. Significant unintended
Congenital abnormalities of metabolism (e.g. Gilbert’s
weight loss may be associated with an underlying
disease, Crigler–Najjar syndrome)
malignancy. Cholangitis should be highly suspected
Medications
in the setting of jaundice, right upper quadrant pain Viral hepatitis
and fever (Charcot’s triad), and expedient investi- Alcoholic hepatitis
gations, treatment and decompression of the biliary Non‐alcoholic steatohepatitis
tree is required. Chronic liver disease/cirrhosis
The patient should also be assessed for risk fac-
tors associated with hepatitis, including a history of Posthepatic (obstructive)
Choledocholithiasis
intravenous drug use, medication history and fam-
Primary sclerosing cholangitis
ily history. The frequency and amount of alcohol
Traumatic biliary strictures
intake should be evaluated. A thorough surgical
Autoimmune pancreatitis
history should also be obtained, as jaundice in a
Malignancy (cholangiocarcinoma, pancreatic
patient having undergone a previous cholecystec-
carcinoma, periampullary tumours)
tomy may represent a late presentation of a biliary
643
644 Problem Solving
Jaundice
History/exam
liver function tests
Hepatocellular Cholestatic
Viral serology
Ultrasound
autoimmune antibodies
+/– liver biopasy
Dilated ducts Non-dilated ducts
Cause identified Cause not identified Consider hepatocellular

causes of jaundice
CT cholangiogram/ Cause identified Cause not identified

MRCP
Choledocholithiasis Mass Stricture Choledocholithiasis Treat accordingly CT cholangiogram/

MRCP
ERCP or EUS ERCP + EUS ERCP or Cause identified Cause not identified
surgery Staging CT/MRI +/–CT surgery
Resectable Not resectable

Treat accordingly Consider liver biopsy
no metastatic disease +/– metastatic disease
fit for surgery +/– not fit for surgery
Surgery Palliative stenting Surgery

ERCP/PTC
Fig. 67.1 Diagnostic and therapeutic approach to a patient with jaundice. CT, computed tomography; ERCP,
endoscopic retrograde cholangiopancreatography; EUS, endoscopic ultrasound; MRCP, magnetic resonance
cholangiopancreatography; MRI, magnetic resonance imaging; PTC, percutaneous transhepatic cholangiography.
evaluating the size of the liver. The presence of should also be performed and if there is evidence of
ascites is assessed, as is any lymphadenopathy. coagulopathy secondary to hepatic impairment,
Courvoisier’s law states that in the presence of a this should be corrected with vitamin K.
palpable non‐tender gallbladder accompanied by Conjugated and unconjugated bilirubin levels
painless jaundice, the cause is unlikely to be gall- may differentiate between prehepatic and hepatic
stones and suggests a malignant process. causes of jaundice and also diagnose genetic
abnormalities related to bilirubin metabolism

(e.g. Gilbert’s disease).
Investigations If liver function tests suggest a hepatocellular pro-
cess, then viral hepatitis serology, autoimmune anti-
Liver function tests bodies and a metabolic screen should be performed
(iron studies for haemochromatosis, serum caerulo-
The pattern of abnormal liver function tests should
plasmin for Wilson’s disease, and α1‐antitrypsin
be noted. Significant elevations of alanine ami-
levels for α1‐antitrypsin deficiency). A liver biopsy
notransferase (ALT) and aspartate aminotrans-
may be required for confirmation.
ferase (AST) are in keeping with hepatocellular
injury, while derangements of alkaline phosphatase
(ALP) and gamma‐glutamyltranspeptidase (γ‐GT),
Ultrasonography and computed tomography
which are enzymes primarily produced by the epi-
thelial cells of the biliary tract, are more consistent Ultrasound is a routine and readily available initial
with biliary obstruction. It should be remembered investigation to evaluate the liver and biliary tree.
that ALP levels can also be elevated in bone diseases Particular note should be made of the calibre of the
such as Paget’s disease or certain types of bony biliary tree with any associated intrahepatic ductal
metastases, while abnormal γ‐GT levels may repre- dilatation, and the presence or absence of gallstones.
sent excess alcohol intake. Coagulation studies A common bile duct diameter in excess of 5 mm is
67: Obstructive jaundice 645
considered abnormal, although this figure rises with generally not be used in cases where the bilirubin is
increasing age and in patients who have previously above 30 mmol/L.
undergone a cholecystectomy. Intraoperative cholangiography is often per-
Ultrasonography may also demonstrate an formed by direct cannulation of the cystic duct at
obstructive mass either within the head of the pan- the time of cholecystectomy (Figure 67.3). If chole-
creas or along the biliary tree. If ultrasound or chol- docholithiasis is identified during intraoperative
angiography demonstrates a mass, then the next cholangiography, this is managed by either an intra-
step is computed tomography (CT) to further eval- operative bile duct exploration (transcystic or via
uate the lesion and to determine if it is potentially choledochotomy) or by postoperative ERCP.
surgically resectable. Imaging including arterial and
venous phases is needed. These scans are often per- Endoscopic ultrasound and endoscopic
formed in conjunction with ERCP/endoscopic retrograde cholangiopancreatography
ultrasound (EUS) to manage and determine the
EUS is an important adjunct in the investigation of
nature of the obstruction.
obstructive jaundice. It is particularly sensitive for
evaluating very small tumours and also allows sam-
Cholangiography
pling of any masses by fine‐needle aspirate. The
Significant advances have been made in the past procedure may provide the diagnosis of autoim-
decade that has allowed non‐invasive techniques to mune pancreatitis, a rare but important cause of
specifically evaluate the biliary tree. CT cholangio- obstructive jaundice that is managed with steroids
graphy relies on hepatobiliary excreted contrast rather than surgery.
agent (e.g. Biliscopin™), while magnetic resonance ERCP is an endoscopic procedure that is both
cholangiopancreatography (MRCP) utilises the diagnostic and therapeutic, the main risks being
fluid within the biliary system as a contrast agent by bleeding, perforation and pancreatitis. If the cause
acquiring heavily T2‐weighted images (Figure 67.2). of the obstructive jaundice is due to choledocho-
As CT cholangiography depends on adequate hepa- lithiasis, the calculi can often be extracted by ERCP,
tobiliary excretion of a contrast agent, it should usually in conjunction with a sphincterotomy of the
Fig. 67.2 MRCP demonstrating a dilated biliary system and gallbladder due to a common bile duct stricture (arrow)
caused by adenocarcinoma at the head of pancreas.
646 Problem Solving
Fig. 67.3 Intraoperative cholangiogram demonstrating choledocholithiasis visualised as filling defects in the common
bile duct (arrows).
ampulla of Vater. Following this, the patient is is expected to live beyond 6 months. This is because
treated by a cholecystectomy, provided that the stents tend to occlude within 6 months, with the
individual is fit for operation. If ERCP demon- resultant septic episodes secondary to cholangitis
strates a benign stricture, this is dilated or stented having a significant impact on the patient’s chemo-
to improve the patient’s clinical condition and then therapy treatment and quality of life.
a decision should be made as to whether repeated
dilatations should be performed or whether a surgi-
cal bypass/resection should be undertaken. Further reading
Malignant causes of obstructive jaundice may
Addley J, Mitchell RM. Advances in the investigation
occur anywhere along the biliary tree, and include
of obstructive jaundice. Curr Gastroenterol Rep
cholangiocarcinoma (intrahepatic, hilar or extrahe-
2012;14:511–19.
patic), pancreatic carcinoma and periampullary Kinney T. Evidence‐based imaging of pancreatic malig-
tumours. Distal biliary tumours are more likely to be nancies. Surg Clin North Am 2010;90:235–49.
amenable to stenting by ERCP, while more proximal Tazuma S, Unno M, Igarashi Y et al. Evidence‐based
tumours may require percutaneous transhepatic chol- clinical practice guidelines for cholelithiasis 2016.

angiography (PTC). This transhepatic approach may J Gastroenterol 2017;52:276–300.
also be required if the ampulla cannot be accessed by
ERCP due to technical difficulties (previous gastrec-
tomy, duodenal diverticulum). Stenting can be per- MCQs
formed with plastic (temporary) stents or with metal
stents, which are far more difficult to remove but
have less problems with early occlusion. Once the
tumour is stented, an assessment must be made about
the resectability of the tumour (based on its anatomi- 1 Which of the following investigations does not
cal features), the p resence or absence of metastatic require injection of contrast?
disease and the patient’s fitness for surgery. a endoscopic retrograde
If the tumour is unresectable, a surgical bypass cholangiopancreatography
may provide better palliation, provided the patient b magnetic resonance cholangiopancreatography
67: Obstructive jaundice 647
c computed tomography cholangiography d post‐sphincterotomy stricture

d percutaneous transhepatic cholangiography e cholangiocarcinoma
e intraoperative cholangiography
3 Which of the following is not a component of
2 A malignant cause for obstructive jaundice Charcot’s triad?
includes: a palpable gallbladder
a primary sclerosing cholangitis b right upper quadrant pain
b autoimmune pancreatitis c fever
c choledocholithiasis d jaundice
68 The acute abdomen, peritonitis
and intra‐abdominal abscesses
Paul Cashin1, Michael Levitt2 and the late Joe J. Tjandra3
1
2
St. John of God Healthcare, Subiaco, Perth, Western Australia
3
The acute abdomen
Establishing a differential diagnosis or a definitive
The aim of this section is to provide a broad set of diagnosis of the acute abdomen by history and
guidelines for the management of patients pre- examination is achieved by two processes. The first
senting an acute abdomen. The detailed clinical, is pattern recognition, drawn from clinical experi-
laboratory and radiological features of the numerous ence, and the second is probability, based on the
causative conditions are provided elsewhere in this theoretical knowledge of what is most likely to be
book. the cause given the circumstances.
The term ‘acute abdomen’ should be confined to The pattern of the pain is a very important factor
those patients with both acute abdominal pain and to explore in the history. The acuteness of onset,
examination findings consistent with peritonitis. periodicity, site, radiation and aggravating factors
These findings often constitute a surgical emer- are features that give hints as to cause. These need to
gency and should be managed as such. The term is be explored in detail. Information with regard to this
not interchangeable with acute abdominal pain and may need to be sought from multiple sources (e.g.
it specifically implies the highest level of abdominal family) in the case of a severely ill patient. This
surgical emergency. accurate history taking also often brings to light pre-
The management of patients with an acute cipitating factors that give clues to the likely cause.
abdomen comprises three concurrent processes – The age, sex and past medical history of the
differential diagnosis, resuscitation and definitive patient give helpful indications as to the likely cause
therapy – culminating in the decision to operate when establishing a differential diagnosis. Specific
or to observe (Box 68.1). These processes often examples of clinical patterns in patients with acute
compete with each other in a severely ill patient. abdominal pain include the following.
1 Sudden onset of pain may indicate perforation
of the gut (perforated ulcer, perforated diverticu-
Diagnostic lum, foreign body perforation) or a vascular event
Regardless of the severity of the presenting illness, (ruptured aneurysm, vascular occlusion). The sud-
management of patients with acute abdominal pain den change in nature of the pain (crampy to sudden
depends heavily on early and accurate establish- exacerbation) may indicate a perforation second-
ment of the clinical diagnosis or, at least, a worka- ary to an obstruction. In the case of right iliac fossa
ble differential diagnosis. This clinical diagnosis pain in a female, the sudden onset of pain might
requires accurate history taking, often from a num- be more likely to indicate ovarian pathology (cyst
ber of sources, and careful examination. This is an rupture or bleed) than appendicitis.
important discipline to develop and the label ‘acute 2 Syncope or collapse associated with abdominal
abdomen’ should be regarded as a flag for urgent pain suggests acute blood loss until proven other-
management and not simply for review at a later wise, for example a ruptured aneurysm or ruptured
time. ectopic pregnancy.
649
650 Problem Solving
4 Right upper quadrant pain and tenderness in a

Box 68.1 Management of the acute
30‐year‐old female (acute cholecystitis).
abdomen
It is beyond the scope of this chapter to cover all the
Diagnostic Therapeutic possible clinical scenarios that account for patients
who present with acute abdominal pain. At the
History and examination Resuscitation
heart of their management, however, is a determi-
Assess severity Airway and breathing
nation on the part of the clinician to establish an
Establish a differential control
accurate clinical differential diagnosis on the basis
diagnosis Establish early intrave-
Seek information from nous access
of history and examination and to direct further
multiple sources investigation and/or management. Indeed, an accu-
Symptom control rate history and examination may occasionally
Investigations Analgesia
lead to immediate surgery.
Explore specific Anti‐emesis
diagnoses with directed Nasogastric tube if
investigations indicated Investigations
Preoperative Monitoring the patient It is not possible, at the outset, to anticipate all the
investigations Urinary catheter investigations that might ultimately prove helpful
General investigations Oxygen saturation in patient diagnosis and management. Emergency
Invasive and non‐invasive
surgical management should never be delayed by
monitoring
investigations that may not add to the information
Non‐surgical treatment gathered from history and examination. In the
Blood transfusion/ event of a confident clinical diagnosis (e.g. acute
intravenous fluids appendicitis) in a fit individual, no confirmatory
Intravenous antibiotics or diagnostic investigations may be deemed nec-
Operate or observe essary. Numerous clinical factors affect the choice
of initial diagnostic investigations and some exam-
ples follow.
3 A combination of nausea and vomiting with 1 The severity of the presenting illness:
abdominal pain is more suggestive of gastroen- a FAST (focused assessment using sonography
teritis. Vomiting and distension with abdominal for trauma) in the emergency department if an
pain is more suggestive of obstruction. intra‐abdominal catastrophe is suspected.
4 A colicky nature to the abdominal pain is sugges- b Full blood count and cross‐match if haemor-
tive of obstruction, and examination usually rhage is suspected.
finds a relatively non‐tender abdomen until 2 Specific diagnostic possibilities:
either perforation or gut ischaemia intervene to a Serum β‐human chorionic gonadotropin in
give peritonitis or an acute abdomen. Patients suspected ruptured ectopic pregnancy.
with renal colic are usually non‐tender on exami- b Serum amylase or lipase in suspected acute
nation but have severe loin to groin pain. pancreatitis.
5 A patient lying rigid in bed whereby the pain is c Abdominal ultrasound in cases of suspected
exacerbated by movement and with associated biliary disease, obstructive uropathy, ruptured
tachycardia and often hypotension is indicative abdominal aortic aneurysm.
of peritonitis. d 12‐lead ECG in suspected acute myocardial
6 Pain exacerbated by movement suggests peritoneal infarction.
irritation (e.g. appendicitis or a musculoskeletal e Urine dipstick and midstream urine (MSU)/
cause). catheter specimen of urine (CSU) should be
Specific examples of the application of probability performed, as urinary tract infections often
in the clinical setting include the following. mimic many other abdominal conditions.
1 Recent onset of abdominal pain in the right side 3 If surgery is anticipated, prior to undergoing a
of the abdomen and anorexia in a previously general anaesthesic, certain investigations may
well young man (acute appendicitis). be obtained, particularly in older patients, as a
2 Left iliac fossa pain and tenderness in a 60 year routine. This will vary from centre to centre, but
old (sigmoid diverticulitis). such tests include urea and electrolytes, full blood
3 Upper abdominal pain, back pain and vomiting count, ECG, chest X‐ray as well as cross‐match in
in a known alcoholic (acute pancreatitis). appropriate cases.
68: The acute abdomen, peritonitis and intra‐abdominal abscesses 651
4 General investigations in patients with acute taken. Tachycardia, hypotension, pallor, sweating
abdominal pain of uncertain origin. These inves- and cool extremities all suggest a more severe
tigations may direct further intervention or flag a clinical presentation and the possibility of sepsis
previously unrecognised degree of severity. Even or hypovolaemia. Immediate intravenous access
before a clinical diagnosis is formulated, certain should be established and fluid replacement appro-
diagnostic investigations may have been insti- priate to the clinical setting commenced. Oxygen
gated in anticipation of subsequent need. Many should be administered to maximise vital organ
centres have routine investigation sets performed oxygenation. If conscious state is compromised,
on presentation of the patient to aid efficiency. early airway management should be undertaken.
Amongst these, those most frequently of value In cases of haemorrhagic shock, a blood transfu-
are as follows. sion should commence as soon as practicable.
a Full blood count: elevation of the white cell However, transfusion should not be allowed to
count is a cardinal sign of sepsis but it may also delay the commencement of urgently needed sur-
be raised by the ‘stress’ of pain alone; it is also gery (e.g. ruptured abdominal aortic aneurysm)
mildly elevated during normal pregnancy. In where the need to control the bleeding point out-
general, an elevation of white cell count should weighs the desire to restore intravascular volume
never be dismissed and a very high white cell by transfusion.
count (>30 × 109/L) in the context of a patient
with acute abdominal pain raises the possibility
Symptom control
of intestinal perforation, peritonitis or ischaemia
(hollow viscus perforation, mesenteric infarc- In the acute setting it is easy to overlook the need
tion, closed‐loop small‐bowel obstruction). to provide basic symptom control. Analgesia
b Abdominal X‐ray: a supine abdominal X‐ray should not be withheld pending surgical review.
reveals distension of intra‐abdominal gas Analgesia requirements are usually an excellent
(intestinal obstruction), thickness of intestinal indicator of the degree of pain being suffered by the
wall (mesenteric ischaemia), abnormal calcifi- patient; anti‐emetic therapy usually accompanies
cation (ureteric colic, chronic pancreatitis) opiate analgesics. For repeated vomiting (e.g. intes-
and outlines the psoas shadows (possibly tinal obstruction, acute pancreatitis) a nasogastric
obscured in ruptured abdominal aortic aneu- tube should be passed. This will relieve the symp-
rysm). The erect abdominal/chest X‐ray toms, permit more accurate measurement of fluid
reveals fluid levels or free gas under the loss and protect the patient from the risks of aspi-
diaphragm (confirmation of intestinal obstruc- ration of gastric contents. Urinary retention often
tion or perforation). accompanies the acute abdomen and a urinary
c Ultrasound in experienced hands may reveal catheter should be inserted to also aid fluid balance
free fluid suggestive of haemorrhage or monitoring.
perforation.
d CT may reveal or confirm the diagnosis and is Monitoring the patient
now readily available. A CT scan should not
be performed in an unstable patient (where it In the severely unwell patient, it is important to
delays definitive surgical management or monitor the outcome of resuscitation and fluid
endangers the patient) nor be used to replace replacement. Apart from the standard vital signs
accurate and rigorous clinical history and (pulse rate, blood pressure, temperature), addi-
examination. tional information can be obtained by measuring
urine output (indwelling urinary catheter) and
invasive (arterial line or central venous line) or non‐
Therapeutic invasive cardiovascular monitoring. These meas-
ures are more sensitive to changes in intravascular
At the same time as these diagnostic steps are being fluid status than are the pulse rate and blood
taken, concurrent therapeutic management should be pressure.
undertaken. This includes the following broad groups.
Resuscitation Non‐surgical therapy
Unwell patients may require preliminary resusci- Broad‐spectrum antibiotics should be administered
tation before any practical diagnostic steps can be according to the likely clinical diagnosis. This may
652 Problem Solving
precede the formulation of an accurate clinical diag- generally indicates progression of the underlying
nosis, especially in unwell patients. Agents active pathological process.
against Gram‐negative bacilli (aminoglycosides,
third‐generation cephalosporins) and anaerobic Clinical example
organisms (metronidazole) are generally preferred
in patients presenting with acute abdominal pain. The clinical scenario described in Box 68.2 serves
In cases of suspected peptic ulcer complications, as a demonstration of the dual processes – diag-
intravenous proton pump inhibitors (PPIs) should nostic and therapeutic – in the management of a
be administered. In the anticoagulated patient, patient with acute abdominal pain. Note especially
reversal of anticoagulation may need to be con- the rapid construction of a workable differential
sidered, if possible, when bleeding is suspected or diagnosis to permit subsequent history and exami-
surgery is planned. nation to focus on identifying the most likely
diagnosis.
Surgery versus observation Peritonitis

Ultimately, an assessment needs to be made about
the need for surgery. This may be clear‐cut where Peritonitis is defined as an inflammation of the
a confident clinical diagnosis has been made (e.g. peritoneum of whatever underlying cause. As
appendicitis). previously discussed in the section on the acute
In some cases, advanced age or infirmity might abdomen, peritonitis is an essential feature of this
caution against surgery even where a confident clinical syndrome but is also a feature of other
diagnosis points to a surgical remedy (e.g. rup- more localised diseases of the peritoneal cavity
tured abdominal aortic aneurysm in a frail 90 year causing acute abdominal pain.
old). Significant concerns in this situation about Often the peritonitis is localised to a particular
goals of care, limitations of care and end‐of‐life area of the abdomen and this occurs due to the
care need to be incorporated into the clinical body’s ability to contain the inflammatory process
discussion. by wrapping of the omentum. This containment
Often, however, the precise diagnosis is uncertain may eventually lead to a localised abscess (see section
and the need for urgent surgery is made obvious by Intra‐abdominal abscesses) or progress to generalised
virtue of either the clinical features of generalised peritonitis and an acute abdomen. This progression
peritonitis (e.g. perforated hollow viscus, mesenteric may be accompanied by marked ileus, hypovolaemia,
infarction, closed‐loop small bowel‐obstruction) or toxaemia or even septicaemia.
the severity of the presenting illness (e.g. associated Cardinal signs of peritonitis are tenderness,
shock). In this situation, clinical experience (pattern guarding and rebound over the specific area or the
recognition) enables early identification of the need whole abdomen in the case of diffuse peritonitis
for prompt surgical intervention, often without (see section The acute abdomen). Fever, tachycardia
further investigation. and dehydration are common features and move-
Where the need for surgery is unclear (e.g. some ment generally exacerbates the pain.
cases of right iliac fossa pain or small intestinal
obstruction), observation, resuscitation and non‐ Causes of peritonitis
surgical treatment of the likely diagnosis, rather
Acute primary peritonitis
than exploratory surgery, is appropriate. This
involves regular clinical review conducted at a fre- Acute primary peritonitis is rare and usually occurs
quency appropriate to the severity of the illness; in association with immunosuppression, such as
for example, review in 12 hours for a 20‐year‐old post splenectomy, renal disease or in cirrhosis,
woman with mild right iliac fossa pain and tender- where the proteinaceous ascitic fluid provides a
ness or in 1–2 hours for a 75‐year‐old man with good culture medium for bacteria. Sometimes it
small bowel obstruction and associated abdomi- affects young girls following pelvic inflammatory
nal tenderness. At times, such review may be disease. Commonly involved organisms include
augmented by further laboratory or radiological haemolytic streptococci, Escherichia coli and
investigations. Of these, the white cell count and Klebsiella species. Acute primary peritonitis is often
C‐reactive protein (CRP) are most often of prac- a diagnosis of exclusion and requires aggressive
tical value; a rising white cell count or CRP antibiotic therapy (Box 68.3).
Box 68.2 Clinical scenario
A 65‐year‐old man presents with the sudden onset of generalised abdominal pain and collapse. On examination, he is
pale, sweaty and distressed, with pulse rate of 110 beats/min, blood pressure 90/50 mmHg and temperature 36.0°C
Diagnostic Therapeutic
1 History and examination (establish and explore 1 Resuscitation

the likely differential diagnosis) • Adequate intravenous access (beware of over‐transfusion
• Ruptured abdominal aortic aneurysm in acute myocardial infarction)
◦ Pain radiating to back or groin • Oxygen mask (plus airway support if appropriate)
◦ History of smoking, other vascular diseases • Transfuse if haemoglobin <8 g/dL
◦ Palpate abdomen for pulsatile mass • Beware the normal haemoglobin in patients with
◦ Absent or reduced lower limb peripheral pulses acute haemorrhage: a normal value does not rule
• Mesenteric infarction out acute bleeding
◦ History of palpitations, arrhythmia, digitalis therapy • Consider transfusing if haemoglobin <10 g/dL and
◦ Palpate pulse for atrial fibrillation further bleeding or major surgery is planned
• Perforated peptic ulcer
2 Symptom control
◦ History of dyspepsia, antacid therapy, NSAID ingestion
• Intravenous or intramuscular opiate analgesics
◦ Board‐like abdominal rigidity
• Anti‐emetic therapy
• Acute pancreatitis
• Nasogastric tube if vomiting
◦ Prominent vomiting, pain referred to back
◦ Alcoholic or gallstone aetiology 3 Monitoring the patient
• Acute myocardial infarction • Indwelling urinary catheter
◦ Past history of ischaemic heart disease • Oxygen saturation monitoring
• Non‐invasive or invasive cardiovascular monitoring
2 Investigations
• Full blood count 4 Non‐surgical treatment
◦ Low haemoglobin may indicate haemorrhage, high • Intravenous antibiotics (suspected perforation,
white cell count suggests infection associated with mesenteric ischaemia)
perforation or ischaemia • High‐dose PPIs
• Urea and electrolytes: to guide resuscitation
• Serum lactate and blood gases: measure of organ
damage/ischaemia
• 12‐lead ECG: changes of acute ischaemia
• Abdominal X‐ray, supine and erect
◦ Free intraperitoneal gas, loss of psoas shadow,
calcification of abdominal aortic aneurysm, dilated
loops of small intestine
• Serum amylase/lipase: >1000 U/L diagnostic of acute
pancreatitis
• Cross‐match: if haemorrhage is suspected and/or
major surgery anticipated
• FAST scan: to confirm ruptured abdominal aortic
aneurysm
• Investigations should not delay surgical management
in a deteriorating patient or a patient not responding
to resuscitation
Operate or observe?
• Ruptured abdominal aortic aneurysm: immediate laparotomy or angiographic stenting depending on facility
• Perforated peptic ulcer: immediate operation (occasionally may be treated by antibiotics, PPIs and observation if
abdominal signs are localised)
• Mesenteric infarction: immediate operation to exclude closed‐loop small‐bowel obstruction
• Acute pancreatitis: intravenous fluid replacement, analgesia, oxygen administration, nasogastric tube if vomiting,
urinary catheter for fluid balance monitoring. Observe for progressive abdominal signs, features of intra‐abdominal
sepsis. Monitor full blood count, liver function tests, serum calcium, blood glucose level, arterial blood gases and CRP
• Acute myocardial infarction: monitor patient in critical care facility, specific therapy according to local protocols
654 Problem Solving
gas beneath the diaphragm, indicating a perfo-

Box 68.3 Common varieties
rated viscus and clinical findings may suggest an
of peritonitis
acute abdomen (Figure 68.1).
Acute peritonitis Chemical peritonitis may occur secondary to bile
Primary (spontaneous) (bile leak post laparoscopic cholecystectomy) or
Secondary blood (postoperative bleeding, abdominal trauma).
Acute suppurative (e.g. perforated viscus) Less commonly, urine (ureteric injury in pelvic
Chemical‐induced surgery or intraperitoneal rupture of bladder) may
Chronic (sclerosing) peritonitis also be the cause. Bacterial contamination and
Infections (e.g. tuberculosis, Candida albicans) overgrowth may develop as a secondary event if the
Chemical‐induced (e.g. surgical talc in the gloves, condition goes unrecognised.
chlorhexidine)
Carcinomatosis
Intra‐abdominal abscesses
Intra‐abdominal abscesses are one extreme in the

spectrum of bacterial peritonitis. They are often
related to the body’s attempt or ability to localise
infections by migration of the omentum to the
site of sepsis. They require drainage in addition
to antibiotic therapy. The pathogenesis requires a
polymicrobial infection, often with the presence of
foreign matter facilitating the development of
progressive infection. The bacterial flora of the

gastrointestinal tract varies from small numbers of
aerobic streptococci and facultative Gram‐negative
bacilli in the stomach and proximal small bowel
to larger numbers of these species with an increas-
ing number of anaerobic Gram‐negative bacilli
(Bacteroides spp.) and anaerobic Gram‐positive
flora (streptococci and clostridia) in the distal ileum
and colon. In patients who have received prolonged
antibiotic therapy and in those with extended hospital
stay or long‐term illness, colonisation by yeasts
such as Candida species or a variety of nosocomial
pathogens may occur. Skin flora may be responsible
following penetrating abdominal injuries. Pelvic
abscesses in women may occur as part of pelvic
inflammatory disease. Common organisms include
Fig. 68.1 Erect chest X‐ray showing free gas beneath the Neisseria gonorrhoeae and Chlamydia trachomatis.
right hemidiaphragm indicating likely perforation. There are four functional compartments within
the peritoneal cavity: pelvis, right and left para-
colic gutters and the subdiaphragmatic spaces.
In the recumbent patient, diffuse intraperitoneal
Secondary peritonitis
fluid collects under the diaphragm and in the pelvis.
Secondary peritonitis may be suppurative, chemical These are the common sites for abscess formation.
or chronic sclerosing. More localised abscesses may develop in relation
Acute suppurative peritonitis may occur second- to the affected viscus (e.g. abscesses in the lesser
ary to a disease process of an intra‐abdominal organ, sac secondary to severe pancreatitis or a perforated
i.e. perforation (e.g. peptic ulcer, diverticular disease, peptic ulcer, or a peri‐appendiceal abscess). In the
Crohn’s disease, appendix or gallbladder), infection paracolic gutters, local abscesses often develop in
(e.g. appendix abscess, pyosalpinx) or ischaemia conjunction with small colonic perforations. This
(volvulus, mesenteric ischaemia or strangulated is usually related to diverticular disease or diver-
hernia). Most of these cases will require urgent sur- ticulitis in the left colon. Solitary diverticular per-
gical intervention. Erect chest X‐ray may show free foration and foreign body perforation are more
common in the right colon. Perforated tumours and is vastly operator dependent. Endovaginal
also need to be part of any differential diagnosis in ultrasound is particularly useful for detecting tubo‐
these situations. These conditions demonstrate ovarian abscess complicating pelvic inflammatory
pattern recognition in clinical assessment. disease in women
Laparoscopy is occasionally used if there is diag-
Clinical features nostic uncertainty.
The clinical presentation of an intra‐abdominal
abscess is highly variable. In a patient with predis- Therapy
posing primary intra‐abdominal disease or following
abdominal surgery, persistent abdominal pain, focal Parenteral antibiotics
tenderness, swinging fever, persistent paralytic Parenteral antibiotics should be administered
ileus, elevated CRP and leucocytosis suggest an prior to drainage of the abscess. Initial choice of
intra‐abdominal purulent collection. The patient antibiotics is empirical but should provide a
may simply fail to thrive and may have mildly broad‐spectrum activity against likely organisms as
abnormal liver function secondary to portal sepsis. they pertain to the proposed source of the infection.
With a pelvic abscess, there may be urinary Specific therapy is guided by the results of cultures.
frequency, dysuria, diarrhoea or tenesmus due to With adequate drainage of the abscess, it may
irritation of the anatomically related organs. With a not be necessary to treat each component of the
subphrenic collection, there may be shoulder tip polymicrobial flora. Commonly used antibiotics
pain, hiccups and unexplained pulmonary symp- include metronidazole with a second‐ or third‐
toms (pleural effusion, basal atelectasis). generation cephalosporin or meropenem alone.
Alternatively, combinations of amoxicillin, gen-
Investigations tamicin and metronidazole provide additional cover
Investigations in patients with suspected intra‐ against enterococci as well. In immunosuppressed
abdominal abscess include full blood examination, patients, Candida species may have an important
CRP, urea and electrolytes and liver function tests. pathogenic role, and treatment with antifungals is
Blood cultures and other appropriate cultures indicated.
(urine, sputum, catheter) may also be performed.
CT scan with iodinated soluble oral contrast is Percutaneous drainage
useful. Spiral images are obtained from the dia-
CT scan or ultrasound localises the abscess cavity
phragm to the pelvis. It is particularly useful for
and guides safe access for percutaneous drainage
localising small or deep intra‐abdominal abscesses
(Figure 68.3), avoiding adjacent viscera and blood
(Figure 68.2). Interpretation in postoperative
vessels. A diagnostic needle aspiration is initially
patients can be particularly difficult, as loculated
performed to confirm the presence of the abscess
non‐infected serous collections are common physi-
and to obtain pus for Gram stain and culture.
ological events.
A large‐bore drainage catheter is then placed in the
Ultrasound equipment is mobile and examina-
most dependent position. While percutaneous
tions may be readily performed in a critically ill
drainage is effective in a single unilocular abscess,
patient in the intensive care unit. However, the
quality of such studies is not as good as a CT scan
Fig. 68.3 CT scan of the abdomen showing a large

subphrenic abscess that was aspirated percutaneously
Fig. 68.2 CT scan showing a pelvic abscess. under CT guidance.
656 Problem Solving
it is more limited in a multiloculated abscess,

especially if the contents are tenacious.
Summary
Preliminary percutaneous drainage is sometimes
Many severe intra‐abdominal pathologies can pre-
useful in improving and reducing the sepsis, prior
sent clinically in a variety of ways. The term ‘acute
to definitive surgical treatment. In some cases, as
abdomen’ should be distinguished from acute
for complicated diverticular disease or Crohn’s
abdominal pain and represent those intra‐abdomi-
disease, it may facilitate subsequent single‐stage
nal conditions at the most severe end of the clinical
resection and primary anastomosis, rather than
spectrum, requiring the most urgent treatment.
traditional multistage procedures with diversion.
Pattern recognition and application of probabili-
Repeat imaging with sinography or CT will often
ties, ascertained from rigorous clinical history tak-
help to estimate the size of the residual cavity and
ing and clinical examination, remain the mainstay
any enteric communication.
in the diagnosis and subsequent management of
many of these conditions.
Intraluminal drainage
The development of technology such as endoscopic Further reading
ultrasound has seen the ability to safely drain
intra‐abdominal abscesses into the lumen of the Almeida PRL, Leão GS, Gonçalves CDG, Picon RV,
gut. This is particularly useful in draining infected Tovo CV. Impact of microbiological changes on sponta-
necrotic pancreatic abscesses, following severe neous bacterial peritonitis in three different periods
pancreatitis, into the stomach. This drainage is over 17 years. Arq Gastroenterol 2018;55:23–27.
Colas PA, Duchalais E, Duplay Q et al. Failure of con-
further facilitated by the ability to insert drain
servative treatment of acute diverticulitis. World J Surg
tubes between the abscess and the gastric lumen
2017;41:1890–5.
or to debride necrotic material via endoscopic Constantinides VA, Tekkis PP, Senapati A. Association of
cyst‐gastrotomy. Coloproctology of Great Britain and Ireland. Comparison
of POSSUM scoring systems and the surgical risk scale in
patients undergoing surgery for complicated diverticular
Surgical drainage disease. Dis Colon Rectum 2006;49:1322–31.
Galbraith N, Carter JV, Netz U et al. Laparoscopic lavage
Surgical drainage is mainly undertaken in patients in the management of perforated diverticulitis: a con-
who have not improved with percutaneous drain- temporary meta‐analysis. J Gastrointest Surg 2017;21:
age or in whom the collections are not appropriate 1491–9.
for percutaneous drainage, as in multiple abscesses, Shah TT, Herbert P, Beresford T. An atypical presentation
severe necrotising pancreatitis or interloop of aortic rupture: intuition and investigation can avoid
abscesses with Crohn’s disease. An extraperitoneal disaster. Ann R Coll Surg Engl 2011;93:e125–e128.
approach, if possible, is generally preferred because Shizuma T. Spontaneous bacterial and fungal peritonitis
it limits the risk of further contamination of the in patients with liver cirrhosis: a literature review.
World J Hepatol 2018;10:254–66.
peritoneal cavity. With a distally located pelvic
abscess that is bulging, the drainage may be per-
formed through the rectum or vagina. The loculae
are gently broken down digitally and soft drains are
MCQs
placed in the most dependent position. Laparoscopic Select the single correct answer to each question. The
drainage of singular abscesses has also proven ben- correct answers can be found in the Answers section
eficial in many cases. at the end of the book.
1 Which of the following clinical features is often

Definitive surgery
found in a patient presenting with an acute
Definitive surgery is generally deferred until after abdomen related to generalised peritonitis?
preliminary drainage of the abscess. In some situa- a slow pulse rate
tions, surgery on the offending organ is performed, b extreme restlessness and writhing around in agony
for example appendicectomy for appendiceal c motionless with pain, worse with movement
abscess, unilateral salpingo‐oophorectomy for d normal bowel sounds
tubo‐ovarian abscess, omental patch of a perfo- e deep palpation of most abdominal organs is
rated duodenal ulcer. possible
2 Acute epigastric pain is unusual in which of the underlying pathological process responsible for
following conditions? acute abdominal pain in a patient being initially
a acute pancreatitis managed non‐operatively?
b acute cholecystitis a erythrocyte sedimentation rate
c perforated peptic ulcer b haemoglobin estimation
d acute diverticulitis c white cell count
e ruptured abdominal aortic aneurysm d white cell scan
e serum phosphate
3 Immediate laparotomy would not be recommended
in a patient diagnosed as having which of the 5 Which of the following is a common cause of
following conditions? post‐surgical pelvic abscess?
a mesenteric infarction a cholecystectomy
b perforated peptic ulcer with generalised b appendicectomy
peritonitis c laparoscopic but not conventional open anterior
c acute pancreatitis resection
d small bowel obstruction with peritonism d rectovaginal fistula
e ruptured abdominal aortic aneurysm e use of powdered surgical gloves
4 Which of the following parameters is the most

practical for monitoring progression of the
69 Ascites
David A.K. Watters1,2, Sonal Nagra1,2 and David M.A.
Francis3
1
Deakin University and Barwon Health, Geelong, Victoria, Australia
2
University Hospital Geelong, Geelong, Victoria, Australia
3
to move through pores between the vascular

Introduction endothelial cells of the portal system into the
extravascular space of the liver and intestine.
Ascites is an abnormal accumulation of free fluid
Lymphatic flow is increased proximal to the point
within the peritoneal cavity. The word ‘ascites’ is of
of vascular obstruction and, when the capacity of
Greek origin (askos) and means bag or sac. Ascites is
the lymphatic system is surpassed, the transudate
due to increased portal venous pressure, low plasma
moves across the surfaces of the liver, mesentery
proteins (hypoproteinaemia), chronic peritoneal irri-
and intestine into the peritoneal cavity. Cirrhosis
tation, leakage of lymphatic fluid into the peritoneal
and schistosomal periportal fibrosis are the com-
cavity, or fluid overload (Box 69.1). Three‐quarters
monest causes of portal hypertension.
of cases occur as a result of portal hypertension in the
Any cause of hepatic venous outflow obstruction
setting of liver cirrhosis, with the remainder due to
may cause ascites by increasing portal venous pres-
infective, inflammatory and neoplastic conditions.
sure (Budd–Chiari syndrome). The site of obstruc-
Ascites needs to be differentiated from other causes
tion may be at the hepatic venules (haematological
of abdominal distension including bowel obstruction,
or liver disease), large hepatic veins, inferior vena
bleeding and huge intra‐abdominal masses or cysts.
cava or right atrium (right heart diseases).
Pathophysiology of ascites Hypoproteinaemia

Low concentrations of plasma proteins, particularly
Increased portal venous pressure albumin, reduce the osmotic pressure of plasma. In
(Figure 69.1) health, the relatively high osmotic pressure of intra-
Any cause of increased resistance to hepatic or por- vascular plasma tends to draw extravascular fluid
tal venous blood flow can lead to ascites. Gross back into the intravascular space. The osmotic gra-
ascites occurs when increased pressure within the dient is reduced in hypoproteinaemic states so that
hepatic veins or at the post‐sinusoidal level dramat- less fluid is removed from extravascular sites. When
ically increases hydrostatic pressure within the the capacity of the hepatic and intestinal lymphatics
hepatic sinusoids in the liver, and within the portal to remove fluid from the extravascular interstitial
venous system. Collateral vein formation, shunting space is exceeded, ascites develops. This is well dem-
of blood to the systemic circulation and splanchnic onstrated in kwashiorkor where the hypoalbumi-
vasodilatation (due in part to the local production naemic state results in ascites due to the severe
of nitric oxide) develop particularly in the later protein energy malnutrition.
stages of cirrhosis. Systemic arterial pressure is
Sodium and water retention
maintained by vasoconstriction and antinatriuretic
factors, resulting in sodium and water retention. Reduced circulating plasma volume, as a result of
The increased portal pressure combined with loss of intravascular fluid into the peritoneal cavity
splanchnic vasodilatation alters the capillary pres- and interstitial spaces (third‐space fluid loss) and
sure and permeability, enabling intravascular fluid pooling of blood in the splanchnic vascular space
659
660 Problem Solving
Box 69.1 Causes of ascites Cirrhosis
Increased portal venous pressure

• Prehepatic: portal vein compression or thrombosis, Portal
Hypertension
schistosomiasis
• Hepatic: cirrhosis, acute hepatic necrosis, viral
hepatitis Splanchnic vasodilatation
• Posthepatic: Budd–Chiari syndrome, myeloprolif-
erative disorders, constrictive pericarditis, right
heart failure, hypercoagulable states
Hypoproteinaemia Splanchnic Systemic

• Renal disease causing severe proteinuria: includes capillary pressure arterial filling
nephrotic syndrome
• Malnutrition and malabsorption
• Protein‐losing enteropathy Renin Angiotensin
• Acute or chronic liver disease sympathetic activity
Lymph Intrarenal factors
• Severe acute or chronic illness
Chronic peritoneal inflammation and infection

Plasma Renovasoconstriction
• Chronic infection: tuberculosis, fungal infection
volume Sodium and water retention
• Secondary malignant infiltration (carcinomatosis
peritonei)
• Post irradiation Hepatorenal
• Serositis secondary to inflammation from chronic Ascites syndrome
infection/allergic reaction
Fig. 69.1 The pathophysiology of ascites due to
Leakage of lymphatic fluid (chylous ascites) cirrhosis.
• Congenital
• Surgical trauma: postoperative ileus
• Primary and secondary lymphatic malignancy
the capacity of the lymphatics to reabsorb the fluid
Other fluids is exceeded, it accumulates within the peritoneal
• Pancreatic ascites cavity. The high protein concentration of this peri-
• Bilious ascites toneal fluid further retards fluid reabsorption. As
• Urinary ascites the inflammatory process resolves, and microvascu-
• Hypothyroidism: severe myxoedema lar permeability returns to normal, less peritoneal
fluid is formed and fluid is removed by absorption.
The commonest cause of chronic peritoneal inflam-
secondary to portal venous outflow obstruction,
mation worldwide is abdominal tuberculosis but
reduces renal blood flow and glomerular filtration.
other peritoneal infections and foreign matter may
Decreased renal perfusion stimulates increased
also induce ascites.
renin secretion from the juxtaglomerular apparatus
in the ascending limb of the loop of Henle of the
kidney. The resultant secondary aldosteronism
Malignant infiltration
causes retention of sodium and water. Impairment Metastatic deposits cause ascites by a combination
of renal excretion of water and renal vasoconstric- of inflammation, shedding of cells, exudation, lym-
tion lead to dilutional hyponatraemia and increase phatic obstruction and sometimes bleeding. Gross
the risk of hepatorenal syndrome, which comprises ascites does not usually occur until late. Gastric and
renal failure, portal hypertension and ascites. ovarian cancers (Meigs syndrome) are the most
notorious for causing ascites due to their ease of
Chronic peritoneal inflammation transperitoneal spread, but any peritoneal malig-
nant process may be responsible.
Any chronic inflammatory process within the peri-
toneal cavity results in considerable increases in
flow within peritoneal blood and lymphatic vessels.
Leakage of fluid
Peritoneal microvascular permeability increases Leakage of fluid directly into the peritoneal cavity
markedly with consequent exudation of plasma occurs when intra‐abdominal lymphatics are tran-
proteins and fluid into extravascular spaces. When sected (e.g. abdominal surgery, trauma) or
69: Ascites 661
obstructed (e.g. primary or secondary lymphatic degree of resistance. In cases of chronic inflamma-
malignancy, surgical ligation). Ascites forms when tion, particularly tuberculosis, the abdomen may
the rate of leakage into the peritoneal cavity exceeds feel ‘doughy’. Gross ascites causes tense abdominal
the rate of absorption by peritoneal lymphatics. distension that makes palpation of organomegaly
Exudation of pancreatic fluid from an inflamed challenging. Ascites is confirmed by the presence of
pancreas may occur in acute pancreatitis. If the a fluid thrill and shifting dullness on percussion.
pancreatic duct ruptures due to inflammation or Clinical examination should include a search for
surgical damage, pancreatic ascites may persist as signs of heart failure such as pitting leg oedema and
an internally draining pancreatic fistula. raised jugular venous pressure. Although rare, fea-
Bile leaks may be termed bilious ascites, although tures of peritoneal carcinoma such as Virchow’s
bile is normally very irritant to the peritoneal cavity node or a Sister Mary Joseph nodule may give a
and commonly induces more of a peritonitis/acute cause for the ascites. Virchow’s node is the presence
abdomen‐type reaction. of left supraclavicular lymphadenopathy and
Urine may leak into the peritoneal cavity from results from nodular metastasis from lymphatic
damage to a ureter or the bladder or from an drainage via the thoracic duct draining into the left
obstructed hydronephrotic kidney. subclavian vein. A Sister Mary Joseph nodule is a
palpable nodule at the umbilicus that arises from
metastasis of a malignant cancer in the pelvis or
Postoperative ascites
abdomen.
It is important to ensure all efforts are made to rule Patients with a history of cancer, especially gas-
out bleeding, bile leak, urine leak, bowel injury and trointestinal cancer, are at risk for malignant
anastomotic leak prior to making a diagnosis of ascites. Malignancy‐related ascites is frequently
postoperative ascites. Most commonly, ascites pre- painful, whereas cirrhotic ascites is usually pain-
sents postoperatively due to low albumin states. less. Patients who develop ascites in the setting of
This is more pronounced in patients with liver established diabetes or nephrotic syndrome may
impairment. Although rare, ascites has been attrib- have nephrotic ascites.
uted to inflammation or allergic reaction of the
peritoneal surface. Postoperative patients have a Fluid thrill
negative nitrogen balance; in patients with ascites,
Large amounts of intraperitoneal fluid, either free
this is further worsened with loss of protein‐rich
or encysted, may give rise to a fluid thrill. The abdo-
fluids in drains and through wounds.
men is flicked on one side and the transmitted
shock wave is palpated by the examiner’s other
hand, which has been placed flat on the far side of
Clinical features
the abdomen (Figure 69.2a). An accessory hand
prevents transmission of the shock wave through
Ascites should be suspected from a history of
the subcutaneous fat of the anterior abdominal
abdominal distension. Physiologically, men gener-
wall. A fluid thrill may also be elicited by tapping in
ally have no peritoneal fluid while women can have
the loin and palpating at the front (Figure 69.2b).
up to 20 mL depending on the phase of their men-
To detect a fluid thrill in an abdomen with smaller
strual cycle. Ascites can be detected clinically on
volumes of ascitic fluid, the area of stony dullness is
examination of the abdomen when the volume
first determined by percussion.
reaches approximately 1 L. Inspection of the abdo-
men reveals distension, which may vary from slight
Shifting dullness
fullness laterally in the flanks to gross distension
predominantly in the centre of the abdomen. Free intraperitoneal fluid gravitates to the most
Sometimes a hernial sac protrudes as it becomes full dependent parts of the peritoneal cavity, namely the
of ascitic fluid, particularly at the umbilicus. Other pelvis and paracolic regions, while the gas‐filled
abnormal findings on inspection may include signs intestine tends to ‘float’ uppermost. Fluid‐filled
of liver disease (jaundice, scratch marks because of structures have a stony dull percussion note, while
pruritus, spider naevi, caput medusae and dilated gas‐filled structures are resonant or hyperresonant
veins on the anterior abdominal wall, hepatomeg- on percussion. Thus, when a patient with ascites
aly), para‐umbilical and other abdominal hernias, lies supine, the flanks or lateral parts of the abdo-
pitting oedema and surgical scars. men are stony dull to percussion while the perium-
On palpation the abdomen may feel thicker bilical area is resonant. When the patient lies on one
owing to the fluid asserting more than the expected or other side, ascitic fluid gravitates to that side
662 Problem Solving
(a) Ascites is a multisystem disease and the probable

cause will determine which systems require investi-
gation. The choice includes urinalysis, serum con-
centrations of electrolytes, urea and creatinine,
total proteins and albumin, liver function tests,
serology, abdominal ultrasonography (Figure
69.3a), computed tomography (CT) (Figure 69.3b),
portal vein Doppler scan and echocardiography.
Diagnostic aspiration of a small volume of ascitic
fluid for biochemical (protein and amylase estima-
tion), microbiological (microscopy and culture) and
cytological assessment may be necessary.
Laparoscopy or mini‐laparotomy may be required
to perform a peritoneal biopsy to diagnose abdomi-
nal tuberculosis and other inflammatory condi-
(b) tions. Schistosomiasis may be suspected from a
history of swimming or living in endemic areas and
confirmed by rectal or liver biopsy, ultrasound or
serology. Plain abdominal films are not a method of
diagnosing ascites but sometimes gross ascites give
an appearance of ground glass.
A serum to ascites albumin gradient (SAAG)
above 1.1 g/dL has 97% accuracy for diagnosis of
ascites due to portal hypertension. There has been a
conceptual shift from a definition that categorises
ascites fluid as either transudative or exudative to
one of high albumin gradient and low albumin gra-
dient, respectively, which relate to portal hyperten-
sive (SAAG >1.1 g/dL) and non‐portal hypertensive
Fig. 69.2 (a, b) Clinical examination: palpating for (SAAG <1.1 g/dL) causes. (SAAG = serum albumin
ascites. level – ascitic fluid albumin level in g/dL.)
because it is then the most dependent part of the

abdomen, and so the percussion note over that area Clinical outcome
becomes stony dull, while the other side becomes
resonant. Mild to moderate ascites may cause few symptoms.
Shifting dullness is elicited by percussing the abdo- Large‐volume ascites (more than 3–4 L) is very
men and determining the point at which the percus- unpleasant for patients because it produces a con-
sion note changes from resonant to dull. The patient stant feeling of abdominal fullness and discomfort,
is then asked to roll about 45° to one side, and per- nausea and anorexia, limitation of movement and
cussion is repeated after waiting for a few seconds. leg swelling. Respiratory difficulty and shortness of
Shifting dullness is confirmed by a significant change breath is due to elevation of the diaphragm, atelec-
in position of the area of stony dullness. It should be tasis and pleural effusions. Ascites may be compli-
noted that slight changes in the percussion note may cated by previously unrecognised abdominal
be caused by positional changes in the small hernias and rarely by primary bacterial peritonitis.
intestine. Primary or spontaneous bacterial peritonitis may
be difficult to diagnose, does not always cause a lot
of guarding or rigidity and patients’ immune
Investigation response to the infection may be impaired owing to
their underlying disease, for example liver, renal or
Investigation of a patient with ascites aims to detect malignancy. Sometimes the peritonitis presents
the cause of the fluid accumulation. This is usually with general deterioration (e.g. development of
evident from the history and clinical examination, hepatic encephalopathy or renal failure) rather
including habits and previous travel or domicile. than abdominal signs. Reduced renal blood flow
Specific investigations depend on the likely cause of and glomerular filtration, poor urine output and
the ascites (see Box 69.1). low urinary sodium excretion cause pre‐renal
69: Ascites 663
(a)
Ultrasound showing ascitic fluid (black) around liver on right

and around spleen on left.
(b)
Ascitic fluid
Fig. 69.3 (a) Ultrasound showing fluid (black) around the liver. (b) CT scan showing ascitic fluid, anterior abdominal
distension and contrast in the loops of the bowel.
impairment with increased urea and creatinine, ascites does not respond to high doses of diuretics
which may progress to acute renal failure (hepato- (spironolactone and frusemide). Moderate‐volume
renal syndrome). Development of ascites in patients ascites does not require paracentesis and large‐vol-
with chronic liver disease indicates severe liver ume ascites is controlled by a combination of medi-
impairment, and 1‐year survival of such patients cal treatment and paracentesis.
with intractable ascites is approximately 50%.
Malignant ascites is most commonly due to intra- Medical management
peritoneal metastatic deposits of cancer originating
in the ovary, stomach, breast and colon. Prognosis Specific management of the cause of liver dysfunc-
of these patients is poor, with a median survival of tion, such as antivirals for hepatitis B and C and
about 3 months. alcohol rehabilitation in alcohol‐related cirrhosis,
should be initiated. Dietary sodium is restricted to
approximately one‐third of the normal daily intake
Treatment (i.e. to about 60–90 mEq/day). Diuretic therapy
commences with an aldosterone antagonist such as
Most patients with ascites are treated non‐opera- spironolactone or amiloride. In recurrent or persis-
tively. Ascites can be classified as moderate‐volume, tent ascites, this should be combined with frusem-
high‐volume and refractory with regard to the ide. These two measures are successful in controlling
approach to treatment. By definition, refractory ascites in about 60–70% of patients. In addition, a
664 Problem Solving
thiazide diuretic may be required. Diuretic therapy Transjugular intrahepatic portosystemic shunt
must be monitored closely to ensure that progres-
Transjugular intrahepatic portosystemic shunt
sive renal failure and electrolyte imbalance (potas-
(TIPS) is a radiological procedure where a shunt is
sium, sodium, calcium and magnesium) do not
placed within the liver between the portal vein and
occur. It is important to stop medications such as
hepatic vein via a transjugular route for venous
angiotensin‐converting enzyme inhibitors, non‐ste-
access under image guidance. Accordingly, it creates
roidal anti‐inflammatory drugs and aminoglyco-
a communication between the portal and systemic
sides which can worsen ascites and/or induce renal
circulation. It may stabilise the patient while con-
failure.
sideration is being given to liver transplantation
Prophylactic antibiotics are not required.
and is judged the best management for diuretic‐
Primary or spontaneous peritonitis‐complicating
resistant ascites. It reduces sinusoidal and portal
ascites is treated with appropriate antibiotics,
pressures and therefore reduces the impact of
although sometimes a laparoscopy or laparotomy
refractory ascites and the side effects of high‐dose
is required either for diagnosis or to wash out the
diuretics. Unfortunately, the shunts have a fairly
peritoneal cavity. Specific causes of ascites such as
high rate of blockage or stenosis (up to 75% after
tuberculosis are treated with appropriate antitu-
6–12 months) and the shunt may induce hepatic
berculous chemotherapy according to national
encephalopathy. TIPS does not improve long‐term
guidelines. Surgical intervention is reserved for
survival as compared to repeated paracentesis.
diagnosis and to treat complications such as acute
bowel obstruction, bleeding or perforation due to
intestinal tuberculosis.
Portosystemic shunts
Paracentesis If ascites is due to portal hypertension, portosys-
Paracentesis, or drainage of ascitic fluid, brings temic shunting may be performed in selected
immediate though temporary relief to patients patients to reduce portal venous pressure. Shunting
with symptomatic tense ascites. Paracentesis is per- may be accomplished by TIPS or by making a for-
formed under local anaesthesia and with a strict mal anastomosis between the splenic and renal
aseptic technique by inserting a cannula through veins (lienorenal shunt) or between portal vein and
the anterolateral abdominal wall, avoiding the inferior vena cava (portocaval shunt). These shunts
inferior epigastric artery and the colon. It can often do not address the problem of the underlying liver
be performed under ultrasound or CT control. disease, but do reduce the issues with oesophageal
Fluid is drained into a sterile collecting system and varices. Shunt surgery may be complicated by
the cannula is either removed immediately or left hepatic encephalopathy and hepatorenal syndrome.
in situ for 24–48 hours. Rapid removal of large The presence of ascites in patients undergoing
amounts of ascites may lead to serious hypovolae- shunt surgery for portal hypertension is a poor
mia because the underlying reason for formation prognostic sign.
of ascites has not been eliminated and ascites re‐
forms rapidly with fluid from the extracellular
space (interstitial and intravascular fluid). Volume Peritoneovenous shunts
replacement may be required during paracentesis
Symptomatic relief by draining ascitic fluid from
and is undertaken cautiously with concentrated or
the peritoneal cavity into the systemic venous sys-
normal serum albumin in order to avoid hypovol-
tem can be achieved by way of a peritoneovenous
aemia on the one hand and fluid overload and
shunt (PVS). A PVS (Denver shunt, LeVeen shunt)
rapid re‐accumulation of ascites on the other. The
consists of a silastic tube, with multiple side holes at
complications of infection, intestinal perforation
each end and a one‐way valve situated in the mid-
and bleeding are rare when performed with an
dle. The PVS is placed entirely subcutaneously, with
appropriate sterile technique and a purpose‐built
one end inserted into the peritoneal cavity and the
cannula.
other into the superior vena cava (SVC) via a jugu-
lar or subclavian vein, so that the valve allows flow
Relief of acute hepatic venous obstruction
of ascites from the peritoneal cavity to the venous
When the cause of ascites is due to an acute throm- system. A PVS is indicated when medical therapy
bus, thrombolytic therapy or angioplasty may be has failed to control ascites in patients with
performed. Where these are unsuccessful a porto- (i) intractable ascites in the presence of reasonably
systemic shunt should be considered. good liver function, or (ii) rapidly accumulating
69: Ascites 665
ascites secondary to abdominal carcinomatosis.

Concern about infusing ascitic fluid laden with
MCQs
malignant cells into the circulation is theoretical
because these patients have widely disseminated
malignant disease before insertion of the PVS.
The postoperative mortality of PVS is 10–20%,
reflecting the serious underlying disorder of patients 1 Which of the following statements about portal
requiring the procedure. However, most patients hypertension is correct?
obtain useful palliation. A minor coagulopathy is a there is increased portal blood volume
common postoperatively but can be partly pre- b there is a decrease in portal blood pressure
vented by completely aspirating the ascites and c there is increased splanchnic vasoconstriction
replacing it with warmed normal saline or d there is hypoproteinaemia due to increased renal
Hartmann’s solution when inserting the PVS. Long‐ protein losses
term complications include occlusion of the PVS e there is reduced splanchnic lymphatic flow
(particularly with bloody or highly proteinaceous
or mucoid ascites), SVC thrombosis, bacteraemia 2 Which of the following conditions is typically
and shunt infection, which may lead to subacute associated with ascites?
bacterial endocarditis. a filiariasis
b Gilbert’s disease
Surgery on patients with ascites c abdominal tuberculosis
d large uterine fibroids
Surgery is liable to complications in patients with
e ectopic pregnancy
ascites. Abdominal surgery is prone to infection
and there is a potential for poor wound/anastomotic
3 Which of the following statements about patients
healing. The patient’s management is complicated
with ascites is correct?
by ascitic leak, wound complications, electrolyte
a bacterial peritonitis can be prevented by
and fluid balance difficulties and protein losses.
prophylactic antibiotics
Although not common, patients undergoing
b Leveen shunts may alleviate ascites associated
abdominal surgery may have damage to lymphat-
with portal hypertension
ics, especially after retroperitoneal surgery, which
c pancreatitis may develop
could result in the challenging problem of lymph
d may be relieved by spironolactone
ascites. The underlying liver disease may cause a
e paracentesis gives long periods of relief, often
coagulopathy. Renal failure complicating liver dis-
lasting several months
ease (hepatorenal syndrome) is a major risk that
can be minimised by ensuring optimal renal perfu-
4 Which of the following statements about jaundiced
sion. Patients who have obstructive jaundice are
patients with ascites is correct?
often surgical candidates, at least for some form of
a there is a low risk for hepatorenal syndrome
bypass procedure. The presence of ascites in these
because of splanchnic vasodilatation
patients increases the mortality, particularly from
b coagulation profiles are usually normal
hepatorenal syndrome, and thus less invasive pro-
c systemic blood volume is increased
cedures such as biliary stenting are preferred.
d renal blood flow is increased
e there is a poor prognosis when operating for
malignant disease
Further reading
5 Which of the following cancers are commonly
Fortune B, Cardenas A. Ascites, refractory ascites and
hyponatremia in cirrhosis. Gastroenterol Rep (Oxf) associated with the development of ascites?
2017;5:104–12. a lymphoma
Liou IW, Kim HN. Diagnosis and management of ascites. b endometrial
Hepatitis C Online. University of Washington Infectious c gastrointestinal stromal tumours
Diseases Education and Assessment. Available at http:// d mucus‐secreting villous adenoma
www.hepatitisc.uw.edu/go/management‐cirrhosis‐ e ovarian
related‐complications/ascites‐diagnosis‐management/
core‐concept/all
Tsochatzis E, Gerbes A. Diagnosis and treatment of
ascites. J Hepatol 2017;67:184–5.
70 Neck swellings
Rodney T. Judson
often in obscure sites such as base of tongue or

Introduction tonsil.
• The lymph nodes in the posterior triangle are all
Swellings or lumps in the neck are a common clini-
distributed along the spinal accessory nerve.
cal problem. Patients presenting with neck lumps
These nodes are most commonly involved in
are likely to be fearful that they have cancer. Neck
benign infective conditions (usually viral) in chil-
lumps in children are common although rarely
dren and young adults. Metastatic involvement
malignant, but the situation is quite different in
of posterior triangle (spinal accessory) nodes
adults. Diagnostic efforts should aim for timely
may occur with nasopharyngeal cancer and skin
exclusion of malignancy with avoidance of lengthy
cancers arising on the posterior scalp, neck and
trials of observation or repeated futile courses of
shoulder region.
antibiotics. Diagnosis of neck lumps involves apply-
• Skin cancer is common in Australia and both
ing basic clinical methods of assessment with his-
melanoma and squamous carcinoma can metas-
tory and physical examination followed by selected
tasise to the lymph nodes in the parotid gland,
imaging techniques and finally sampling for cyto-
those in the submandibular triangle and those in
logical or histological examination.
the posterior triangle.
• Approximately 80% of lateral neck lumps in
adults will be due to metastatic cancer. It is
Basic knowledge
important to examine the possible anatomical
primary sites that may lead to metastatic disease
Most neck lumps can, with a little experience, be
in the neck. These include the skin of the head
diagnosed on clinical grounds by applying knowl-
and neck (including the scalp), the lip, the oral
edge of head and neck anatomy and the clinical fea-
cavity, the oropharynx, the post‐nasal space
tures of the usual pathological processes affecting
(especially in Asian patients), the larynx and
the structures in the head and neck (see Chapter 41).
hypopharynx.
The triangles of the neck and the distribution of
• A solitary lump, low in the neck, deep to the ster-
lymph nodes are shown in Figure 70.1. The lymph
nomastoid muscle in the supraclavicular fossa
nodes can be grouped into levels and these are
(level IV) is likely to be a metastasis from a pri-
shown in roman numerals. Level I consists of the
mary cancer below the clavicles, i.e. lung, oesoph-
submandibular and submental lymph nodes. Levels
agus, stomach or pancreas.
II, III and IV are respectively the upper, middle and
lower jugular chain nodes. Level II also contains the
jugulodigastric lymph node. Level V has the lymph
Clinical assessment
nodes of the posterior triangle. The following facts
should be remembered.
History
• The jugulodigastric lymph node, draining the
oral cavity and oropharynx including the tonsils, Evaluation of the patient begins with a careful his-
is commonly enlarged in both inflammatory and tory, taking into account the age of the patient and
malignant conditions. In children, tonsillitis is the the location of the swelling as either in the lateral or
most common cause of swelling in this region of anterior compartment of the neck.
the neck, in young adults glandular fever or lym- The rapidity of onset of the lump provides a val-
phomatous conditions and in adults cancers uable clue as to its likey cause. A short history of
667
668 Problem Solving
Submandibular
nodes
Parotid
Posterior belly
of digastric
Submatal nodes
Upper jugular node
I II
Ant. belly Jugulodigastric node

of digastric Spinal accessory
Hyoid bone nerve and nodes
III
Jugulo-omohyoid node Trapezius
Sternocleidomastoid V
muscle
Omohyoid muscle
IV
Lower
jugular nodes
Fig. 70.1 The triangles, lymph node levels and normal lymph nodes in the neck. Diagram shows the main muscular
anatomy of the neck with the sites of normal, named lymph node groups. In addition, the lymph nodes are subdivided
into levels as follows: level I, submandibular and submental triangle; level II, upper jugular chain lymph nodes (including
the jugulodigastric lymph node); level III, mid‐jugular chain nodes (including the jugulo‐omohyoid node); level IV, lower
jugular chain lymph nodes (including lymph nodes overlying scalenus anterior muscle and those in the supraclavicular
fossa); level V, lymph nodes of the posterior triangle, lying along the course of the spinal accessory nerve.
Physical examination
enlarged tender lymph nodes suggests an infective
or inflammatory process, while multiple small non‐ The usual evaluation of lumps involves clarification
tender nodes, particularly in the posterior triangle, of the following features: site, size, shape, consist-
suggests a subclinical viral infection. Long‐stand- ency, deep and superficial attachments, the nature
ing swellings in children suggest a congenital of the surface and the edge of the lump, and the
problem, possibly cystic hygroma (also called lym- presence of fluctuation, pulsation and translumina-
phangioma). Painless progressive neck swellings tion. In the neck the following issues apply.
in adults are strongly suggestive of a malignant • Which triangle of the neck is involved? Is the
origin. lump in the lateral or anterior compartment of
It is also important to ascertain information the neck?
about general systemic symptoms in potentially • Does it move with swallowing? This indicates it
inflammatory processes and suspected lymphoma. is deep to the pretracheal fascia and likely to be
Weight loss provides a clue to a malignant process thyroid.
arising below the clavicles that has metastasised to • Does it move with protrusion of the tongue? This
a lower cervical lymph node. Patients should also applies to upper anterior neck lumps, and the
be questioned about possible past skin tumours, physical sign refers to thyroglossal cysts.
which may metastasise even years later to parotid, • What is the relationship to the sternomastoid
upper cervical, submental, submandibular and pos- muscle? This point is important for differentiat-
terior triangle nodes. ing lumps in the upper neck. Tumours in the tail
Travel history and country of origin are impor- of the parotid gland will lie superficial to the ster-
tant with regard to the possibility of tuberculosis. nomastoid muscle and, when the muscle is con-
The racial group of the patient may also be impor- tracted by turning the head to the opposite side,
tant as nasopharyngeal cancer is not uncommon in the lump will remain easily palpable. By contrast,
Asian populations. an upper jugular chain (level II) lymph node,
A smoking history is important as mucosal squa- lying deep to the sternomastoid muscle, will
mous cell carcinoma is rare in non‐smokers but become less obvious and more difficult to pal-
would be suspected as a primary site of tumour in a pate when the head is turned to the opposite side.
patient with a history of heavy tobacco and alcohol • Where the neck lump appears to be an enlarged
use who presents with a painless lateral neck lump. lymph node, either benign or malignant, the
70: Neck swellings 669
possible sources of infection or malignancy • Metastatic lymph nodes from an upper aerodi-
should be searched for. gestive tract primary squamous cell carcinoma:
Sites of common anterior compartment swellings moderately fast growth of a painless, usually
are shown in Figure 70.2. firm, often tethered upper lateral lump deep to
sternomastoid occurring in middle‐aged to elderly
Characteristic clinical features of common patients with a strong smoking history.
neck lumps • Benign parotid tumour: long history of a very
slow‐growing, painless, firm, initially mobile
• Thyroglossal cyst: firm, tense, midline, painless
lump behind the angle of the mandible lying
swelling at or below the level of the hyoid bone,
superficial to the sternomastoid muscle.
which elevates on tongue protrusion.
• Carotid body tumour: very slow‐growing, pain-
• Branchial cyst: smooth, often fluctuant swelling
less, deep lump in upper lateral neck with limited
protruding at the anterior border of the sterno-
lateral mobility and characteristic transmitted
mastoid muscle below the jaw (level II). There is
pulsation.
usually rapid painless development of the swell-
ing, although secondary infection and inflamma-
tion may occur.
Investigation
• Plunging ranula: a soft, painless, cystic swelling
in the submandibular region in continuity with a
Fine‐needle aspiration biopsy
swelling in the floor of the mouth due to extrava-
sation through the mylohyoid muscle of mucoid Fine‐needle aspiration biopsy, preferably ultra-
saliva from a disrupted sublingual gland. sound guided, is the single most important test in
• Submandibular salivary gland swelling: painful if the evaluation of neck lumps, particularly in adults
due to obstruction of the gland or painless if due who may have malignancy. It is usually not neces-
to usually benign tumour presenting as a swelling sary to carry out needle biopsy of tender lymph
in the submandibular triangle of the neck, which nodes in children; however, non‐tender swellings in
is easily differentiated from a submandibular the central and lateral compartments of the neck in
lymph node on bimanual palpation. adolescents and adults should be evaluated by
• Thyroid nodules: lower anterior compartment, needle biopsy as the initial investigation. Metastatic
slow‐growing, painless usually smooth lumps malignancy can usually be diagnosed with a very
which move upwards on swallowing. high degree of accuracy. In general, reactive
Submental
node
Submandibular
nodes
Branchial cyst
Hyoid
(or other level II mass
bone
e.g. lymph node)
Thyroid
cartilage Thyroglossal cyst
Pyramidal
lobe of thyroid
Thyroid gland
Thyroid nodules
Sternomastoid
muslce
Trachea
Fig. 70.2 The anterior compartment of the neck showing the trachea, thyroid gland and laryngeal framework
consisting of the thyroid cartilage and hyoid bone. This area is made up of the two anterior triangles of the neck, each
consisting of the area bounded by the jaw superiorly, the anterior board of the sternomastoid muscle posteriorly and
the midline medially. The sites of various anterior and anterolateral neck lumps are shown.
670 Problem Solving
lymphadenopathy can be distinguished from lym- Excision biopsy

phoma on needle biopsy; however, occasionally
If a diagnosis cannot be confirmed on fine‐needle
atypical lymphocytes are identified and it is neces-
aspiration biopsy, an excision biopsy may be nec-
sary to carry out an excision biopsy of the node to
essary to confirm or exclude malignancy. Care
clarify the diagnosis. Branchial cysts mainly occur
should be taken not to spill tissue or break up a
in young adults and when they are aspirated thick
lymph node in the course of biopsy to prevent
creamy fluid is removed along with benign squa-
malignant cells being implanted into the sur-
mous cells. Under the microscope cholesterol crys-
rounding tissue. The biopsy incision should be
tals and cellular debris are visible. Branchial cysts
oriented in a natural skin crease in such a way
occasionally occur in middle‐aged adults, otherwise
that the biopsy scar can be excised in a subse-
at risk of metastatic cancer, and it can sometimes be
quent operation. Furthermore, care must be taken
difficult to distinguish between metastatic squa-
not to damage related anatomical structures, for
mous carcinoma with central necrosis and a benign
example the spinal accessory nerve in the poste-
branchial cyst on cytology. Excision of the lump
rior triangle and the marginal mandibular nerve
may be necessary.
in the submandibular triangle, during excision
Fine‐needle biopsy is also the best initial investi-
biopsy procedures.
gation of thyroid swellings. The presence of col-
loid, normal follicle cells and haemosiderin‐laden
macrophages is consistent with the presence of a
Chest X‐ray
colloid nodule. The presence of papillary struc- Chest radiology is important in young adults, when
tures raises the possibility of papillary carcinoma, lymphoma is the possibility, and in all adults. It
while a finding of multiple follicle cells in a micro- may demonstrate mediastinal widening or primary
follicular pattern with very little colloid indicates or secondary lung neoplasms. It should be remem-
that the nodule is a solid follicular lesion. In this bered that lung cancers are more common than
setting it is necessary to completely remove the mouth and throat cancers and that smokers, who
lump (by thyroid lobectomy) to differentiate between are at risk for head and neck cancers, are also at
follicular adenoma and follicular carcinoma. risk of having lung cancer.
Fine‐needle aspiration biopsy is very safe and the
risk of tumour implantation along the needle tract
is negligible. Treatment
The management algorithm for neck lumps is sum-

Ultrasound marised in the decision‐making flowchart shown in
Figure 70.4. Following the history, physical exami-
Apart from the investigation of thyroid nodules,
nation and investigations, a diagnosis can usually
ultrasound is not particularly useful in the evalua-
be made. Excision of the lump may be necessary
tion of head and neck lumps. Ultrasound can dif-
and if the lump proves to be benign, then excision
ferentiate between solid and cystic masses and can
biopsy is likely to be curative. Some benign lumps
indicate whether there are multiple enlarged lymph
(e.g. reactive lymph nodes, lipomas and sebaceous
nodes or multiple nodules in the thyroid gland.
cysts) may be simply observed and left untreated.
While ultrasound is highly sensitive, being able to
Other benign lumps require removal for patient
detect nodules or lymph nodes less than 1 cm in
comfort, cosmesis or to avoid future problems.
size, it is rarely diagnostic.
Branchial cysts, thyroglossal cysts, plunging ranu-
las, dermoid cysts, some lipomas and sebacous
cysts, and benign salivary and thyroid swellings fall
Computed tomography
into this category.
Computed tomography (CT) is far more helpful Once a diagnosis of malignancy is made, defini-
than ultrasound in assisting with the diagnosis of tive treatment is necessary. Lymphoma requires
neck swellings, especially when they are larger than further staging investigations and treatment by
2 cm. CT scanning can provide an idea of the con- chemotherapy, radiotherapy or both.
sistency of a lump along with its size and anatomi- The treatment of metastatic cancer depends on
cal relations. Figure 70.3 shows a series of CT scans the type of cancer and whether or not the primary
of common neck lumps, demonstrating the typical site can be identified. If the primary cancer is found
radiological appearance. (skin or mucosa of the upper aerodigestive tract), it
(a) (b)
(c) (d)
(e) (f)
Fig. 70.3 Computed tomography scans showing common pathological processes in the neck. Each has a typical
appearance. (a) Large lipoma neck deep to sternomastoid muscle and impinging on the parapharyngeal region. Note that
the lesion is black, the same as the subcutaneous fat. (b) Thyroglossal cyst. Note the smooth‐walled, well‐circumscribed
cystic mass closely attached to the anterior part of the right thyroid cartilage lamina. (c) Branchial cyst. This is a
smooth‐walled, well‐circumscribed cyst deep to the sternomastoid muscle in the right neck in a young patient. It must be
differentiated from metastatic squamous carcinoma with cystic degeneration [see (e)]. (d) Plunging ranula. This cystic
swelling is more dense than subcutaneous fat but less dense than the soft tissue of the adjacent submandibular salivary
gland (small black arrow). It is due to extravasation of mucoid saliva from the sublingual gland into the submandibular
space and through the mylohoid muscle. (e) Metastatic squamous carcinoma of the neck with cystic degeneration. Note
that this is also cystic but, unlike the branchial cyst (c), the wall of the lesion is irregular. (f) Large mass of metastatic
squamous carcinoma in the right neck. This is a predominantly solid mass with little cystic degeneration.
672 Problem Solving
Neck swelling (excluding thyroid)
History
physical examination
Child/ Adult
adolescent Uncommon
Likely malignant
Likely benign diagnosis
diagnosis
Benign FNAB Malignant
Inflammatory
Congenital/
or infected Lymphoma
cystic mass Metastatic cancer
nodes Observe +
others
Primary Primary
Observe FNAB Resolves Persists known unknown
CT
State: EUA
Biopsy chest X-ray endoscopy
Remove CT scan, etc. biopsy, CT
Still occult
Treat
Treat neck
Fig. 70.4 Management algorithm for neck lumps. EUA, examination under anaesthetic; FNAB, fine‐needle
aspiration biopsy.
should be treated definitively with the metastatic

neck disease. If a primary cancer cannot be found
Further reading
and the fine‐needle aspiration biopsy shows meta-
Ridge JA, Glisson BS, Horwitz EM, Lango NM. Head and
static squamous carcinoma, a thorough investigation neck tumors. Cancer Network. Available at https://
of the upper aerodigestive tract should be carried out www.cancernetwork.com/articles/head‐and‐neck‐
with biopsies of potential occult primary sites. These tumors
include the nasopharynx, tonsil and tongue base. Shah JP, Patel SG (eds) Cancer of the Head and Neck.
When the primary site is still not identified, the meta- Hamilton, Ontario: BC Decker, 2001, chapters
static disease in the neck requires treatment. This 13–17.
may be achieved by surgery or radiotherapy or Thompson LDR, Bishop JA (eds) Head and Neck
sequential surgery followed by radiotherapy. Pathology, 3rd edn. Philadelphia: Elsevier, 2018.
When metastatic adenocarcinoma is identified by
fine‐needle aspiration biopsy, an attempt should be
made to determine whether there is a treatable pri-
mary cancer, for example in the thyroid gland or a
MCQs
salivary gland. Adenocarcinomas from the prostate,
breast or abdomen that metastasise to the neck lymph
nodes are not curable and so radical treatment to
the neck may not be warranted. The operation used to
treat cancer in the neck is called neck dissection. Neck 1 Which of the following neck lumps is always
dissections can vary in extent and according to which fluctuant?
anatomical structures are preserved (see Chapter 41). a carotid body tumour
Radiotherapy is given after surgery when multiple b haemangioma
lymph nodes are involved with metastatic disease or c cystic hygroma
when there is evidence of spread outside the lymph d branchial cyst
node capsule (extracapsular spread). e thyroid cyst
70: Neck swellings 673
2 Which of the following is the most informative 4 Which of the following is the most common cause
imaging technique for the assessment of a neck lump? of enlargement of the jugulodigastric lymph node
a ultrasound in a child aged 9 years?
b angiography a Hodgkin’s disease
c CT scan b glandular fever
d positron emission tomography c tonsillitis
e radionuclide scanning d non‐Hodgkin’s lymphoma
e metastatic Wilms’ tumour
3 Which of the following statements about lymph
node swellings in the neck is correct? 5 Metastatic involvement of the posterior triangle
a they are always characterised by their oval shape nodes in the neck is most likely due to which of the
b multiple bilateral nodes are suspicious of following?
lymphoma rather than a secondary carcinoma a nasopharyngeal carcinoma
c are commonly associated with all skin cancers of b basal cell carcinoma of the shoulder region
the head and neck c laryngeal carcinoma
d cystic lymph node swellings are always benign d squamous cell carcinoma of the posterior scalp
e thyroglossal cysts do not move on swallowing e carcinoma of the oesophagus
71 Acute airway problems
Stephen O’Leary
mylohyoid muscle. Infection spreads into the

Introduction subcutaneous tissue, pushing the tongue back-

wards, such that the tongue base obstructs the
Definition hypopharynx. Tumours of the base of the tongue
Acute airway problems present as difficulty with can on occasion cause airway obstruction, but
breathing. The latter may be caused by anything this is seldom an acute presentation. The lingual
that interferes with oxygenation, including respira- tonsils can cause acute airway obstruction in the
tory or cardiovascular disease or pending airway context of acute infection or lymphoma.
obstruction. The surgeon’s primary role is to recog- Epiglottitis is the classical cause of airway
nise airway obstruction, determine its site within obstruction in the supraglottic region. While once
the airway, secure the airway and then treat the caused primarily by Haemophilus influenzae type B
underlying problem. (HiB), since the widespread introduction of HiB
vaccination Streptococcus pneumoniae is now the
Significance most prevalent pathogen. This too may change with
the recent introduction of universal pneumococcal
Initial management of an acute airway problem can
vaccination in children in many countries. The air-
determine the patient’s survival. A multidisciplinary
way obstruction from epiglottitis is caused by
team of ear, nose and throat surgeons, anaesthetists
swelling of the epiglottis, which narrows the glottic
and intensivists is required to manage acute airway
inlet. Critical swelling of the supraglottic airways,
obstruction. The surgeon must always be prepared
causing acute airway distress, may also occur
to provide an urgent surgical airway, such as a tra-
during anaphylaxis, such as to bee stings or food
cheostomy, if required.
allergens. It is important to recognise that these
conditions can also cause acute bronchospasm and
exudation of the airways, requiring management
Causes
in addition to the pending airway obstruction.
Supraglottic neoplasia may also present as an acute
Acute asthma and acute cardiovascular insuffi-
airway emergency. A supraglottic tumour can be
ciency (such as myocardial infarction) are medical
relatively asympomatic, especially compared with
causes of sudden breathing difficulty, and should
laryngeal cancer, where the airway is narrower and
always be considered. However, the emphasis of
vocal cord fixation is likely to cause other symp-
this chapter will be the identification and manage-
toms such as hoarseness of the voice.
ment of more surgically related aetiologies.
Acute airway obstruction at the level of the vocal
cords can arise from neoplasia, inhaled foreign
Airway obstruction, including foreign bodies
bodies or following acute bilateral vocal cord palsy.
Airway obstruction can occur anywhere from the The glottis is the narrowest part of the airway,
base of the tongue through to the trachea. Acute which is why foreign bodies are prone to obstruct
obstruction at the level of the tongue base is most the airway at this level. Neoplasia may present as
often caused by Ludwig’s angina, an infection of acute airway obstruction at the glottic level, but
the floor of the soft tissue of the anterior neck. This there have usually been previous indications of dis-
arises from dental infection involving the molars, ease, such as bleeding, vocal hoarseness or stridor.
where the dental roots can extend beneath the Acute bilateral vocal cord palsy may arise from
675
676 Problem Solving
surgery to the neck, typically following total thy- interventions to control a post‐tonsillectomy bleed.
roidectomy. In neck surgery, the recurrent laryngeal Another classical cause of airway compromise
nerve may be vulnerable. When paralysed, the vocal immediately after adenoidectomy or tonsillectomy
cords come to lie in a paramedian position, which is the so‐called ‘coroner’s clot’, namely a clot left in
significantly narrows the airway, causing acute the postnasal space after the operation that is
obstruction. Caution must be exercised during inhaled causing asphyxiation.
surgery on one side of the neck, given that the con- Bleeding into the neck following thyroidectomy
tralateral vocal cord may be paralysed prior to sur- carries a specific risk to the airway. This can lead to
gery. Therefore, it is routine to assess vocal cord compression of the airway that can only be relieved
function prior to operations that may put the recur- by opening the wound and expelling the clot.
rent laryngeal nerve at risk, such as hemithyroid- Nasal packs, placed to control nasal bleeding
ectomy or anterior surgical approaches to the during epistaxis or after nasal surgery or trauma,
cervical spine. can if displaced obstruct the airway. Airway com-
Acute airway obstruction at the level of the tra- promise occurs when the pack is dislodged posteri-
chea is unusual, but can arise from a foreign body orly when it may act as a foreign body. It has been
in the oesophagus, particularly in children. The said that all packs have been associated with at
posterior wall of the tracheal is soft tissue, with the least one fatality, so their management is of para-
oesophagus further posterior again. Therefore, a mount importance in postoperative care.
foreign body that is obstructed in the oesophagus
can cause the anterior oesophageal wall to bulge
forward, potentially causing a partial obstruction Assessment
of the trachea. Foreign bodies further down the air-
way within a main bronchus can cause asthma‐like The key to management of the airway is to establish
symptoms. Consequently, a bronchial foreign body the level of the obstruction within the airway. The
needs always to be considered in the newly diag- clinical presentation will give a good indication of
nosed asthmatic, particularly if the clinical signs are the site of the obstruction.
unilateral. The right main bronchus is most likely The presumptive diagnosis of an airway foreign
that affected, because its vertical orientation will body in a child is made on the basis of clinical
more likely impact a foreign body than the left. suspicion. A sudden onset of airway distress, even
when foreign body aspiration is not observed, is
Post‐traumatic airway obstruction sufficient grounds to consider this diagnosis. As
described, airway distress may arise after either
The airway may be compromised after trauma due
swallowing or inspiring a foreign body. If the
to bleeding within the respiratory tract, direct
child is gagging, the foreign body is more likely to
trauma to the neck, or burns. Although securing the
be in the hypopharynx. If a child cannot swallow
airway is a first priority in stabilising the patient, it
their own saliva, then the foreign body is more
must be seen in the broader context of other trauma
likely to be in the oesophagus. Batteries are of
which, with airway trauma, may include injury to
particular concern, given that they can erode
the cervical spine. In this situation, the need to keep
through the oesophageal or tracheal lumen within
the neck stable may necessitate the creation of a
hours, so these must be removed immediately if
surgical airway.
suspected.
Airway compromise may be delayed after burns,
Additional points of history include a past his-
presenting 12–24 hours after the trauma. This
tory of asthma, recent exposure to an allergen or
means that high‐dependency monitoring is essential
agent known to cause anaphylaxis, or a history of
for at least a day after the injury.
smoking. Progressive dysphagia, the production of
blood, or dysphagia might suggest neoplasia.
Post‐surgical airway obstruction
Patients with airway obstruction at any location
The most serious risk associated with secondary between the tongue base (e.g. Ludwig’s angina) and
bleeding following nasal surgery or a tonsillectomy the larynx are distressed when lying down. They
is loss of control of the airway. Securing the airway present sitting upright and leaning forward to brace
in an obtunded or anaesthetised patient is made the shoulders in order to maintain an airway.
particularly difficult because in this situation Stridor is a hallmark of airway obstruction, and
blood in the pharynx obscures visualisation of the its character can help to identify the site of lesion.
larynx. Most deaths associated with tonsillectomy Inspiratory stridor is caused by an obstruction
are caused by loss of the airway during surgical above the level of the larynx. Biphasic stridor arises
71: Acute airway problems 677
from an obstruction at the laryngeal level or in the If an acute airway compromise occurs in a patient
trachea. Expiratory stridor typically arises from with a nasal pack, it must be assumed that the pack
lower airway obstruction. itself has dislodged into the pharynx and is causing
The upper airway is best assessed via nasendos- the airway obstruction. An examination of the
copy. This allows visualisation and identification of mouth may reveal a pack ‘hanging down’ from
airway lesions to the level of the glottis, and can be the post‐nasal space. Urgent removal of a pack on
done safely in most situations. Nasendoscopy is the ward is required if it is believed to have become
preferred over examination of the larynx with a displaced. All packs should be taped to the face,
mirror, especially in cases such as epiglottitis, when providing a draw‐cord for the rapid removal of the
manipulation of the airway can precipitate airway pack in this circumstance.
obstruction. Prior to the definitive procedure to secure the
airway, it is imperative that all preparations have
been made meticulously. The time of greatest risk
Investigation is when an anaesthetic is given, such that the
patient ceases to maintain their own airway.
Imaging is seldom indicated in the initial manage- This means that the team must have discussed
ment of acute airway distress. Lesions above the all possible scenarios in advance, and have the
glottis can be diagnosed via nasendoscopy. Foreign equipment within the operating theatre before
bodies are managed on the basis of history alone. the procedure commences. This is a circumstance
Unless an imaging facility is integrated into the where team planning and communication is
emergency department, imaging can be dangerous essential.
and even life‐threatening, because in the event of The approach to securing the airway will depend
rapid progression to airway obstruction, resuscita- on the level of the obstruction. A nasopharyngeal
tion may not be available or optimal within the tube will control an obstruction at the level of the
department. The better time for imaging is after the tongue base. Awake fibre‐optic intubation, when a
airway has been secured. nasotracheal tube is introduced through the vocal
cords over an intubating bronchoscope that has
been passed through the vocal cords, is an excel-
Securing the airway lent technique when there is concern that the air-
way may be lost on induction of anaesthesia. This
Any patient with an acute airway should be given may be indicated for either supraglottic tumours,
oxygen and their saturation monitored with pulse when there is blood in the airway, or with airway
oximetry. Intravenous access is obtained, unless a distress in a patient with a difficult (to intubate)
foreign body is being considered in a young child airway.
when cannulation may cause distress and provoke A tracheostomy is required when there is a
acute airway obstruction. mass such as a tumour obstructing the glottis,
In most cases, the airway will best be secured in in cases of bilateral vocal cord paralysis or when
the operating theatre, so early mobilisation of an the neck cannot be moved as in suspected cervi-
experienced surgical team is necessary. Most cal fracture. Urgent tracheostomy under local
patients will require admission to intensive care, so anaesthesia remains the gold standard for the per-
it is prudent to involve the intensivist in the early ilous airway that cannot be secured in another
management. way. However, a range of new techniques can
Prior to surgery to secure the airway, it is impor- be considered as alternatives to conventional
tant to keep the patient conscious if at all possible, tracheostomy, such as kits for intubation via a
so that the person can maintain their own airway. cricothyroidotomy.
The management to achieve this will depend on When the lesion is in the lower airway bronchos-
the specific context. For example, during a post‐ copy will be required. Rigid bronchoscopes are
tonsillectomy bleed there is blood in the airway designed to allow the surgeon to operate in one
and the patient may become hypovolaemic. Loss main bronchus and simultaneously ventilate the
of consciousness will arise if the patient loses too other. It is also possible to draw a foreign body into
much blood, so the best preoperative management the rigid bronchoscope and thus remove it without
(if the bleeding cannot be controlled by local the risk of causing further trauma to the airway on
measures such as cauterisation of the tonsillar egress of the scope. These characteristics provide
bed) is to ensure that there has been adequate fluid distinct advantages over flexible bronchoscopy in
resuscitation. many circumstances.
678 Problem Solving
2 Which of the following types of airway support is

Further reading most appropriate in the emergency setting for a
patient with Ludwig’s angina and acute airway
American College of Surgeons. Advanced Trauma Life
distress?
Support, 10th edn. Chicago: ACS, 2018.
Kenneth M, Grundfast LF, Isolaco JL. The 10 command- a Guedel’s airway
ments of management for acute upper airway obstruc- b nasopharyngeal airway
tion in infants and children. JAMA Otolaryngol Head c positive end‐expiratory pressure
Neck Surg 2017;143:539–40. d laryngeal mask
e cricothyroidotomy
MCQs 3 What is the safest way to maintain a patient’s

airway prior to definitive management (in the
Select the single correct answer to each question. The emergency setting) during a severe post‐
correct answers can be found in the Answers section tonsillectomy bleed?
at the end of the book. a keep them conscious through adequate fluid
1 Which of the following is not appropriate resuscitation
management for a child with suspected epiglottitis? b anaesthetise and introduce a laryngeal mask
a provide oxygen c perform a cricothyroidotomy
b organise urgent review by ENT, anaesthetics and d introduce a nasopharyngeal airway
intensive care e provide sedation
c examine the child’s mouth with a tongue
depressor
d enquire about their immunisation status
e keep the child calm, avoiding unnecessary
distress
72 Dysphagia
Wendy A. Brown
Monash University Department of Surgery, Alfred Health, Melbourne, Victoria, Australia
Introduction Box 72.1 Symptoms associated

with dysphagia
Definition
• Chest pain due to reflux oesophagitis.
Dysphagia is defined as difficulty in swallowing. It • Odynophagia or pain on swallowing: may be
is a common and important symptom. Two types associated with oesophagitis or oesophageal
are recognised. spasm.
• Oropharyngeal: involving the transfer of food • Physical reflux of food or bile into the mouth,
from the mouth into the upper oesophagus. associated with severe gastro‐oesophageal reflux.
• Oesophageal: involving the transport of food • Coughing and aspiration of food, indicating
down the oesophagus and into the stomach. possible recurrent laryngeal nerve or bulbar palsy.
• Palatal incompetence, with food being regurgitated
Significance through the nose on attempted swallowing: this is
associated with bulbar palsy following cerebrovas-
The significance of this condition relates to its mul- cular accident.
titude of causes. Dysphagia may be caused by mild • Loss of weight and anorexia often indicates a
muscular spasm or incoordination due to psycho- malignant obstruction.
logical causes or, at the other end of the spectrum, • Hoarseness of voice due to malignant involvement
may be progressive, associated with loss of weight of the larynx or recurrent laryngeal nerve
and due to a malignant obstruction of the oesopha- compression.
gus. Consequently, any patient complaining of the
symptom of dysphagia requires full investigation to
exclude malignancy and to effectively treat the
condition. Causes of dysphagia
Problems within the mouth may cause difficulties

Incidence
in swallowing food. Simple examples include pain-
Dysphagia is a common symptom affecting most ful ulceration or abscesses, severe tonsillitis, lack of
individuals transiently at some time in life. One of teeth, or deformity after head and neck surgery.
the important causes of dysphagia is adenocarci- Many of these problems can easily be excluded, and
noma of the lower oesophagus. This is a tumour the causes of dysphagia that raise concern relate to
that is increasing in incidence throughout the west- the pharyngo‐oesophageal area and the oesophagus
ern world and often occurs in middle‐aged males. It itself (Box 72.2).
is associated with long‐standing gastro‐oesopha-
geal reflux and the development of Barrett’s mucosa
in the oesophagus (see Chapter 14). Diagnosis of the causes of dysphagia
Associated symptoms Clinical features

There are a variety of other symptoms that may The clinical history can give a major lead to the
accompany the presence of dysphagia (Box 72.1). diagnosis of the cause of dysphagia. For example,
The presence of these symptoms helps in making a difficulty in swallowing fluids rather than solids
clinical diagnosis. suggests a muscular incoordination problem.
679
680 Problem Solving
diagnosis is difficult or obscure, the whole gamut of

Box 72.2 Causes of dysphagia
investigations may be needed (Figure 72.1).
Pharyngo‐oesophageal disorders
• Diminished pharyngeal propulsion: motor neurone Radiological examination
disease; myasthenia gravis; cerebrovascular
accident with dysfunction of ninth, tenth and The barium swallow examination provides good
twelfth cranial nerves. views of the upper oesophagus and helps makes the
• Relaxation anomalies: upper oesophageal diagnosis of pharyngeal pouch, webs and strictures.
achalasia or cricopharyngeal spasm; However, a negative barium swallow examination
cricopharyngeal bar. in the presence of persistent dysphagia demands
• Incoordination: cerebrovascular accident resulting further investigation by endoscopy.
in ninth, tenth and twelfth cranial nerve palsy;
gastro‐oesophageal reflux with cricopharyngeal Oesophagoscopy and gastroscopy
spasm; pharyngeal diverticulum with cricopharyn-
geal spasm. This is usually the first investigation for dysphagia
and is done using flexible endoscopes under intra-
Oesophageal causes
venous sedation. Care has to be taken to avoid per-
• Motor disorders: achalasia of the oesophagus,
foration, particularly if there is suspicion of a
diffuse oesophageal spasm, scleroderma.
pharyngeal pouch or if a stricture is present. The
• Mechanical causes: luminal obstruction due to a
large food bolus or bone impaction; mucosal
oesophagus is carefully examined for abnormalities
strictures; webs (e.g. Patterson–Brown–Kelly such as inflammation and stricture. A stricture can
syndrome, Schatzki ring); fibrous strictures (which usually be easily determined as being benign or
result from inflammation and scarring from malignant. In the absence of stricture, features such
long‐standing gastro‐oesophageal reflux); as oesophageal dilatation with food residue may
ingestion of caustics (which causes fibrous scarring suggest achalasia. Rarely, rigid oesophagoscopy is
and predisposes to malignancy); squamous cell necessary if flexible endoscopy is unsuccessful.
carcinoma; adenocarcinoma; rare tumours
including lymphoma and metastatic tumours; Radiological staging
benign tumours (rarely).
Radiological staging includes computed tomogra-
Extrinsic pressure on the oesophagus phy (CT) examination and, less commonly, mag-
• Retrosternal goitre. netic resonance imaging (MRI). This can help
• Pharyngeal diverticulum. make the diagnosis in obscure cases, but its major
• Vascular abnormalities (right subclavian artery and
role is helping to stage the extent of malignant
right‐sided aortic arteries).
disease.
• Any mediastinal mass may cause oesophageal
compression.
Endoscopic ultrasound
Endoscopic ultrasound is a very effective way of
Progressive dysphagia for solids suggests a malig-
diagnosing abnormalities within the oesophageal
nant cause. Dysphagia in the presence of retros-
wall. It is not useful if there is a tight narrowing in
ternal pain, associated with regurgitation of
the proximal oesophagus that prevents the passage
fluids, may indicate the stricture or carcinoma
of the instrument. It is the most precise method for
associated with reflux. Coughing or the aspira-
detecting the depth of penetration of a cancer into
tion of fluid into the larynx will give a guide to
or through the wall of the oesophagus.
lesions such as cranial nerve palsies. Loss of
weight is one of the most important accompany-
ing symptoms of dysphagia and indicates malig- Oesophageal transit studies
nancy. Lymph node and other masses may be Radiolabelled (99mTc and 111In) liquid, scrambled
palpable in the neck. However, physical signs are egg or porridge is given to the patient to swallow. A
usually absent. scintigram is performed and the level of tracer
within the oesophagus is recorded at various time
Investigations points until the tracer has disappeared. This allows
Not all investigations need to be carried out in all a calculation to be made of the effectiveness of
cases of dysphagia, but in those cases where the oesophageal transit.
72: Dysphagia 681
Patient presents
with dysphagia
Associated with
pulmonary
aspiration and/or PEG feeding
nasal regurgitation rehabilitation
and/or signs of
cerebrovascular
accident-
no investigations
Endoscopy required
NAD Abnormal
Observe/reassure Biopsy
Continuing Benign stricture Probably

symptoms associated with malignant stricture
reflux
Oesophageal
CT exam (staging
manometry Treat with PPIs
exclude motility of disease)
and dilation
disorder
Anti-reflux Possible EUS

Achalasia Spasm/ surgery in younger (small lesion)
scleroderma age group and
symptomatic on
Assessment of
Myotomy Conservative medical treatment cardiopulmonary
management status and decide
on treatment
alternatives
Surgery Chemoradiation Palliative

therapy treatment
e.g. stenting
Fig. 72.1 Management of dysphagia. EUS, endoscopic ultrasound; PEG, percutaneous endoscopic gastrostomy; NAD,
no abnormality detected; PPI, proton pump inhibitor.
Oesophageal motility studies

Specific causes of dysphagia
These are done via a multilumen catheter inserted
into the oesophagus via the nose. Propulsive waves Transfer or pharyngo‐oesophageal dysphagia
in the oesophagus can easily be measured and the
More correctly this is an inability to swallow and is
response to a swallowing effort detected.
associated with aspiration, coughing and nasal
Abnormalities can be identified in achalasia, sclero-
regurgitation. The common cause of this type of
derma and oesophageal spasm.
problem is a cerebrovascular accident. It produces
major problems when attempting to rehabilitate a
stroke patient with a bulbar palsy. Feeding via
Other investigations nasogastric tubes or gastrotomy tubes (percutane-
ous endoscopic gastrostomy) may be necessary to
Monitoring of pH over 24 hours will help docu-
provide nourishment.
ment the degree of oesophageal reflux. Gastro‐
oesophageal reflux studies using nuclear scan
techniques can be helpful in difficult cases. Reflux
Motility disorders of the oesophagus
may be associated with fibrous stricture or oesoph-
ageal spasm, thereby causing dysphagia. See Chapter 14.
682 Problem Solving
Achalasia Symptoms
The patient complains of dysphagia that is often
Achalasia of the oesophagus is also known as car-
worse for liquids, is intermittent and is noted in the
diospasm and is often associated with the pres-
mid‐sternal region. Pain, which is retrosternal and
ence of a so‐called mega‐oesophagus. It occurs
severe, is also common, is sometimes misdiagnosed as
most commonly in the young to middle‐aged (30–
being cardiac in origin, and is worse under emotional
60 years). The incidence is 1 in 100 000 people.
stress. There is rarely any weight loss. There is marked
There are associated neural abnormalities in the
belching and other indigestion‐type symptoms.
ganglia but the exact cause is not known. The dys-
phagia is intermittent, but progressive in the
Diagnosis
longer term. It is detected by the patient as being
The diagnosis is made on X‐ray, which shows ter-
suprasternal in position and occurs for both liq-
tiary contractions in the oesophagus, and motility
uids and solids. Regurgitation is postural and
studies, which show simultaneous, vigorous, repeti-
aspiration pneumonitis may occur. Usually only
tive waves in the oesophageal body when the lower
weak oesophageal contractions occur and the con-
oesophageal sphincter relaxes.
dition is painless. In 10% of cases a condition
known as ‘vigorous achalasia’ exists. This is
Therapy
regarded as an early stage of the disease and is
Therapy is generally simple, using simple bougien-
associated with pain. Oesophageal manometry
age without rupturing oesophageal muscle, and
reveals markedly elevated lower oesophageal
medication.
sphincter pressures and diminished oesophageal
contractions.
Scleroderma
Complications This systemic connective tissue disorder is charac-
In the chronic long‐standing case, weight loss and terised by muscle atrophy, dilatation of the oesoph-
chest pain occur. Pulmonary disease from aspira- agus and smooth muscle fibrosis. It is diagnosed
tion of oesophageal content and the development by motility studies that show a non‐contractile
of carcinoma within the dilated oesophagus are sig- oesophagus. Oesophageal reflux is often a contrib-
nificant complications. uting and secondary factor causing strictures. No
satisfactory therapy exists.
Diagnosis and treatment
Chest X‐ray, barium meal and manometry exami-
Chagas’ disease
nations help to confirm the diagnosis, which may
be difficult to determine. Treatment is by surgical This is a parasitic infection, common in South
division (myotomy) of the hyperactive lower America. It produces destruction of the ganglia of
oesophageal sphincter, usually approached lapa- the oesophagus and an achalasia‐type stricture.
roscopically. A thoracoscopic approach can also
be used. Reflux is a complication after myotomy
and an anti‐reflux procedure at the time of Mechanical causes of dysphagia
surgery is commonly performed. An alternative
The mechanical causes of dysphagia are those that
treatment is by manometric dilatation using a
are most commonly the province of the surgeon.
balloon placed across the hypertensive lower
The diagnosis depends on taking a clinical history
oesophageal sphincter, which is then expanded
and often requires a full investigation (see previous
causing disruption of the sphincter. The results of
section) to make the diagnosis. The difficult diagno-
both methods of treatment are good in about
sis is often between a benign and a malignant stric-
90% of cases.
ture in the oesophagus (see Chapter 14). Repeated
biopsies may be necessary to make this distinction.
Diffuse oesophageal spasm
Malignant obstruction in the lower oesophagus
This is usually a primary disorder but may be sec- demands either extensive surgery or combined sur-
ondary and associated with: gery and chemoradiation if curative therapy is indi-
• peptic oesophageal reflux cated. However, in about 30% of patients with
• ingestion of irritants malignancy, palliative treatment only is indicated.
• emotion and tension Intubation of the tumour or laser ablation are two
• possibly an underlying carcinoma. effective methods of palliation.
72: Dysphagia 683
c associated with altered motility of the

Further reading oesophagus
d achalasia is a disease primarily of the oesopha-
Gidwaney NG, Bajpai M, Chokhavatia SS. Gastrointestinal
dysmotility in the elderly. J Clin Gastroenterol 2016;
geal musculature and is coexistent with gastro‐
50:819–27. oesophageal reflux
Moawad FJ, Cheng E, Schoepfer A et al. Eosinophilic e associated with an adenocarcinoma of the
esophagitis: current perspectives from diagnosis to mucosal lining
management. Ann NY Acad Sci 2016:1380:204–17.
Philpott H, Sweis R. Hiatus hernia as a cause of dyspha- 3 Which of the following methods for identifying the
gia. Curr Gastroenterol Rep 2017;19:40. causes of dysphagia is incorrect?
Schlottmann F, Neto RM, Herbella FA, Patti MG. a upper gastrointestinal endoscopy
Esophageal achalasia: pathophysiology, clinical presen- b barium swallow examination
tation and diagnostic evaluation. Am Surg 2018; 84:
c upper abdominal ultrasound examination
467–72.
d CT examination of the chest
e oesophageal manometry
MCQs
4 With regard to patients with dysphagia, which of
Select the single correct answer to each question. The the following complaints is incorrect?
correct answers can be found in the Answers section a regurgitation of fluid and food when recumbent
at the end of the book. at night
b difficulty with swallowing fluids more than solid
1 Which of the following symptoms of dysphagia is food
incorrect? c difficulty with swallowing solid food more than
a very common and thus can be ignored in most liquids
cases d may have significant weight loss
b may be associated with reflux symptoms e may have no weight loss
c may be associated with significant pain f their partner may complain of snoring
d can present acutely with total obstruction of the
oesophagus 5 Which of the following causes of dysphagia is
e may be associated with diminished pharyngeal incorrect?
propulsion a benign strictures in the oesophagus
b squamous carcinoma of the oesophagus
2 Which of the following causes of dysphagia is c pharyngeal diverticulum
incorrect? d oesophageal spasm
a classified as pharyngo‐oesophageal and e uncomplicated sliding hiatus hernia
oesophageal
b pharyngo‐oesophageal causes are often
neurological in origin, e.g. cerebrovascular
accident
73 Leg swelling and ulcers
Alan C. Saunder1, Steven T.F. Chan2 and David
M.A. Francis3
1
Monash University and Surgery and Interventional Services Program, Monash Health , Melbourne,
Victoria, Australia
2
University of Melbourne and Western Health, Melbourne, Victoria, Australia
3
Introduction Box 73.1 Commoner causes of leg swelling
Systemic causes
Leg swelling and leg ulcers are increasingly com-
• Congestive cardiac failure
mon patient presentations, especially in our ageing
• Renal disease
populations. Most frequently, venous dysfunction,
• Hypoproteinaemia
in the form of swelling, ulcers and/or varicose veins,
may be immediately obvious in a coexistent way. Local causes
Conversely, ulceration may occur without swelling Venous conditions
that the patient has noticed. In either situation, it is • Occlusion or compression: deep vein thrombosis,
imperative to diagnose all contributing factors and abdominal or pelvic tumour, trauma, ligation,
determine if the leg presentation is part of a sys- inferior vena cava plication, retroperitoneal fibrosis,
temic condition(s) or a local leg issue only. This ascites
chapter outlines the common causes of both leg • Stagnation: dependent position
• Valve incompetence: most common and need to
swelling and ulceration, acknowledging that there
determine superficial, deep or a combination
is some clinical overlap between the two presenta-
• Arterialisation: arteriovenous fistula
tions and with arterial disease (see Chapter 55).
This is especially the case with diabetic foot disease, Lymphatic causes
presenting as Charcot foot or with foot ulcers. • Primary: congenital lymphoedema, lymphoedema
It is essential that a thorough history and examina- praecox, lymphoedema tarda
tion is done looking at the patient as a whole as well as • Secondary: neoplastic obstruction, irradiation
the afflicted limb(s). This is a very appropriate scenario damage, surgical excision, insect bite
to apply the following classic surgical paradigm. Inflammatory causes
• What is it (i.e. the diagnosis)? • Acute infections (streptococci, staphylococci)
• What else might it be (differential diagnosis)? • Chronic infections (fungi, filariasis, mycobacteria)
• What are you going to do about it (the plan for
investigations and management)?
Such an approach is an easy way to communicate
unilateral. The commoner causes of leg swelling
with patients, families and staff what the plan is to
are summarised in Box 73.1. Lesions that result in
establish a diagnosis and therefore treat the swell-
discrete leg swellings are not discussed in this
ing and/or ulcer.
chapter. Systemic causes generally result in bilateral
leg swelling and these causes should be excluded.
Leg swelling Localised causes may result in either unilateral or
bilateral swelling depending on the site of the
Leg swelling generally occurs because of an abnor- ‘localised problem’. The most common localised
mal accumulation of interstitial fluid – oedema – of cause of a unilateral leg swelling is venous disease.
the lower extremity and it may be bilateral or Lymphoedema is almost always secondary to a
685
686 Problem Solving
Capillary Plasma colloid

pressure osmotic pressure
Interstitial Interstitial colloid

fluid pressure osmotic pressure
Fig. 73.1 Pressures influencing net movement of fluid in and out of capillaries. Source: Guyton AG, Hall JE. Textbook
of Medical Physiology, 10th edn. Philadelphia: WB Saunders, 2000. Reproduced with permission of Elsevier.
disorder of lymph nodes since primary lymphoedema Systemic causes of leg swelling
is a rarity (see Chapter 57).
Congestive cardiac failure
Congestive cardiac failure (right heart failure) is a
Pathophysiology of leg swelling
common cause of bilateral leg swelling. Venous
There is normally a balance between the inflow pressure is increased due to the failing right heart, as
and outflow of extracellular fluid as blood flows demonstrated clinically by raised jugular and central
through capillaries. Figure 73.1 shows the four venous pressures. Consequently, post‐capillary venous
basic forces that determine the rate of accumulation pressure and intravascular hydrostatic pressure are
of interstitial fluid: increased. Also, fluid may be retained because of
• capillary pressure reduced glomerular filtration and secondary aldo-
• interstitial fluid pressure steronism. Excessive fluid intake, which may be
• plasma colloid osmotic pressure iatrogenic, and hypoproteinaemia also contribute
• interstitial fluid colloid osmotic pressure. to leg swelling.
The capillary and interstitial fluid pressure are
opposed by an oncotic gradient that is determined
Renal disease
by the different protein concentrations of the
interstitial and intravascular fluid compartments. Renal failure results in the inability to excrete water
About 90% of the fluid that leaks from the capil- and expansion of the extracellular fluid compart-
laries is estimated to return to the post‐capillary ment, unless fluid restriction is instituted. If renal
venules, while the remaining 10% enters the lym- disease is complicated by the nephrotic syndrome,
phatic system. hypoproteinaemia is an additional factor contributing
Oedema can be caused by the following. to leg swelling.
• Increased filtration pressure as a result of:
–– Arteriole dilatation
Hypoproteinaemia
–– Venule constriction
–– Raised venous pressure A low concentration of plasma proteins, particularly
• Reduced oncotic pressure: albumin, is a common cause of leg swelling in
–– Hypoproteinaemia hospitalised patients. Hypoproteinaemia reduces
–– Accumulation in interstitial space plasma osmotic pressure and so alters the balance
• Increased capillary permeability of opposing forces across the capillary wall in
• Reduced lymphatic removal of exudate favour of fluid leaking out of capillaries into the
73: Leg swelling and ulcers 687
interstitial space. Hypoproteinaemia causes a addition to cells, leak out of capillaries into the inter-
generalised oedema, but is more apparent in regions stitial space and cause swelling. Oedema may be lim-
of increased hydrostatic pressure, especially gravity‐ ited to the inflamed area but may drain by gravity to
dependent limbs. Hypoproteinaemia is due to the dependent part of the limb, often causing circum-
increased protein loss (extensive burns, tissue ferential swelling of the leg and swelling of the dor-
catabolism, proteinuria, protein‐losing enteropathy, sum of the foot. Repeated acute infections (cellulitis,
gastrointestinal fistulas, paracentesis), decreased lymphangitis) or chronic infections (fungal infec-
synthesis by the liver (acute or chronic liver disease, tions, filariasis, tuberculosis) produce secondary
malnutrition, malabsorption) or fluid overload. lymphoedema because of lymphatic obstruction.
Lymphoedema and chronic leg swelling may be
complicated by infection, which increases swelling of
Local causes of leg swelling the limb.
Venous disorders
Venous hypertension or obstruction increases intra- Assessment of the swollen leg
vascular hydrostatic pressure and reduces move-
ment of fluid into the venous end of capillaries, As with all medical problems, assessment relies
with subsequent accumulation of dilute interstitial on the history, examination and appropriate
fluid. Varicose veins secondary to saphenofemoral investigations.
incompetence can be associated with lower leg
oedema. Furthermore, failure of the normal calf History
muscle pump, due to valvular incompetence or
deep vein obstruction, results in failure of the Specific inquiry is made for symptoms suggesting
normal reduction of hydrostatic pressure within disorders of the heart (chest pain, dyspnoea, parox-
superficial veins that occurs with exercise. ysmal nocturnal dyspnoea, palpitations, haemopty-
Incompetence of several perforating veins leads to sis, hypertension), gastrointestinal tract (abdominal
only mild oedema because the calf pump mecha- pain and distension, indigestion, vomiting, haema-
nism can still lower superficial venous pressures to temesis, diarrhoea, rectal bleeding, alcohol intake,
some extent. Gross unilateral oedema results from drug ingestion, jaundice) and kidneys (back pain,
occlusion, such as after an occlusive iliofemoral dysuria, haematuria, nocturia, urine volume, frothy
venous thrombosis or stenosis of the femoral or urine, tiredness, lethargy). Recent nutritional intake
iliac veins. Bilateral swelling results from occlusion must be considered, especially in hospitalised
or extrinsic pressure on the inferior vena cava or patients who may become malnourished because of
major pelvic veins and is uncommon. Deep vein long periods of anorexia, nausea, vomiting, gastro-
thrombosis is discussed in Chapter 57. intestinal dysfunction, or fasting for investigations
and treatment. Similarly, in hospitalised patients,
the volume of intravenous fluid infusions must be
Lymphatic disorders reviewed. The duration and rapidity of onset of leg
Lymphatic obstruction reduces the clearance of swelling must be ascertained. Family history of
fluid and protein from the interstitial space, resulting similar problems may be relevant. Past history of
in an increased amount of interstitial fluid with a varicose veins, malignant disease, radiotherapy, sur-
relatively high protein concentration (lymphoedema). gery, previous episodes of leg swelling or infection,
Lymphoedema usually develops slowly. The high or deep vein thrombosis (perhaps complicating sur-
protein content of lymphoedema eventually leads gery or childbirth) must be identified.
to subcutaneous fibrosis. Movement of fluid and
protein in and out of capillaries is essentially
Examination
normal. Lymphatic disorders are discussed in

Chapter 57. A full physical examination must be performed.
General points of examination include the patient’s
nutritional status, and abnormal pigmentation of
Inflammatory disorders
the skin, sclera and mucous membranes. Look at
As part of the inflammatory response to injury, vaso- the abdomen and lower limbs for the presence of
active amines and peptides are released from dam- suspicious skin lesions and vascular abnormalities,
aged cells and produce vasodilatation and increased surgical scars, and signs suggestive of radiotherapy
capillary permeability. Fluid and plasma proteins, in (skin atrophy, telangiectasia, scaly skin).
688 Problem Solving
Swelling of one or both legs is confirmed by along medical lines. Protein deficiency is treated by
inspection and measurement at a designated point. nutritional supplementation, either orally, enterally
Remember that the swollen limb may be tender to or intravenously (see Chapter 7). Infective condi-
touch. Pitting oedema is determined by slow gentle tions are treated with antibiotics with or without
pressure over the medial malleolus or the shaft of surgical drainage. Specific treatments of venous and
the tibia. Lymphoedema is characterised by non‐ lymphatic diseases are discussed in Chapter 57.
pitting swelling of the leg and the foot, as well as Non‐specific measures that help in the treatment of
swelling of the toes. Intradermal vesicles, weeping the swollen leg include elastic support stockings,
of the skin, dry and scaly skin and an ‘elephant elevation and massage.
skin’ appearance occur in long‐standing cases. The
legs are examined for signs of venous disease (vari-
Elastic stockings
cose veins, venous flares, pigmentation, lipoderma-
tosclerosis, eczema, venous ulceration). An The use of elastic stockings is described in Chapter 57.
arteriovenous fistula is characterised by a pulse,
thrill and machinery bruit over dilated veins. The
Elevation
hip, knee and ankle joints should be examined,
together with the popliteal fossa. Regional lymph Simple elevation of the leg relieves oedema by reduc-
node groups must be examined. Rectal and pelvic ing intravascular hydrostatic pressure. The principle
examinations may be indicated. is to avoid having the swollen leg in a dependent
Signs of inflammation (erythema, heat, tender- position and to avoid having it still. First, patients
ness, swelling, reduced movement) with or without must keep off their feet as much as possible, and
infection (pus) should be noted. Tinea pedis between elevate the affected limb above the level of the hip
the toes and on the soles of the feet leads to crack- whenever sitting. The limb should be raised above
ing and breakdown of the skin, and may produce the horizontal whenever possible and, ideally, the
the portal of entry for bacteria causing cellulitis of patient should lie on the floor with the legs vertically
the legs and feet (see Chapter 9). against a wall for 15–20 minutes several times each
day. This may not be practical for many patients but
Investigations should be advised and encouraged. Second, when
patients are standing, they should avoid standing still
These should include full blood examination, liver and should be encouraged to exercise the calf mus-
function tests and measurement of erythrocyte sedi- cles and to walk with a support stocking (usually calf
mentation rate and levels of serum creatinine, urea length will suffice). Third, the foot of the bed should
and electrolytes, glucose, plasma proteins and albu- be elevated by at least 10 cm.
min. An ECG and chest X‐ray are performed.
Urinalysis for sugar, blood and protein is per-
formed. Abdominal ultrasound scan or computed Massage
axial tomography is required to define organomeg- Massage of the limb towards the hip, using a surface
aly or tumour mass if this is suspected. skin oil, reduces subcutaneous tissue swelling and
If venous disease is suspected, a Doppler study is helps keep the skin and subcutaneous tissues soft
performed to detect patency and the pattern of and supple. This is especially so with lymphoedema.
underlying venous incompetence. Venography is
rarely required but can be used in a targeted way to
demonstrate the deep veins, the extent of stenosis Diuretic therapy and fluid restriction
or obstruction, the presence of collateral circulation Diuretic therapy and fluid restriction are indicated
and some endovenous treatment options. in congestive heart failure and in some renal and
Lymphangiography may be attempted when hepatic diseases, and may be of value in some cases
venous and other diseases have been excluded. This of limb swelling due to local causes. However, care
is done using a nuclear medicine technique with must be taken not to induce significant electrolyte
technetium which provides good functional assess- abnormalities or dehydration.
ment of lymphatic drainage.
Venous treatment options

Treatment
The duplex scan may have disclosed underlying
The treatment of leg swelling depends on the cause. issues in a number of cases and, if suitable, the
Cardiac, hepatic and renal disorders are treated patient’s venous status can be improved in many
instances by ablating incompetent superficial Development of collateral pathways

veins, especially the great saphenous vein, using Small venules and veins dilate in the subcutaneous
one of laser, radiofrequency, glue and less often venous system and may collateralise. The walls of
surgery. Major deep vein thromboses, especially these veins are fragile and the veins are exposed to
acute iliofemoral disease, may be suitable for high pressure, so they may bleed externally or
endovenous treatment and subsequent stenting
rupture in the subcutaneous tissue, leading to skin
under the cover of anticoagulation. pigmentation.
Impaired nutrition of the skin and subcutaneous

Leg ulcers tissue
With sustained ambulatory venous hypertension in
Epidemiological studies have shown that leg the lower extremity, there is impaired tissue perfu-
ulcers are present in 3–4% of the population sion. Atrophy and fibrosis results in progressive
aged more than 65 years old. Management of induration of the subcutaneous tissue of the lower
such ulcers is often suboptimal and recurrence is one‐third of the leg, giving an ‘inverted champagne
common because the underlying pathophysio- bottle’ appearance.
logical mechanisms have not been correctly diag-
nosed and therefore treated comprehensively. Ulcers
Consequently, ulcers result in considerable disability Minor injury, which may be unrecognised, can
and expense to the patient and the healthcare initiate leg ulceration. Healing is poor because of
system. Improved results will follow a rigorous the impaired nutrition of the tissues and tissue
diagnostic approach, more specialised medical breakdown follows. Ulceration can be compounded
care and appropriate compression to facilitate by infection, particularly streptococcal cellulitis,
healing, in the commonest cause, namely venous coincident arterial disease or diabetes.
incompetence.
Aetiology and pathogenesis Arterial disease

Venous disease This is the predominant cause of about 20% of leg
ulcer cases and a contributing factor, with venous
More than 80% of lower leg ulcers will have a
disease, in a further 20%. As arterial insufficiency
venous component and understanding normal
can often be corrected, it is important that arterial
venous return and hence its perturbations will allow
perfusion is checked even if the clinical appearance
targeted treatment to facilitate rapid healing in most
of an ulcer is typically venous.
cases. Musculo‐venous pumps, the most important
of which is the calf muscle pump, augment venous
return to the heart. The pumps work best when the
Other causes
veins are patent, the valves competent and the pump
used by regular exercise. There is a miscellaneous group that comprises only
Venous insufficiency results from failure of the 10% of patients with ulcers. Ulcers associated with
normal mechanisms returning venous blood from hypertension (Martorell’s ulcers) occur predomi-
the lower limb, particularly incompetence of nantly on the anterior and lateral aspects of the
valves. Incompetence of the deep venous system calf. The ulcers are distinguished from arterial
may follow deep vein thrombosis (DVT) or occur ulcers by their site. Multiple ulcers may occur and
spontaneously. Incompetence of the venous valves may be painful. Treatment is conservative with
causes a reduction in the volume of blood expelled healing often delayed.
by the calf muscle pump. The calf muscle pump A common injury is a fall that lifts a distally based
may also be impaired by limited ankle joint mobility skin flap which can leave a post‐traumatic ulcer.
caused by arthritis. With increasing obesity and a Diabetic foot ulcers are discussed in Chapter 55
sedentary lifestyle in an ageing population, the calf and highlight the importance of considering periph-
muscle pump may be simply not used. eral neuropathy in the genesis of foot ulcers.
The common pathway is ambulatory venous Several systemic diseases are associated with leg
hypertension, which leads to soft tissue damage in ulceration including rheumatoid arthritis, inflam-
the leg and eventually ulceration. The overlap of leg matory bowel disease and vasculitis.
swelling and ulceration is considerable due to Finally, but most important, malignant change
venous incompetence. (so‐called Marjolin’s ulcer), usually squamous cell
690 Problem Solving
carcinoma, should be suspected in any long‐stand- With atypical ulcers or non‐healing ulcers, markers
ing ulcer or one with an atypical appearance or that for connective tissue disorders such as rheumatoid
fails to heal despite adequate management. Biopsy serology should be considered and a biopsy is
of the ulcer edge is then indicated. mandatory.
Clinical presentation Local investigations

Chronic venous insufficiency Measurement of ankle blood pressure
The patient presents with ulcers, often recurrent, Measurement of the ankle–brachial pressure index
and the history may extend over many years. The (ABI) should be performed to check the arterial cir-
ulcers may be painful in the early stages, relieved culation. If the ABI is abnormal, duplex ultrasound
by elevation of the leg. The most common site is should be used to determine the site and severity of
on the medial side of the lower third of the calf. any arterial disease present. Angiography can then
On examination, the ulcer is usually irregular in be performed on an intention‐to‐treat basis, aiming
outline and surrounded by eczematous and/or to restore arterial perfusion to normality by angio-
pigmented skin with a base of granulation tissue. plasty or bypass surgery.
Careful serial measurement, ideally using digital
photography, of the size of the ulcer will help
determine if healing or progressive ulceration is Venous duplex ultrasound
occurring. This test has supplanted venography in the assess-
ment of chronic venous insufficiency. The veins are
examined to determine the venous anatomy,
Arterial disease
patency and valvular competence. It is important
The ulcer may be anywhere on the lower leg, char- to determine the pattern of venous incompetence
acteristically over bony prominences such as the present, as superficial incompetence can be treated
malleoli. The pain is worse when the leg is elevated very efficaciously.
and relieved when the leg is hanging down. The
ankle pulses are absent.
Treatment
Investigations The principles of treatment have come to be applied
more aggressively in recent years (Box 73.2). Such
General investigations
treatment should be directed to correcting the
These should include a full blood examination, fast- underlying cause of the ulcer, optimising healing
ing blood glucose and serum albumin estimation. and preventing recurrence.
Box 73.2 Management algorithm for leg ulcers
1 Define and treat cause If saphenofemoral and/or short‐saphenopopliteal

Measure ABI veins incompetent, and the deep veins are patent,
If ABI <0.5 consider surgery to correct superficial venous
Do not apply compression bandaging incompetence
Arterial duplex scan If iliac vein stenosed/occluded, consider stenting or
Improve arterial inflow venous bypass
Angioplasty ± bypass surgery
3 Biopsy
If ABI >0.9
Long‐standing ulcers
Apply compression: class I–II surgical stocking or
Ulcers with atypical appearance
four‐layered banding
Ulcers that recur despite adequate initial management
2 Determine venous patency and competence Remember, a leg ulcer may be malignant de novo
Venous duplex scan
4 Prevent recurrence
Check deep vein patency and competence
Nutritional support
Check saphenofemoral and short‐saphenopopliteal
Perseverance with surgical stocking support
competence
Treatment of the underlying cause elastic stockings are now available with applica-
tion devices to make it easier for patients to put
Venous insufficiency
them on. These stockings are designed to provide
An immediate concern is to control oedema of the
graduated compression, greatest around the ankle,
subcutaneous tissue and to minimise the sequelae.
less proximally. Graduated compression should be
This is best done by keeping the patient ambulatory
applied with a 40 mmHg pressure gradient at the
by wearing elastic stockings or using compression
ankle level, tapering to 20 mmHg at the knee. The
bandaging, although occasionally bed rest with
ankle arterial pressure should be measured before
elevation of the leg is required. Neglected or inade-
compression bandaging is applied to ensure that
quate lower extremity compression is the common-
there will be no compromise of arterial inflow.
est reason for failed healing or early ulcer recurrence.
In most cases a below‐knee stocking provides
Elderly patients need considerable physical and
adequate support.
emotional support to help them persevere with
stockings, particularly for those with arthritis or
limited mobility. It is essential that an adequate
Provide conditions to allow healing
arterial supply is proven before instituting com-
pression therapy. Careful attention should be given to nutrition as
Surgery has a limited place in relieving venous elderly immobile patients with painful ulcers may
obstruction and restoring valvular competence. neglect themselves.
Targeted surgery, using the duplex as a ‘road map’,
can deal with superficial venous insufficiency or Treat infection
perforating veins. Superficial varicose veins should In addition to these general measures, local skin
be treated, unless they are forming important col- care and antibiotic therapy for any associated
lateral around obstructed deep veins. Patients with c ellulitis will help control infection and provide
only superficial incompetence and normal deep optimal local conditions for healing. It is impor-
veins are an important group to identify as their tant to distinguish between invasive infection
tendency to ulceration can be largely controlled by and contamination of the wound. Prolonged
a combination of endovenous or surgical proce- courses of antibiotics should not be given
dures. Incompetent calf perforating veins, commu- because this will usually result in colonisation of
nicating between the deep and superficial venous the wound by strains of bacteria resistant to the
systems, can be treated by sclerotherapy or by antibiotics.
endoscopic surgery.
Attempts have been made to relieve venous
Provide and maintain optimum conditions
obstruction or restore valve function by surgical
for healing
means. The most successful procedure has been
The two major elements of this are to remove dead
femoro‐femoral vein bypass to relieve unilateral
tissue and to apply appropriate dressings. Dead
iliac venous obstruction. Procedures to restore
tissue can be removed enzymatically or surgically.
valve function by applying cuffs to restore valvular
Although correct application of external compres-
competence or autotransplantion of vein segments
sion is the most important therapeutic measure,
containing competent valves into an incompetent
dressings are important as wounds heal best in
deep vein have met with very limited success. These
warm moist conditions. There are now a large num-
measures are applicable to only about 1–2% of
ber of products available to provide and maintain
patients with venous ulceration.
optimum conditions for healing. The choice of
Skin grafting can hasten healing, but in almost
dressing will depend on the depth of the wound and
all patients it is unnecessary. Performance of a
the amount of exudate.
skin graft does not remove the need for the other
measures described; in particular, the need to
wear supporting stockings remains an essential
Prevention of recurrence
component of postoperative care.
The most important therapeutic measure for Treatment that results in healing of an ulcer is not
healing venous ulcers, supported by level 1 evidence, sufficient. The next objective is to prevent recur-
is external compression preferably by stockings or, rence by general measures, such as lifestyle change
alternatively, well‐applied elastic bandaging. The encouraging greater mobility and weight loss, and
choice of dressing is far less important, other than local measures, the most important of which is
to cover the ulcer and protect the skin. A variety of perseverance with surgical stocking support.
692 Problem Solving
Arterial disease 4 Eight days following a low anterior resection for

carcinoma of the rectum, a 65‐year‐old man
The treatment of arterial disease and diabetic foot
developed unilateral gross swelling of his right
ulcers is covered in Chapters 55 and 58.
lower limb. Which of the following statements is
correct?
a a diagnosis of deep venous thrombosis
Further reading
can confidently be made on the basis of
Fitridge RA, Thompson MM (eds) The Mechanisms of clinical signs
Vascular Disease: A Reference Book for Vascular b deep venous thrombosis is unlikely as the patient
Specialists. Adelaide: University of Adelaide Press, 2011. had received perioperative prophylactic subcuta-
Perler BA, Sidawy AN (eds) Rutherford’s Vascular Surgery neous heparin
and Endovascular Therapy, 9th edn. Philadelphia: c a past history of superficial thrombophlebitis in
Elsevier, 2018. this patient is almost certainly related to deep
venous thrombosis
d the short saphenous vein is usually the site of
MCQs origin of deep venous thrombosis
e ilio‐femoral thrombosis is likely as it commonly
Select the single correct answer to each question. follows pelvic surgery
The correct answers can be found in the Answers
section at the end of the book. 5 A 65‐year‐old woman has a chronic leg ulcer.
1 Which of the following causes of bilateral leg Which of the following is the least likely cause?
swelling with pitting oedema s incorrect? a squamous cell carcinoma
a reduced lymphatic removal of exudate b giant cell arteritis
b increased capillary permeability c superficial venous valvular incompetence
c decreased filtration pressure at the arteriolar end d deep venous valvular incompetence
d reduced oncotic pressure e trauma
e excessive fluid intake
6 Which of the following is the most important
2 A 75‐year‐old female underwent a right‐sided total measure for healing a chronic venous ulcer?
hip replacement. On postoperative day 10, she a apply a dressing
complained of discomfort and swelling over her b stop smoking
right thigh and calf. She has been ambulating c apply compression bandaging/stockings
satisfactorily. Which of the following statements is d surgery to excise the ulcer
true? e counselling
a bed rest and diuretic therapy should be
prescribed 7 Which of the following statements about chronic
b CT scan of the lower pelvis and right hip should leg ulcers is correct?
be done a they are generally well managed
c Doppler study of the lower limb deep venous b 80% are due to superficial venous insufficiency
system should be performed c a biopsy is best done of the ulcer edge
d local complications of surgery are the most likely d basal cell carcinoma is the commonest malig-
cause for the swelling nancy in the leg
e a plain X‐ray of the right hip is most informative e arterial and venous ulcers are easily distinguished
3 Which of the following statements about acute 8 Which of the following statements about the calf
lymphangitis of the lower limb is incorrect? muscle pump is correct?
a improperly managed, it may lead to a it plays no part in venous return to the heart
lymphadenitis b it cannot work if the valves are incompetent
b lymphangiography is the investigation of choice c it is the only musculo‐venous pump
in the management d it depends on good ankle movement
c rest and elevation of the affected limb is e it cannot work if arterial disease is present
appropriate
d cellulitis may be the initiating cause
e appropriate antibiotics should include cover for
streptococcal infection
74 Haematuria
Kenny Rao1 and Shomik Sengupta2
1
2
genitalia (Table 74.1). Consideration needs to be

Introduction given particularly to the serious and common
causes.
Classification
Haematuria refers to the presence of blood in the Medical renal disease
urine. It may be ‘macroscopic’ when it is visible to
A range of intrinsic diseases of the kidney can also
the naked eye (also known as ‘gross’ or ‘frank’) or
cause haematuria but are usually managed by neph-
‘microscopic’ when it is only detectable on dipstick
rologists (renal physicians). Typically, the presenta-
or laboratory examination of the urine. Only a
tion is with microscopic rather than visible
small amount of blood is needed to change the col-
haematuria, and can be associated with other
our of urine, and thus it is common to overestimate
features such as hypertension, renal impairment,

the amount of bleeding. Fresh active bleeding causes
proteinuria or oedema. The key distinction between
the urine to look bright red while old blood or clot
renal diseases and surgical causes of haematuria is
results in a dark yellow or brown discoloration.
that in the former the red cells have come from
within the glomeruli and on microscopy usually
Significance have a dysmorphic appearance as a result. There
may also be associated red cell casts, and if these
In most cases, haematuria results from benign or
diagnoses are suspected, referral to a renal physi-
indeterminate causes, but it can also be the cardinal
cian is required. Occasionally, low‐level micro-
symptom of serious conditions such as urinary tract
scopic haematuria may be difficult to classify
malignancy. Hence, the presence of blood in the
accurately, and both urological and nephrological
urine should never be taken lightly and almost
evaluation maybe warranted.
always warrants further investigation.
Asymptomatic microscopic haematuria in low‐
risk patients (age <45 years, non‐smoker) does not
Neoplasm
usually require further investigation. Neither does Tumours arising from any part of the genitourinary
haematuria in females that is clearly attributable to tract can present with haematuria, and thus repre-
an uncomplicated urinary tract infection (UTI) and sent the most serious potential cause of this symp-
resolves with its successful treatment. It should be tom. Therefore, the assessment of the patient with
noted that recurrent UTIs or UTIs in males usually haematuria is aimed, in large part, to the detection
requires further investigation for potential predis- of any underlying neoplasm. While this is particu-
posing causes. larly important if the patient has risk factors such as
smoking, metabolic syndrome, a family history or
environmental exposure, such pathology can arise
Differential diagnosis even in those who do not. It is crucial to note that
the presence of non‐malignant causes of haematu-
A systematic approach is necessary to assessing a ria, such as infection, does not exclude concurrent
patient presenting with haematuria, since various malignancy as a cause for haematuria. Therefore, a
pathologies can occur anywhere along the genitou- systematic protocol‐based assessment is key to
rinary tract from the kidneys to the external avoid missing serious causes of haematuria.
693
694 Problem Solving
Table 74.1 Differential diagnoses of underlying causes of haematuria.
Kidney Ureter Bladder Prostate Urethra
Neoplasm Renal call carcinoma Urothelial Urothelial Adenocarcinoma Urothelial

Angiomyolipoma carcinoma carcinoma carcinoma
Oncocytoma Solitary fibrous Adenocarcinoma
Urothelial carcinoma tumour Squamous
carcinoma
Inflammation Pyelonephritis UTI Prostatitis Urethritis
Radiation cystitis
Congenital Arteriovenous Arteriovenous Arteriovenous
malformation malformation malformation
Trauma Renal contusion or Ureteric injury Bladder rupture Urethral
laceration injury
Calculi Renal Ureteric Bladder
Other Glomerulonephritis Benign prostatic Stricture
Cyst hyperplasia
Bladder cancer Infection and inflammation

Haematuria is the most common presentation of UTI is one of the most common causes of haematu-
bladder cancer. It may be microscopic or macro- ria, particularly in young adults. This can affect the
scopic and is often isolated or episodic rather than bladder (cystitis) or the kidneys (pyelonephritis).
continuous. It may also be associated with dysuria, The resultant inflammation and oedema can cause
recurrent UTIs, pelvic pain and voiding frequency. bleeding from the epithelium and into urine. The
Bladder cancer can progress rapidly, and delays in more typical symptoms of UTI are dysuria and
diagnosis are known to significantly worsen out- LUTS, and if involving the kidney flank pain, fever
comes and thus prompt investigation is crucial. and constitutional symptoms.
Various non‐infective causes of cystitis can also
lead to a similar presentation as UTI. Radiation ther-
Renal tumours apy, often used to treat cancers of the pelvic viscera, is
the commonest cause of such chronic haemorrhagic
Various renal neoplasms can cause haematuria
cystitis. Other causes include drug‐induced (e.g. the
including renal cell carcinoma, urothelial cell carci-
immunosuppressant cyclophosphamide) or infiltra-
noma, angiomyolipoma and cystic diseases. Other
tive (interstitial or eosinophilic) cystitis. Inflammation
associated symptoms can include flank pain or a
of the bladder mucosa causes friable neovascularisa-
palpable mass. In current practice, however, the
tion which can bleed easily and be difficult to control.
majority of renal malignancies are discovered inci-
Haemorrhagic cystitis is often episodic in presenta-
dentally on radiological imaging rather than due to
tion, but when severe can be life‐threatening and
symptoms.
require urgent and major intervention.
Prostate pathology Calculi (stones)

Prostate cancer and benign prostatic hyperplasia Urinary calculi commonly originate in the renal col-
(BPH) can each result in increased vascularity over lecting system, where they can remain asymptomatic
the surface of the prostate which surrounds the ure- for lengthy periods, but presentation can be with
thra. These vessels are friable and may spontane- pain or haematuria. Sometimes, stones can travel
ously bleed. Patients may also have concomitant along the urinary tract, and typically present with
lower urinary tract symptoms (LUTS) including fre- flank pain (renal colic) caused by urinary obstruc-
quency, intermittency, dribbling, hesitancy, incom- tion. Renal colic is commonly associated with hae-
plete emptying, nocturia and urgency. However, maturia, often microscopic, but sometimes visible.
prostate cancer is most commonly diagnosed at an Bladder stones usually arise as a result of bladder
asymptomatic stage based on elevation of the serum outlet obstruction and urinary stasis, and thus are
marker PSA (prostate‐specific antigen). often identified during assessment of the associated
74: Haematuria 695
LUTS, but again visible or invisible haematuria can However, it should be noted that the presence of
coexist. blood in the bladder can itself provoke irritative
LUTS, while obstructive symptoms may be caused
Urethral strictures or exacerbated by clots.
Flank pain in association with haematuria may
Strictures arise as a result of scarring of the urethra,
indicate renal inflammation from pyelonephritis or
which may be secondary to prior trauma, infection
obstruction from calculi or clots within the ureter.
or instrumentation. Strictures impair bladder emp-
Fever, malaise and related symptoms can be indica-
tying and commonly present with LUTS but can
tive of sepsis from infection. Weight loss, cachexia
also cause haematuria.
and bony pain are symptoms that raise the concern
of advanced malignancy. Renal cell carcinoma can
Trauma
additionally lead to a variety of paraneoplastic syn-
The mechanism of injury usually alerts the clinician dromes, including fever.
to potential genitourinary trauma as a cause of hae- Exposure to risk factors for genitourinary malig-
maturia. Blunt trauma from falls, motor vehicle nancies should be assessed. Smoking is associated
accidents or sports injury are most common in with both urothelial cancers and renal cell carci-
Australia, but penetrating injuries from gunshots or noma. Environmental exposure to aniline dyes and
stabbings need specific consideration. aromatic amines are also risk factors for urothelial
Renal trauma occurs in a spectrum of grades, cancers and employment in the textile, dry cleaning,
ranging from simple contusion to a completely shat- petrochemical, rubber and other chemical indus-
tered or avulsed kidney. The extent of haematuria tries, trucking, painting and printing are of poten-
may not provide an accurate assessment of the sever- tial concern.
ity of injury since a major component of the bleeding Family history may be of particular significance
may be confined to the retroperitoneum. Appropriate for some malignancies, notably prostate cancer and
imaging by CT is the key to diagnosis and underpins renal cell carcinoma, especially in the context of
further management. known cancer syndromes such as von Hippel–
Pelvic fractures can be associated with bladder Lindau and Birt–Hogg–Dubé syndromes. Urolithiasis
and urethral injuries that can sometimes remain and BPH can also be associated with a familial
undiagnosed without appropriate imaging. There tendency.
needs to be a high index of suspicion, with blood at Past medical history, such as urolithiasis, malig-
the urethral meatus being a pathognomonic sign. nancy, radiation therapy and surgery, can obviously
Again, appropriate imaging by way of retrograde be particularly important in directing clinical diag-
urethrogram and cystogram is crucial for making nosis. Comorbidities, particularly cardiovascular
the diagnosis. Urological involvement is important disease, may lead to treatment with anticoagulant
for avoiding further exacerbation of the injury dur- and antiplatelet medications which can precipitate
ing attempted catheter placement. or worsen haematuria. It should be noted that even
among patients on such medications, haematuria
can be associated with underlying pathology and
Assessment therefore appropriate clinical assessment and inves-
tigation is imperative.
History
Haematuria may be reported by the patient on vis-
Examination
ualising their urine or be picked up incidentally on
urine microscopy. The pattern of haematuria may In most cases, other than visible haematuria on a
sometimes provide clues to the source; initial or ter- urine sample, there are few signs visible on exami-
minal bleeding is suggestive of prostatic or urethral nation. Significant blood loss or infection can pre-
pathology. The extent of haematuria, including the sent with hypovolaemic or septic shock. Chronic
presence of clots and resulting difficulties in passing blood loss may occasionally manifest as signs of
urine (sometimes resulting in so‐called ‘clot reten- anaemia.
tion’), may have implications for management Abdominal examination can reveal masses or ten-
including the potential need for catheterisation to derness, which may be indicative of renal pathology
drain and wash out the bladder. (if in the flank) or lower urinary tract pathology
The presence of associated LUTS may provide including a full bladder or large pelvic malignancy. A
suggestive evidence of lower urinary tract pathol- digital rectal examination (DRE) in males is helpful
ogy, especially if they pre‐date the haematuria. in assessing the prostate for size and possible cancer.
696 Problem Solving
The DRE (or a vaginal examination in females) can underlying pathology. Abdominopelvic CT scans
also give clues on other pelvic malignancies. are undertaken prior to, during and after admin-
Examination of the genitalia in either sex helps iden- istration of intravenous contrast. This allows the
tify potential external sources of bleeding. detection of the full range of possible pathology
In the context of trauma, it is vital to rule out a (Figure 74.1): urolithiasis, renal and bladder
palpable pulsatile retroperitoneal mass as this is an masses and abnormalities along the collecting
indication for urgent surgery for renal bleeding. system (possibly indicating tumour, calculi, clots,
Blood at the meatus is a sign of possible urethral or etc.). The administration of intravenous contrast
bladder injury, as previously discussed. is contraindicated in patients who have an allergy
to it or inadequate renal function (usually, esti-
mated glomerular filtration rate <45 mL/min per
Investigations 1.73 m2).
• Non‐contrast CT: can be used if contrast
Blood tests
administration is contraindicated. However, the
• Full blood examination: searching for anaemia, assessment of renal masses and collecting sys-
infection or platelet abnormalities. tem abnormalities is very inadequate in such a
• Electrolytes, urea and creatinine: important for scan.
assessing renal function. • Renal tract ultrasound: provides an alternative to
• Coagulation studies: assessing for bleeding CT that avoids the risks of radiation and contrast
diathesis. exposure, of particular utility in pregnant or
young females. However, ultrasound has more
limited resolution than CT and can be dependant
Urine tests
on operator skill and body habitus. Good at
• Urine dipstick: can be quick and convenient but detecting renal masses and stones as well as the
has limitations of false positives and false nega- presence of hydronephrosis, but limited in assess-
tives. Provides additional information about the ing ureteric abnormalities. Provides fairly good
presence of leucocytes/nitrates (indicative of anatomical detail of the lower urinary tract.
infection), glycosuria, etc. Ultrasound can be used for initial imaging for
• Midstream urine: attention needed for appropri- patients considered to have a low risk for under-
ate collection to avoid contamination. Urine lying pathology.
microscopy allows the detection of red cells (indic- • Magnetic resonance imaging (MRI): provides
ative of bleeding), while morphology is important another alternative modality for high‐resolution
in distinguishing nephrological causes of bleeding. cross‐sectional imaging, although used rela-
White cells are indicative of infection or inflam- tively infrequently. Useful for patients who can-
mation, microorganisms (bacteria or fungi) of not have CT contrast administration due to
colonisation or infection, casts of nephrological allergy (for those with inadequate renal func-
conditions, and crystals of risk for stone formation, gadolinium MRI contrast also poses sig-
tion. Culture and sensitivity analysis provides nificant risks and is contraindicated). Sometimes
information on possible infectious agents and thus utilised if findings on CT and/or ultrasound are
guide appropriate antibiotic therapy. equivocal.
• Urine cytology: allows assessment for malignant • Retrograde urethrogram: undertaken by instill-
or atypical cells shed in the urine, typically indic- ing contrast into the urethra. Relatively rare as
ative of high‐grade urothelial cancer. However, an investigation for haematuria, but used if ure-
relatively few cancers are actually associated thral stricture or injury are suspected, as dis-
with positive urine cytology, and the analysis is cussed previously.
significantly operator‐dependent and prone to • Retrograde pyelogram: undertaken by instilling
both false‐negative and false‐positive results. contrast into the collecting system at the time of
cystoscopy (see next section). A specialised test
that is utilised for assessment of the collecting
Imaging studies
system usually undertaken if other imaging stud-
• CT intravenous pyelography (CT‐IVP) is the ies have shown suspicious findings or inadequate
gold standard for radiological investigation of visualisation of the collecting system. May often
haematuria, and is usually recommended for lead on to endoscopic examination of the collecting
patients considered to be at risk of serious system if indicated (see next section).
74: Haematuria 697
(a)
(b)
(c) (d)
Fig. 74.1 Representative CT images: (a) calculus (arrow) within the lower pole of right kidney; (b) renal mass (arrow)
consistent with renal cell carcinoma arising from right kidney; (c) filling defect within bladder lumen (arrow) suggestive
of bladder tumour; (d) filling defect within left ureteric lumen (arrow) suggestive of ureteric tumour.
(a) (b)
Fig. 74.2 Cystoscopic images: (a) bladder tumour; (b) enlarged prostatic lobes.
Procedural investigations
The most important role of cystoscopy in hae-
• Cystoscopy (Figure 74.2): examination of the maturia is to exclude bladder tumour, but the
lower urinary tract using an endoscope. This can procedure also provides additional useful infor-
be carried out under local anaesthetic or seda- mation on anatomy and pathology of the lower
tion using a flexible endoscope or under general urinary tract. Biopsy or resection of tumours,
anaesthetic using a rigid endoscope (which removal of bladder calculi and performance of
allows more interventions to be undertaken). retrograde pyelogram (see previous section) can
698 Problem Solving
Haematuria Further reading
Chiong E, Grossman HB. Hematuria, gross and micro-

History scopic, adult. In: Gomella LG (ed.) The 5‐Minute
Urology Consult, 2nd edn. Philadelphia: Wolters
Kluwer/Lippincott Williams & Wilkins, 2010.
Ngo B, Papa N, Perera M, Bolton D, Sengupta S. Factors
Examination
affecting the timeliness and adequacy of haematuria
assessment in bladder cancer: a systematic review. BJU
Int 2017;119(Suppl 5):10–18.
Urine dipstick Sharp VJ, Barnes KT, Erickson BA. Assessment of asymp-
tomatic microscopic hematuria in adults. Am Fam
Physician 2013;88:747–54.
Investigations
• Blood tests
• Midstream urine microscopy MCQs
• CT IVP/Ultrasound
Select the single correct answer to each question.
• Urine cytology x3
section at the end of the book.
1 Which of the following patients presenting with
Urology referral haematuria does not need further investigation?
a single episode of visible haematuria in a 70‐year‐
old male who has never smoked
Cystoscopy b a 55‐year‐old male who is admitted via emer-
gency with clot retention
Fig. 74.3 Flowchart illustrating clinical assessment of c a 20‐year‐old female who has haematuria with a
patients with haematuria. proven UTI that resolves after antibiotic
treatment
also be carried out at the time of cystoscopy as d a 60‐year‐old ex‐smoker who is found to have
indicated. microscopic haematuria on his urine tests during
• Ureteroscopy and/or pyeloscopy: endoscopic a health check
examination of the upper urinary tract. This is not
a routine investigation for haematuria, but would 2 CT scan done for radiological assessment of the
be undertaken if a stone or upper tract tumour urinary tract in patients presenting with haematuria
was found on imaging. Biopsies or laser destruc- should:
tion of tumours and extraction or fragmentation a include pre‐ and post‐contrast scans with early
of calculi can be undertaken as indicated. and delayed phases
b is done for patients who cannot have an
ultrasound scan
Conclusion c should cover the chest abdomen and pelvis
d all of the above
Haematuria is a common presenting symptom that
can sometimes be indicative of serious underlying 3 Cystosopic assessment of the lower urinary tract:
pathology. Every patient needs careful and system- a is essential to complete investigation of
atic assessment, by way of careful history and haematuria
examination and appropriate further investigation b is the best way to assess for bladder tumour
(Figure 74.3). With limited exceptions, all patients c allows for initial treatment by resection of
with haematuria should undergo imaging of the bladder tumours
urinary tract and cystoscopic examination. d all of the above
75 Postoperative complications
Peter Devitt
Department of Surgery, University of Adelaide and Royal Adelaide Hospital, Adelaide,
South Australia, Australia
Introduction Box 75.1 Common and important

postoperative problems
The management of postoperative complications
Cardiorespiratory
can be approached in a number of ways. Perhaps
Atelectasis
the most practical way is to consider the frequency
Pneumonia
with which various complications may occur
Congestive failure
(Box 75.1). Another strategy is to consider the
Arrhythmias
problems that relate directly to the procedure and
those that are more general and patient‐related Infection
(Box 75.2). Chest
This chapter will take the former approach, Operative site and wound
but obviously it is sensible that in managing any Urinary
patient with a postoperative problem, the doctor Catheters and other lines
considers: Venous thromboembolism
• the procedure Deep vein thrombosis
• the general state of health of the patient before Pulmonary embolism
the illness/operation
• progress since the procedure.
Thus, the questions to be asked should include the
Box 75.2 Categorisation of potential
following.
postoperative complications
• What procedure was done, when was it done and
why was it done? Those related to the procedure
• Is there any coexisting illness (i.e. is there a past For example
medical history of note, such as chronic respira- • Laparoscopy: air embolism
tory disease)? • Pancreatic leak after pancreaticoduodenectomy
• Is the patient on any medication? • Sympathetic ophthalmia after eye surgery (very rare)
• What has now happened to the patient to demand
Those related to specific patients
your attention? For example
• What investigations have been done (both before • Increased risk of infection in the immunocompro-
and after procedure)? mised individual
These will then be followed by the following • Consequence of infection in a patient with a
questions. synthetic heart valve
• Is the cause of the problem clear‐cut? • Bleeding in a patient with a coagulation disorder
• If yes, how should I proceed with management?
General problems
• If no, what will I need to do to make a clear
For example
diagnosis?
• Cardiorespiratory
This chapter contains a number of examples of
• Venous thromboembolism
postoperative complications. A model answer is
• Infection
provided for each scenario. As a learning exercise,
699
700 Problem Solving
cover each model answer and provide your own be attached for monitoring and consideration
answer. Put yourself in the position of the intern. should be given to further management on a high‐
dependency unit.
You have excluded hypoxia as a cause for the
Confusion confusion and the patient does not appear to be sep-
tic. There is no apparent electrolyte disturbance and
Example: A 67‐year‐old man becomes confused you are reasonably confident that the patient is suf-
2 days after a laparotomy for a perforated peptic fering alcohol withdrawal symptoms (delerium tre-
ulcer. The operation was uneventful and 2 L of gas- mens). Describe your initial plan of management.
tric contents were evacuated from the peritoneal Move the patient to a quiet well‐lit room. Arrange
cavity. Lavage was performed and the perforation continuous nursing care, preferably with a nurse
closed. What critical piece of information would familiar to the patient. Institute an alcohol with-
help you determine the cause of the confusion? drawal program. The protocol for this program will
How would you approach the problem? stipulate regular observations of the patient’s symp-
toms, allocating a score to various symptom group-
Model answer: Hypoxia is the most important and
ings and correlating the amount of sedation (if any)
common cause of confusion. If this patient has a
that needs to be given according to the score.
chest infection, you may have the quick explana-
Symptoms to be scored include nausea, anxiety,
tion for his confusion.
visual disturbances and agitation. The preferred
To approach the problem, gain all the information sedative is oral diazepam.
you can about the patient’s preoperative state of
health, the details of the procedure and progress
since the operation. From the case notes you will Chest pain
hopefully glean information about the patient’s past
medical history, medications, examination findings Example: Five days after a bilateral salpingo‐
and general fitness. From the past history, look for oophorectomy and total abdominal hysterectomy,
evidence of chronic respiratory disease and sus- you are asked to see a 62‐year‐old patient who
tained alcohol consumption. Various investigations complains of breathlessness and right‐sided chest
may have been undertaken (e.g. blood biochemis- pain. What are the thoughts that go through your
try) that may give clues as to the current problem. mind and how would you approach this problem?
Any problems associated with the operation (the
Model answer: If she has had a major pulmonary
procedure itself or the anaesthetic) should be noted.
embolism, the patient may have circulatory col-
The case records and the nursing observations since
lapse and require resuscitation.
the procedure may help determine the cause of the
current problem. Note any investigations that have You will obviously want to know more about the
been performed since the procedure. current symptoms, including the type of pain, the
Take a history from the patient, if his state of mode of onset and severity. Her medical history will
confusion allows. Examine the patient, looking par- be important, particularly any pre‐existing cardi-
ticularly for evidence of hypoxia. A chest infection orespiratory problems. Ideally, you will want to
may explain the confusion. There may be other look at the case record, nursing observations and
causes of hypoxia to consider (e.g. opiate toxicity, drug charts before you proceed with the history
cardiac failure). If the patient is not obviously and physical examination. The conditions you will
hypoxic, he may be septic, have a fluid and electro- need consider include:
lyte disturbance, be suffering a drug complication • pulmonary embolism
or be in alcohol withdrawal. • chest infection
To test some of these hypotheses, several investiga- • pneumothorax
tions may be required. These may include arterial • pleural effusion
blood gas analysis, serum biochemistry, blood cul- • cardiac problems.
ture, an electrocardiogram (ECG) and a chest X‐ray. Your priority will be an assessment of her cardiovas-
Before you start the investigations, some simple cular system. Provided the patient is normotensive
measures can be adopted. Ensure that the patient is and not hypoxic, you can proceed with your investi-
given supplemental oxygen through a face mask gations. These will include an ECG, arterial blood
and that intravenous fluids are being given. If sepsis gas analysis, a chest X‐ray and possibly a CT pulmo-
is likely, you may want to start the patient on a nary angiogram (CTPA). The CTPA will allow accu-
broad‐spectrum antibiotic. A pulse oximeter must rate definition of the major pulmonary vasculature
75: Postoperative complications 701
and can detect filling defects and obstruction. The antibiotics, Provided that there is a rapid response
scans are undertaken after rapid bolus administra- to this treatment, consideration can then be given
tion of 100–140 mL of non‐ionic contrast. This tech- to looking for the underlying cause of the problem.
nique can be used to detect 3–4 mm clots in the The patient will almost certainly have an intra‐
second‐, third‐ and fourth‐order branches of the pul- abdominal collection and this can usually be both
monary vasculature. identified and drained percutaneously under CT
On the assumption that the diagnosis of pulmo- guidance.
nary embolism has been confirmed, the patient Initial assessment of a patient with suspected sepsis
should be started on intravenous heparin. must include an appreciation of the type of procedure
Clinical examination of a patient with suspected undertaken and the risk of infection from that proce-
deep venous thrombosis (DVT) or pulmonary embo- dure. Also to be considered are the consequences
lism is relatively inaccurate and should not be relied should infection in that particular patient occur, for
on to determine diagnosis or treatment. example reduced resistance to infection in an immu-
nocompromised individual. The type of procedure
and the pattern of fever will give important clues as
Fever to the site of sepsis and the causative organism.
Investigations to be considered include those to:
Example: A previously well 45‐year‐old man • identify the site of infection
undergoes a laparotomy and oversewing of a perfo- • diagnose the type of infection.
rated duodenal ulcer. Peritoneal lavage is performed
to deal with the contamination from the perfora-
tion. Postoperative progress is slowed by the devel- Oliguria
opment of a paralytic ileus. On day 6, he is noted to
have a temperature of 38.5°C, blood pressure of Example: A 68‐year‐old patient is reviewed on the
110/60 mmHg, pulse rate of 100/min and a respira- ward some 6 hours after he returned from the oper-
tory rate of 20/min. Describe how this situation ating suite for a sigmoid colectomy performed for
should be managed. perforated diverticular disease. The nursing obser-
vation charts show that he has accumulated a total
Model answer: The measurements on the nursing
of 50 mL of urine in the catheter bag since his
chart indicate systemic inflammatory response syn-
return. The patient looks comfortable, with a blood
drome (SIRS). In this case, the SIRS almost certainly
pressure of 110/75 mmHg and pulse of 90/min.
has an infectious aetiology and, considering the tim-
Describe an appropriate plan of management.
ing of onset with response to the laparotomy, the
site of origin of sepsis is most like to have originated Model answer: While it is possible that this man’s
at the site of the operation (rather than the chest). problem may be fluid retention and pump failure, it
is more likely that he has received inadequate fluid
First, there must be an overall assessment of the
replacement, either during or immediately after the
general state of health of the patient. It appears that
operation and you are dealing with an under‐filled
he is about to slip into septic shock. The patient’s
patient.
progress since the operation must be reviewed and
information sought on any pre‐existing problems Ideally, his urine output should be about 1 mL/kg
(e.g. diabetes) that might predispose the patient to per hour. This patient has a poor urine output and
infection. The nursing observation chart and pat- there are many reasons to consider:
tern of the fever and pulse rate may give clues as to • inadequate filling
the likely cause. A spiking fever over several days • inadequate output
could be due to an intra‐abdominal abscess. • renal tract obstruction.
Although a chest infection may not be the cause Most cases of postoperative oliguria are due to
of the fever, the chest must be examined carefully. under‐filling, either during or immediately after
After that, the abdomen should be inspected and surgery. The case notes should be studied, looking
the wound examined. Cannula and drain sites for evidence of pre‐existing renal or cardiac disease.
should also be examined for evidence of infection. Any recent laboratory investigations (serum bio-
Occasionally, a DVT will be accompanied by a low‐ chemistry) should be assessed. Details of the surgi-
grade fever, and the legs should be examined. cal procedure should be noted, with a calculation
In this instance, the patient will require prompt of how much fluid was lost during the operation
resuscitation with oxygen by face mask, a bolus of and how much was given. The amount of fluid
intravenous fluid and empirical broad‐spectrum given since the time of the operation should be
702 Problem Solving
noted and any discharge from drains or a nasogas- in intra‐abdominal pressure, such as a chest infec-
tric tube measured. Given the scenario, this patient tion or paralytic ileus.
may have lost a considerable amount of fluid as a During this process the patient must be kept fully
result of the peritonitis and may still be losing fluid informed and warned that he may need to be taken
into the peritoneal cavity. Not all fluid lost by a back to the operating theatre (for the wound to be
patient may be readily evident. Patients with para- resutured) if the wound has indeed disrupted. The
lytic ileus and/or peritonitis can accumulate many wound must be carefully inspected. A non‐inflamed
litres of fluid within the peritoneal cavity, so‐called wound with seepage of pink fluid is highly sugges-
‘third space’ losses. tive of acute failure of the wound. Extensive bruis-
Whilst less likely, a blocked catheter could be a ing around the wound might suggest discharge of a
simple explanation and a bedside bladder scan will seroma, while a red angry wound would be in keep-
provide rapid information; however, considering ing with infection.
his recent surgery, this might not be a very practical If there is any doubt as to the nature of the prob-
manoeuvre. lem, the wound should be gently probed (with ster-
It is unlikely that this patient would have been ile instruments). If intestine becomes visible, there
sent directly back to the ward if there had been should be no further local exploration and the
(preoperative or perioperative) concerns about patient prepared for formal wound closure in the
coexisting conditions that might have had a major operating room.
impact on his recovery. On the assumption that the There are a number of factors that can contribute
patient does not have pre‐existing renal impairment to deep wound dehiscence (acute wound failure).
or cardiac failure (the latter backed up by physical • Local: poor suturing techniques, poor tissue heal-
examination), in most instances it will be relatively ing (infection, necrosis, malignancy, foreign bod-
safe to manage the problem at the bedside. The first ies), increased intra‐abdominal pressure.
step will be to give a bolus infusion of 500 mL of • General: malnutrition, diabetes mellitus.
isotonic saline rapidly and observe the effect on In most instances, acute wound failure is due to a
urine output over the next few hours. Further local factor. The hallmark of deep wound dehis-
boluses of fluid may be required and a diuretic cence is the presence of a serosanguineous discharge
should only be given once it can be confidently some 5–7 days after the initial surgery.
judged that the patient has had adequate fluid
replacement. In more complex cases, the resources
of an intensive care unit may be required to help Bleeding
determine the nature of the underlying problem.
Example: A 27‐year‐old man is being reviewed on
the ward, having recently undergone a splenectomy
Wound discharge for trauma. The nursing staff report fresh blood in
the drain. How should this problem be approached?
Example: Five days after undergoing a laparotomy
Model answer: Further information is needed. The
and small bowel resection following an episode of
bleeding may be localised or generalised. It may be
adhesive obstruction, a 73‐year‐old patient devel-
reactionary, primary or secondary. How long ago
ops a pinkish discharge from the wound. Describe
was the operation and how much blood is in the
how the problem should be managed.
drain? A small amount of fresh blood a few hours
Model answer: While there are a number of causes after the operation may be of little consequence. Is
of wound discharge, the most urgent to consider is the bleeding confined to the drain or is there evi-
the possibility that this is the harbinger of disrup- dence of bleeding at other sites (wound, intrave-
tion of the deep layers, with the consequent risk of nous cannula)? If the former, the problem may be
complete wound failure. haemorrhage from the operative site; if the latter,
the patient may have a disorder of coagulation.
First, the wound should be covered with a sterile
dressing in the event of sudden complete disrup- The initial assessment must include a review of the
tion. The next action must be to ascertain if the charts. In what circumstances was the operation
patient has any risk factors for wound failure. The performed? If the patient had a massive and rapid
case records should provide information on his pre- transfusion to maintain his circulatory state, then
operative nutritional status. His progress since the the problem may be one of a coagulation defect.
operation should be assessed and any problems What has happened since the operation? A rising
sought that might have led to an untoward increase pulse and falling blood pressure would suggest that
the patient is still bleeding, and what is seen in the Once these things have been done, stand back and
drain may only be the tip of the iceberg. In other review the situation. Look at the charts. Is there a his-
words, there could be a considerable volume of tory of ischaemic heart disease or other cardiac prob-
blood collecting at the operative site, with only a lems? Did the patient come in with urinary retention
little escaping into the drain. Remember that when and could he have infected urine and the present
a drain drains, positive information may be gleaned; problem be septic in origin? How major was the pro-
however, an empty drain means little. cedure that was performed and how much fluid was
Examine the patient and look for evidence of cir- used during the procedure, both intravenous admin-
culatory insufficiency. The material in the drain istration and as irrigation? What is in the urine drain-
tube and drainage bag may be fresh and not clotted, age bag? A large volume of fresh blood would suggest
or it may be serosanguineous. A normotensive hypovolaemia as the cause of the collapse. Were there
patient with old clot in the drain is probably a sta- any complications during the procedure? How has
ble patient. It is more important to pay attention to the patient progressed since the operation? It is
the general state of the patient, rather than the con- important to know if this has been a sudden collapse
tents of the drainage bag. or a steady deterioration since the procedure.
In summary, the clinical assessment of this case In this case there is nothing of significance from
should include: the medical history, except that the patient pre-
• the severity of the bleed sented in acute urinary retention after a series of
• the site of the bleed urinary tract infections. The operation itself was
• the cause of the bleed uneventful and associated with minimal blood loss.
• the need for further action (e.g. coagulation studies, The fluid in the bladder irrigation system is tinged
cross‐matching blood, contacting senior staff). with blood and there are no blood clots. The
patient’s vital signs were within normal limits until
about 15 minutes before the call was made. The
Shock ECG monitor does not show any acute changes.
Describe the further management.
Example: A call is made to review a 66‐year‐old The cause of the problem appears not to be
man on the ward who is hypotensive and con- hypovolaemia. It is either septicaemia or a cardiac
fused. Twelve hours earlier he had a transurethral event. A normal ECG does not exclude an acute
prostatectomy. Describe an appropriate plan of myocardial problem and the enzyme assays and
management. troponin levels must be studied.
It would be prudent to work on the assumption
Model answer: The priority will be resuscitation and
that the patient is in septic shock. In addition to the
to do this effectively it is important to have a clear
oxygen by face mask and fluid loading, antibiotics
idea of the likely cause of his collapse. The causes of
should be given. The choice of antibiotics will depend
shock to consider in these circumstances are:
on the likely organisms. Gram‐negative aerobes are
• pump failure (cardiogenic)
an important and common cause of urinary infection,
• haemorrhage (hypovolaemia)
and in this case it would be logical to assume that the
• sepsis (septicaemia)
presumed sepsis has originated from the urinary tract.
• anaphylaxis (drug reaction).
The trio of an aminoglycoside (gentamicin), metroni-
Make a rapid assessment of the state of the patient. dazole and amoxicillin remains perhaps the most
How profound is the hypotension and it real or a effective antibiotic combination in the management of
statutory call based on a nursing chart algorithm? patients with Gram‐negative septic shock.
The patient may be connected to a monitor, facili-
tating any changes in the ECG to be noted.
Ensure that the patient has an oxygen mask in
Leg swelling
place, running at 6 L/min, and that a pulse oximeter
is attached. On the assumption that the cause of the
Example: Five days after a low anterior resection
problem is not cardiac failure, run in 500 mL of
for a carcinoma of the rectum, a 75‐year‐old man
isotonic saline rapidly. While this is happening, take
complains of pain and swelling in his right leg.
blood samples for assay of cardiac enzymes (cre-
Discuss the initial assessment of the problem.
atine kinase), myocardial breakdown proteins (tro-
ponin), haematological and biochemical screens, Model answer: Of prime concern is whether this
blood cross‐match and culture. Arterial blood gas patient has a DVT. Before the patient is examined,
analysis should be considered. information should be sought on any medical
704 Problem Solving
history of venous thromboembolic disorders and factor Xa inhibitor (e.g. apixaban) or a direct throm-
any risk factors for DVT. Apart from the nature of bin inhibitor (e.g. dabigatran). The direct oral anti-
the recent surgery, were appropriate prophylactic coagulants do not require monitoring, but care must
measures taken to minimise the risk of clot forma- taken in patients with any renal impairment and in
tion? The changes that may bring about DVT those where there could be interactions with other
(Virchow’s triad) focus on: drugs.
• change in flow
• change in the vessel wall
• change in the constituents of the blood. Further reading
Apart from DVT, other conditions to consider include
congestive cardiac failure, dependent oedema and Stubbs MJ. Deep vein thrombosis. BMJ 2018;360:k351.
cellulitis. The clinical assessment for the presence of
DVT is at best unreliable, but a tender swollen calf
suggests that the patient may have a DVT. MCQs
In this case, the patient has an unremarkable medi- Select the single correct answer to each question.
cal history and in particular there is no history of The correct answers can be found in the Answers
thromboembolic problems or cardiac disease. He is section at the end of the book.
not overweight and had been mobile before the
operation. The patient had been classified as having 1 A 19‐year‐old man is injured in motorbike crash in
a low risk for DVT and immediately before the which his right femur is fractured. This is treated by
operation had been given a dose of an unfraction- internal fixation and early mobilisation is encour-
ated heparin preparation. A calf vein compression aged. He makes satisfactory postoperative progress
device had been used during the procedure. The but on day 5 complains of sudden left‐sided chest
operation itself had been uncomplicated and the pain which makes him catch his breath. A friction
patient has started to mobilise. rub can be heard on the left side on auscultation.
On examination, there is some swelling of most Which one of the following is the most likely
of the leg, with calf tenderness and some pitting diagnosis?
oedema. From this assessment it is suspected the a fat embolism
patient may have a DVT, based on a Wells score b pneumonia
of 4. Describe the next step in management. c pulmonary embolism
An ultrasonographic examination of the deep d pneumothorax
veins of the thigh and leg should confirm or refute e cough fracture
the diagnosis. If the patient has a DVT, it will be
important to document the extent of the clot and 2 A 55‐year‐old man with type 2 diabetes and
the degree of luminal occlusion. Extension of the chronic obstructive pulmonary disease undergoes
clot into the femoral vein increases the risk of a sigmoid colectomy and end‐colostomy for
detachment and pulmonary embolism. perforated diverticular disease. His body mass
If clot is present and extends into the popliteal index is 34. Five days after the operation a
vein or beyond, heparin should be started and copious serosanguineous discharge is noted from
graded compression stockings applied if there is a the lower part of the abdominal wound. The
substantial amount of leg swelling. There is no evi- discharge soaks through the dressing. The wound
dence that long‐term use of graded compression has some thickening and erythema at the margins.
stockings will reduce the risk of post‐thrombotic Which one of the following is the most likely
syndrome. If conventional heparin is to be used, a diagnosis?
typical regimen is a loading dose of 5000 units fol- a staphylococcal wound infection
lowed by 1000 units/hour. The patient will require b streptococcal wound infection
monitoring with serial activated partial thrombo- c small bowel fistula
plastin time (APTT) measurements. Alternatively, a d wound dehiscence
low‐molecular‐weight heparin can be given. This e liquified wound haematoma
does not require APTT estimations and can there-
fore be used on an outpatient basis. 3 You are asked to see a 65‐year‐old woman who
Traditionally, this patient would have been antico- feels unwell and faint. Seven days previously she
agulated with warfarin for 3–6 months; however, underwent an elective sigmoid colectomy for
with the advent of the direct oral anticoagulants, carcinoma. The procedure was uncomplicated and,
such patients now tend to be treated with a direct until now, she had been making an uneventful
recovery. On examination she has a temperature of 4 An otherwise fit 57‐year‐old man spikes a tempera-
39.5°C, a pulse rate of 100/min and blood ture of 39°C 5 days after an open appendicectomy
pressure of 90/60 mmHg. Her respiratory rate is for acute appendicitis. There is a tender, reddened
15 breaths/min. She has cool clammy peripheries. and fluctuant swelling at the medial end of the
Her abdomen is tender in the left iliac fossa, wound. What is the most appropriate initial action
around the wound site. Which of the following is to take?
the most reasonable explanation for her current a arrange a CT scan of the abdomen
problem? b arrange an ultrasound scan of the wound and
a myocardial infarction anterior abdominal wall
b pneumonia c start the patient on oral antibiotics
c secondary haemorrhage d open the wound to allow free drainage
d pulmonary embolus e send off blood samples for a white cell count and
e septic shock culture
76 Massive haemoptysis
Julian A. Smith
Department of Surgery, Monash University and Department of Cardiothoracic Surgery,
Monash Health, Melbourne, Victoria, Australia
Introduction Surgical pathology
Massive haemoptysis is rare but carries with it a The source of bleeding is nearly always the high‐
high mortality. Any amount of blood loss in excess pressure bronchial circulation. These vessels are
of 100 mL in 24 hours may constitute massive often enlarged in response to the primary pathol
haemoptysis. Some patients may expectorate sev ogy (e.g. bronchiectasis) or are involved in the
eral litres of blood per day. The risk to life is from inflammatory or necrotic process (e.g. tuberculo
respiratory compromise due to the tracheobron sis). The pulmonary arterial circulation is the source
chial tree filling with blood rather than from hypo of bleeding from arteriovenous malformations.
volaemia and haemodynamic deterioration. The
term ‘life‐threatening haemoptysis’ may be more
appropriate. Clinical evaluation
A thorough history and examination is required

Aetiology of massive haemoptysis bearing the possible causes in mind. Epistaxis and
haematemesis must be excluded. Any anticoagulant
The causes of massive haemoptysis are listed in intake should be established. A history of fever,
Box 76.1. The majority are benign inflammatory or night sweats, weight loss, previous tuberculosis or
infective lung disorders. Malignancy seldom pre exposure to tuberculosis may suggest active tuber
sents with massive bleeding (<5%). culosis. Recurrent pulmonary infections may point
to bronchiectasis. Helpful physical signs may
include finger clubbing, peripheral or cervical lym
Box 76.1 Causes of massive phadenopathy and localised wheeze, crepitations or
haemoptysis consolidation. Abnormal respiratory signs may be
absent if the blood is effectively expectorated.
Infective lung conditions
Tuberculosis
Bronchiectasis
Lung abscess Box 76.2 Investigations of massive
Aspergillosis haemoptysis
Cystic fibrosis
Pulmonary neoplasms Haemoglobin level
Pulmonary embolus Arterial blood gases
Trauma Coagulation studies
Pulmonary artery catheter injury Sputum microscopy and culture
Penetrating or blunt external Chest X‐ray
Arteriovenous malformation Bronchoscopy
Cardiac valve disease Computed tomography
Mitral stenosis Radionuclide perfusion scanning
Infective endocarditis Angiography (CT or digital subtraction)
707
708 Problem Solving
Definitive therapy may include one or more of

Investigations the following.
• Medical therapy: antibiotics, reversal of anti
The investigations for massive haemoptysis are
coagulation.
listed in Box 76.2. A chest X‐ray may be com
• Rigid bronchoscopic control (local coagulation
pletely normal if little blood is retained within the
therapies).
airway. Infection or tumour may be localised but
• Surgical resection: immediate or after initial con
shadows of aspiration may be confusing. Serial
trol of bleeding source.
chest X‐rays may be helpful. Bronchoscopy, per
• Angiography and arterial embolisation for arte
formed while bleeding is occurring, is the best way
riovenous malformations: up to 20% incidence
to localise the source (achieved in over 70% of
of rebleeding, so should be followed with surgi
cases). The rigid instrument provides a superior
cal resection.
view and facilitates airway suction and bronchial
• Radiotherapy: for non‐resectable tumours or if
toilet. Occasionally the flexible instrument may be
the patient is unfit for surgery.
passed through the rigid bronchoscope to visual
Massive rebleeding can occur following the initial
ise more peripheral lung lesions. If the patient is
establishment of control. Surgical resection of the
fit enough to tolerate computed tomography
lesion therefore offers the best hope of cure. All
(CT) scanning, the majority of causes of massive
endobronchial and angiographic therapies should
haemoptysis will be demonstrated. CT or digital
be considered temporary answers to this problem.
subtraction bronchial or pulmonary branch angi
Surgical resection is contraindicated in patients
ography and possible embolisation may have a
with severe cardiorespiratory dysfunction, uncor
role in high‐risk surgical patients where initial
rectable coagulopathy, unresectable cancer and in
bronchoscopy has been unhelpful.
those in whom the bleeding site is impossible to
localise by any method.
Management plan
The key principles in the management of this poten Further reading

tially fatal condition are:
• prompt early resuscitation Ibrahim WH. Massive haemoptysis: the definition should
• precise localisation of the bleeding source and be revised. Eur Respir J 2008;32:1131–2.
airway protection Jean‐Baptiste E. Clinical assessment and management of
• definitive therapy. massive hemoptysis. Crit Care Med 2000;28:1642–7.
The patient requires intensive care monitoring of Jougon J, Ballester M, Decambre F et al. Massive haemop
tysis: What place for medical and surgical treatment.
vital signs and oxygen saturation. The patient
Eur J Cardiothorac Surg 2002;22:345–51.
should be positioned head down and bleeding side
Sakr L, Dutau H. Massive hemoptysis: an update on the
down (if known). Adequate amounts of blood role of bronchoscopy in diagnosis and management.
should be available for administration via a large‐ Respiration 2010;80:38–58.
bore intravenous line based on haemodynamic
parameters rather than the amount of blood lost
(notoriously unreliable). Broad‐spectrum antibiot
ics should be given pending results of sputum cul MCQs
tures. Specific antituberculosis therapy is added in
the presence of active tuberculosis.
Rigid bronchoscopy is vital for maintaining the
airway, aspirating blood and secretions from the air
way and for ventilation. After localising the source 1 From which of the following blood vessels does the
of bleeding, control may be obtained by ice‐cold bleeding in a patient with massive haemopytsis
saline lavage (leading to vasospasm) or placement of usually occur?
an endobronchial balloon blocker and endotracheal a pulmonary artery
intubation. Patients are ventilated (with positive end‐ b pulmonary vein
expiratory pressure) and bronchoscopy is repeated c bronchial artery
12–24 hours later to assess ongoing bleeding prior to d bronchial vein
definitive therapy. e thoracic aorta
76: Massive haemoptysis 709
2 Which of the following lung conditions is not a c radionuclide lung scan

common cause of massive haemoptysis? d bronchoscopy
a carcinoma of the lung e pulmonary angiogram
b pulmonary arteriovenous malformation
c tuberculosis 4 Definitive therapy in a patient with massive
d lung abscess haemoptysis may include which of the following?
e aspergillosis a broad‐spectrum antiobiotics
b surgical resection of the bleeding source
3 Which of the following investigations will most c pulmonary arterial embolisation
reliably determine the site of bleeding in a patient d radiotherapy
with massive haemoptysis? e all of the above
a chest X‐ray
b CT scan of the chest
77 Epistaxis
Robert J.S. Briggs
Primary tumours are a rare cause of epistaxis in

Introduction children that should be considered. Rhabdo
myosarcoma is a malignant tumour occurring in the
Nasal bleeding or epistaxis is the most common
paediatric population which sometimes involves the
otolaryngologic emergency and may occur in either
nasal cavity and presents with epistaxis. Juvenile
the paediatric or adult patient. Epistaxis may be
nasopharyngeal angiofibroma is a benign, highly
minor or more severe, requiring hospitalisation,
vascular tumour that involves the posterior nasal
resuscitation and surgical control. In the majority
cavity, typically affecting adolescent males and pre
of cases the aetiology is idiopathic, although other
senting with epistaxis. The diagnosis must be consid
causes such as primary neoplasms or trauma need
ered because biopsy of the tumour is contraindicated
to be identified.
due to the potential for severe haemorrhage. The
appearance on CT imaging and angiography is
diagnostic.
Vascular anatomy
The nasal cavity and its mucosa is extremely vascu

lar, with supply from terminal branches of both the Epistaxis in adults
internal and external carotid arteries and frequent
anastomoses between the systems. The anterior sep The most common site for bleeding in adults is also
tum is the most frequent site for bleeding, with a the anterior septum, Little’s area. Bleeding usually
plexus of vessels known as Kiesselbach’s area or stops spontaneously and this may be facilitated by
Little’s area supplied by both systems. local pressure, applied by pinching the alar carti
lages to occlude the nasal airway. Bleeding sites
more posterior in the nasal cavity are more often
Epistaxis in children associated with severe bleeding and likely to
require hospitalisation, particularly in patients with
Nose bleeds in children most often occur from hypertension.
Little’s area on the septum. Bleeding is usually minor A common predisposing factor in adults with
and stops spontaneously. The site of bleeding can epistaxis is the use of blood thinning agents for
frequently be cauterised with silver nitrate using thromboembolic prophylaxis. Aspirin, warfarin
local anaesthetic. For uncooperative or younger and clopidogrel in particular are often taken alone
children, general anaesthesia is required and electro or in combination and may complicate manage
cautery may be used. ment of epistaxis. A high alcohol intake is also asso
For recurrent or more severe epistaxis, it is ciated with a higher incidence of epistaxis.
important to exclude conditions that may cause Epistaxis may occur secondary to a variety of
abnormal bleeding. These include acute leukaemia, local or systemic factors affecting the nasal mucosa.
thrombocytopenia and clotting factor deficiencies. • Trauma, such as nose picking or nasal fracture.
As many as 5–10% of children with recurrent • Inflammatory conditions: allergic, viral or bacte
epistaxis may have undiagnosed von Willibrands’s rial rhino‐sinusitis.
disease. • Granulomatous diseases.
711
712 Problem Solving
• Environmental irritation. may allow identification and control of the bleed

• Iatrogenic: following nasal or sinus surgery. ing site. During examination, unusual conditions
• Primary neoplasms: benign or malignant. such as tumours can be identified and dealt with
• Drugs: topical nasal steroids or cocaine abuse. after acute bleeding is controlled.
• Osler’s disease or hereditary haemorrhagic
telangectasia. Endoscopic sphenopalatine artery ligation
Assessment of patients with epistaxis must include
If bleeding cannot be controlled after endoscopic
adequate history, examination and investigation to
examination and cautery and/or nasal packing,
exclude such conditions.
then treatment under general anaesthesia may be
necessary. This provides the opportunity for better
examination of the nasal cavity. In the past it was
Management
the opportunity to insert a firmer nasal pack.
Currently, if direct cautery of bleeding points is not
Initial assessment should include estimation of the
effective, then clipping or diathermy of the spheno
amount of blood loss and whether there is a need
palatine artery is the accepted treatment for man
for immediate resuscitation and blood volume
agement of persistent posterior epistaxis.
replacement. Cardiac status and circulating blood
volume should be assessed and intravenous access Embolisation
obtained if necessary. Checking and correcting any
hypotension, anaemia or clotting deficiencies should Arterial embolisation can also be effective for con
be performed as required. trol of intractable epistaxis. The procedure carries
The key to controlling epistaxis is to establish risk of significant complications and so is reserved
both the site and the cause of bleeding so that the for patients with refractory epistaxis who are unfit
bleeding can be stopped and the cause treated. for surgery or in whom surgery has failed to control
the bleeding.
Headlight examination with local
anaesthesia
Further reading
Thorough examination of the nose with adequate
light and instrumentation is necessary. When bleed McGarry GW. Epistaxis. In: Gleeson M (ed.) Scott‐
ing is minor, or even when more severe, often the Brown’s Otolaryngology Head and Neck Surgery, 7th
bleeding site can be identified and controlled. edn, Vol 2. London: Hodder‐Arnold, 2008:1596–608.
Simmen DB, Jones NS. Epistaxis. In: Flint PW, Haughey
Chemical cautery with silver nitrate can be used, par
BH (eds) Cummings Otolaryngology Head and Neck
ticularly for anterior septal vessels; however, bipolar
Surgery, 6th edn, Vol 1. Philadelphia: Elsevier Saunders,
or even monopolar diathermy is more effective. 2015:678–90.
If the site for bleeding cannot be seen and con
trolled, then packing the nasal cavity usually pro
vides control. Most emergency departments have MCQs
specialised packing devices, inflatable balloons or
packing material for this purpose. Thorough topi Select the single correct answer to each question.
cal anaesthesia is required for nasal packing, other The correct answers can be found in the Answers
wise the procedure can be very painful. The pack is section at the end of the book.
usually left in place for 2 days and prophylactic
antibiotics administered. 1 Which of the following is the most common site for
bleeding in minor epistaxis?
a posterior septum
Nasal endoscopy
b inferior turbinate
Examination of the nasal cavity using rigid or flex c anterior septum
ible fibre‐optic endoscopes is now standard when d sphenopalatine artery
managing epistaxis. Whilst anterior sites for bleed
ing can be seen and controlled with a headlight, 2 Recurrent epistaxis in an elderly patient is not
nasal endoscopes have a vital role in defining and usually associated with which of the following?
treating posterior epistaxis. a hypertension
In acute epistaxis management, active bleeding b cardiac failure
is often reduced or stopped after initial topical c aspirin
anaesthesia and skilled endoscopic examination d clopidogrel
77: Epistaxis 713
3 Which of the following is the most likely cause for 4 For a patient with intractable bleeding, which of
epistaxis in a child? the following is not a treatment option?
a juvenile nasopharyngeal angiofibroma a ascending pharyngeal artery ligation
b rhabdomyosarcoma b nasal packing under general anaesthesia
c nasal fracture c angiography with embolisation
d a blood vessel on Little’s area d sphenopalatine artery ligation
78 Low back and leg pain
Jin W. Tee1,2,4 and Jeffrey V. Rosenfeld1,3
1
Alfred Health, Melbourne, Victoria, Australia
2
3
Monash Institute of Medical Engineering, Melbourne, Victoria, Australia
4
National Trauma Research Institute, Melbourne, Victoria, Australia
professions with repetitive lifting or very physical

Introduction work such as labourers, firefighters, paramedics,
nurses, police and army personnel. It is therefore an
Low back and leg pain, isolated or in conjunction,
important public health issue. Prevention is therefore
are amongst the most common reasons for general
the most important strategy to reduce the prevalence
practice consultations. They are mainly degenera-
of low back pain.
tive in cause but in some instances may be trau-
Leg pain in a dermatomal pattern is often due to
matic, oncological and infectious. These latter
nerve root compression and in most patients is
aetiologies are deemed ‘red flag’ conditions or neu-
benign and self‐limiting. Anatomically, the leg refers
rosurgical emergencies, and awareness of red flag
to that part of the lower limb below the knee,
symptoms and signs are paramount in ensuring safe
although when discussing leg pain, it commonly
and timely medical care.
refers to any part of the lower limb, i.e. the buttock,
This chapter covers the management principles
thigh, leg and foot.
required to assess and treat these conditions, both
There are a few terms that are regularly used
in the short and long term. The most important
when discussing leg pain: sciatica, claudication and
consideration regarding the successful long‐term
antalgic gait being the important ones.
management of low back and leg pain is that the
• Sciatica is a symptom not a disease. It is a syn-
spinal vertebrae and soft tissue structures (disc, lig-
drome characterised by pain radiating from the
aments, facet joint capsule) deteriorate with age.
back into the buttock and into the lower extrem-
Acute stressors of the spine are cumulative and
ity along its posterior or lateral aspect; the term
often in an active person, accelerate a natural ten-
is also used to describe pain in the distribution of
dency to symptomatic osteoarthritic degeneration.
the sciatic nerve.
As such, treating physicians must also be aware
• Claudication is a condition where the patient suf-
that genetic factors, underlying structural anoma-
fers lower limb pain on walking, possibly associ-
lies, occupation, pain tolerance, psychological fac-
ated with lameness or limping. It usually resolves
tors and social circumstances all contribute to the
on rest. A neural cause is likely when the patient
origin, persistence and success of the long‐term
has a stooped posture when ambulating, and
management of low back and leg pain.
when the symptoms dissipate on sitting and not
There are many possible pain generators in the
on standing. A vascular cause is likely when the
spine, including discs, ligaments, facet (zygapophy-
symptoms dissipate on standing alone.
seal) joints, nerve roots, paraspinal muscles and
• An antalgic gait is a limping gait as a result of a
extraspinal structures. It is often difficult to identify
painful lower limb and with avoidance of
the exact cause of back pain in particular, as the
mechanical stress on the affected side.
pain is often emanating from multiple structures at
multiple segmental levels in the spine. This makes
the treatment of low back pain especially problem-
atic, particularly as much of the treatment given for Applied anatomy
back pain is not based on a strong evidence base.
Importantly, low back pain results in a large finan- There are seven cervical vertebrae, twelve thoracic
cial cost to the community, especially as it afflicts vertebrae, five lumbar vertebrae and five sacral
715
716 Problem Solving
vertebrae. The spinal cord terminates in the adult at

Box 78.1 Differential diagnosis of low
the LI–L2 disc level, where it becomes the filum ter-
back pain
minale. The nerve roots of the cauda equina arise
from the conus medullaris and pass through the • Pancreatic disease, e.g. pancreatitis (high lumbar
lumbar and sacral canal. region)
The spinal nerve roots exit through the interver- • Renal disease, e.g. hydronephrosis (usually lateral
tebral foramina. There are eight cervical spinal loin pain)
nerve roots, so for example C7 passes across the • Abdominal aortic aneurysm
C6–C7 disc and exits the C6–C7 intervertebral • Pelvic disease
foramen. A posterolateral C6–C7 disc prolapse will • Rectum, bladder, gynaecological disease
therefore compress the C7 nerve root. As there are • Hip disease: there is pain on moving the hip; the
eight cervical roots and with C8 passing in the C7– pain may radiate to the buttock and posterior or
T1 foramen, the T1 nerve root passes out in the lateral thigh down to the knee
T1–T2 foramen. • Sacroiliitis
In the lumbar spine, each nerve root passes under • Lumbosacral plexus pathology
the pedicle of its numbered level, so for example the • Peripheral nerve pathology, e.g. schwannoma,
L5 nerve root passes inferiorly across the back of entrapment, inflammation
L4–L5 intervertebral disc to exit below the L5 pedi-
cle. Therefore, a posterolateral disc prolapse at L4–
with chronic back pain. Table 78.1 lists the com-
L5 will compress the L5 nerve root. A posterolateral
mon causes of leg pain.
disc prolapse at L5–S1 will compress the S1 nerve
root. A ‘far’ lateral disc prolapse may compress the
lumbar root passing beneath the pedicle above, so Musculo‐ligamentous strain
for example a far lateral disc prolapse at L4–L5 This is the commonest cause of acute back pain.
may compress the L4 nerve root. Usually there is an acute event such as a twisting,
bending or lifting motion. The pain is localised but
may spread to the buttock and upper thigh if from
Pain generators the lumbar region. There is spinal stiffness, local
paraspinal muscle tenderness but no abnormal neu-
Pain arising from the bones of the spine, ligaments, rological signs.
muscles or intervertebral discs is often called
mechanical back pain. There is a lot of crossover in
Intervertebral disc prolapse
segmental nerve supply in the lumbar spine between
different structures. The annulus of the interverte- This is a common problem. There is usually a back-
bral disc and the facet joints are supplied with nerve ground of pre‐existing weakening of spinal struc-
fibres. Pain from the disc (discogenic pain) or facet tures due to degeneration, and coupled with
joints is felt in the back centrally (somatic pain) but occurrences of high intra‐abdominal pressure and
may radiate to the buttock and upper thigh (somatic sudden flexion of the lumbar spine (repeated strain-
referred pain). Somatic back pain may also emanate ing and coughing) could lead to intervertebral disc
from musculoskeletal structures, bone and extraspi- prolapse. The fibrous annulus of the disc tears,
nal or paraspinal structures. Box 78.1 lists the com- allowing the softer nucleus of the disc to herniate or
mon differential diagnoses of low back pain. prolapse. If the prolapsed nucleus separates from the
Nerve root compression or irritation results in disc, it becomes a sequestrated fragment and may
radicular pain, which is sharp lancinating pain radi- not resolve with expectant treatment. The interver-
ating down the lower limb and which may pass into tebral disc usually prolapses in the posterolateral
the foot or down the arm into the hand. It may not direction and may compress the exiting spinal nerve
follow an exact dermatomal pattern. As the facet root, which is adjacent to it, and cause sciatica. In
joints are innervated by the nerve roots of that level the acute phase, the back pain is usually a minor
and the level above, it is often difficult to distin- component. Much less common is the central disc
guish somatic referred pain from radicular pain. prolapse, which compresses the spinal cord or the
The overall clinical assessment and correlation with cauda equina nerve roots depending on the spinal
the radiological findings is important. Local anaes- level. Cauda equina syndrome is a clinical syndrome
thetic facet joint blocks, which suppress facet joint that ensues as a result a major compressive lesion
pain, and intradiscal injections have also been used within the spinal canal, in this instance an acute disc
to identify the principal pain generators in patients prolapse. Based on the level of compression, this
78: Low back and leg pain 717
Table 78.1 Differential diagnosis of leg pain.
Clinical problem Presentation Region of pathology Pathology
Neural: spinal
Sciatica Radiating leg pain Nerve root Disc prolapse
compression in spinal Lateral recess stenosis
canal or exit foramen Osteophyte
Synovial cyst
Spondylolisthesis
Foraminal stenosis
Tumour
Neurogenic Bilateral leg pain, pins and Multiple roots under Lumbar canal stenosis
claudication needles, heaviness compression in the Facet hypertrophy
spinal canal Ligamentum flavum hypertrophy
Diffuse disc bulge
Spondylolisthesis
Venous hypertension Dural arteriovenous fistula
or ischaemia of the
spinal cord
Neural: peripheral nerve
Meralgia Burning pain, numbness Lateral cutaneous Entrapment under inguinal
paresthetica anterolateral thigh nerve of thigh ligament medial to anterior
superior iliac spine
Piriformis syndrome Pain in sciatic distribution Sciatic nerve Entrapment by piriformis muscle
Common peroneal Weak ankle dorsiflexion and Common peroneal Trapped as it winds around the
nerve entrapment anterolateral leg pain nerve head of fibula
Tarsal tunnel Burning pain in the plantar Posterior tibial nerve Flexor retinaculum from medial
syndrome surface of foot malleolus to calcaneus
Morton’s neuralgia Pain in third web space of foot Digital nerve in foot Compression between metatarsal
and adjacent toes heads
Vascular Acute vascular compromise
Vascular claudication
Varicose vein/venous insufficiency
Deep vein thrombosis
Joint/bony Degenerative arthritis
Rheumatoid arthritis
Bony pathology: fracture, infection,
malignancy
Soft tissue: muscle
Ligament
Joints: facet, sacroiliac, symphysis
pubis, hip, knee, ankle, foot
Referred Retroperitoneal pathology
Appendicitis
Inguinal hernia
Aortic dissection
Renal colic
Pelvic disease
causes severe bilateral sciatica, lower limb weak- common. Disc bulging (protrusion) occurs where
ness, paraesthesia or dysaesthesia, loss of proprio- there is no prolapse (or extrusion) of nucleus. This
ception, and bowel and bladder dysfunction. The is a common finding on CT or MRI and is not nec-
patient may develop acute urinary retention. essarily the cause of back pain and sciatica. Also,
Disc prolapse (Figure 78.1) is most frequent in thoracic disc prolapse may compress an intercostal
the lower lumbar spine (L4–L5, L5–S1) and in the nerve laterally and cause radiating pain in the dis-
lower cervical spine (C5–C6, C6–C7). These are tribution of that nerve or may cause spinal cord
also the levels where degenerative changes are most compression when central.
718 Problem Solving
(a) into the spinal epidural space by a needle puncture

or placement of an epidural catheter for analgesia.
This problem has been reported following child-
birth, with the mother developing severe back pain
and possibly neurological deficit in the weeks fol-
lowing the placement of an epidural catheter for
analgesia during labour. Discitis caused by a bacte-
rial infection following surgery or systemic bacte-
raemia may also cause acute (and chronic) back
pain.
Trauma
Trauma to the spine (Figure 78.2) may cause verte-
bral fractures, which may be unstable and may
cause neurological injury. These injuries cause acute
and often severe local pain and tenderness.
Vertebral collapse
Crushing of the anterior portion of the vertebral
body in the thoracic or lumbar region is common
following a hyperflexion injury to the spine. This
causes wedging of the affected vertebral bodies and
acute pain (severe, unrelenting). Wedging and verte-
bral collapse is also common in elderly patients and
(b) may be due to neoplastic infiltration (Figure 78.3),
osteoporosis or, less commonly, infection.
Haematoma
An acute subdural or epidural haematoma in the
thoracic spinal canal may cause acute cord com-
pression with severe back pain and paraparesis. The
cause of the bleed may be a ruptured vascular mal-
formation or a spontaneous bleed in a patient on
anticoagulants such as warfarin.
Spinal stroke
Fig. 78.1 (a) T2‐weighted sagittal MRI of lumbar spine Thrombotic occlusion of the anterior spinal artery
showing a smaller disc prolapse at L4/L5 and a larger usually in a patient with diffuse atherosclerotic vas-
disc prolapse at L5/S1. (b) T2‐weighted axial MRI of cular disease causes an acute paraplegia, with severe
lumbar spine showing a right‐sided posterolateral disc acute back pain in the thoracic region. Myelogram
prolapse (green arrow) compressing the S1 nerve root. or MRI does not show any compressive lesion but
MRI may show cord signal hyperintensity, which
Infection indicates oedema or developing infarction.
Osteomyelitis may be due to pyogenic infection

usually by haematogenous spread, or due to tuber- Clinical presentation
culosis. This will cause acute back pain (severe,
unrelenting) and may cause neurological deficit due History
to vertebral deformity, bony instability or second-
ary epidural abscess. Again, acute and severe com- A detailed history will provide a likely cause of the
pression of the thecal sac is a neurosurgical patient’s low back and leg pain, and should help to
emergency. distinguish mechanical, radicular and long tract
Primary epidural abscess may occur without symptoms. The age of the patient is an important
osteomyelitis, particularly if bacteria are introduced factor in the analysis of cause of back pain. Back
(a) (b)
Fig. 78.2 (a) Sagittal midline CT of lumbar spine (bone windows setting) showing an L1 vertebral body compression
fracture with distraction injury of the posterior elements (note the increase in superior–inferior dimensions of the T12
and L1 spinous processes and lamina). (b) T2‐weighted sagittal midline MRI of lumbar spine showing the L1 fracture
and distraction injury, which can be clearly seen as a hyperintensity between the T12 and L1 posterior elements.
pain can be caused by disorders of organs that are

not part of the musculoskeletal system (Box 78.1).
Degenerative spinal disorders

The commonest cause of sciatica is entrapment of
the nerve root in the lumbar spinal canal or the
exiting foramen by a disc prolapse or foraminal ste-
nosis secondary to degeneration. The pain is usually
unilateral and commonly involves one or more of
the nerves from L4 to S1. Patients complain of
sharp shooting pain, often originating in the but-
tock and radiating down the leg in the distribution
of the nerve root under pressure (the sciatic nerve is
not under pressure, rather a nerve root that contrib-
utes to the formation of the sciatic nerve). The pain
is often associated with numbness, pins and needles
and tingling, typically in a dermatomal pattern (see
Fig. 78.3 T2‐weighted sagittal midline MRI of lumbar Figure 78.4a for dermatomal patterns). Patients can
spine showing a destructive sacral hepatocellular go on to develop weakness (see Figure 78.4b for
carcinoma metastases and pathological fracture with myotomal patterns) in the distribution of the nerve
complete lumbar canal obliteration. root. Patients may occasionally develop leg pain as
720 Problem Solving
Lumbar segments
L2-Medial thigh
(a) L3-Medial knee
L4-Medial ankle, Great toe
L5-Dorsum of foot
T11 Social segments

T12 S1-Lateral foot
S1-Posteromedial thigh
L1
S2 S3-4,5-Perianal area
S3 L2 T12
L1
L2
L3
L4
L3 L5
S1
S3 S2
S4
L4 5
L5
S1
(b)
Function Muscles Segments
Hip adductors Adductor longus L2,3

and brevis
Knee extensors Quadriceps L3,4
Ankle dorsiflexors Tibialis anterior L4,5
Ankle Gastrocnemius
S1,2
plantarflexors soleus
Extensor hallucis
Great toe extensor L5,S1
longus
Sphincter ani
Anal sphincter S2,3,4
externus
Fig. 78.4 (a) Dermatomal pattern of sensory supply. Source: adapted from Netter FH. The CIBA Collection of Medical
Illustrations, Vol 1. Nervous System, Part II: Neurologic and Neuromuscular Disorders, p. 183. Reproduced with
permission of Elsevier. (b) Nerve root supply of muscles. Source: adapted from Netter FH. The CIBA Collection of
Medical Illustrations, Vol 1. Nervous System, Part II: Neurologic and Neuromuscular Disorders, p. 182. Reproduced with
a result of pressure on the L3 and rarely L2 nerve gravitational congestion of the leg. This results in
root, and this will radiate to the anterior thigh and a painful, achy, swollen leg that improves with
knee. rest and elevation of the leg. A major associated
The patient presents with an antalgic gait (where complication is thrombophlebitis and conse-
the gait is shortened on the painful side) and avoids quent risk of deep vein thrombosis. Surgery is
sitting or does so with the leg straightened at the hip indicated for major vascular incompetence.
and flexed at the knee. This posture tends to relieve
the stretch on the nerve and reduces pain levels. Joint/bone pain
Examination reveals limitation of straight leg
Joint pain as a result of acute inflammation, as seen
raising, limited back movements, altered sensation,
in rheumatoid disease, connective tissue disease,
and numbness or weakness in the distribution of
gout or septic arthritis, is often acute and associated
the nerve root. An absent reflex aids significantly in
with swelling, redness and tenderness of the joint
confirming the root involved.
with radiation up or down the leg.
Neurogenic claudication is characterised by bilat-
• Gout is a metabolic disorder characterised by an
eral leg pain, worse with walking but can be present
excess of uric acid in the blood. It usually pre-
when upright and standing still and improves with a
sents in middle‐aged men with rapid‐onset pain-
change in posture (as compared with vascular clau-
ful swelling of a joint, usually the first
dication, which resolves with rest, irrespective of the
metacarpophalangeal joint, which is red, hot and
posture of the patient). The pain is an ache‐like dis-
associated with proximal and distal pain. It must
comfort, often with pins and needles, heaviness and
be differentiated from septic arthritis and other
tiredness of the legs, with variable numbness and a
causes of leg pain.
sense of weakness with walking. Lumbar canal ste-
• Septic arthritis is often bacterial in origin, pre-
nosis is the commonest cause. Examination is often
sents with pain, swelling, redness and tenderness
unremarkable and hyporeflexia may be the only
of a joint with radiation. Inflammatory markers
finding. A vascular examination of skin circulation,
are abnormal and patients require antibiotics
and peripheral pulses is also required.
and possibly aspiration or irrigation of the joint.
Thoracic or cervical myelopathy is a rare cause of
• Pain from wearing down of the cartilage of the
leg pain. Occasionally compression or pathology in
articular surface is a progressive event and thus
the spinal cord in the thoracic or cervical spine can
the pain has an insidious nature and progresses
result in a syringomyelia (a cavity in the spinal
over a long period.
cord) that may result in leg pain.
• An injury or inflammation of the joint capsule,
tendon and muscle around a joint can also simu-
Vascular late joint pathology with secondary leg pain.
The vascular causes are described in greater detail Both muscle and joint pain can occur from meta-
in Chapters 55 and 57. bolic and connective tissue disorder, and thus
• Acute arterial vascular compromise: caused by these patients may require a blood screen with
trauma or acute arterial occlusion of a diseased measurement of erythrocyte sedimentation rate
artery by a thrombotic or embolic event. The (ESR), rheumatoid factor and antinuclear factor
patient presents with leg pain and paraesthesia and a rheumatology review.
with coldness, absence of pulses and pallor. Acute • Sacroiliitis and arthritic changes in the hip, knee,
intervention to restore circulation is vital to pre- ankle or arch of foot will cause local and radiat-
serve limb function. ing pain. Sacroiliac joint pain can radiate from
• Vascular claudication: a well‐recognised and the buttock into the upper thigh. Hip joint pain
common problem of leg pain, often calf pain. The can radiate down to the knee.
pain is worse with walking and improves with
rest. The pain is often a cramp‐like pain in the
Entrapment neuropathies
muscles of the legs with a sense of tiredness and The pain is restricted to the distribution of the nerve
fatigue. Pain at rest is present with very severe root and thus a good history and examination can
disease. This is a result of progressive arterioscle- often provide the diagnosis. These syndromes (mer-
rotic disease and the distribution of the pain algia paresthetica, piriformis syndrome, tarsal tunnel
reflects the site of arterial disease. Patients may syndrome, Morton’s neuralgia) present primarily
benefit from bypass surgery. with pain restricted to the distribution of the nerve
• Venous disease: incompetence of the valves of the under pressure (Table 78.1). Medical therapies with
veins of the lower limb results in progressive an anticonvulsant (carbamazepine) or antidepressant
722 Problem Solving
(amitriptyline) can provide good control of their Urgent MRI of the spine is mandated with any
symptoms. The alternative is a diagnostic and thera- patient complaining of saddle area numbness or dif-
peutic block with local anaesthesia and steroids. ficulty initiating micturition or incontinence. In these
Should this fail, surgical decompression of the nerve situations, a large disc prolapse or tumour causing
should be considered. cauda equina syndrome (compression of the cauda
equina – the lumbosacral nerve roots in the lumbar
Extraspinal pathology spine – resulting in sacral anaesthesia plus bowel and
bladder disturbance) needs exclusion. A cauda
Pathology of any of the structures in the abdomen,
equina syndrome is a neurosurgical emergency and
retroperitoneum and pelvis may cause local and
requires urgent neural decompressive surgery.
referred pain. In most of these patients, the referred
pain is likely to be non‐radiculopathic, with no der-
matomal pattern unless there is involvement of the
Examination
lumbosacral plexus.
The examination is done in the erect, prone and
Emergencies
supine positions. It is important to differentiate
The attending physician should always be on the between upper and lower motor neurone lesions
look out for red flag conditions presenting with and to identify the level of spinal pathology.
acute low back and/or leg pain (Box 78.2) These
conditions need urgent neurosurgical review, as Spine and joints
they are likely to require emergency surgical decom-
Standing
pression to treat neurological deficits, and fixation
to treat instability. Nocturnal pain and pain at rest Inspection for midline skin lesions such as a pit,
may indicate neural ischaemia from significant sinus, hairy patch, lipoma, naevus or angioma over
mechanical compression. A history of recent trauma the spine. These may indicate underlying occult spi-
and worsening pain on ambulation requires the nal bifida, spinal dysraphism or tethering of the spi-
exclusion of fracture. A history of weight loss and nal cord.
solid organ primary tumours implies metastatic Assess general posture and spinal alignment, par-
spread or primary lesions unless proven otherwise. ticularly for scoliosis or kyphosis. Are both feet
Fever, night sweats and rigors are symptoms sug- planted symmetrically on the ground? The cervical
gestive of an infection or haematological malig- spine and the lumbar spine normally have a lordo-
nancy including lymphoma. sis (forward curve).
A red flag is raised if the patient has bilateral lower Range of movement includes forward flexion,
limb symptoms such as numbness, weakness or pain. lateral flexion, rotation and extension. Examine the
shoulders and upper limbs if the patient has neck
pain.
Box 78.2 Key points and pitfalls
• Most back pain is benign in nature and cause, and Supine

usually resolves, even without treatment, in 3–4
weeks. Examine the movements of the hips and knees.
• It is important to try to differentiate radicular pain Examine the sacroiliac joint by adduction and
from musculoskeletal spinal pain and spinal cord internal rotation of the flexed hip.
compression.
• Hip pain may mimic sciatica due to compression of
Prone
a spinal nerve root.
• Back pain in children should not be ignored as it Palpate the back for tenderness, paraspinal mass,
often has a serious underlying cause. paraspinal muscle spasm. Percuss the spine for ten-
• Negative plain radiographs or CT scans do not derness. Complete the examination of the hip joint
exclude the presence of serious spinal pathology. with extension.
• Make sure adequate investigation of back pain is
undertaken at an early stage so that serious
Motor function
pathology is not missed.
• In patients with signs of spinal cord compression, Neurological examination
do not forget to examine perineal sensation or to
Even in the absence of limb pain a careful examina-
percuss the bladder.
tion must be made of the limbs, as the neurological
signs that may be detected will often lead you to the Anal reflex (S4–S5) involves contraction of the
precise site of pathology in or around the spine. subcutaneous portion of the external sphincter in
response to scratching the perianal skin.
Sacral sparing may occur within a widespread
Gait area of sensory loss caused by an intramedullary
Observe for limping, rate of movement, length of spinal cord lesion, and is due to the laminar arrange-
stride and need for walking aid. This will give many ment of the fibres in the spinothalamic tract. The
clues as to what is wrong and the severity. sacral segments are lateral in the tract. It thus means
there is an incomplete spinal cord problem and may
be the only sign of this.
Muscles
Muscle wasting and fasciculation imply denerva-
General examination
tion of muscles – examine all the muscle groups The examination includes chest, abdomen and
including the shoulder girdle and gluteal region. lymph nodes. Rectal and internal pelvic examina-
Muscle tone, power and reflexes including the plan- tions are done when relevant. In a patient with back
tars are measured to determine whether it is an or radicular pain always consider intra‐abdominal
upper or lower motor neurone problem, or a mixed and other pathologies as a cause for pain. Assess the
picture (see Figure 78.4). adequacy of the arterial circulation in the lower
limbs in the older patient.
Sensation
If you suspect a spinal cord lesion, then full sensory Investigation
testing should be performed. Test pain with pin-
prick (spinothalamic tracts) and light touch and Plain X‐rays
proprioception (dorsal columns). Figure 78.4 shows
the dermatomal distribution from T11 to S5. Do Plain X‐rays are often done as an initial screen for
not forget to test sacral, perianal and scrotal/vulval patients with back pain but have a low sensitivity.
sensation when relevant. Establish a sensory level Plain cervical X‐rays are also used as a routine
on the trunk for a suspected case of spinal cord screen in multiple trauma patients and other regions
compression. This will help with the localisation of of the spine if clinically indicated.
the pathology.
Dynamic (flexion–extension) views
Special tests These are plain radiographs, fluoroscopy or MRI
scans used to demonstrate mechanical instability of
Straight leg raising is normally to 90° with the
spinal segments.
patient in the supine position. Lift the whole
lower limb passively whilst it is straight, flexing at
Computed tomography
the hip joint. This stretches sciatic nerve roots.
Record the angle at which sciatica stops the Computed tomography is often ordered as the initial
movement. investigation for back pain. It shows the bony anat-
Lasègue’s stretch test is a test of pressure on the omy and the facet joints very clearly but is of variable
sciatic nerve. The ankle is dorsiflexed with the and often inferior quality at showing the soft tissues,
lower limb outstretched and flexed at the hip, plac- including the discs and intraspinal pathology.
ing extra stress on the sciatic nerve which, if already
tethered by some pathology such as a disc prolapse, Magnetic resonance imaging
will cause a sharp jab of pain.
MRI is now the main modality for spinal imaging
Femoral stretch test is a test of pressure on the
and has virtually replaced CT myelography because
upper lumbar nerve roots. The patient is prone and
it is non‐invasive and because of the extensive
the lower limb is extended at the hip, placing ten-
information provided in different projections
sion on the upper lumbar roots.
including the sagittal.
Rectal examination includes prostate and pelvis,
anal tone, external sphincter contraction (the
Myelography
patient tightens the anus with the gloved finger in
the rectum), perianal and perineal sensation. Assess The introduction of intrathecal contrast produces a
the abdomen for bladder fullness. myelogram that outlines the spinal roots and cord
724 Problem Solving
and is a dynamic study which can demonstrate a managed conservatively and surgery should be con-
spinal block of the subarachnoid space by a mass sidered as a last resort unless there is significant neu-
lesion. Myelography is often followed by CT (CT rological deficits causing functional impairment.
myelography) which shows the contrast on the Conservative treatments for acute back pain usu-
axial (horizontal) CT images. This modality is espe- ally trialled include rest and physiotherapy, which
cially useful in patients with previous metal compo- may include massage, traction, interferential heat
nents (obscures MRI images) and especially those treatment and manipulation. Chiropractic treat-
with MRI‐incompatible cardiac pacemakers and ment and acupuncture are alternatives, but should
deep brain stimulators. not be recommended when there is a spinal deform-
ity or significant radicular symptoms. Drugs include
SPECT‐CT nuclear medicine bone scan non‐steroidal anti‐inflammatory drugs (NSAIDs),
analgesics including opiates, nerve membrane stabi-
Single photon emission computed tomography lisers, muscle relaxants and steroids. Exercises such
(SPECT)‐CT is a fusion between a technetium‐ as Pilates are often not useful in treating acute back
labelled nuclear medicine bone scan and CT spine pain, but have a role once it has largely settled so as
imaging. The radionuclide is detected by a gamma to strengthen the paraspinal and abdominal mus-
camera. The cameras rotate over a 360° arc around cles, which are often weakened in patients with
the patient, allowing for reconstruction of images degenerative spinal disease and disc prolapse.
in three dimensions. This allows identification of More than 80% of patients with sciatica respond
hotspots, which if correlated with clinical history to non‐operative treatment. Patients also need to
and examination can lead to higher accuracy of spi- avoid factors that will exacerbate the pain, so should
nal element pain generators. These areas are then avoid heavy lifting, repetitive bending and twisting.
injected with local anaesthetic and corticosteroids The role of physiotherapy is to re‐educate the patient
to assess response. in terms of posture, exercises to strengthen back,
abdominal and pelvic muscles, and stretches.
Discography The role of warm/cold therapy, massage, acu-
Discography involves injection of the intervertebral puncture or hydrotherapy in the acute stage is
disc with contrast, which may show internal uncertain and unpredictable. The patient must be
derangement of the disc and may be used as a pro- cautioned against manipulation as it may precipi-
vocative test to identify the origin of back pain. This tate a larger disc prolapse and a cauda equina syn-
test has rapidly gone out of favour with poor evi- drome. In the acute setting the benefit from epidural
dence for its use. Instead, injection of local anaes- or foraminal steroids is not predictable and more
thetic and corticosteroid into the disc space is used likely to succeed in patients who have a small disc
occasionally to diagnose discal pain generators. bulge or a foraminal disc prolapse.
The role of non‐surgical treatment for neurogenic
claudication is limited in patients with significant
Biopsy and needle aspirate of vertebral or
symptoms. They may have some benefit from anal-
paraspinal disease
gesia, NSAIDs, physiotherapy and hydrotherapy;
Biopsy and needle aspirate under CT guidance is a however, in view of the mechanical compression,
useful diagnostic technique that may be used when decompression offers the best long‐term result.
open surgery is not indicated and provides speci-
mens for histopathology and microbiology analysis.
Operative treatment
Blood tests Surgical intervention is indicated in patients with
intractable pain, in those who fail to respond to
Blood tests, including blood cultures, full blood
medical therapy, and in those who have a neuro-
examination and inflammatory markers are per-
logical deficit. Patients are usually treated conserva-
formed selectively.
tively for a minimum of 6 weeks unless they present
with red flag conditions.
Microdiscectomy and neurolysis (freeing up the
Treatment
nerve root) are indicated for patients who have a
disc prolapse and have failed non‐operative treat-
Non‐operative treatment
ment. The microdiscectomy is done with magnifica-
Most back pain aetiologies are benign in nature, and tion of the surgeon’s view, a small skin incision,
usually resolve in 3–4 weeks with no treatment. minimal paraspinal muscle disruption, and minimal
Degenerative disease and disc prolapse are initially bony removal of lamina and adjacent ligament.
This surgery has a better than 90% success rate for relieve pain. This treatment remains controversial
control of the leg pain provided the clinical picture based on a conflicting evidence base.
matches the imaging.
Patients with lumbar canal stenosis require a
decompressive laminectomy, lateral recess decom- Further reading
pression (the lateral part of the spinal canal
where the nerve roots are compressed) and neu- Koes BW, van Tulder M, Lin C‐WC, Macedo LG, McAuley
rolysis. In either situation, the presence or poten- J, Maher C. An updated overview of clinical guidelines
for the management of non‐specific low back pain in
tial of instability will require consideration of an
primary care. Eur Spine J 2010;19:2075–94.
instrumented fusion in addition to the surgical
Lewis RA, Williams NH, Sutton AJ et al. Comparative
decompression. clinical effectiveness of management strategies for sci-
The potential success of spinal surgery for atica: systematic review and network meta‐analyses.
degenerative conditions depends on many factors. Spine J 2015;15:1461–77.
Predictors of a poor outcome are smokers, patients Lurie JD, Tosteson TD, Tosteson ANA et al. Surgical ver-
undergoing active litigation or those who are sus non‐operative treatment for lumbar disc herniation:
claiming compensation within the work‐cover sys- eight‐year results for the Spine Patient Outcomes
tem and having a predominant back pain symp- Research Trial (SPORT). Spine 2014;39:3–16.
tomatology. It is crucial that all patients are given Samanta J, Kendall J, Samanta A. 10‐minute consultation:
chronic low back pain. BMJ 2003;326(7388):535.
the full range of conservative management prior to
surgical intervention. This will include chronic
pain management if their symptoms are chronic
and disabling and where the surgical indications
MCQs
are uncertain. They would also need to be well
counselled regarding the goal of surgery, the poten-
tial complications, the lifestyle modification
required to ensure longevity of their spine con-
struct and, finally, appropriate expectations. 1 An L5–S1 posterolateral disc prolapse is most likely
It is pertinent that red flag conditions are diag- to cause which of the following?
nosed and treated emergently. Neural decompres- a pain from the buttock radiating down the back
sion, restoration of neural deficits and augmentation of the thigh and to the sole of the foot
of spinal structures conferring stability remain the b an L5 radiculopathy
mainstay of treatment of these conditions. c weakness of foot dorsiflexion
Acute or subacute spinal cord compression and d weakness of extensor hallucis longus
cauda equina syndrome are serious problems e an absent knee jerk
that require urgent referral to a neurosurgeon.
Emergency decompressive surgery may be required 2 Which of the following statements about cauda
to preserve neurological function and reverse neu- equina syndrome is correct?
rological deficit. Whether the decompression of a it is a benign clinical problem
the spinal canal is done via a posterior approach b requires urgent decompression
(laminectomy or costotransversectomy) or via an c has no influence on bladder function
anterior approach (anterior cervical, thoracotomy d can only be present if the patient has severe
or transabdominal) depends on the nature and site leg pain
of the pathology and the experience of the sur- e can be managed best with manipulation
geon. A diseased vertebral body may require exci-
sion and replacement by a prosthesis (intervertebral 3 A 30‐year‐old man presents with 1 week of right
‘cage’) and the stability of the spine may need sciatica and has numbness on the dorsum of his
to be restored with metallic internal fixation right foot and weak dorsiflexion at the ankle.
using rods, plates, pedicle screws and bone Which of the following is true?
grafts. Following such spinal surgery the patient a he probably has an L4–L5 disc prolapse, with
may require radiotherapy or chemotherapy for a compression of the L4 nerve root
neoplasm or prolonged antibiotic therapy for an b he needs an urgent CT myelogram
infection. c he can be managed initially with rest and
An osteoporotic vertebral collapse could be analgesics
treated with an injection of acrylic cement into the d he is likely to require surgery
affected vertebral body under radiological guidance e he should be encouraged to undertake spinal
to restore the volume and strength of the bone and extension exercises
726 Problem Solving
4 A 35‐year‐old woman presents with acute lumbar 5 A 30‐year‐old diabetic presents with a severe mid
back pain, bilateral sciatica, difficulty in voiding and lower thoracic pain, radiation of the pain to the
and on examination has weakness in the ankles mid‐abdomen, and on examination is tender in the
and feet, absent ankle reflexes and decreased thoracic spine at the level of T10, has weak lower
sensation in the soles of both feet. Which of the limbs and finds it difficult to walk. Which of the
following statements is incorrect? following statements is incorrect?
a she has developed an acute cauda equina a CT scan will be helpful as an initial investigation
compression b he should have a full blood examination
b she has developed an acute spinal cord and ESR
compression c he may have a dissecting aneursym of the aorta
c central disc prolapse at L5–S1 is a likely cause d a needle biopsy is indicated initially
d urgent MRI is required e MRI is indicated and urgent surgery should be
e urgent surgery will be required considered
79 Acute scrotal pain
Anthony Dat1 and Shomik Sengupta2
1,2
2
Scrotal ultrasound, if undertaken, may demon

Introduction and anatomy strate reduction of blood flow (Figure 79.2).
There are two types of torsion: intravaginal and
The scrotum is the pouch of skin that contains the
extravaginal. Intravaginal torsion is by far the most
testes, spermatic cords and associated structures
common type (95%) with torsion of the spermatic
(Figure 79.1). Embryologically, the scrotum devel
cord within the tunica vaginalis. Extravaginal tor
ops by fusion of the labioscrotal swellings and the
sion occurs almost exclusively in newborns as the
urogenital folds in the midline. The scrotum contains
tunica vaginalis is not adherent to the dartos. Thus,
the dartos muscle, a smooth muscle underlying the
the spermatic cord and tunica vaginalis can twist as
skin which contributes to its rugosity. Deep to this
a unit. Predisposing factors for torsion include
are the following layers covering the testes and sper
undescended testis (cryptorchidism) and the bell
matic cord: external spermatic fascia, cremasteric
clapper deformity (12% of the male population).
muscle (over the cord) and fascia, internal spermatic
This is a congenital abnormality where the tunica
fascia, tunica vaginalis and tunica albuginea. The
vaginalis has an abnormal fixation proximally on
cremaster muscle, supplied by the genital branch of
the spermatic cord, allowing greater mobility and
the genitofemoral nerve, allows the raising and
hence risk of torsion.
lowering of the testicle. This function allows for
Testicular torsion is a true surgical emergency
temperature regulation to optimise spermatogenesis
because viability of the testis is inversely related to
(which requires a temperature slightly lower than
duration of ischaemia. Ischaemia greater than
core body temperature). The contents of the sper
6 hours usually results in irreversible damage and
matic cord (vas deferens, testicular artery, pampini
loss of the testis. Thus, the diagnosis of torsion needs
form plexus, nerves and lymphatics) enter the
to be based mainly on clinical suspicion and should
scrotum via the inguinal canal.
lead to urgent surgical intervention to untwist the
Acute scrotal pain is a presenting complaint that
testicle and restore vascularity. This is usually under
requires a timely diagnosis. There are a number of
taken by surgical exploration of the scrotum,
differential diagnoses, ranging from the emergent
although external detorsion can also be attempted,
such as testicular torsion and incarcerated ingui
especially if there are unavoidable delays in organis
nal hernia to epididymo‐orchitis and varicocele.
ing surgery. Possible complications of testicular tor
A presumptive diagnosis can be obtained on history
sion include testicular infarction and atrophy or the
and physical examination in most cases.
development of anti‐sperm antibody, both of which
can lead to subfertility.
Torsion of appendages
Testicular torsion
Torsion of testicular appendages is the most common
Testicular torsion occurs due to twisting of the sper cause of acute scrotal pain in prepubertal children.
matic cord, a surgical emergency with an incidence The appendix testis (hydatid of Morgagni) is a rem
of 1 in 4000 in males under than the age of 25 nant of the paramesonephric or Müllerian duct and
years. Testicular torsion leads to vascular com is present in 92% of cases and found at the superior
promise, initially causing venous occlusion with pole of the testis. The appendix of the epididymis is
subsequent arterial ischaemia and infarction. a remnant of the mesonephric or Wolffian duct and
727
728 Problem Solving
(a)
Testicular
artery
Pampiniform
plexus
Vas deferens
Epididymis
Tunica
vaginalis
Testis
(b)
Dartos muscle in Scrotal skin
superficial fascia
External spermatic
Cremaster muscle in fascia
cremasteric fascia
Internal spermatic
Parietal
fascia
lamina of the
tunica vaginalis Visceral lamina of
the tunica vaginalis
Tunica albuginea Lobules of the
Septula testis testis
Mediastinum testis
Sinus epididymis Testicular veins
Epididymis
Artery of the vas
Testicular artery deferens
Vas deferens
Fig. 79.1 (a) Diagrammatic view of scrotal anatomy. (b) Cross‐section of testicular anatomy. Source: Ellis H,
Mahadevan V. Clinical Anatomy: Applied Anatomy for Students and Junior Doctors, 13th edn. Oxford: Wiley
Blackwell, 2013. Reproduced with permission of John Wiley & Sons.
79: Acute scrotal pain 729
Fig. 79.2 Ultrasound images demonstrating a reduction in blood flow in the right testicle consistent with testicular
torsion.
is present in about 25% of cases, usually near the Depending on the area of involvement, temporary
head of the epididymis. The clinical presentation can urinary diversion (either urethral or preferably
be similar to testicular torsion but with a peak age suprapubic catheter) or diverting colostomy or
of incidence between 7 and 12 years old. Torsion of rectal tube may be required. Anatomically, the
appendages can sometimes present with the ‘blue infection is usually superficial to Colles’ fascia of
dot’ sign, the blue infarcted appendage seen through the perineum, the dartos fascia of the scrotum
the scrotal skin. This sign occurs in 20% of people and Scarpa’s fascia of the anterior abdomen.
and mainly in those with fair skin. This condition is Orchidectomy is usually not required as the testes
usually self‐limiting with no adverse sequelae to have their own blood supply (testicular arteries and
fertility, although scrotal exploration is often under veins) independent to that of the scrotum.
taken if there is any diagnostic uncertainty.
Epididymo‐orchitis
Fournier’s gangrene Epididymo‐orchitis occurs due to an ascending
infection from the lower urinary tract. Most cases
Fournier’s gangrene is a form of necrotising fasciitis
in younger men are due to sexually transmitted
that is a surgical emergency requiring urgent debride
organisms such as Neisseria gonorrhoeae and
ment and broad‐spectrum antibiotics. It is potentially
Chlamydia trachomatis. Urethritis is usually pre
life‐threatening and most commonly arises secondar
sent in those with a sexually transmitted infection
ily from infections of the skin, anorectal region or
(STI)‐related cause. In older men, it is usually
urethra. Risk factors include diabetes mellitus, immu
due to Gram‐negative urinary pathogens such as
nosuppression or recent urethral instrumentation. It is
Escherichia coli. Epididymo‐orchitis can also occur
usually polymicrobial with a mixture of anaerobic
secondary to a number of systemic bacterial infec
and aerobic bacteria. Clinically, it starts as cellulitis
tions such as extrapulmonary tuberculosis, syphilis,
that rapidly spreads. Extreme pain, fever and evi
melioidosis and viral infections (e.g. mumps). On
dence of septic shock are key findings. Crepitus can
scrotal ultrasonogaphy, patients with epididymo‐
be felt secondary to gas gangrene. A high clinical sus
orchitis have increased blood flow to the epididymis
picion is necessary if there is a systemic inflammatory
or testicle (Figure 79.3). A reactive hydrocele may
response syndrome or septic shock out of proportion
also be present. Antibiotics are the mainstay of
to local findings.
treatment. Untreated epididymo‐orchitis can lead
Management involves intravenous fluid resuscita
to abscess formation, pyocele and infertility.
tion, intravenous broad‐spectrum antibiotics and
immediate surgical debridement of all necrotic
Inguinal hernia
tissue. A second look for further debridement and
washout should be performed 24–48 hours after A complicated inguinal hernia must be considered as
the initial procedure to assess further tissue viability. part of the work‐up of acute scrotal pain. Reducible
730 Problem Solving
Fig. 79.3 Ultrasound images demonstrating oedema and swelling of the epididymis (E) and testis (T) and a reactive
hydrocele (arrow) resulting from epididymo‐orchitis.
Testicular or paratesticular tumour

hernias can cause discomfort, but acute pain and ten
derness associated with an irreducible mass is con Characteristically, testicular or paratesticular
cerning for an incarcerated inguinal hernia. Bowel tumours present as a painless scrotal mass, although
contents within the hernia sac can infarct if emer a minority can present with pain particularly if
gency inguinal herniorrhaphy is not undertaken. A there is acute haemorrhage or infarction within the
history of known hernias or previous hernia surgery tumour. Testicular ultrasound should be used to
may exist. Key physical examination findings to sug further characterise if there is suspicion of malig
gest an inguinal hernia as cause of a scrotal mass nancy. Differentiation from an inflammatory mass
include the inability to get above the scrotal mass can sometimes be difficult, in which case close tem
and presence of bowel sounds over the mass. poral follow‐up with repeat imaging may be needed.
Hydrocele vehicle accidents. Penetrating injuries are secondary

to a projectile such as a gunshot wound. Degloving
This is a serous fluid collection sometimes resulting
(avulsion) injuries are the least common, with scrotal
from a defect in the tunica vaginalis, although most
skin being sheared off, for example, from clothing
adult hydroceles are idiopathic. It should be noted
getting caught in machinery. In the blunt trauma set
that some hydroceles can occur in those with a tes
ting, ultrasound can be useful for demonstrating evi
ticular tumour. In addition, a reactive hydrocele can
dence of testicular rupture. If testicular rupture is
form secondary to infection (e.g. orchitis). Thus,
present, the goal of surgery is to debride devascular
clinical and radiographic examination of the under
ised tissue and ensure closure of the tunica albuginea.
lying testicle and scrotal ultrasound is essential.
The aim is to preserve as much testicle as possible for
Clinical presentation is usually with swelling and
endocrine function and spermatogenesis.
subacute discomfort, with acute painful presenta
tion suggesting infection or haemorrhage. In those
patients with ongoing pain and discomfort, surgery Referred pain
can be undertaken, whereby the hydrocele sac is Referred pain from the abdomen, lower back or
excised and everted to prevent recurrence. upper thigh can present with scrotal pain and is
usually duller and not easily localised. Classic
Epididymal cyst or sperm granuloma examples of this are pain from ureteric colic caus
These epididymal pathologies are quite common, ing the typical ‘loin to groin’ pain or nerve root
and typically present with a palpable lump, occa pain arising from intervertebral disc prolapse.
sionally with mild discomfort. Acute pain occurs
rarely and may be indicative of infection or haem
orrhage. The diagnosis is usually obvious on clinical Assessment
examination, but may be confirmed by scrotal
ultrasound. Surgical excision is indicated only if History
symptoms are bothersome.
The following structure can be used as a template
for history taking.
Varicocele
Varicocele refers to the dilatation and tortuosity of
History of presenting complaint
the pampiniform plexus and should be seen as the
testicular version of varicose veins. It can occur in • Onset and duration of pain (testicular torsion is
up to 10% of men and is due to incompetent valves sudden onset and intense, epididymo‐orchitis is
in the testicular veins. The majority of varicoceles gradual and progresses from mild to more
occur on the left side. The pathophysiology is thought severe). Duration is key for prognosis in those
to be due to increased venous pressure within the with torsion
left renal vein and increased risk of valvular incom • Prior episodes (may indicate previous intermit
petence at the junction between the left testicular tent torsion that resolves)
vein and the left renal vein. Occasionally, it can be • History of trauma or symptoms of urinary tract
a presenting feature of a left renal tumour, hence infection (UTI) such as dysuria and frequency
the kidneys are usually assessed sonographically if • Presence of vomiting
a varicocele is found. An additional concern about • Concurrent fevers, chills and rigors (suggests
varicoceles is that they can be associated with infective cause)
subfertility due to increased testicular temperature • Patient fasting status, if need for theatre
secondary to vein dilatation. Treatment in the form
of a varicocelectomy or embolisation should be
considered for those with demonstrably impaired Past medical/surgical/medications history
sperm quality or quantity and ongoing severe pain. • Comorbidities and regular medications (e.g. anti
coagulants/antiplatelet medication due to bleed
Testicular trauma
ing risk)
The mechanism of testicular trauma can be divided • History of prior testicular pathologies (e.g.
into blunt, penetrating or degloving. In the Australian tumour, varicocele)
setting, it is predominantly blunt secondary to • Previous scrotal surgery
assaults, sporting injuries or, infrequently, motor • History of inguinal hernia
732 Problem Solving
Family history present with an intact cremasteric reflex. Thus the

presence of a cremasteric reflex does not neces
• Family history of testicular cancer
sarily rule out a diagnosis of torsion, especially if
there are other strong clinical findings of torsion
Social history present.
• Sexual history in those with suspected STI‐ Investigations

induced epididymo‐orchitis
In the setting of acute scrotal pain with clinical sus
picion of testicular torsion, investigations should
Examination not delay emergency scrotal exploration. In those
where diagnosis is uncertain and a timely ultra
Systematic examination includes the abdomen, sound Doppler of the scrotum can be sought, it
inguinal region and finally the perineum and scro has a sensitivity of 86–100% and specificity of
tum. Inspection should be followed by palpation. 75–100%. Findings consistent with torsion include
testicular parenchymal heterogeneity and reduced
Inspection or absent Doppler colour flow compared with the
contralateral testis. Scrotal ultrasound is most use
• Perineal or scrotal masses or wounds
ful in confirming diagnoses other than torsion, such
• Previous scrotal and inguinal hernia surgical scars
as epididymo‐orchitis.
• Presence of erythema, crepitus and swelling
Besides this, investigations that are useful include
(marking the extent of erythema is useful in
midstream urine for microscopy, culture and sensi
assessing response to treatment)
tivity for UTI; first‐void urine sample for nucleic acid
• Dilated varicosities for varicocele (‘bag of
amplification testing (polymerase chain reaction,
worms’); can perform Valsalva manoeuvre to
PCR) for C. trachomatis and N. gonorrhoeae;
enlarge varicosities
and urethral swab for Gram stain and culture for
• Lie of testicle (should be vertical)
N. gonorrhoeae if there is suspicion of STI.
• Check for urethral discharge
Management
Palpation
• If scrotal mass present, characterise size, location, When findings support or raise suspicion for tes
consistency (e.g. hard, fluctuant), transillumina ticular torsion, emergency scrotal exploration and
tion with a pen torch (in case of hydrocele) and detorsion is indicated and should not be delayed, as
presence of concurrent tenderness discussed previously. If the testicle is viable, both
• Check inguinal ring for presence of hernia and testes should be surgically fixed to the scrotum
whether reducible (orchidopexy). Orchidectomy is reserved for non‐
• Palpate testes and epididymis for tenderness and viable testicles. Time is critical in successful salvage
lie (note that patients with torsion will do every rates. Detorsion within 6 hours results in a salvage
thing they can to prevent you from examining rate of 90% and higher. This falls significantly to
due to pain) 20% after 12 hours and 0–10% after 24 hours.
• Elicit cremasteric reflex (see following) For epididymo‐orchitis, antibiotic treatment
Testicular torsion is characterised by a high‐lying against the causative organisms is the mainstay, with
testicle that is exquisitely tender and which may selection of agents guided by local antibiotic guide
preclude full examination. The affected testis may lines. Sexually acquired infection should be treated
also be in a horizontal orientation due to the tor with ceftriaxone 500 mg i.v. stat plus azithromycin
sion as opposed to the normal vertical lie. Testicular 1 g oral stat. Subsequent maintenance treatment is
torsion has been associated with an absent cremas doxycycline 100 mg oral 12‐hourly for 2 weeks or
teric reflex. This reflex, mediated by the genitofem azithromycin 1 g oral as a single dose 1 week later
oral nerve which supplies the cremaster muscle, (if the patient is suspected to be non‐adherent to dox
normally presents after the age of 2 years and is ycycline). For those with non‐sexually acquired infec
elicited by scratching the medial thigh with result tions, trimethoprim or a quinolone (e.g. ciprofloxacin,
ant testis elevation. It is thought that the reflex cor norfloxacin) for 2 weeks is required. Symptomatic
relates with normal testicular perfusion. However, relief may be provided by scrotal support and anal
up to 10% of men with testicular torsion can gesics or anti‐inflammatories.
1 Which of the following symptoms and signs is not

Conclusions commonly found in testicular torsion?
a high‐riding testicle
Acute scrotal pain has a limited range of differentials. b vomiting
Despite this, it has a number of important diagnoses c transverse lie of testicle
that require timely surgical management. These d haematuria
include testicular torsion, Fournier’s gangrene, tes e acute severe testicular pain
ticular rupture and incarcerated inguinal hernia. If
clinically indicated, management should not be 2 Which of the following is the most appropriate next
delayed by ultrasound imaging as ‘time is testis’. step for a clinically suspected testicular torsion?
a organise Doppler testicular ultrasound
b start on intravenous antibiotics and review again
Further reading in 24 hours
c proceed to scrotal exploration and orchidopexy
Jaison A, Mitra B, Cameron P, Sengupta S. Use of ultra
sound and surgery in adults with acute scrotal pain. d organise computed tomography of the scrotum
ANZ J Surg 2011;81:366–70. e discharge the patient and organise review in
Metzdorf M, Barthold JS. Torsion, testis and testicular outpatient clinic in 2 weeks
appendages. In: Gomella LG (ed.) The 5‐Minute Urology
Consult, 2nd edn. Philadelphia: Wolters Kluwer/Lippincott 3 Which of the following is not associated with
Williams and Wilkins, 2010. epididymo‐orchitis?
Srinath H. Acute scrotal pain. Aust Fam Physician a bell clapper deformity
2013;42:790–2. b fever
c history of urinary tract infection
d recent urethral instrumentation
MCQs e sexually transmitted infection

80 Post‐traumatic confusion
John Laidlaw
irreversible, and given an optimal cellular environ

Introduction ment some or many of these cells can recover.
Even after relatively minor trauma, a very signifi
The term ‘confusion’ is widely used but not dis
cant head injury can occur. Indeed, it is often not
cretely defined. In medical situations confusion
recognised that a fall from a standing position
typically refers to a disordered state characterised
resulting in direct head impact can commonly cause
by lack of clear and orderly thought and/or behav
a fatal brain injury. Therefore, post‐traumatic con
iour. Common features include inattentiveness and
fusion must always raise a high degree of suspicion
altered perception of the world (disorientation in
for a significant head injury, with altered brain
time, place and/or person, and occasionally halluci
function immediately after the trauma being highly
nations) with these features commonly resulting in
suggestive of a primary brain injury, and delayed
the patient demonstrating uncooperative behaviour
onset suggesting secondary brain injury (e.g. hypoxia,
and agitation. Although the term ‘delirium’ is also
poor cerebral perfusion, expanding intracranial
often used interchangeably with the term ‘acute
haematoma).
confusional state’, this adds further confusion and
Although a normal CT scan of the brain follow
will not be used further in this chapter.
ing trauma is somewhat reassuring, it needs to be
It must be appreciated therefore that post‐
remembered that this does not exclude a significant
traumatic confusion is a clinical finding, but not in
brain injury; indeed, DAI may have a normal early
itself a diagnosis. It is not confined to patients with
CT scan (if present, the ‘pathognomonic’ petechial
brain injuries and is not uncommon following other
haemorrhages seen in the subcortical regions,
injuries. It can occur at any age, although is more
splenium and tectal plate are a result of small vessel
commonly identified in very young and also elderly
shear injury, and the axonal injury is implied but
patients. Being a clear demonstration of abnormal
not directly demonstrable on the scan).
brain function, the need to identify and treat the
It is also important to remember that a minor
pathology underlying post‐traumatic confusion is
traumatic brain injury (mTBI) can sometimes fail
of critical importance.
to be identified, particularly in intoxicated
patients but also in those with multiple other inju
ries. The terms ‘concussion’ and ‘post‐traumatic
Aetiology and pathogenesis (Box 80.1)
amnesia’ (PTA) are often applied to mTBI patients
with post‐traumatic confusion and a brain CT that
Primary brain injury
is normal or only has minor changes. These terms
Primary brain injury occurs at the time of the are not strictly interchangeable, and there is insti
trauma. This includes direct neuroglial injury that tutional variability in the defining criteria.
can be relatively focal at the major points of impact Concussion is generally considered to be a pre
or can occur throughout the brain following blunt dominantly transient alteration in neurological
head trauma, the diffuse form being referred to as function following head trauma, with the cerebral
diffuse axonal injury (DAI). Direct damage to the injury being predominantly functional rather than
cortical vessels causing haemorrhagic contusions is structural. Its major features are confusion and
also usually included in the primary brain injury amnesia following cerebral trauma, often follow
group. One of the main principles of brain injury ing a brief period of loss of consciousness, usually
management is that not all damage to neurones is associated with minimal evidence of structural
735
736 Problem Solving
Box 80.1 Causes of post‐traumatic confusion
Head injury • Subdural empyema

Primary brain injury • Intracerebral abscess
• Diffuse axonal injury • Septic venous sinus thrombosis
• Cerebral contusions
General/metabolic
Secondary brain injury • Hypoxia
Hypoxia • Hypercapnia
• Hypoxaemia due to respiratory causes • Acid–base problems (particularly acidosis)
–– Aspiration –– Metabolic
–– Pulmonary contusions ▪▪ Renal failure
–– Pulmonary oedema ▪▪ Lactic acidosis
–– Pulmonary thromboembolism ▪▪ Diabetic ketoacidosis
–– Pulmonary fat embolism –– Respiratory
–– Hypoxaemia due to anaemia • Electrolyte imbalance
–– Sodium
Cerebral ischaemia
▪▪ Hyponatraemia
• Shock
▪▪ Hypernatraemia (unusual to cause confusion)
• Vascular injury (particularly arterial dissection)
–– Calcium
• Thromboembolism
▪▪ Hypocalcaemia
–– Thromboembolic
• Glucose
–– Cerebral fat emboli
–– Diabetic hyperglycaemia/ketoacidosis
–– Disseminated intravascular coagulation
–– Hypoglycaemia (usually seen in treated diabetics)
• Raised ICP (CPP = MAP – ICP)
• Infection
–– Intracranial haematoma
–– Septicaemia
▪▪ EDH
▪▪ Primary (iatrogenic, i.v. lines, etc.)
▪▪ Acute SDH
▪▪ Secondary (to other infection)
▪▪ Intracerebral haematoma and enlarging
–– Pulmonary
contusions
–– Urinary
▪▪ Chronic SDH
–– Wound
–– Hydrocephalus
• Nutritional
▪▪ Obstructive
–– Vitamin B12 deficiency
▪▪ Communicating
–– Brain swelling Drug intoxication/withdrawal
▪▪ Vascular • Medication
Vasodilatation –– Sedatives and tranquillisers
–– Post‐traumatic (usually children) –– Analgesics (particularly narcotics)
–– Hypercapnia –– Steroids (although not usually indicated in trauma)
Venous engorgement –– Anticonvulsants
–– Jugular compression or obstruction –– Hypoglycaemic agents
–– Sinus thrombosis or obstruction • Non‐medicinal
▪▪ Oedema –– Alcohol
• Vasogenic –– Narcotic
• Cytotoxic –– Hallucinogens
• Hyponatraemia –– Cocaine
–– Solvents
Infection
• Meningitis CPP, cerebral perfusion pressure; MAP, mean arterial pressure;
• Epidural abscess EDH, extradural haematoma; SDH, subdural haematoma.
cerebral injury on imaging, and typically has a necessarily imply a good prognosis. These terms
good prognosis for spontaneous recovery. PTA has (concussion and PTA) have been mentioned
similar clinical features, but occurs also after more because of their widespread usage, but I would
significant brain injuries, and does not imply mini encourage clinicians in the acute clinical settings to
mal structural brain injury and nor does it avoid their use when possible.
80: Post‐traumatic confusion 737
Secondary brain injury Scale (GCS; Table 80.1). Please note that ‘confused’
is not an adequate descriptor of conscious state,
Secondary brain injury occurs after the trauma, and
and conscious state assessment demands the GCS
its prevention is the primary focus of most therapy
be documented (eye opening, best motor response,
for brain injury. The most common preventable
and verbal response). If previous GCS has been
causes are hypoxia, cerebral ischaemia secondary to
charted, the degree and rapidity of the change
hypotension or vascular injury, raised intracranial
should be noted. A very rapid assessment for later
pressure (most commonly due to intracranial hae
alising neurological signs should then be performed
matomas and brain swelling) and seizures. A host of
(particularly looking for pupillary inequality, gaze
other factors can also contribute to secondary
palsies, and obvious differences in motor function
brain injury, and these include fever, infection,
on one side).
hyperglycaemia, hyponatraemia and other meta
At this point the clinician should be aware whether
bolic conditions. It is also recognised that complex
urgent action is required, or if a more detailed clini
biochemical cascades are activated at a cellular level
cal assessment is appropriate. Inadequate airway,
following trauma, and these events (e.g. free radical
respiratory failure, or a GCS score below 9 demand
formation) are significant contributing factors to
urgent attention to the airway (optimally, immediate
secondary brain injury. An important principle to
endotracheal intubation). Circulatory failure
recognise is the increased susceptibility of the
requires urgent investigation and support, with par
recently injured brain to secondary insults; rela
ticular attention to cardiac, thromboembolic and
tively mild hypoxia or hypotension that would be
concealed blood loss in a post‐trauma patient. New
readily tolerated by a normal brain can cause sig
lateralising neurological signs and/or a rapid fall in
nificant further damage to an injured brain.
GCS score of 2 points or more require an urgent
brain CT.
Causes of post‐traumatic confusion not However, the vast majority of patients do not
directly related to brain injury have these sentinel indicators, and in each a
Even in the absence of a brain injury, a broad range methodical and detailed examination should be
of pathologies can cause confusion in a patient fol performed. This includes a detailed general exami
lowing trauma. These include hypoxia and hypo nation, with particular attention to the respiratory
tension, infections, medication, non‐prescribed system and also looking for evidence of infection,
drugs (substance effect and withdrawal), electrolyte and a full neurological examination (also of course
abnormalities and metabolic problems. Confusion looking for any evidence of meningism). The drug
is commonly the first presentation and the underly charts should be examined and considered, and if
ing pathology not necessarily clinically obvious, possible a history of alcohol and substance abuse
necessitating a high level of suspicion and appropri and/or withdrawal should also be considered.
ate investigation.
Investigation
Management of patient with post‐
The investigations and their urgency are dictated
traumatic confusion (Box 80.2)
by the clinical assessment findings. However, the
majority of cases of post‐traumatic confusion
Clinical assessment
require strong consideration for the following
Post‐traumatic confusion is not uncommonly a sen investigations.
tinel for serious underlying pathology and demands • Arterial blood gas examination: note that normal
rapid and detailed medical assessment. Immediate oxygen saturation monitoring is usually not
attention to ‘ABC’ is of course required: adequacy adequate alone, and measurement of Pao2, Paco2,
of the patient’s airway (which must not only be pat bicarbonate, pH and base excess provide evi
ent but protected by a good cough or gag), breath dence not just for respiratory failure but are also
ing (including oxygen saturation and arterial blood rapidly available indicators suggesting other
gas in most cases) and circulatory sufficiency (heart serious pathologies (e.g. pulmonary embolus,
rate and rhythm, peripheral perfusion and chest sepsis, diabetic ketoacidosis).
auscultation). The vital signs chart provides much • Venepuncture: full blood examination (haemo
but not all of the necessary information for this globin, red cell count, white cell count and platelet
immediate assessment. The patient’s conscious state count), electrolytes, urea and creatinine, liver
needs formal assessment using the Glasgow Coma function, calcium and phosphate, blood glucose.
738 Problem Solving
Box 80.2 Management of post‐traumatic confusion
Clinical assessment –– Recognition of legal incompetency

• Physical examination –– Relevancy to consent and refusal of treatment
–– Airway, breathing, circulation immediately, then
general examination Specific management of the cause of confusion
• Neurological examination • Intracranial lesions
–– Particularly note GCS, papillary inequality or other –– Immediate neurosurgical opinion for all
focal neurological deficit, and meningism –– Usually surgical decompression if mass effect, and
relatively urgent if a patient is developing lateralising
Investigation signs or deteriorating GCS
• CT scan brain (urgent if GCS score falls >2 points, or –– Consider arterial dissection if lateralising neurology
focal neurological signs) and normal CT/infarction
• Arterial blood gas analysis (Pao2, Paco2, bicarbonate, –– Perform lumbar puncture and urgent CSF analysis
pH, base excess) for meningitis (check CT normal first) if no other
• Full blood examination (haemoglobin, RCC, WCC, cause of confusion or risk factors for meningitis
platelets) (compound fracture, skull base fracture, CSF leak,
• Urea, creatinine and electrolytes pneumocephalus, ICP monitor, ventricular drain,
• Calcium/phosphate cranial surgery)
• Septic work‐up (wound swabs, blood cultures, urine • Hypoxia and respiratory disturbance
analysis and culture, chest X‐ray, ± CSF analysis) –– Oxygen supplementation
–– Immediate intubation if:
General management of confused patient ▪▪ Airway not patent and protected (cough and
• Environmental gag)
–– Close monitoring and supervision ▪▪ Respiratory failure
–– Protection ▪▪ Note spinal precautions for all intubations, but do
–– Quiet environment if possible not delay for spinal investigation

• Sedation avoided if at all possible • Electrolyte disturbance
–– If absolutely required, best to use only short‐acting –– Appropriate fluid and electrolyte therapy
parenteral (i.v.) sedatives in small doses titrated to • Infection
effect, closely supervised –– Appropriate antibiotic therapy instituted immedi-
• Analgesia if required ately after cultures, and modified when culture and
–– If narcotic, only small frequent i.v. doses (e.g. sensitivities known
morphine 1–2 mg p.r.n.) titrated carefully, with the • Medications and non‐medicinal drugs
patient closely supervised (not intramuscular or –– Medications scrutinised
subcutaneous) –– Drug and alcohol history determined
Table 80.1 Glasgow Coma Scale.
Score Best eye opening (E) Best verbal (V) Best motor (M)
6 Obeys
5 Orientated Localises pain
4 Spontaneous Confused Withdraws to pain
3 To speech Inappropriate words Abnormal flexion to pain (‘decorticate’)
2 To pain Incomprehensible sounds Extension to pain (‘decerebrate’)
1 None None None
GCS = E + V + M.
Worst score is 3, best is 15.
Use best response if differences between sides for eye opening or motor function.
GCS measures only conscious state, not neurological deficit.
• CT brain: this is urgent if there is a rapid fall in Patients with post‐traumatic confusion are also
GCS score of 2 points or more, or if there are commonly very sensitive to sedatives, and on occa
localising (lateralising) neurological signs. sion a relatively small incremental dose increase
• Septic work‐up: blood cultures, urine microscopy can cause respiratory depression and compromise
and culture, chest X‐ray and sputum culture, airway protection. Also, in patients with raised
changing intravenous lines, wound swabs, and intracranial pressure (ICP) the effect of the sedation
lumbar puncture if meningism and CT shows no controlling the agitation causes a reduction in the
intracranial mass lesion. associated hyperventilation, and in doing so can
trigger a cascade of escalating intracranial hyperten
sion and cerebral herniation. Therefore, if sedation
General management of the confused patient is to be used in these patients it needs to be deter
mined that the appropriate level of vigilance and
The primary management goals are always to diag the appropriate facilities for emergency airway
nose the causative pathology and then treat appro support are available.
priately. However, there are a number of general A major concern with sedation is that it can mask
management strategies for confused patients that neurological deterioration from other causes. It is
warrant further discussion. therefore unwise to use sedation in confused
patients who have not had dangerous intracranial
Environmental (such as expanding intracranial haematoma, brain
swelling, hydrocephalus, meningitis) or metabolic
A safe environment for a confused patient requires (particularly hypoxic) problems excluded, and
close supervision by experienced nursing and medi even then staff should be cautioned regarding the
cal staff in order to protect the patient from harm dangers of attributing any significant deteriora
and also to detect any further neurological deterio tion in conscious state or any other neurological
ration in a timely manner. A busy ward environ deterioration to the sedative. If sedation is con
ment often causes more agitation and a quiet sidered necessary in the acute post‐traumatic
environment is optimal, but this should not be at period, then a shorter‐acting benzodiazepine such
the expense of close supervision. Confused patients as clonazepam in small doses intravenously that
are often agitated, and this often responds to calm can be titrated for immediate effect has signifi
reassurance with minimal extraneous stimulation. cantly less risk than longer‐acting medication (e.g.
Falls are a significant risk for confused patients, diazepam) or medication given by other routes
and padded bed‐sides and other protective strate (oral or intramuscular).
gies must be employed. A Craig bed, allowing a
confused patient to be nursed at floor level with
padded safety barriers, is useful for those who are Analgesia
medically and orthopaedically stable in the post‐ Analgesia is an important in management of the
acute period. patient with post‐traumatic confusion, particularly
On occasions physical restraint is required for in those with multisystem trauma. Inadequate anal
patient safety, although these restraints can often gesia is unlikely to cause confusion but is likely to
frighten the patient, lead to more agitation and are cause a confused patient to become agitated and
not without risk. Restrained confused patients are uncooperative.
at risk of becoming entangled, experiencing respira Patients with isolated head injuries often have
tory restriction, or sustaining pressure injury or headache, but it should be recognised that severe
other injuries arising from the restraint itself. It headache is the exception rather than the rule. Oral
must be stressed that if a patient is restrained, there or intravenous paracetamol is commonly very effi
is a need for closer supervision not less. cacious for these headaches, and its regular use in
the early post‐traumatic period is recommended.
Non‐steroidal anti‐inflammatory agents used in
Sedation
combination with paracetamol can also be very
Sedation is best avoided in confused patients if at all effective after the acute period, although their anti
possible and should be used only when there are platelet affect and gastric ulceration side effects
serious concerns that patient agitation poses a sig usually preclude their consideration in the first
nificant risk of harm to the patient. Sedatives them week or so after a significant trauma.
selves may cause confusion, and sedation might Narcotic agents may themselves cause confusion
aggravate the situation in a confused patient. but are at times necessary in the acute post‐trauma
740 Problem Solving
period. It needs to be remembered that narcotic use The inability of the confused patient to provide
in head injured patients has significant risks, includ valid medical consent also of course implies that
ing the sedative effect masking deteriorating con the patient’s ability to make a valid decision to
scious state from other causes, the analgesic effect refuse treatment is also compromised. If a confused
hiding the headache associated with raised ICP or patient refuses necessary treatment or threatens to
meningitis, and the respiratory depression (with abscond or discharge themselves against medical
secondary rise in ICP), vomiting (with aspiration in advice, the same procedural steps should be fol
a poorly protected airway) and pupillary constriction. lowed as for obtaining consent in the jurisdiction.
Therefore, if narcotics are used I would recomend It should be stressed that refusal of treatment by a
frequent small intravenous doses that are rapid in confused patient in no way absolves the clinician of
onset and which can be titrated for immediate the responsibility for that patient’s ongoing welfare.
effect and have a predictable and short duration of Although at times formal declarations of legal
action that allows for assessment of neurological incompetence and compulsory treatment orders are
deterioration. For these same reasons I would required, most situations can be resolved with quiet
strongly argue against the use of oral, subcutaneous reassurance of the confused patient, particularly if
or intramuscular narcotics in the post‐traumatic the assistance of a trusted friend or family member
confused patient. can be a obtained.
Orthopaedic injuries require significant analge
sia, usually narcotic, at presentation. However, it
must be remembered that the simple act of bracing Specific management of the cause
and stabilising a fracture will provide very effective of confusion
pain control. Failure to provide adequate pain relief Identification of the cause and its appropriate
to those with painful chest and abdominal injuries treatment is the primary management goal in post‐
will predispose to respiratory compromise and traumatic confusion.
chest infection. Clinical input from a specialist
anaesthetist regarding the potential use of intercos
Intracranial lesions
tal blocks and epidural analgesia is also valuable in
these situations. In a multisystem trauma patient A CT scan of the brain is required for any patient
who has a head injury and/or is confused, my com with significant post‐traumatic confusion, and con
ments regarding analgesia are still very valid. sideration should be given to repeating that scan if
Narcotics typically are required in these cases, but there is further deterioration in the absence of
their associated risks are not only those mentioned another cause being identified. CT will identify the
in reference to the head injury, but also of obscuring majority of readily treatable intracranial patholo
the worsening pain that should alert clinicians to gies causing post‐traumatic confusion, including
abdominal complications or compartment syn intracranial haematomas (extradural, subdural,
dromes. Therefore, I reiterate the recommendation intracerebral and cerebral contusions), pneumo
that narcotics be used only by the intravenous route cephalus and hydrocephalus. These conditions typi
in the acute period. cally require surgical treatment and necessitate
urgent neurosurgical consultation. Acute haemato
mas typically are composed of solid clot and there
Legal competency
fore require a craniotomy (rather than a burr‐hole)
A confused patient is not legally competent and for evacuation. Hydrocephalus is recognised by ven
therefore cannot provide valid consent for medical tricular enlargement and needs a burr‐hole for cere
procedures. Almost all legal jurisdictions have pro brospinal fluid (CSF) diversion (e.g. a ventricular
visions to allow necessary urgent procedures to be drain or ventriculoperitoneal shunt). The urgency of
performed in the absence of consent, and therefore the surgery is dictated by the patient’s clinical condi
any urgent treatment required for the welfare of a tion, the rapidity of clinical deterioration and, for
confused patient should not be withheld because of unilateral lesions, the mass effect of the lesion (par
the absence of consent. There are provisions for ticularly the amount of midline shift on an axial CT
another person/legal authority to be authorised to scan). Pneumocephalus, unlike the other conditions,
make medical decisions on the patient’s behalf. rarely causes major mass effect and therefore does
However, the qualifications of that person and their not usually require surgery for evacuation. However,
relationship to the patient vary between jurisdictions it is very important to note (even if only one or two
and it is required that practitioners are aware of tiny intracranial air bubbles) on a post‐trauma CT
local requirements. in that it implies a compound skull fracture,
typically through the paranasal sinuses. These skull complete arterial occlusion and immediate stroke,
base fractures might not be obvious on a standard it is not uncommon for the intimal flap to be caus
axial CT of the brain. Pneumocephalus (or the clini ing only arterial stenosis and/or platelet aggrega
cal findings of CSF rhinorrhoea/otorrhoea or CT tion for some time, with later arterial occlusion or
evidence of skull base fractures) indicates that the thromboembolism causing delayed stroke. It is
patient is at risk of meningitis, the onset of which therefore important to consider this diagnosis,
may be weeks, months or years after the head injury particularly if there are unilateral neurological
and after the resolution of all other clinical findings. symptoms/signs and a normal brain scan, because
There is some controversy as to whether prophylac recognition of a dissection (often using CT angi
tic antibiotics are appropriate, with their use ography) and timely treatment may prevent an
becoming less common in the absence of infection. established stroke. Acute cerebral infarction
However, pneumocephalus and/or skull base frac (stroke) typically does not show abnormalities on a
ture indicates the need for nasopharyngeal swabs to CT scan in the first few hours, except if detailed
identify potential pathogens, and also avoidance of perfusion scans are requested. After the first few
positive pressure mask ventilation or blowing of hours, when the infarct is established, there is
nose (both of which can increase the risks of menin hypodensity identified in the area with, typically,
gitis and also of tension pneumocephalus). swelling of this infarcted brain occurring 12–48
Nasopharyngeal tubes are also typically avoided hours after the event. If this is a large area of the
with skull base fractures, particularly those through brain, the swelling itself might cause dramatic neuro
the anterior fossa floor. logical deterioration and herniation and require
There are also a few important intracranial con surgical decompression for preservation of life.
ditions that are not recognised on CT, including Meningitis (see section Infection) is also an
DAI, acute cerebral infarction and meningitis. DAI important and dangerous intracranial cause of
is a common association with severe head injuries post‐traumatic confusion that is expected not to
and is caused by differential movement in the outer cause CT scan abnormalities.
layers of the brain and the deeper layers during A point should be made regarding MRI, which is
rotational acceleration (which commonly occurs in now widely available and demonstrates some
car accidents for example). This results in shear pathologies that are poorly demonstrated on CT
injuries to the axons (particularly the subcortical (particularly in the case of post‐traumatic confusion,
regions of the hemispheres, but also elsewhere early cerebral ischaemia and widespread changes
including the splenium and tectal plate region). often associated with DAI). However, the require
It has a poor prognosis and patients with DAI have ment for the patient to remain still, the long duration
a high mortality and survivors a relatively high risk of the scan and the difficulty in monitoring patients
of significant neurological disabilities. DAI itself is in the scanner are such that it is rarely used in the
not recognisable on CT scan, although often there assessment of post‐traumatic confusion. For these
are similar shear injuries to penetrating vessels in reasons, CT is the primary diagnostic imaging tool in
those regions, and the secondary ‘petechial haemor the acute post‐traumatic period.
rhages’ identifiable on CT scan are often said to be
pathognomonic of DAI. There is no specific treat
Hypoxia and respiratory disturbance
ment of DAI other than supportive measures and
prevention of secondary brain injury. Survivors The patient’s airway and breathing must be imme
with significant DAI typically have prolonged and diately assessed, and if there is cause for concern
often severe cognitive impairment, including confu then ventilatory support and/or airway protection
sion. However, my main point here is to remind the immediately instituted (see section Clinical assess
reader that the patient’s clinical state is the most ment). If the cervical spine is unstable or its status
important prognostic factor after a head injury, and unknown, then this should not delay endotracheal
a normal CT scan does not necessarily rule out very intubation, but necessitates the head and neck being
severe primary brain injury. held in a neutral position during the procedure.
Acute cerebral infarction is a diagnosis often All patients with post‐traumatic confusion should
overlooked in trauma patients, and when it does be administered supplemental oxygen and, even if
occur it is usually secondary to arterial dissection oxygen saturation monitoring demonstrates no
(a tear in the inner layers usually caused by a abnormality, arterial blood gases should be assessed
stretch‐type mechanism at the time of trauma) of as a matter of priority (see section Investigations).
the carotid and/or vertebral arteries either in the Considering the increased susceptibility of an
neck or in the head. Although this might cause injured brain to relatively mild secondary insults,
742 Problem Solving
therapy should aim for Pao2 above 100 mmHg and However, clinicians must also be aware that many
Paco2 35–45 mmHg, and normal pH. Hyperven of these classic symptoms might initially be absent,
tilation is not recommended as although this and particularly in trauma patients the onset can be
reduces ICP it does so because of vasoconstriction, heralded by post‐traumatic confusion, not uncom
which can cause secondary cerebral ischaemia. monly with no clinical evidence of infection. A CT
scan would not be expected to show any abnormal
ity in early meningitis, but it should be performed
Electrolyte and metabolic disturbances to rule out lesions causing intracranial hypertension
prior to performing a lumbar puncture. If meningi
A full electrolyte and renal function screen should
tis is suspected (and it should be, particularly if
be assessed. Sodium abnormalities can cause sig
there has been a history of skull base fracture/CSF
nificant confusion and are common in acute post‐
rhinorrhoea/pneumocephalus, compound skull
trauma patients. Acute hyponatraemia in particular
fractures or any intracranial surgery including ven
can cause significant cerebral swelling, seizures and
tricular drainage, CSF shunt or ICP monitoring),
confusion, and should be treated with fluid restric
then a lumbar puncture must be performed after
tion and/or hypertonic saline (typically the former,
the negative CT brain as a matter of urgency. The
but this depends on hydration status and underlying
CSF must be immediately analysed for cell counts,
cause). Iatrogenic water overload is quite a com
protein and glucose, and Gram stain microscopy
mon cause of post‐traumatic hyponatraemia, the
for organisms, with a specimen being sent for
syndrome of inappropriate secretion of antidiuretic
culture. CSF with a high protein and low glucose
hormone (which causes increased total body water)
concentration (<50% of blood glucose) and a raised
less common, and salt wasting syndrome (associ
proportion of white cells to red cells (more than 1
ated with total body water deficit) even more
in 700) makes the diagnosis likely and necessitates
unusual. Differentiation is clinically difficult and
institution of parenteral antibiotics (assuming
specialist advice recommended. A point of caution
blood and urine cultures have been collected),
is that rapid correction of chronic hyponatraemia
which should be continued until after final culture
has been associated with central pontine myelino
results have been assessed. As mentioned previously,
sis, and therefore if the patient has had long‐stand
meningitis secondary to a skull base fracture (dural
ing hyponatraemia (often due to medication) or if
fistula) can be very delayed, and once the meningi
this is unknown but considered likely, then the
tis has been treated elective surgical repair of the
correction should be slow (over 24–48 hours). In
dural fistula is required to prevent recurrence.
other cases a more rapid correction is appropriate.
If infection of any type is suspected clinically,
Other electrolyte abnormalities, particularly hyper
then antibiotics should be commenced as soon as
calcaemia, are less common causes of confusion.
the culture specimens have been taken and modi
fied if required when culture and sensitivity results
are available.
Infection
Infection is a very common cause of post‐traumatic
confusion, and confusion is often the only early sign
Medication and non‐medicinal drugs
even in the absence of fever. Therefore, any post‐
traumatic patient with new‐onset or worsening con Thorough assessment of the patient’s recent medi
fusion should have a full septic work‐up, including cation is necessary for any confused patient, as is
chest examination and chest X‐ray, inspection of all the history of chronic medication, alcohol or other
intravenous sites and wounds (swabbing as neces non‐prescribed drugs that have been withheld. As
sary), changing of all intravenous lines, and urine discussed, sedative and narcotic use in hospital and
microscopy and culture. Meningitis must also be also their withdrawal can cause confusion. Alcohol
seriously considered and if suggested in any way withdrawal is also not uncommon and should be
clinically or in the presence of risk factors, the patient considered. Other medications, such as anticon
must have an urgent lumbar puncture performed vulsants, can also cause or exacerbate confusion.
(after CT brain demonstrates it safe to do so). One important point is that these medication/
Meningitis classically presents with sepsis, drug causes of post‐traumatic confusion must be
altered conscious state and meningism (headache, presumptive only, and the diagnosis made only
photophobia and neck stiffness), and can be rapidly after other serious causes (particularly intracranial
fatal and cause major morbidity in survivors. pathology and hypoxia) have been excluded.
2 In a patient with multisystem trauma demonstrating

Further reading significant post‐traumatic confusion, which of the
following is the most immediate requirement?
Behrouz R, Godoy DA, Azarpazhooh MR, Di Napoli M.
Altered mental status in the neurocritical care unit.
a a brain CT scan
J Crit Care 2015;30:1272–7. b formal assessment of the GCS
Sharp DJ, Jenkins PO. Concussion is confusing us all. c assessment of respiratory and circulatory
Pract Neurol 2015;15:172–86. sufficiency
Zaal IJ, Devlin JW, Peelen LM, Slooter AJC. A systematic d exclusion of papilloedema
review of risk factors for delirium in the ICU. Crit Care e detailed neurological examination
Med 2015;43:40–7.
3 Which of the following are typically always
associated with abnormal findings on standard axial
MCQs CT brain?
a diffuse axonal injury
b acute cerebral infarction
c meningitis
d cerebral contusion
1 Post‐traumatic confusion: e skull‐base fracture
a indicates significant brain injury
b indicates a concussional state
c is always associated with an altered conscious
state (GCS <15)
d indicates the need to keep the patient in a quiet
room with minimal disturbance
e is rare in the absence of a direct head injury
81 Sudden‐onset severe headache
Alexios A. Adamides
University of Melbourne and Royal Melbourne Hospital, Melbourne,
Victoria, Australia
latter occurs instantly and is of maximal intensity

Introduction at onset (thunderclap headache). Patients often
describe the headache of a subarachnoid haemor-
Headache is a very common symptom, the cause
rhage as ‘the worst headache of my life’ or that it
often benign, the diagnosis often presumptive and
resembles ‘being shot in the head’ or ‘hit on the
the course usually self‐limiting. This is not the case
back of the head with a bat’. A patient described the
for sudden‐onset severe headache where the under-
moment of a subarachnoid haemorrhage as fol-
lying cause can be a serious life‐threatening condi-
lows: ‘I was in the pub having a drink when all of a
tion that must be diagnosed expeditiously and
sudden I had a massive headache and I thought
treated appropriately (Box 81.1). Any patient pre-
someone punched me at the back of the head. I
senting with a sudden‐onset headache must be
turned around to see who it was but there was no‐
assessed promptly with a detailed history and full
one there.’
neurological examination, followed by targeted
Cerebral aneurysms usually develop at branching
investigations dictated by the clinical findings
points of arteries from changes due to wear and
(Box 81.2).
tear and therefore their prevalence and rupture
rates increase with age. Sudden‐onset severe head-
ache may be associated with collapse and loss of
Subarachnoid haemorrhage
The most common cause of non‐traumatic suba-

Box 81.2 Initial management and
rachnoid haemorrhage is rupture of an aneurysm
investigations for abrupt‐onset
with extravasation of blood within the subarach-
severe headache
noid space. If the patient is conscious and able to
give a history, it is important to elicit whether the • Initial resuscitation with attention to airway,
headache was of gradual or sudden onset. The breathing and circulation
• Vital observations: pulse rate, temperature, blood
pressure, oxygen saturations
Box 81.1 Causes of abrupt onset severe • CT brain
headache • Lumbar puncture if no contraindication on CT brain
(four tubes for red cell count, oxyhaemoglobin,
• Intracranial haemorrhage: subarachnoid, subdural bilirubin, differential cell count, microscopy for
or intracerebral haemorrhage secondary to an Gram stain, culture and sensitivities, protein,
underlying lesion such as a ruptured aneurysm, glucose)
arteriovenous malformation, cavernous malforma- • Blood tests: full blood count, coagulation, urea and
tion, arterial dissection, dural arteriovenous fistula, electrolytes, group and save, cross‐match,
vasculitis erythrocyte sedimentation rate (ESR), C‐reactive
• Primary intracerebral haematoma protein (CRP), pituitary hormones
• Bacterial or viral meningitis • Depending on history/examination and findings
• Giant cell (temporal) arteritis from the above investigations, additional investiga-
• Reversible cerebral vasoconstriction syndrome tions may include CT angiography, magnetic
• Reversible posterior leucoencephalopathy resonance (MR) angiography, digital subtraction
• Pituitary apoplexy angiography CT/MR venogram
745
746 Problem Solving
consciousness, drowsiness, confusion, nausea and accurate than the visual detection of xanthochromia
vomiting, meningism (neck stiffness, photophobia) (yellow coloration). The number of red blood cells in
or seizures. There may be focal neurological signs each tube must also be recorded and CSF must be
such as ipsilateral third nerve palsy with ptosis and sent to microbiology for a differential cell count,
a fixed dilated pupil from direct compression of the Gram stain, cultures and sensitivities, protein and
oculomotor nerve by the dome of an aneurysm aris- glucose to exclude other pathologies such as bacte-
ing from the junction of the internal carotid and rial or viral meningitis. CT angiography and/or digi-
posterior communicating arteries. Occasionally, an tal subtraction angiography are only useful in
unruptured but acutely enlarging posterior commu- identifying the source of haemorrhage but are of no
nicating artery aneurysm may present with a pain- use in establishing whether a haemorrhage is present
ful third nerve palsy. Although the majority of or not.
ruptured aneurysms cause a subarachnoid haemor-
rhage, some aneurysms may rupture within the sub-
dural space, causing a subdural haematoma, or Initial management of aneurysmal
within the brain parenchyma, causing an intracere- subarachnoid haemorrhage
bral haematoma, with or without subarachnoid Once the diagnosis of subarachnoid haemorrhage
blood. Associated hydrocephalus from blood is established, it is important to secure the aneu-
within the ventricular system often accompanies rysm as soon as practicable, either by craniotomy
subarachnoid haemorrhage. and clipping or by endovascular coiling so as to
prevent rebleeding. Until the aneurysm is secured it
Investigations for the diagnosis is important to control systolic blood pressure to
of subarachnoid haemorrhage less than 140 mmHg using antihypertensives.
Patients with hydrocephalus who deteriorate neu-
An urgent non‐contrast CT scan of the brain will rologically may require insertion of a ventriculos-
typically demonstrate blood (hyperdensity) within tomy catheter to drain CSF but the sudden change
the subarachnoid space, including the basal cisterns in transmural pressure on drainage may precipitate
and/or fissures in the majority of cases. Even a small rebleeding and therefore CSF diversion before the
amount of blood on a CT scan is adequate to con- aneurysm is secured must only be performed if clin-
firm the diagnosis. Occasionally, in cases where the ically necessary.
haemorrhage is small or if the patient presents late
there may not be visible blood on CT scan (98% of
patients with subarachnoid haemorrhage will have Non‐aneurysmal causes of subarachnoid
blood on a CT scan performed within the first day haemorrhage
from the onset of symptoms, whereas 7 days after Subarachnoid haemorrhage may also be secondary
subarachnoid haemorrhage only 50% of patients to arterial dissection, either spontaneous or trau-
will have visible blood on CT scan). In such cases, if matic. Occasionally, subarachnoid haemorrhage
the history is suggestive of subarachnoid haemor- may be caused by rupture of an arteriovenous mal-
rhage but the CT scan is normal, a lumbar puncture formation (AVM), although typically an AVM pre-
is necessary before subarachnoid haemorrhage can sents with an intracerebral haemorrhage or a
be excluded. The initial lumbar puncture is often the seizure. AVMs are generally thought to be congeni-
one and only opportunity to establish the correct tal lesions and are therefore an important cause of
diagnosis and must be performed by an experienced abrupt‐onset headache in children and young adults.
practitioner, using a fine needle and adequate local Convexity subarachnoid haemorrhage, with
anaesthesia so as not to precipitate rebleeding, which blood in a sulcal distribution and remote from the
is a common and usually fatal early complication of basal cisterns or fissures, is unlikely to be aneurys-
subarachnoid haemorrhage. Ten drops of cerebro- mal. Often this is due to trauma or may be second-
spinal fluid (CSF) are collected sequentially in four ary to vasculitis, dural venous sinus thrombosis,
separate tubes which must be labelled according to reversible cerebral vasoconstriction syndrome and
the sequence of collection. The CSF specimen must reversible posterior leucoencephalopathy.
be protected from light exposure and must be hand‐
delivered immediately to the pathology department
Reversible cerebral vasoconstriction syndrome
for the sample to be centrifuged before red blood cell
lysis occurs. The supernatant must be tested for oxy- This is an entity that has been described relatively
haemoglobin and bilirubin (products of red blood recently, also known as Call–Fleming syndrome. It
cell lysis) using spectrophotometry as this is more is characterised by abrupt‐onset severe headache,
81: Sudden-onset severe headache 747
often recurrent, that may be associated with focal young patients and in elderly patients in whom the
neurological deficits and angiographic evidence of haematoma is in a location atypical of a hypertensive
multifocal segmental cerebral artery constriction haemorrhage (e.g. if the haematoma extends into the
that is reversible within 12 weeks. It is commoner sylvian or interhemispheric fissures), CT angiogra-
in women, often early postpartum, and has also phy or digital subtraction angiography may be nec-
been associated with the use of drugs such as selec- essary to exclude an underlying vascular lesion.
tive serotonin reuptake inhibitors, cocaine, ecstasy Less common causes of intracranial haemorrhage
(MDMA), amphetamines and cannabis. There may include bleeding from a cavernous malformation,
be subarachnoid blood on CT scan in a sulcal dis- arteriovenous fistula, or hypervascular intracranial
tribution (but not in the basal cisterns). The vaso- tumours such as haemangioblastoma, melanoma or
constriction can lead to ischaemic complications renal cell metastases.
such as transient ischaemic attack and stroke.
Treatment is with avoidance of precipitants and Giant cell arteritis
with calcium channel blockers such as nimodipine.
This is primarily seen in middle‐aged/elderly
Caucasian patients and is twice as common in women
Posterior reversible encephalopathy syndrome compared with men. It is a chronic vasculitis primar-
Posterior reversible encephalopathy syndrome, also ily involving the cranial branches arising from the
known as reversible posterior leucoencephalopathy aortic arch and if untreated may lead to blindness,
syndrome, results in vasogenic oedema preferentially stroke or arterial dissection. Headache associated
affecting the white matter of the posterior cerebral with giant cell arteritis is usually of insidious onset,
hemispheres, hence the name. Patients present although occasionally it may occur abruptly. It may
with severe headache which can be of acute onset be generalised or located in the temporal region and
and associated symptoms include confusion, visual there may be associated tenderness over the course of
changes and seizures. CT or MRI of the brain may the superficial temporal arteries (hence the previous
demonstrate the characteristic pattern of widespread name ‘temporal arteritis’). Associated features may
vasogenic oedema predominantly affecting the include a variety of visual symptoms and signs,
parietal and occipital regions and there may be
including ocular pain, amaurosis fugax (painless
associated subarachnoid blood in a sulcal distribu- transient visual loss), visual field deficits and blind-
tion. The syndrome has been associated with hyper- ness (due to occlusion of branches of the ophthalmic/
tensive encephalopathy, eclampsia/pre‐eclampsia, posterior ciliary arteries). There may be associated
autoimmune conditions and immunosuppression.
jaw claudication. Systemic symptoms may include
Management is by treatment of the underlying cause, fever, weight loss, fatigue, myalgia, joint pain and
such as control of hypertension, delivery of the baby peripheral neuropathies. Inflammatory markers (ESR
or withholding of immunosuppressive medication. and CRP) are elevated and the diagnosis is confirmed
with a temporal artery biopsy. Early treatment with
corticosteroids is critical for preventing blindness.
Other causes of intracranial Pituitary apoplexy
haemorrhage
Pituitary apoplexy occurs due to sudden expansion of
The commonest cause of an intracerebral haemor- a mass within the sella turcica, usually from haemor-
rhage in middle‐aged/elderly patients is a sponta- rhage or infarction within a pre‐existing pituitary
neous intracerebral haemorrhage, often associated adenoma. Patients often present with abrupt‐onset
with hypertension or amyloid angiopathy. Long‐ severe headache with associated visual disturbance,
standing, poorly controlled hypertension may lead to typically bitemporal hemianopia but also ophthalmo-
micro‐aneurysms of perforating arteries (Charcot– plegias, diplopia, deteriorating visual acuity or blind-
Buchard aneurysms) and a typical hypertensive ness. There may be drowsiness, confusion or loss of
haemorrhage is usually located in the basal ganglia, consciousness from hydrocephalus. If the haemor-
internal capsule, pons or cerebellum. Amyloid angi- rhage ruptures through the tumour capsule and the
opathy is a common cause of lobar haemorrhage in arachnoid membrane and into the chiasmatic systern,
elderly patients. All patients with an intracerebral there may be symptoms and signs of subarachnoid
haemorrhage must be resuscitated and their hyper- haemorrhage such as nausea and vomiting, neck stiff-
tension controlled and may require craniotomy and ness and photophobia. Associated endocrinological
evacuation of the haematoma if there is significant abnormalities may result in hypotension or diabetes
mass effect and/or deteriorating consciousness. In all insipidus. CT or MRI of the brain will demonstrate
748 Problem Solving
haemorrhage in the sella region and CT or MR angi- dysphasia and right‐hand clumsiness. A CT scan of
ography are usually the minimum investigations the brain does not show intracranial haemorrhage.
required to exclude subarachnoid haemorrhage from Which of the following is correct?
a ruptured aneurysm. There may be associated a he requires urgent thrombolysis
compression of the optic chiasm or hydrocephalus b he requires urgent empirical antibiotics for
from obstruction of the third ventricle. Management meningitis
includes corticosteroid administration and urgent sur- c the most likely diagnosis is reversible cerebral
gical decompression if there is sudden constriction of vasoconstriction syndrome
visual fields or deterioration of visual acuity from d the most likely diagnosis is posterior reversible
compression of the visual apparatus. encephalopathy syndrome
e the most likely diagnosis is delayed cerebral
Meningitis ischaemia after aneurysmal subarachnoid
haemorrhage and a lumbar puncture is likely to
Bacterial meningitis is a potentially life‐threatening
show elevated oxyhaemoglobin and bilirubin on
infection of the meninges that must be diagnosed
spectrophotometry
and treated expeditiously with antibiotics. Viral
meningitis is usually self‐limiting and often requires
2 A 21‐year‐old woman presents with a 3‐day history
supportive therapy only. Clinical features of menin-
of sudden‐onset headache. A CT scan of the brain
gitis include headache, which can be of sudden
shows a 2.5‐cm right temporal intracerebral
onset, nausea/vomiting, meningism (neck stiffness,
haemorrhage but a CT angiogram does not show
photophobia), fever, petechial rash, drowsiness,
any underlying lesion. While in the scanner she has
confusion and coma. There may be associated fea-
a generalised tonic–clonic seizure. Which of the
tures of the original source of infection, such as
following is correct?
upper respiratory tract symptoms, sinusitis, otitis
a a lumbar puncture must be performed to exclude
media, mastoiditis or features of bacterial endocar-
subarachnoid haemorrhage
ditis. The diagnosis is by microbiological examina-
b a CT angiogram of the circle of Willis is adequate
tion of CSF obtained by lumbar puncture. Treatment
to exclude an underlying vascular lesion
with empirical antibiotics should be administered
c she requires immediate craniotomy and evacua-
immediately on suspicion of bacterial meningitis,
tion of the haematoma
even before a lumbar puncture is performed.
d the clinical priority is to secure her airway and
administer anticonvulsants to terminate the seizure
e the most likely cause of the haemorrhage is
Further reading amyloid angiopathy
Connolly ES Jr, Rabinstein, AA, Carhuapoma JR et al.
3 A 55‐year‐old man presents to a small country
Guidelines for the management of aneurysmal suba-
rachnoid haemorrhage: a guideline for healthcare pro- hospital with a history of headache. While in the
fessionals from the American Heart Association/ emergency department he collapses unconscious
American Stroke Association. Stroke 2012;43:1711–37. and is found to have a fixed and dilated right pupil.
Laidlaw JD, Siu KH. Ultra‐early surgery for aneurysmal A brain CT scan shows a large right temporal
subarachnoid haemorrhage: outcomes for a consecutive intracerebral haematoma and a CT angiogram
series of 391 patients not selected by grade or age. shows a right middle cerebral artery aneurysm. He
J Neurosurg 2002;97:250–8. is air‐lifted to a neurosurgical centre intubated and
Tunkel, AR, Hartman J, Kaplan SL et al. Practice guide- ventilated. Which of the following is the most
lines for the management of bacterial meningitis. Clin
appropriate management?
Infect Dis 2004;39:1267–84.
a urgent cerebral angiogram and coiling of the
aneurysm followed by craniotomy and evacua-
tion of the haematoma
MCQs b urgent craniotomy and clipping of the aneurysm
and evacuation of the haematoma
c urgent craniotomy and evacuation of the
haematoma followed by cerebral angiography
and coiling of the aneurysm
1 A 49‐year‐old male smoker with poorly controlled d transfer to intensive care to wean sedation and
hypertension presents with a 5‐day history of assess neurology
sudden‐onset severe headache and neck stiffness. e transfer to a palliative care ward for comfort
On examination he is found to have expressive measures
82 The red eye
Christine Chen
Monash University and Department of Ophthalmology, Monash Health, Melbourne,
Victoria, Australia
Introduction Basic anatomy of the eye
Ophthalmology is the diagnosis and management of See Figure 82.1.

conditions affecting the eye, orbit and visual neural
pathways. To cover the entire field of ophthalmology
is beyond the scope of this book, so the aim of this
and the following chapter is to provide a solid foun- The red and/or painful eye
dation for recognising both common and serious con-
ditions presenting with red eye and diplopia and for The red eye is one of the most common ophthal-
understanding the appropriate primary management mic presentations to general practitioners and
prior to referral to an ophthalmologist. At the end of accident and emergency departments (Table 82.1).
these chapters you should have an understanding of It is usually accompanied by some degree of pain
the relevant anatomy of the eye (see Figure 82.1), be or discomfort and possibly discharge. It is impor-
able to take a targeted ophthalmic history based on tant to differentiate the benign self‐limiting causes
the presenting problem and undertake a basic oph- such as viral conjunctivitis and subconjunctival
thalmic examination to identify and describe pathol- haemorrhage from sight‐threatening conditions
ogy. Most importantly, you should be able to identify such as microbial keratitis and angle closure
life‐threatening, eye‐threatening and sight‐threaten- glaucoma.
ing conditions and undertake emergency ophthalmic Remember the golden rule: Beware of the unilat-
investigation and treatment where appropriate. eral red eye.
Lens
Retina
Iris
Macula
Cornea
Vitreous Optic nerve
Pupil
Aqueous
Conjunctiva
Sclera
Fig. 82.1 Basic anatomy of the eye.
749
750 Problem Solving
Associated symptoms
Table 82.1 Common systemic causes of red eye.
• Vision loss: most benign causes of a red painful
Causes of red eye Associated systemic conditions eye such as conjunctivitis should not affect vision.
Conjunctivitis Upper respiratory tract viral • Discharge: watery or purulent.
infection • Photophobia: associated with corneal pathology
Chlamydia such as keratitis or ocular inflammation such as
Scleritis Connective tissue disorders, e.g. uveitis.
rheumatoid arthritis, systemic • Headache: associated with ocular inflammation
lupus erythematosus or raised intraocular pressure (IOP).
Infectious causes: herpes zoster
ophthalmicus
Uveitis Paediatric: Previous ophthalmic history
• TORCH infection • Contact lens wearers are at higher risk of infec-
• Juvenile arthritis
tive keratitis.
Adults:
• Uveitis can be recurrent and many patients will
• Any autoimmune condition,
e.g. serum‐negative
have a prior history of similar episodes.
arthropathies, sarcoidosis, • Recurrent corneal erosion syndrome is a condi-
inflammatory bowel disease tion where previous minor corneal trauma,
• Systemic infections, e.g. such as a fingernail scratch, results in a healed
tuberculosis, syphilis but unstable corneal epithelium. Subsequent
Dry eye Sjögren’s syndrome very minor trauma (such as rubbing or even
Thyroid eye disease opening of the eyes first thing in the morning)
can lead to repeated, painful, corneal epithelial
defects.
• Those with long‐sightedness and people of
History Asian descent are predisposed to angle closure
Duration of symptoms glaucoma.
Patients with eye trauma will generally seek medi-

Previous medical history
cal attention immediately.
Patients with viral conjunctivitis will generally Hypertension and anticoagulants predispose to
present within the first 1–2 weeks after failing with subconjunctival haemorrhage.
over‐the‐counter medications such as chloram-
phenicol drops or ocular lubricants. Viral conjunc-
tivitis will often start unilaterally and spread to the The basic eye examination
fellow eye. There is often a history of viral illness or Visual acuity
contact with people with viral conjunctivitis or
viral illness. Visual acuity represents the global function of the
Chronic conjunctivitis is defined as conjunctivitis eye and visual system and is the single most impor-
lasting for more than 4 weeks. The most common tant part of the eye examination.
cause of chronic conjunctivitis is chlamydial inclu-
sion conjunctivitis in sexually active young adults. Distance visual acuity testing and recording
A sexual history is therefore important. Distance visual acuity is obtained one eye at a time
by occluding the fellow eye (Figure 82.2). This
measures the patient’s ‘best corrected vision’, which
means that vision should be tested with the patient’s
Description of pain
habitual distance glasses (many patients over 50
• Foreign body sensation is usually associated with years old may have separate distance and near/
foreign bodies or conjunctivitis. reading glasses). The eye not being tested is occluded
• Burning watery eyes and itchy eyelids are symp- with an occluder or the patient’s palm. The test is
toms of blepharitis. then repeated with a pinhole over the eye being
• Severe pain, not relieved by rest or simple analge- tested.
sia, can indicate more sinister pathology such as The patient should be encouraged to read the
keratitis. smaller letters or the next line even if they are not
82: The red eye 751
and the numerator then changes, e.g. 3/x, 1/x. The

denominator (x) corresponds to the smallest letter
line that a patient is able to read correctly. Each letter
line is assigned a number (Figure 82.3). This number
represents the distance at which a person without a
visual deficit should be able to read those letters.
For example, vision of 6/12 is interpreted as fol-
lows. The patient was tested with a chart calibrated to
be read at 6 m. He or she was only able to see the line
that should be read at 12 m, i.e. the patient can see at
6 m what can be read at 12 m by a person without a
visual deficit. If the patient is unable to read the top
letter of the chart (60), reduce the distance to 3 m
(3/60), then 2 m (2/60) and then 1 m (1/60).
If the patient is unable to read the top letter of the
chart at 1 m, test their ability to count fingers at 1
m (CF), then hand movement (HM), and then the
ability to perceive a very bright light source (LP).
If the patient is unable to perceive a bright light
source, then this is recorded as no perception of
light (NPL).
An ‘E’ chart should be used for patients who do
not recognise English alphabet characters. The
Fig. 82.2 Occlusion with palm.
patient is asked in which direction the ‘arms’ of the
E are pointing. A picture chart can be used for chil-
dren unfamiliar with alphabetical symbols.
confident of the letters. The distance visual acuity is
recorded as a fraction, with the numerator as the dis-
Gross examination of the eye and adnexae
tance at which the chart is positioned from the patient
(in metres for Australia). Each chart is calibrated to Inspect the eyelids and the surrounding tissue
be read at a certain distance, most commonly 6 m, • Inspect the cornea for clarity.
and the fraction is 6/x. The distance can be changed • Inspect the conjunctiva and sclera for redness.
Fig. 82.3 Standard Snellen visual acuity chart, ‘C’ chart and ‘E’ chart.
752 Problem Solving
Additional tests therefore hand hygiene and meticulous cleaning of

• Tonometry to measure IOP: use a slit lamp‐ the examination room and instruments is manda-
mounted Goldmann tonometer or a hand‐held tory to prevent spreading of infection.
electronic tonometer such as the Tonopen™. If chlamydial conjunctivitis is suspected, azithro-
• Colour vision testing: with Ishihara colour plates. mycin 1 g orally should be administered immedi-
• Fluorescein staining: to detect corneal epithelial ately. It is important to take conjunctival swabs for
defects or penetrating eye injuries. A cobalt blue polymerase chain reaction (PCR). The patient must
illumination source, as found on direct ophthal- be reviewed to check the results and contact tracing
moscopes or slit lamps, is used to identify the instituted in confirmed cases.
fluorescein dye.
• Eversion of the upper lid: for foreign bodies.
Keratitis
• Examination of the eye and adnexae: a great deal
of pathology can be detected on gross inspection Keratitis describes the inflammation of the cornea
and with a direct ophthalmoscope. caused by either infection or inflammation
(Table 82.2). Microbial keratitis is a serious and
potentially sight‐threatening condition. It is usually
Primary management associated with decreased vision, sensitivity to light
(photophobia) and pain. Examination may confirm
Subconjunctival haemorrhage
reduced visual acuity, fluorescein staining and cor-
Subconjunctival haemorrhage is a haemorrhage neal infiltrate (Figure 82.4).
into the potential space between the conjunctiva Pathogens include viruses such as herpes simplex
and sclera (Table 82.2). Blood pressure should be types 1 and 2 and herpes zoster ophthalmicus; bac-
checked. The condition is self‐limiting but can take teria such as Staphylococcus, Streptococcus and
several weeks for complete resolution of the blood. Pseudomonas; and Acanthamoeba. These infec-
Ocular lubricant may alleviate the foreign body tions often occur on a background of predisposing
sensation. factors which could be ocular (contact lens use or
ocular trauma) or systemic (diabetes or rheumatoid
arthritis).
Blepharitis
Primary management of microbial keratitis
Blepharitis or inflammation of the eyelid due to includes prompt referral to ophthalmologists for
either staphylococcal infection or meibomian gland microbiological work‐up and empirical anti‐infec-
dysfunction causes symptoms disproportionate to tive treatment.
the underlying pathology (Table 82.2). Stye and
chalazion can develop as a complication of blephar-
Episcleritis
itis. Treatment options include:
• lid hygiene, with scrubbing of eyelid margin with Episcleritis is inflammation of the episclera (super-
a mild, very dilute shampoo such as ‘no tear’ ficial layer of the sclera), which can be either local-
shampoo ised or diffuse and is often idiopathic (Table 82.2).
• hot compress It is often self‐limiting and can be treated with
• ocular lubricant. ocular lubricant and topical non‐steroidal anti‐
The patient may be referred to an ophthalmologist inflammatory drugs (NSAIDs). Scleritis is a more
if the symptoms are not responsive to these s imple severe condition that may be associated with sys-
measures. temic disease. It is c lassified into non‐necrotising
and necrotising and requires treatment with high‐
dose systemic anti‐inflammatory agents such as
Conjunctivitis
NSAIDs or steroids and investigation and treat-
Most mild cases of conjunctivitis are managed with ment of the underlying associated systemic condi-
simple ocular lubricant and reassurance (Table 82.2). tions (see Table 82.1).
The typical course of viral conjunctivitis is much
like a viral upper respiratory infection, with worsen-
Uveitis
ing of symptoms without visual disturbance in the
first 7–10 days and subsequent involvement of the Uveitis describes inflammation of the uveal tract,
fellow eye. The symptoms will start to improve after which includes the iris, ciliary body and choroid
7–10 days with resolution expected within 3 weeks. (see Table 82.2). An anatomical classification, grad-
Viral conjunctivitis is extremely contagious and ing system and diagnostic criteria is published by
Table 82.2 Common differential diagnosis for a red eye.
Differential Visual Anterior

diagnosis Discharge Pain acuity Pupil Conjunctiva Cornea Chamber IOP Refer
Subconjunctival No No, FBS Unaffected Normal Localised redness Clear Quiet Normal No, if visual
haemorrhage acuity is normal
Blepharitis Dry crusts No, FBS Unaffected Normal Diffuse redness Clear. May have pinpoint Quiet Normal No, if visual
Often bilateral staining with fluorescein acuity is normal
Conjunctivitis Yes No, FBS Can be Normal Diffuse redness Clear. May have pinpoint Quiet Normal No, if visual
Viral: affected Often bilateral staining with fluorescein acuity is normal
watery
Bacterial:
purulent
Foreign body Yes, watery Can be Can be Normal Localised redness Foreign body or abrasion Quiet Normal Yes, if unable to
affected Unilateral with fluorescein staining remove foreign
body
Keratitis Yes, watery Yes Affected Normal Diffuse redness Localised opacity with Possible Normal Yes
Unilateral fluorescein staining cells
Uveitis No Yes Affected May be sluggish Diffuse redness Keratic precipitates (localised Cells and Normal or Yes
and constricted Unilateral deposits on endothelium) flare increased
without fluorescein staining
Episcleritis/ No Yes Can be Normal Localised or Clear Possible Normal Yes
scleritis affected diffuse redness cells
Unilateral
Angle closure No Yes Affected May be sluggish Diffuse redness Diffuse cloudiness due to Shallow Increased Yes
glaucoma and dilated Unilateral corneal oedema without Cells
fluorescein staining
FBS, foreign body sensation.

Source: adapted from Smith JA, Fox JG, Saunder AC, Yii MK. Hunt & Marshall’s Clinical Problems in Surgery, 3rd edn. Chatswood, NSW: Elsevier Australia, 2016. Reproduced
with permission of Elsevier.
0004427829.INDD 753 10/1/2019 9:50:59 AM

754 Problem Solving
such as acetazolamide and topical medication such

as ocular antihypertensives including alpha‐ago-
nists, beta‐blockers, prostaglandin analogues and
miotics such as pilocarpine 2–4% as well as analge-
sia and anti‐emetics. Definitive treatment consists
of peripheral laser iridotomy to re‐establish com-
munication between posterior and anterior cham-
bers. In some cases surgical treatment is required
which may involve a peripheral iridectomy or cata-
ract surgery. Prophylactic laser iridotomy for the
fellow eye and screening of first‐degree relatives
should also be considered.
Herpes simplex virus dendrite Further reading

Fig. 82.4 Corneal dendrite caused by herpes simplex
virus demonstrated by fluorescein staining. Source: Bagheri N, Wajda B (eds) The Will’s Eye Manual: Office
Friedman NJ, Kaiser PK. Essentials of Ophthalmology. and Emergency Room Diagnosis and Treatment of Eye
Philadelphia: Saunders Elsevier, 2007. Reproduced with Disease, 7th edn. Philadelphia: Wolters Kluwer, 2017.
permission of Elsevier. Bowling B. Kanski’s Clinical Ophthalmology: A Systematic
Approach, 8th edn. Elsevier, 2016.
James B, Bron A, Parulekar MV. Lecture Notes in
the Standardization of Uveitis Nomenclature (SUN) Ophthalmology, 12th edn. Oxford: Wiley Blackwell,
Working Group to establish a framework for this 2016.
vast and diverse condition. The patient with uveitis Khaw PT, Shah P, Elkington AR. ABC of Eyes, 4th edn.
usually presents with a painful red eye, photopho- London: BMJ Publishing Group, 2004.
bia and reduced vision. There may be associated
systemic autoimmune conditions, most commonly
ankylosing spondylitis or infectious conditions MCQs
such as HIV. Refer to an ophthalmologist for fur-
ther assessment, investigation and management.
Acute angle closure glaucoma
1 A 70‐year‐old man with a history of recent cold
Acute angle closure glaucoma is a sight‐threatening and anticoagulant use presented with a red eye and
emergency presenting as sudden painful loss of no other symptoms. On examination there is a
vision due to sudden and total closure of the irido- sector of one eye that is solid red without injection
corneal angle (see Table 82.2). It is more common of the conjunctival vessels. What is the most likely
in patients with hypermetropia or long‐sightedness, diagnosis?
advancing age, of Asian race, and a positive family a uveitis
history. The patient usually presents with sudden b keratitis
onset of severe ocular pain and headache, blurred c subconjunctival haemorrhage
vision with halos around lights, nausea and vomit- d conjunctivitis
ing. Examination will reveal high IOP (50–100
mmHg); mid‐dilated, sluggish and irregular pupil; 2 A 45‐year‐old Asian woman presented with a
corneal epithelial oedema with or without stromal history of sudden‐onset right painful red eye,
oedema; red eye from congested episcleral and con- blurred vision with halos around the lights, nausea
junctival blood vessels; shallow anterior chamber; and vomiting. She usually wears glasses for
mild amount of aqueous flare and cells; and the reading. Tonometry revealed an intraocular
optic nerve may be swollen during an attack. A pressure of 55 mmHg in the right eye and 18
definitive diagnosis depends on gonioscopy, which mmHg in the left. What is the most likely
requires a specialised contact lens to examine the diagnosis?
iridocorneal angle and confirm that it is closed by a conjunctivitis
the iris. b scleritis
Prompt referral to an ophthalmologist is required. c acute angle closure glaucoma
Emergency treatment includes systemic medication d corneal foreign body
82: The red eye 755
3 A 27‐year‐old man with a history of ankylosing 4 What is the definition of chronic conjunctivitis?
spondylitis presented with bilateral red eye, a conjunctivitis >1 week
photophobia and reduced vision. On examination, b conjunctivitis >2 weeks
there are cells in both anterior chambers. What is c conjunctivitis >3 weeks
the most likely diagnosis? d conjunctivitis >4 weeks
a scleritis
b conjunctivitis
c anterior uveitis
d keratitis
83 Double vision
Christine Chen
Monash University and Department of Ophthalmology, Monash Health, Melbourne,
Victoria, Australia
cranial nerve supplies the lateral rectus. It is essen-

Basic extraocular muscle anatomy tial to understand the nerve pathways that supply
the extraocular muscles and the pupil, a full
The extraocular muscles are divided into two
description of which is beyond the scope of this
groups. The first group arises from the apex of the
chapter.
orbit to attach to the sclera anterior to the equator
Extraocular muscle actions can be simply repre-
of the eye. Included in this group are the rectus
sented diagrammatically (Figure 83.1). The hori-
muscles: medial, lateral, superior and inferior. The
zontal recti abduct (away from nose) or adduct
second group consists of the oblique muscles. The
(towards the nose). The vertical recti elevate and
superior oblique arises from the apex of the orbit
depress the eye in abduction. The superior oblique
and is deviated through a pulley (the trochlear liga-
causes depression in adduction and the inferior
ment) in the anterior orbit so that it passes back-
oblique causes elevation in adduction. In addition,
wards and laterally above the globe to attach to the
the vertical muscles have secondary actions of
posterolateral area of the upper surface of the eye.
intorsion and extorsion.
The inferior oblique arises in the anterior orbit and
passes backwards and laterally under the globe to
attach to the posterolateral quadrant of the eye Diplopia
inferiorly.
The extraocular muscles are supplied by three Double vision (diplopia) is divided into two catego-
cranial nerves (Table 83.1). The third cranial nerve ries: monocular diplopia and binocular diplopia. It
passes forward in the lateral wall of the cavernous is important to identify the diplopia due to neuro-
sinus and divides anteriorly into the superior and surgical causes.
inferior divisions, which enter the orbit through the
superior orbital fissure. The superior division sup-
Monocular diplopia
plies the levator and superior rectus, while the infe-
rior division supplies the medial and inferior recti Double vision persists in the affected eye when the
and the inferior oblique. The fourth cranial nerve unaffected eye is occluded, usually due to benign
supplies the superior oblique muscle, and the sixth causes.
Table 83.1 Cardinal position of gaze, extraocular muscles and their cranial nerve supply.
Right and up Left and up

• Right superior rectus III • Left superior rectus III
• Left inferior oblique III • Right inferior oblique III
Right Left
• Right lateral rectus VI • Left lateral rectus VI
• Left medial rectus III • Right medial rectus III
Right and down Left and down
• Right inferior rectus III • Left inferior rectus III
• Left superior oblique IV • Right superior oblique IV
757
758 Problem Solving
RSR LIO>LSR RSR>RIO LSR>LIO RIO>RSR LSR
RLR LMR Primary position RMR LLR
RIR LSO > LIR RIR>RSO LIR>LSO RSO > RIR LIR
Fig. 83.1 Cardinal eye positions of gaze. The primary muscles active in each position are indicated below the associated
eye. First letter indicates right (R) or left (L), and the next two letters specify the muscle. SR, superior rectus; LR, lateral
rectus; IR, inferior rectus; MR, medial rectus; IO, inferior oblique; SO, superior oblique. Note the superior and inferior
rectus muscles contribute to vertical eye movements in all positions of gaze. Contributions from the oblique muscles are
greatest in adduction. Source: Mackay DD, Prasad S. Eye movements. In: eLS, July 2012. Chichester: John Wiley & Sons.
DOI: 10.1002/9780470015902.a0024018. Reproduced with permission of John Wiley & Sons.
Differential diagnosis –– Intermittent or constant: is the double vision

present all the time?
• Refractive error: astigmatism
–– Horizontal or vertical: are the two images side
• Cornea: opacity or irregularity
by side or one on top of the other?
• Lens: cataract, decentred natural or artificial
• Associated symptoms:
intraocular lens
–– Headache: a dilated pupil with third nerve
palsy and headache is a sign of cerebral aneu-
Binocular diplopia
rysm until proven otherwise
Double vision is eliminated when either eye is • History of trauma: orbital fracture or false local-
occluded. A neurosurgical lesion must be excluded. ising sign due to head injury
• Previous ophthalmic history: history of squint or
squint surgery
• Previous medical history: cardiovascular risk fac-
Intermittent tors, Graves’ disease, multiple sclerosis, myasthe-
• Myasthenia gravis nia gravis
• Intermittent decompensation of an existing stra-
bismus (squint)
Examination
Constant
Visual acuity (see Chapter 82)
• Isolated cranial nerve palsy: III, IV, VI
–– Pupil‐involving third nerve palsy is highly sug- Pinhole placed in front of the affected eye will elim-
gestive of a compressive lesion such as cerebral inate the double vision for most acquired causes of
aneurysm monocular diplopia.
–– Cranial nerve palsy can be a false localising
sign due to cranial space‐occupying lesions
such as tumour or haemorrhage Pupil
• Other central nervous system (CNS) lesions: inter- It is important to examine the pupil carefully for
nuclear ophthalmoplegia due to multiple sclerosis both direct and consensual responses. Pupils
• Orbital disease: thyroid eye disease, orbital inflam- should be tested with the patient fixating on a dis-
mation or tumour, trauma tant target and a bright pen torch. Next to vision,
this is perhaps the most important and easily elic-
History
ited sign.
• Nature of the double vision: • Observe the pupil:
–– Monocular or binocular: does the double –– round or irregular
vision persist when one eye is occluded? –– equal size in both eyes
83: Double vision 759
Inspection
No light
Observe for head posture, ptosis and eyelid swelling.
To observe corneal reflections, hold the pen torch
Direct response Consensual response 30 cm in the midline in front of the patient and observe
Response to the corneal reflections. The corneal light reflections
light should be positioned symmetrically on the patient’s
eye. If they are not, it indicates a likely deviation.
Equal response Equal response Cover test

Swinging Determine monocular or binocular diplopia.
light test
• In binocular diplopia, double vision is elimi-
nated when the occluder is placed in front of
either eye.
Fig. 83.2 Normal direct and consensual response. • In monocular diplopia, double vision persists
when the occluder is placed in front of the unaf-
fected eye, and is eliminated when the occluder is
No light placed in front of the affected eye.
Eye movements
Direct response Consensual response
Response to The patient is asked to follow an object in six direc-
light tions, the cardinal fields of gaze. This can be best
done by drawing a large imaginary ‘H’ in the air
between the patient and yourself. If there is an obvi-
Dilation Paradoxical dilation
ous abnormality, the examiner should also test each
eye individually, with the opposite eye occluded by
Swinging the patient’s palm.
light test
If the patient is an adult, a target such as a finger
or pen will suffice. If the patient is a child, a more
interesting target such as a toy is required for
Fig. 83.3 Swinging light reflex showing relative afferent cooperation.
pupil defect. In binocular diplopia, determine the following.
• Nature: horizontal, vertical or torsional diplopia.
–– associated eyelid and or eye position/move- Ask the patient if the two images are side by side,
ment abnormalities one on top of the other, or rotated.
• Direct and consensual response (Figure 83.2) • Where: in which direction of gaze is the diplopia
most pronounced?
Swinging light reflex (Figure 83.3)
This is to look for a difference in the afferent Cranial nerve examination
response of the optic nerves. It is an objective test of
optic nerve function and measures the strength of Identification of any other cranial nerve involved
one optic nerve relative to the other. may localise any underlying intracranial pathology.
• If one optic nerve is damaged, on direct illumina-
tion it will transmit a lesser signal to the brain- Third nerve palsy
stem which will result in a lesser constriction of In third nerve palsy, one or more of the muscles that
both pupils. the third nerve innervates can be affected to any
• When swinging the light from the unaffected to degree in any combination (Figure 83.4).
the affected side, both pupils will therefore dilate • Exotropia: medial rectus weakness
initially. • Hypertropia: inferior rectus weakness
• When swinging the light from the affected to the • Hypotropia: superior rectus ± inferior oblique
unaffected side, both pupils will constrict because weakness
of the stronger light signal received by the • Ptosis: levator palpebrae superioris weakness
brainstem. • Enlarged pupil: sphincter pupillae weakness
760 Problem Solving
Fig. 83.4 Patient with a right third cranial nerve palsy. In the upper picture he is attempting to look up: the right eye
fails to elevate. In the lower picture when he attempts to look down the upper lid elevates owing to misdirection of
nerve fibres from aberrant regeneration. In this case, fibres intended for the inferior rectus are innervating the levator
muscle of the upper lid.
• There may be signs of aberrant regeneration where should be sought, with advice from the neurosurgi-
there are changes in pupil size or eyelid position on cal team to exclude cerebral aneurysm. MRI or CT
attempted elevation, depression or adduction. brain with contrast should be obtained if a mass‐
In an isolated ischaemic third nerve palsy on the occupying lesion is suspected. CT for orbital frac-
affected side, the palsy should be complete: com- ture needs to specify CT orbit with fine cuts.
plete ptosis, no movement on attempted elevation, Presumed microvascular cranial nerve palsy
depression or adduction, with entirely normal pupil does not generally require neuroimaging. Be very
and fourth and sixth nerve function. careful to exclude possible neurosurgical causes
before making this diagnosis. The patient should
Fourth nerve palsy be referred to a physician and ophthalmologist for
The patient prefers their head tilted away from the follow‐up.
hypertropic eye. On cover testing, there is a vertical
and/or oblique deviation in the primary position.
Blood examination
On motility testing there is hypertropia in primary
position, which increases with ipsilateral head turn Full blood examination with measurement of eryth-
and ipsilateral head tilt. In the hypertropic eye, rocyte sedimentation rate (ESR) and C‐reactive
there is superior oblique underaction (limitation of protein (CRP) for presence of giant cell arteritis, a
depression in adduction) and inferior oblique over- bilateral blinding disease and a great masquerade.
action (upshoot in adduction). In the fixing (appar- Patients presenting with binocular diplopia or
ently hypotropic) eye, motility examination is reduced vision and aged over 60 years should have
entirely normal. In congenital fourth nerve palsy, blood tests to exclude giant cell arteritis.
there is often mild facial asymmetry. Targeted blood tests for other causes such as thy-
roid eye disease, myasthenia gravis and cardiovas-
Sixth nerve palsy cular risk factors (e.g. fasting blood sugar and lipid
The patient exhibits horizontal diplopia that is profile) should be undertaken by physicians.
worse for distance than near. In primary position,
there is esotropia and unilateral restriction of Ongoing management
abduction with slow abduction saccades apparent
on testing movement to the side of the lesion. Monocular diplopia which resolves with pinhole
can be referred to community eye care providers,
Primary management such as optometrists, for follow‐up. Binocular
diplopia not caused by neurosurgical causes should
It is important to remember that binocular diplopia be referred to physicians and/or ophthalmologists.
can be caused by life‐threatening neurosurgical
causes such as cerebral aneurysm.
Surgery for diplopia
At the end of the history and examination, one
must determine whether urgent neuroimaging and Surgery for diplopia is performed if reversible
neurosurgical referral is required. Magnetic reso- causes have not been identified, spontaneous reso-
nance or computed tomography (CT) angiography lution has not occurred after at least 6 months and
83: Double vision 761
the condition has stabilised. The principles of sur- b in abduction, the inferior rectus depresses
gery for double vision are: the eye
• to strengthen weak muscles by shortening them c in adduction, the inferior oblique muscle intorts
• to weaken overacting muscles by effectively the eye
lengthening them. d in abduction, the inferior oblique muscle intorts
A muscle is strengthened by excising some of the the eye
tendon and then re‐suturing it to its original inser-
tion. A muscle is weakened by removing it from the 2 Which of the following conditions can cause
globe and re‐attaching it closer to its origin. monocular diplopia?
The primary intention is to at least gain single a refractive error
vision in the primary and depressed positions, b cataract
which are the most commonly used areas of gaze, c corneal irregularities
while diplopia may still remain in other position of d all of the above
gaze.
3 If a patient is suspected to have a third nerve palsy,
what is the most appropriate management?
Further reading a refer patient to emergency department urgently
for further assessment and investigations
Bowling B. Kanski’s Clinical Ophthalmology: A b refer patient to physician for cardiovascular risk
Systematic Approach, 8th edn. Elsevier, 2016. factors work‐up
James B, Bron A, Parulekar MV. Lecture Notes in c assure patient that the double vision will resolve
Ophthalmology, 12th edn. Oxford: Wiley Blackwell,
within 6 months
2016.
d refer patient to ophthalmologist for squint
Pane A, Miller NR, Burdon M. Neuro‐Ophthalmology
Survival Guide, 2nd edn. Elsevier, 2018. surgery
Snell RS, Lemp MA. Clinical Anatomy of the Eye, 2nd
edn. Oxford: Wiley Blackwell, 2016. 4 A 37‐year‐old nurse with new‐onset headache
is unable to abduct the right eye and has
horizontal diplopia. The diplopia resolves when
MCQs she covers either eye. Which of the following is
correct?
Select the single correct answer to each question. The a she may have a right sixth nerve palsy as a false
correct answers can be found in the Answers section localising sign
at the end of the book. b she has a right exotropia
c she has thyroid eye disease
1 With reference to the actions of the extraocular
d she has a microvascular right sixth nerve palsy
muscles, which of the following is correct?
a in adduction, the superior oblique elevates
the eye
Answers to MCQs
Chapter 1 Chapter 2 Chapter 3 Chapter 4

1 d 1 e 1 b 1 d
2 c 2 d 2 d 2 c
3 a 3 e 3 a 3 c
4 c 4 d 4 e

1 c 1 c 1 c 1 c
2 d 2 d 2 c 2 e
3 a 3 b 3 d 3 a
4 a 4 d 4 d
5 a 5 b

1 b 1 c 1 b 1 b
2 b 2 a 2 c 2 e
3 e 3 e 3 c 3 e
4 e 4 c 4 e 4 b
5 d 5 d
6 c

1 b 1 a 1 a 1 b
2 e 2 b 2 c 2 d
3 c 3 c 3 d 3 c
4 c
5 d
763
764 Answers to MCQs

1 b 1 b 1 d 1 c
2 a 2 d 2 e 2 e
3 b 3 c 3 d 3 e
4 a 4 e
5 b 5 a

1 d 1 d 1 b 1 d
2 b 2 b 2 b 2 c
3 d 3 e 3 c 3 b
4 b 4 b 4 d 4 a
5 d 5 e 5 c
6 d 6 c

1 a 1 d 1 b 1 d
2 c 2 e 2 d 2 d
3 b 3 d 3 c 3 b
4 a 4 d 4 b 4 c

1 e 1 d 1 c 1 e
2 b 2 c 2 b 2 d
3 b 3 b 3 c 3 b
4 e 4 e 4 d 4 e

1 a 1 b 1 c 1 c
2 e 2 e 2 b 2 d
3 d 3 a 3 d 3 a
4 a 4 c 4 d 4 d

1 d 1 a 1 b 1 d
2 a 2 b 2 d 2 b
3 c 3 e 3 e 3 c
4 b 4 b 4 a
5 e 5 d 5 c
Answers to MCQs 765

1 b 1 d 1 a 1 c
2 b 2 d 2 d 2 b
3 e 3 c 3 c 3 a
4 b 4 e
5 c 5 d

1 c 1 a 1 b 1 d
2 d 2 e 2 c 2 b
3 e 3 c 3 e 3 e
4 b 4 d 4 e 4 a
5 e 5 e

1 e 1 a 1 a 1 b
2 d 2 c 2 b 2 a
3 a 3 a 3 a 3 b
4 e 4 d 4 a 4 a
5 b 5 c

1 c 1 d 1 b 1 d
2 d 2 c 2 a 2 b
3 a 3 c 3 e 3 a
4 c 4 c 4 e 4 b
5 d 5 b
6 d

1 d 1 c 1 c 1 c
2 a 2 a 2 e 2 d
3 e 3 c 3 c 3 d
4 d 4 e 4 d 4 d
5 e 5 b 5 c

1 a 1 d 1 a 1 e
2 b 2 c 2 c 2 e
3 e 3 a 3 b 3 b
4 e 4 d 4 b 4 e
5 e
766 Answers to MCQs

1 d 1 c 1 b 1 c
2 b 2 d 2 e 2 d
3 b 3 a 3 c
4 a 4 c
5 c 5 b

1 a 1 c 1 c 1 a
2 c 2 c 2 b 2 d
3 d 3 b 3 a 3 c
4 e 4 c 4 f
5 e 5 d 5 e

1 c 1 c 1 c 1 c
2 c 2 a 2 d 2 a
3 b 3 d 3 e 3 b
4 e 4 d 4 e
5 b
6 c
7 c
8 d

1 c 1 d 1 d 1 c
2 b 2 b 2 c 2 c
3 d 3 c 3 a 3 d
4 a 4 b
5 d
Chapter 81 Chapter 82 Chapter 83

1 e 1 c 1 b
2 d 2 c 2 d
3 b 3 c 3 a
4 d 4 a
Index
Page numbers in italic refer to figures.

Page numbers in bold refer to tables or boxes.
abdomen subperiosteal, 465 acute pancreatitis, 199–205

abscesses, 654–656 wounds, 30 positron emission tomography, 211
distension, 661 see also intra‐abdominal acute peripancreatic fluid collection,
pressure, 382–383 collections 201, 202
see also acute abdomen; intra‐ absorbable sutures, 41 acute primary peritonitis, 652
abdominal collections accessory nerve acute surgical units, 109
abdominal aortic aneurysms, lymph nodes, 667 adalimumab
528–529 neck dissection, 364 Crohn’s disease, 263
devices to exclude, 555 acetazolamide, intraocular ulcerative colitis, 258
endovascular management, 556–557 pressure, 356 Addisonian crisis, 349
rupture, 653 acetylcholinesterase inhibitors, 291 adenocarcinoma
abdominal wall achalasia, 682 chronic pancreatitis, 205
causes of pain, 111 achondroplasia, 474 ethmoid sinus, 363
weaknesses, 382 acid‐base balance, gastrointestinal lung, 610
abdominoperineal resection, rectal tract, 237 metastases to neck, 672
cancer, 278, 280 acids, chemical burns, 447 oesophagus, 123, 124–125
ablation aciduria, paradoxical, 140 parotid gland, 374
hepatocellular carcinoma, 182 acinic cell tumour, 374 small bowel, 245
prostate carcinoma, 579–580 acoustic neuromas, 500–501 stomach, 143–147
renal cell carcinoma, 582–583 acral lentiginous melanoma, 401 adenoid cystic carcinoma, 374
varicose veins, 549 acromegaly, 502 adenoidectomy, airway
abrupt‐onset severe headache, ACTH see adrenocorticotropic obstruction, 676
745–748 hormone adenoids, 363
abscesses actinic keratosis, 398 adenolymphoma, 373–374
brain, 507–508 active surveillance, prostate adenoma–carcinoma pathway,
Crohn’s disease, 263, 266 carcinoma, 579 colorectal carcinoma, 273
diverticulitis, 269, 270 ACTS‐GC trial, gastric adenomas
percutaneous drainage, 269–270 carcinoma, 147 aldosterone‐producing, 347, 348
epidural, 718 acute abdomen, 111, 649–652, colorectal, 281
extremities, 416–417 653, 656 pleomorphic, 373, 374
intra‐abdominal, 654–656 acute cholecystitis, 165, 170 thyroid, 370
kidney, 570 appendicitis vs, 251 adenomatous polyposis coli gene,
liver Tokyo guidelines, 166 273, 282
amoebic, 193 acute colonic pseudo‐obstruction, adenosquamous carcinoma, lung, 610
pyogenic, 191–193 290–291 adhesions
perineal, 301–302 acute limb ischaemia, 533–534, 535 division, postoperative
peritonsillar (quinsy), 363 endovascular procedures, 559–560 management, 233
pilonidal sinus, 305 Rutherford classification, 560 small bowel obstruction, 245
right iliac fossa mass, 252 acute necrotic collection, pancreatitis, adhesives
skin cancer vs, 369–372 201, 202 cyanoacrylate, 41
spinal, 520 acute pain medicine, 23–24 drapes, 103
767
768 Index
adjuvant therapy, 88 benign prostatic hyperplasia, anal intraepithelial neoplasia,

breast carcinoma, 325–326 568–569 298–299
gastric carcinoma, 147 kidney stones, 566 anal plugs, 628
gliomas, 496 alpha‐fetoprotein (AFP) anal reflex, 723
melanomas, 401–402 germinomas, 503 anal verge, 293
pancreatic cancer, 215 hepatocellular carcinoma, 181 anaphylaxis, airway obstruction, 675
rectal cancer, 280 ALPPS procedure, 189 anaplastic high‐grade neuroendocrine
adrenal cortex, 345 Altemeier procedure, 299 tumours, 148–149
carcinomas, 347 alternate pathway, bile acids, 163 anaplastic thyroid carcinomas, 334
tumours, 346, 347–348 altruistic donors, 76 anastomoses
adrenalectomy, 349 alveolar cell carcinoma, lung, 610 bowel surgery, 231, 232–233
adrenal glands, 345 alveolar echinococcosis, 195–196 diverticulitis, 270–271
tumours, 345–349 amaurosis fugax, 538 large bowel obstruction, 289
adrenaline, 61 ambivalence, approach–avoidance, 93 rectal cancer, 278, 279
adrenal medulla, 345 ambulatory venous ileal pouch–anal, 283
adrenocorticotropic hormone hypertension, 689 ileorectal, colectomy with,
(ACTH) American College of Surgeons, online 260, 265
levels, 348 risk calculator, 22 oesophagectomy, leaks, 129–130
tumours producing, 502–503 American Society of portosystemic, 219, 219–220, 664
afterload‐reducing agents, 599 Anesthesiologists, risk scoring androgen deprivation therapy, 580
AIDS system, 14–15, 22 andropause, 580
cachexia, 51 aminosalicylates, 256, 262 aneurysms, 527–529
see also HIV ammonia, hepatic aortic arch, cardiopulmonary
airflow, operating rooms, 101 encephalopathy, 223 bypass for surgery, 587
air‐fluid levels, 244, 245 amnesia aortic dissection, 598
airway concussion, 484 cerebral, 503–506, 745–746, 758
intraoperative interventions, 23 post‐traumatic, 735 devices to exclude, 555
obstruction, 675–678 amoebic liver abscess, 193 endovascular management,
preoperative assessment, 19, 20 ampicillin, 467 556–557
trauma, 436, 490, 737 AMPLE (mnemonic), 450 false, 527, 534
AJCC/UICC staging ampulla of Vater, familial left ventricle, 591
cholangiocarcinoma, 177 adenomatous polyposis, 283 thoracic aorta, 597–598
gallbladder carcinoma, 179 Amyand’s hernia, 382 see also abdominal aortic
hepatocellular carcinoma, 182 amylase aneurysms
see also TNM staging pancreatic cystic diseases, 217 angina, 589
alanine aminotransferase, 644 pancreatitis, 203, 653 surgical risk, 16
alarm symptoms, gastro‐oesophageal anaemia, preoperative management, angiofibroma, juvenile, 363, 711
reflux disease, 118 10, 21 angiography, 530–531, 556
albendazole, hydatid cysts, 195 anaerobic bacteria, colon, 66 carotid, 539, 540
ALBI grade, hepatocellular anaesthesia, 19–24, 97–98 computed tomography
carcinoma, 181 airway obstruction, 677 abdominal aortic
albumin, 52 epidural, on stress response, 55 aneurysms, 528
ascites, 659 preoperative assessment, 15–16, massive rectal bleeding, 634–635
gradient to serum, 662 19–22 pulmonary, 700–701
large bowel obstruction, 286 risks, 5 coronary, valvular heart
resuscitation solutions, 60 anaesthesia machines, monitoring disease, 593
alcohol with, 23 mesenteric, 635
breast carcinoma, 317 anal canal, 293, 294 small bowel ischaemia, 246–247
pancreatitis, 200, 205, 206 manometry, 294 angiography suites, 553–556
withdrawal, 31, 700 SECCA therapy, 631 angiomyolipoma, 582
alcohol (antiseptics), 36, 47, 102 sepsis, 301–306 embolisation, 561
aldosterone, adenomas producing, squamous cell carcinoma, 298–299 angiomyoma, 404
347, 348 anal fissure, 296 angioplasty, 531
aldosteronism, secondary, 660 Crohn’s disease, 266 carotid, 541
alkaline phosphatase, 644 analgesia coronary, 589
alkalis, chemical burns, 447–448 chest trauma, 740 stenting, 554–555
allergies, preoperative multimodal, 23–24 angiosarcoma, head and neck,
management, 8 post‐traumatic confusion, 739 371, 376
allografts, heart valves, 595 anal glands, 301 angiotensin‐converting enzyme
alpha‐blockers anal incontinence, 625 inhibitors, 599
Index 769
angle closure glaucoma, 753, 754 antiplatelet therapy arteriovenous malformations, 505
predisposing factors, 750 epistaxis, 711 massive haemoptysis, 708
anismus, 620 preoperative management, 9 subarachnoid haemorrhage,
ankle–brachial index, 530, 690 bowel surgery, 229 503, 746
annuloplasty antiseptics, 36, 46–47, 102 arthritides, 467–471
mitral valve, 594 antithyroid drugs, 335 leg pain, 721
tricuspid valve, 596 anti‐TNF agents arthrodesis, 469
anorectal complex, 625 Crohn’s disease, 263, 266 arthroscopy, 39
anorectal manometry, 621, 628 ulcerative colitis, 258 articular cartilages, wear, 721
antacids antrectomy, 135, 136 artificial bowel sphincter, 629
gastro‐oesophageal reflux anus see anal canal; anorectal ARTIST trial, Korea, gastric
disease, 120 complex carcinoma, 147
peptic ulcer disease, 135 anxiety, preoperative ASA (American Society of
antalgic gait, 715, 721 management, 11 Anesthesiologists), risk scoring
anterior anal sphincter repair, 629 aorta system, 14–15, 22
anterior cervical cord syndrome, 522 aneurysms see abdominal aortic ascariasis, biliary, 197
anterior mediastinotomy, 605 aneurysms ascites, 219, 659–665
anterior resections, rectal cancer, 278 coarctation, 597 surgery and, 665
anthropometry, 52 dissection, 589 treatment, 220–221, 663–665
antiandrogen agents, 580 aneurysms, 598 asepsis, 35–36
antibiotics aortic arch aneurysm, Ashkenazi Jews, breast
abdominal abscess, 655 cardiopulmonary bypass for carcinoma, 318
acute abdomen, 651–652 surgery, 587 aspartate aminotransferase, 644
cellulitis, 419 aortic valve disease, 592 aspiration
epididymo‐orchitis, 732 aortic valve surgery, 593 joints, 467, 468
Helicobacter pylori prostheses, 595, 596 liver abscess, 192
eradication, 135 aorto‐enteric fistula, 529 pleural effusions, 605
liver abscess, 192 aorto‐iliac disease, 530 aspiration (pulmonary), risk of, 20
meningitis, 506–507 APACHE scoring systems, 15, 61 aspiration thromboembolectomy, 559
open fractures, 460–461 APC gene, 273, 282 assistants, 35, 100
osteomyelitis, 466 Apfel risk score, PONV, 21 asthma, preoperative management,
perianal Crohn’s disease, 265–266 apixaban, 9, 704 9, 20
prophylactic, 6, 46, 67–68, 101 apnoea–hypopnoea index, 152 astrocytoma, 493–496
appendicectomy, 252 apocrine sweat glands, 419–420 cerebellum, 498
colorectal carcinoma, 276 appendicectomy, 251–252 spinal cord, 519
pancreatitis and, 204 surgical risk, 14 asymptomatic bacteriuria, 570
transplant patients, 85 appendicitis, 249–252 pregnancy, 571
pseudomembranous colitis, 70 appendix Asymptomatic Carotid
resistance see antimicrobial in hernias, 382 Atherosclerosis Study, 540
resistance retrocaecal, 250 atherosclerosis, 527
septic arthritis, 467 appendix of the epididymis, carotid bifurcation, 537
septic shock, 703 727–729 coronary arteries, 588
stewardship, 71–72 appendix testis, 573, 727–729 athlete’s foot (tinea pedis), 415–416,
ventilator‐associated pneumonia, 70 approach–avoidance ambivalence, 93 551, 688
antibody‐mediated transplant arginine, 55 atrial fibrillation
rejection, 82 aromatase inhibitors, 326, 327 mitral valve disease, 594
anticoagulants arrhythmias, surgery for, small bowel ischaemia, 246
cardiac valve surgery, 596 598–599 atrial septal defect, 597
direct oral, 704 arterial blood gases, 603, 737, atypical ductal hyperplasia, breast,
epistaxis, 711 741–742 315, 322
preoperative management, 9 arteries atypical lipomas, 403
bowel surgery, 229 catheterisation, 556 atypical lobular hyperplasia,
anticonvulsants, for pain, 24 disorders, 527–535 breast, 315
anti‐CTLA4, 402 leg ulcers, 689, 690 atypical symptoms, gastro‐
antidiuretic hormone, 32 leg pain, 721 oesophageal reflux
anti‐integrin agent, ulcerative repair, 535 disease, 118
colitis, 258 trauma, 440, 534–535 auditory prostheses, bone‐
antimicrobial resistance, 71–72 arteriography see angiography conducting, 361
Helicobacter pylori, 135 arteriovenous fistulas, 534 Australian Paired Kidney Exchange
Staphylococcus aureus, 416 leg swelling, 688 program, 76
770 Index
autoclaves, 36 balloon valvuloplasty, binocular diplopia, 758–761

autoimmune pancreatitis, 206, 645 percutaneous, 593 Biobrane™, 453
autonomic neuropathy, 533 bandaging biofeedback
autotransplantation, parathyroid leg ulcers, 691 constipation, 621
glands, 342–343 varicose vein surgery, 548 faecal incontinence, 628
awake fibre‐optic intubation, 677 bariatric surgery, 151–159 biological therapies, 88
axillary dissection, 325 gastro‐oesophageal reflux Crohn’s disease, 263
axillary lymph nodes disease, 120 pre‐immune suppression
breast carcinoma, 319 barium enemas, constipation, 619 screen, 258
surgery, 325 barium meals, 136 ulcerative colitis, 258
axonotmesis, 511 barium swallows, 119 see also molecular therapy
axons, 511 Barrett’s oesophagus, 116, 123–124 biomarkers
azathioprine, 81, 257–258, 262 sleeve gastrectomy, 155 colorectal liver metastases, 187
azithromycin, 357 barrier protection, gastrointestinal sepsis, 58
chlamydial conjunctivitis, 752 mucosa, 133 biopsy
epididymo‐orchitis, 732 barrier protection (Universal bone sarcomas, 478
Precautions), 35–36, 37 breast, 311–312
bacillus Calmette–Guérin, basal cell carcinoma, 398 breast carcinoma, sentinel
intravesical, 581 head and neck, 371, 372 node, 325
back pain, 715–726 basal‐like breast carcinoma, 324 cancer, 89
bacteraemia Bascom’s procedure, 306 chest, 605
defined, 59 batteries, airway obstruction, 676 endobronchial, 604
portal vein, 191 Beger procedure, 207 hepatobiliary malignancy, 176
bacteria bell clapper deformity, 573, 727 kidney, 581
brain abscesses, 508 benign prostatic hyperplasia, neck lumps, 669–670
central line‐associated bloodstream 568–569 osteoporosis, 475
infections, 68 haematuria, 694 pancreatic cancer, 211
colon, 101 benzylpenicillin, meningitis, 507 pleura, 605, 608
drug‐resistant, 71 beri‐beri, sleeve gastrectomy, 155 prostate, 578
Helicobacter pylori, 135 β‐human chorionic soft tissue tumours, 409,
Staphylococcus aureus, 416 gonadotrophin, 503 410–411
empyema of gallbladder, 165 Bethesda classification, thyroid bipolar diathermy, 100
gastrointestinal tract, 654 nodules, 332 birth injuries, 512
infections of extremities, bevacizumab, colorectal liver birthmarks, 404
416–422 metastases, 187 Birt–Hogg–Dubé syndrome, 582
infective endocarditis, 68 bicarbonate bite wounds, organisms, 418
keratitis, 752 ICF and ECF, 27 bladder
meningitis, 506 in secretions, 28 anatomy, 565
necrotising fasciitis, 71 see also sodium bicarbonate carcinoma, 580, 581
prostatitis, 570 bile haematuria, 694
sepsis, 58 electrolytes, 28 stones, 694–695
stomach, 66 leak into peritoneum, 661 bladder outlet obstruction, 568
surgical site infections, 67 production, 163–164 bleeding
see also flora bile acids, 163–164 gastrointestinal, 137–138,
bacterial infections short‐gut syndrome, 240 221–223
liver, 191–193 bile duct injury, laparoscopic haemorrhoids, 297–298
peritonitis, 219 cholecystectomy, 169–170 perianal, 293–294
bacteriuria, 72 biliary colic, 165 postoperative, 702–703
asymptomatic, 570 biliary tract rectal, 137, 293–294, 633–635
pregnancy, 571 ascariasis, 197 see also haemorrhage
Bairnsdale ulcer, 420 ascending infections, 191 blepharitis, 750, 752, 753
balanced salt solutions, 60 stenting, distal tumours, 646 blisters, burns, 444
balanitis xerotica obliterans, 572 ultrasound, 644–645 blood cultures
balloon angioplasty, 531, 554 see also cholangiocarcinoma; osteomyelitis, 465
balloon‐expandable stents, 555 cholangitis; cholelithiasis septic arthritis, 467
balloon expulsion test, rectum, 621 biliopancreatic diversion with blood gases, 603, 737, 741–742
balloon‐occluded retrograde duodenal switch, 158 blood pressure, organ failure, 203
transvenous obliteration, bilirubin, 644 blood supply, 424, 426
bleeding varices, 222 Biliscopin, 174 colon, 231
balloon pumps, intra‐aortic, 599 Billroth II gastrectomy, 136, 137 nasal cavity, 711
Index 771
blood transfusion reconstruction, 424 perforation, 251

acute abdomen, 651, 653 reduction surgery, 427 volvulus, 290
haematemesis, 638 breast carcinoma, 317–328 CagA‐positive H. pylori, gastric
massive haemoptysis, 708 assessment, 309–312 carcinoma, 143
preoperative, 10 follow‐up, 91, 327 calcification
blow‐out fracture, orbit, 354–355 genetics, 318 hyperparathyroidism, 341
blue dot sign, 729 histopathology, 319–324 mammography, 323
blunt injury, 433 incidence, 317 calcineurin inhibitors, 81
arteries, 534 molecular subtypes, 322–324 calciphylaxis, 341
head, 483 prevention, 318 calcium
body composition, 49–50, 52 risk factors, 317–318 dietary requirements, 50
body mass index (BMI) risk from benign disease, 315 ICF and ECF, 27
indications for bariatric screening, 318 pancreatitis, 200, 205
surgery, 152 spread, 318–319 24‐hour urine collection, 340
malnutrition, 50 staging, 319, 320, 321 calcium channel blockers, 599
obesity, 151 treatment, 324–327 anal fissure, 296
body water, 27 breathing calcium gluconate, 33, 448
Bolam test, 3 acute problems, 675–678 calculi see cholelithiasis; kidney
bone(s) burns, 448 stones
cancer, 478–480 head injuries, 489 calf compression devices, 7
hyperparathyroidism, 341, 472 monitoring, 439 calf muscle pump, 546, 687, 689
hyperthyroidism, 471–472 primary survey, 437 Call–Fleming syndrome, 746–747
infections, 465–467 see also respiratory disease Cameron’s ulcers, 117
Paget’s disease, 474–475 brochures see patient explanatory canal wall‐down mastoidectomy,
prostate carcinoma brochures 360, 361
metastases, 577 bronchi, foreign bodies, 676 canal wall‐up mastoidectomy,
scans, elderly patients, 457 bronchiectasis, 707 360–361
tumours, 473–474, 478–480 bronchoscopy, 38, 604 cancer
head and neck, 371, 376 airway obstruction, 677 ascites, 660, 661, 663
bone‐conducting auditory inhalation injury, 448 Crohn’s disease, 261
prostheses, 361 massive haemoptysis, 708 haematuria, 693–694
bone mineral density Brown–Séquard syndrome, 522 from immunosuppression, 83
hyperparathyroidism, 340 bruits, carotid, 538, 540 lymphoedema, 550
scans, 475 bubonocele, 385 malnutrition, 51
botulinum toxin, anal fissure, 296 Budd–Chiari syndrome, 219, 659 see also oncology; specific sites and
bowel function, rectal cancer budesonide, 257 tumours
surgery, 278 bulbar palsy, 679 candy cane Roux syndrome, 157
bowel preparation, 230 bulking agents (dietary), 628 cannulas, intravenous access, 22–23, 43
bowel sounds, large bowel bulking agents (injectable), 629 capecitabine, pancreatic cancer, 215
obstruction, 286 bundle of care, 101 capittonage, 195
brachial plexus injury, 512–513, 514 buried mucous fistula, 289 capsule endoscopy, 635
brachytherapy, 88 burns, 443–454 caput medusae, 220
prostate carcinoma, 579 from antiseptics, 102 carbohydrate antigen 19‐9,
BRAF inhibitors, 402 classification, 444–445 pancreatic cancer, 211
BRAF mutations, colorectal liver eyelids, 356 carbohydrates, 49–50
metastases, 187 mechanism, 445–448 dietary requirements, 240
brain death, 77, 78, 82 on metabolism, 51–52 drinks, 54
brain injury, 735, 738, 740–741 systemic effects, 451 carbon dioxide
secondary, 737 teamwork, 453–454 as contrast medium, 556
see also head injuries wound care, 450–453 expired, monitoring, 23
brainstem tumours, clinical burns units, indications for transfer heart surgery operative field, 593
features, 498 to, 450 saturation, postoperative, 29
brain tumours see intracranial Buruli ulcer, 420 carcinoembryonic antigen (CEA)
tumours bypass grafts, 531 colorectal carcinoma, 275
branchial cysts, 669, 670, 671 see also coronary artery bypass pancreatic cystic diseases, 217
breast grafting surveillance after hepatectomy, 189
anatomy, 309 carcinoid syndrome, 216, 246
normal ducts, 322 cachexia, 50, 51 carcinoma
assessment, 309–312 caecopexy, 290 neuroendocrine, 216
benign disease, 312–316 caecum see also specific sites and tumours
772 Index
cardiac arrest cefalotin, 460, 466 colorectal liver metastases,

extracorporeal membrane cefotaxime, meningitis, 507 184–185, 186–187
oxygenation, 600 ceftriaxone, 461 gastric carcinoma, 146–147
imminent, 438 epididymo‐orchitis, 732 gliomas, 496
induced for surgery, 587–588 meningitis, 507 on liver, 173
cardiac failure cellulitis, 418–419, 551, 688 lung carcinoma, 611–612
leg swelling, 686 lymphatics, 420 melanomas, 401
postoperative, 32 central cord syndrome, 522 pancreatic cancer, 214–215
surgical risk, 16 central lines, 23, 43, 55 rectal cancer, 280
cardiac surgery, 587–601 bloodstream infection, 68–69 soft tissue sarcomas, 412–413
cardiac transplantation, 600 long‐term, 43 chest
results, 84 central sterile and supply analgesia for trauma, 740
cardiac valve surgery, 592–596 departments (CSSD), 104–106 empyema, 608
cardinal positions of gaze, 757, central venous pressure, 25 imaging, 603–604
758, 759 cerebellum, astrocytoma, 498 see also thoracic surgery
cardiogenic shock, 591 cerebral aneurysm, 503–506, chest pain, 589
cardioplegia solution, 588 745–746, 758 postoperative, 700–701
cardiopulmonary bypass, 587 cerebral contusion, 483 chest tubes, 605–606, 609
cardiovascular disease cerebral oedema, from fluid chest wall, disorders, 607
preoperative management, 8–9, replacement, 449 childbirth
20–21 cerebral swelling, 483 epidural abscess, 718
surgical risk, 5, 16 cerebral vasospasm, 505 obstetric injury, 626, 631
C‐arms, angiography, 553 cerebrospinal fluid Child–Pugh score, 173, 181,
carotid angiography, 539, 540 meningitis, 506 223–224
carotid artery stenting, 541 post‐traumatic confusion, 738, 742 children
carotid body tumours, 375, 538, 669 rhinorrhoea, 362, 491 airway obstruction, 676
carotid disease shunts, 498 burns, fluid management, 449
atherosclerosis, 537 subarachnoid haemorrhage, 504, cochlear implants, 361–362
post‐traumatic, 741 745, 746 epistaxis, 711
preoperative management, 9 cerebrovascular disease, 537–543 inguinal hernia, 387
carotid endarterectomy, 539–542 see also stroke intracranial tumours, 497–498
carpal tunnel syndrome, 513–515 cervical lymph nodes, 366–367, 369, juvenile naevus, 400
castration, medical, 580 667, 668, 669–670 malnutrition, 50
catabolism, 51–52 upper aerodigestive tract meningitis, 506
catecholamines, 346–347 cancer, 364 obstructive sleep apnoea, 363
catgut, 41 cervical myelopathy, 520–521, 721 oesophageal foreign body, 676
catheter(s), intravenous, 23, 43 cervical nerve roots, 716 rhabdomyosarcomas, 376
catheter‐associated urinary tract tumours, 375 subarachnoid haemorrhage, 503
infections, 70 cervical oesophagus, cancer total body surface area, 444, 446
catheter‐directed thrombolysis, 559 surgery, 127 umbilical hernia, 391
catheterisation cervical screening, 89 chlamydial conjunctivitis, 752
arteries, 556 cervical spine, trauma, 435, 490, Chlamydia trachomatis, 357
urinary 521, 522 chloramphenicol ointment, for eye
burn patients, 449 Chagas’ disease, 682 injuries, 356, 357
trauma, 438 Charcot’s disease, 476 chlorhexidine, 36, 102
catheter laboratories, 553–556 Charcot’s triad, 166, 643 chloride
cationic trypsinogen gene, 200 checklists, 37, 99, 106 ICF and ECF, 27
Cattell–Braasch manoeuvre, 79 chemical injuries, 446–448 in secretions, 28
cauda equina, 716 eye, 354 cholangiocarcinoma, 176–178, 646
compression, 519 chemical peritonitis, 654 perihilar
cauda equina syndrome, 716–717, chemoembolisation, 560 imaging, 175–176
722, 725 TACE, 183 treatment, 178
cautery, 100 chemoprevention, breast cholangiography, 645
epistaxis, 712 carcinoma, 318 computed tomography, 174, 645
caval filters, 31–32 chemoradiotherapy, rectal cancer, intraoperative, 646
C chart, 751 278, 280, 289 percutaneous transhepatic, 646
CD4‐positive T cells, 82 chemotherapy, 88 see also endoscopic retrograde
CD8‐positive T cells, 82 bowel surgery, 229 cholangiopancreatography
CDH1 gene, gastric carcinoma, 143 breast carcinoma, 326 cholangitis, 166
CDKN2A gene, 400 cholangiocarcinoma, 178 bacterial, 191
Index 773
Clonorchis sinensis, 196 circulation familial adenomatous polyposis, 283

Tokyo guidelines, 167 burns, 448–449 with ileorectal anastomosis,
cholecystectomy, 169 monitoring, 439 260, 265
after gallstone pancreatitis, 205 primary survey, 437 left hemicolectomy, 277
incidentally discovered gallbladder circulatory death, 77–78 patients with cirrhosis, 225
cancer, 179–180 circulatory support, 599–600 subtotal, 260–261
patients with cirrhosis, 224, 225 circumferential burns, 448, 450 toxic megacolon, 260–261
see also under laparoscopic cirrhosis see also proctocolectomy; right
surgery cholelithiasis, 164–165 hemicolectomy
cholecystitis see acute cholecystitis portal hypertension, 219 colic, 650
cholecystostomy, 170 signs, 220 colitis
choledocholithiasis surgery on patients with, 223–225 ischaemic, 247
endoscopic ultrasound, 168 Clark’s levels of invasion, see also inflammatory bowel
ERCP, 645–646 melanomas, 401 disease
magnetic resonance classic pathway, bile acids, 163 collapse (pulmonary), 611
cholangiopancreatography, CLASSIC trial, gastric signs, 604
169 carcinoma, 147 collapse (vertebral), 725
obstructive jaundice, 166, 168 claudication, 529, 531, 532, 557, Colles fracture, 458
pancreatitis, 204 715, 717, 721, 724 colloid cyst of third ventricle, 501
ultrasound, 168 claw hand, 516 colloids, 60
cholelithiasis, 163–171 clean‐contaminated wounds, 6, colon
Crohn’s disease, 164, 262 46, 67 bacteria, 66, 101
diagnosis, 167–169 clean procedures, 6 blood supply, 231
Roux‐en‐Y gastric bypass, 157 clean wounds, 46, 67 cancer see colorectal carcinoma
short‐gut syndrome, 240 clear fluids, preoperative, 20 diverticular disease, 267–272
treatment, 169–170 clinically relevant postoperative elective surgery, 271–272
cholesteatoma, 360–361 pancreatic fistula strictures, 285, 290
cholesterol, gallstones, 164 (CR‐POPF), 212 Gardner’s syndrome, 406
cholesterol 7α‐hydroxylase, 163 clinical trials, 91 motility, 617
chondrosarcomas, 478–479 clips nutritional function, 238
chordae, mitral valve, haemostatic, 40 obstruction see large bowel
replacement, 594 mitral valve, 596 obstruction
choroidal rupture, 356 cloacas, 465 short‐gut syndrome and, 240
chromic catgut, 41 Clonorchis sinensis, 196 surgery, 229–235
chromoendoscopy, 145 closed cardiac surgery, 588 mobility, 232
chromogranin A, gastric mitral valvotomy, 593 see also colectomy
neuroendocrine tumours, 148 closed drainage, 42 transit testing, 619–620
chromosomal instability, colorectal closed fractures, 457, 459 colonoscopy
carcinoma, 273 closed gloving, 103 acute colonic pseudo‐obstruction,
chronic conjunctivitis, 750 closed injury, arteries, 534 290–291
chronic infective arthritis, 468 Clostridium (spp.), 421 adenomas, 281, 282
chronic kidney disease Clostridium difficile infection, 70, 72 colorectal carcinoma, 275
hyperparathyroidism, 341, 342 closure devices, arteriography, 556 Crohn’s disease, 262
preoperative management, 10, 21 CMM2 gene, 400 diverticulosis, 268
chronic limb ischaemia, 529–533 coagulation disorder perianal disorders, 295
endovascular procedures, 557–560 large bowel obstruction, 286–287 preoperative, 230
chronic obstructive pulmonary liver disease, 10 rectal bleeding, 294, 633, 634
disease, preoperative peritoneovenous shunts, 665 sigmoid volvulus, 290
management, 9, 20 coarctation of the aorta, 597 surveillance after hepatectomy, 189
chronic otitis media, 359–361 cochlear implants, 361–362 ulcerative colitis, 256
chronic pancreatitis, 205–207 codeine, short‐gut syndrome, 240 colorectal carcinoma, 273–284
pancreatic cancer, 209 coeliac axis, pancreatic cancer, 212 aetiology, 273, 274
chronic pelvic pain, 570 coffee‐ground vomit, 137 bleeding, 293–294
chronic transplant dysfunction, 82 coils (embolic), 554 constipation, 619
chylothorax, 130, 608 cerebral aneurysm, 506 epidemiology, 273
ciclosporin, 81 coin lesions, 611 follow‐up, 91, 280–281
cinacalcet, 342 see also solitary pulmonary inflammatory bowel disease and,
circle of Willis, 537 nodule 255–256
circular staplers, 233 colectomy, 276–278 large bowel obstruction, 286,
circulating nurses, 98 Crohn’s colitis, 265 289–290
774 Index
colorectal carcinoma (cont’d ) liver tumours, 174 coronary angiography, valvular heart
liver metastases, 176, 184–189, 281 MRI vs, 175–176 disease, 593
pathology, 274 Meckel’s diverticulum, 252 coronary angioplasty, 589
from polyps, 281, 282 neck lumps, 670, 671 coronary arteries, surgery, 588–592
presentation, 274–275 pancreatic cancer, 211 coronary artery bypass grafting,
prognosis, 274 pancreatitis, 202, 203 589–592
screening, 281 parathyroid gland localisation, 341 patient explanatory brochure,
staging, 90, 185–186, 274 post‐traumatic confusion, 740 95–96
treatment, 231, 275–281 pulmonary angiography, 700–701 surgical risk, 14
colorectal polyps, 281–284 renal cell carcinoma, 582 coroner’s clot, 676
colostomy, 238, 271, 289, 631 small bowel obstruction, 244 corticosteroids
colovesical fistulas, 271 soft tissue tumours, 409 Crohn’s disease, 262
commensals, skin, 101 subarachnoid haemorrhage, 746 preoperative management, 9
common bile duct subdural haematoma, 487, 488 transplantation, 81, 85
diameter, 644–645 surveillance after hepatectomy, 189 ulcerative colitis, 257
distal cholangiocarcinoma, 178 trauma, 439 see also glucocorticoids
common peroneal nerve entrapment, urothelial cancer, 580 cortisol, 348
5, 717 concretions, pancreatitis, 205 cosmetic surgery, 426–428
communication, 26, 104 concussion, 484, 735–737 cough impulse, 386
see also consent; discussion with conductive hearing impairment, 361 counselling see discussion with
patient confusion patient
compartment syndrome, 462 management, 739–740 counting of instruments, 98
complement, 66 postoperative, 30–31, 700 Courvoisier’s law, 644
complex sclerosing lesions, trauma, 735–743 covered endovascular repair of the
breast, 315 congenital heart disease, 596–597 aortic bifurcation (CERAB),
composite flaps, 426 congestive cardiac failure, leg 559
composite grafts, 425 swelling, 686 covered stents, 555
compound naevi, 399 conjunctiva, injuries, 353 see also stent‐grafts
compression ischaemia, nerve conjunctivitis, 357, 750, 752, 753 cover test, 759
injuries, 513 Conn’s syndrome, 346, 347 Craig beds, 739
compression stockings, 7, 691, 704 hypokalaemia, 347, 348 cranial nerves
lymphoedema, 551 consciousness carotid endarterectomy, 542
see also elastic stockings head injuries, 489 head injuries, 484–485
computed tomography trauma, 737 microvascular palsy, 760
abdominal abscess, 655 consent, 3–4, 36, 94–97 tumours, 375–376
angiography confused patients, 740 see also fourth cranial nerve; sixth
abdominal aortic risk assessment for, 13, 14 cranial nerve; third cranial
aneurysms, 528 urgent surgery, 7 nerve
massive rectal bleeding, 634–635 conservation surgery, breast, 324 craniectomy, 491
appendicitis, 250 consolidation (pulmonary), 611 craniotomy, 486–487, 488,
cerebrovascular disease, 539 signs, 604 505–506
chest, 603–604 constipation, 617–623 crazy pavement, Paget’s disease, 474
cholangiography, 174, 645 management, 621–622 C‐reactive protein
cholelithiasis, 168 consultant‐led care, emergencies, 109 acute abdomen, 652
colonic obstruction, 287 contaminated wounds, 6, 46, 67 appendicitis, 250
colonography, diverticular disease, contrast enema, large bowel large bowel obstruction, 286
268, 269 obstruction, 287 creatinine, organ failure, 203
colorectal carcinoma, 275 contrast media, arteriography, 556 cremaster, 727
colorectal surgery, 230 contrecoup injury, 483 cremasteric reflex, 732
Crohn’s disease, 261–262 convexity meningiomas, 499 critical illness, 57–63
extradural haematoma, 486 convexity subarachnoid management, 62
fractures, 457–459 haemorrhage, 746 critical limb ischaemia, 530,
functional liver remnant, 173 core biopsy 531, 557
gastro‐oesophageal reflux disease, breast lumps, 311 Crohn’s disease, 261–266
119–120 soft tissue sarcoma, 409, 410–411 cholelithiasis, 164, 262
haematuria, 696, 697 cornea colitis, 265
head and neck cancer, 365 eye injuries, 356–357 complications, 262
head injuries, 490, 735 recurrent corneal erosion perianal, 265–266, 303
intracranial tumours, 495 syndrome, 750 surgery, 263–265
kidney stones, 566, 697 reflections, 759 ulcerative colitis vs, 255, 265
Index 775
cross‐matching, blood transfusion, 638 deceased donors, 77–79 dexamethasone

CROSS trial, gastric carcinoma, 147 procurement operations, 78–79 meningitis, 507
cryptogenic liver abscess, 192 decerebrate posture, 489 spinal injuries, 522
crypto‐glandular hypothesis, 301 decompression dexamethasone suppression test, 348
cryptorchidism, 727 acute colonic pseudo‐obstruction, diabetes mellitus
crystal arthropathies, 476 291 bariatric surgery on, 152
crystalloids, 60 laminectomy, 725 foot, 532–533
head injuries and, 490 small bowel obstruction, 245 pancreatic cancer, 209, 211
cubital tunnel, 515 urinary tract, 567 preoperative management, 8, 21
Cullen’s sign, 201 use of drains, 28 dialysis, extended‐hour, 342
curative surgery, cancer, 90 deep dermal burns, 444, 446, diaphragm, free gas under, 139, 654
Curling’s ulcer, 133–134 447, 451 diaphyseal aclasis, 473–474
Cushing response, 486 deep dorsal vein, penis, 571 diarrhoea
Cushing’s disease, 502–503 deep veins of calf, 545 appendicitis, 249
Cushing’s syndrome, 346, 348 deep vein thrombosis, 6–7, 31–32, bile acid excretion, 164
subclinical, 347 546, 689, 703–704 Crohn’s disease, 263
Cushing’s ulcer, 133–134 defecating proctography, 295 electrolytes, 28
cutting staplers, 233 defecation, 293, 617 short‐gut syndrome, 240
cyanoacrylate disorders of, 620–621 treatment, 628
adhesives, 41 pain, 296 ulcerative colitis, 256
embolic agents, 554 definitive care, trauma, 434, 439 diathermy, 37, 100
cyclical mastalgia, 312 de Garengeot’s hernia, 382 dietary factors
cyclopentolate, 356 degenerative arthritis, 468–469, 470 cholelithiasis, 164
cylindroma, 374 degenerative spinal disorders, colorectal carcinoma, 273
cystectomy, radical, 581 719–721, 724 diverticulosis, 267
cysteine stones, 566 degloving injuries, scrotum, 731 gastric carcinoma, 143
cystic fibrosis, cholelithiasis, 164 dehiscence, 30, 702 diethylenetriaminepentaacetic
cystitis, haematuria, 694 avoidance, 42 acid‐galactosyl HSA,
cystoscopy, 697–698 dehydration, 27 99m
Tc‐labelled, 173
cysts short‐gut syndrome, 240 diffuse axonal injury, 735, 741
branchial, 669, 670, 671 dehydroepiandrosterone diffuse large B‐cell lymphoma,
breast, 313, 314 (DHEAS), 348 stomach, 149
epididymal, 573–574, 731 delayed primary wound closure, 47, diffuse oesophageal spasm, 682
hydatid disease, 193–196 424–425 digital subtraction angiography, 553
kidney, 582 delayed union, fractures, 462 diltiazem, anal fissure, 296
neck, 669 delirium, 30 2,3‐diphosphoglycerate, 10
ovary, torsion, 251 Delorme procedure, 299 Diphoterine®, 448
skin, 397 dental tumours, 371 diplopia, 757–761
thyroglossal, 331–332, 669, 671 dentate line, 293 blow‐out fracture of orbit, 355
thyroid, 332, 333 Denver shunt, 664–665 raised ICP, 495
vocal folds, 363 depressed skull fracture, 485, 491 direct inguinal hernias, 384,
cytokines De Quervain’s thyroiditis, 335, 336 385–386
inflammatory response, 66 Dercum’s disease, 403 direct oral anticoagulants, 704
pancreatitis, 200 dermatofibromas, head and direct wound closure, 424–425
protein catabolism, 52 neck, 371 dirty wounds, 6, 46, 67
cytology dermatofibrosarcoma disability prevention, trauma,
urine, 580, 696 protuberans, 376 433, 434
see also fine‐needle aspiration dermatomes, 720 disaster management, 433
cytology dermatophytes, 415 discharge
cytomegalovirus, transplant dermis, 443 anal, 294
patients, 82 dermoid cysts, 397 ear, 359–360
cytotoxic T‐lymphocyte‐associated de‐roofing, hydatid cysts, 195 nasal, 362
protein 4, 402 desmoid tumours, 406 nipple, 313–314
familial adenomatous wounds, 702
dabigatran, 9, 704 polyposis, 283 discogenic pain, 716
dartos, 727 Determinant‐based Classification, discography, 724
deafness see hearing impairment pancreatitis, 201 disc prolapse (intervertebral),
debridement devascularisation, portal 519–520, 716–717, 718, 724
burns, 451 hypertension, 223 discussion among staff, operating
open fractures, 460 deviation, septal, 362 rooms, 37
776 Index
discussion with patient drainage dysplastic naevi, 400

breast carcinoma, 327 abscesses, 269–270, 655–656 dyspnoea, 592
cholelithiasis, 169 chronic pancreatitis, 207 dysrhythmias, surgery for, 598–599
oncology, 87 see also percutaneous drainage dyssynergia, rectum, 620
postoperative care, 26 drains, 28, 42, 195
preoperative management, 3–4, anal fistula, 304 ear
25, 94 chest tubes, 605–606, 609 skin cancer, 369
disimpaction, fractures, 459 early removal, 68 see also otology
dislocations, 462–463 drapes, 36, 103 early gastric cancer, 145
spine, 522 dress code, 101 early goal‐directed therapy, 58
dissecting scissors, 100 dressings, 47 early‐stage hepatocellular
dissection burns, 450–451 carcinoma, 182
aorta, 589 leg ulcers, 691 E‐cadherin CDH1 gene, gastric
aneurysms, 598 open fractures, 460 carcinoma, 143
carotid, 538, 741 drowsiness, head injuries, 486 E charts, 751
intimal, 534 drug‐eluting stents, coronary Echinococcus spp., 193
vertebral arteries, 741 arteries, 589 E. granulosus, 193–195
dissection (surgical), 40 drug resistance see antimicrobial E. multilocularis, 195
disseminated intravascular resistance echocardiography, valvular heart
coagulation, drugs (illicit), reversible cerebral disease, 593
N. meningitidis, 507 vasoconstriction ectopic parathyroid glands, 339
distal cholangiocarcinoma, syndrome, 747 ectopic pregnancy, 251
treatment, 178 drugs (therapeutic) elastic stockings, 547, 691
distal spleno‐renal shunt, 223 cholelithiasis, 165 see also compression stockings
distance visual acuity, 750–751 constipation from, 620 elderly patients
diuretics pancreatitis from, 199 bone scans, 457
ascites, 663–664 postoperative, 25 cholelithiasis, 163
leg swelling, 688 post‐traumatic confusion, 742 Glasgow Coma Scale, 489
diverticular disease, 267–272 drugs of addiction, 98 meningitis, 506
elective surgery, 271–272 dry heat sterilization, 36 preoperative assessment, 5
strictures, 285, 290 ductal carcinoma in situ, breast, 318, surgical risk, 16
diverticulitis, 268–271 319–320, 322, 323 urgent surgery, consent, 7
appendicitis vs, 251 Dukes’ staging, colorectal elective lymph node dissection
strictures, 285 carcinoma, 274 (ELND), melanomas, 401
diverticulosis, 267–268 dumb‐bell tumours, 375, 519 electrical injuries, 445–446
diverting loop colostomy, 271, 289 dumping syndromes, 136 electrocardiography, ischaemic heart
diverting loop ileostomy, 260, Roux‐en‐Y gastric bypass, 157 disease, 589
270, 271 duodenal juice, electrolytes, 28 electrocautery, 100
D‐lactic acidosis, 240 duodenal ulcers, 134–136 electrolytes, 27, 28
documentation bleeding, 638 gastrointestinal tract, 237
informed consent, 4 perforation, 139 electro‐stimulated graciloplasty, 629
operative, 104 duodenum, familial adenomatous elevation of leg, 688
dogs, E. granulosus, 193–194 polyposis, 283 embolic agents, 554
donors, organs for transplant, 76–79 duplex ultrasound embolic theory, cerebrovascular
donor skin, split‐thickness skin carotid arteries, 539 disease, 537
grafts, 452–453 deep vein thrombosis, 31 embolisation (therapeutic)
Doppler ultrasound leg ulcers, 690 angiomyolipoma, 561
limb ischaemia, 530 limb ischaemia, 530 epistaxis, 712
scrotum, 732 lymphoedema, 550–551 for haemorrhage, 560
double gloving, 102 varicose veins, 547 peptic ulcer bleeding, 138
double‐stapled anastomoses, 233 dutasteride, 569 portal vein, 173
doublet chemotherapy dynamic views, spine, 723 ruptured hepatocellular
colorectal liver metastases, 187 dyschondroplasia, 473 carcinoma, 183
rectal cancer, 280 dyslipidaemia, bariatric surgery see also chemoembolisation
double vision see diplopia on, 152 embolism
down‐staging dysphagia, 679–683 acute limb ischaemia, 533
lung carcinoma, 612 oesophageal carcinoma, 125, 130 cardiac valve surgery, 596
pancreatic cancer, 214 dysphasia, stroke, 538 complicating carotid
liver metastases, 187, 189 dysplasia, inflammatory bowel endarterectomy, 542
doxycycline, epididymo‐orchitis, 732 disease, 255–256, 259 pulmonary, 32, 700–701
Index 777
small bowel, 246 endoluminal procedures see energy stores, 50

see also venous thromboembolism endovascular procedures enhanced recovery after surgery
embryology endoluminal repair, aneurysms, 529 (ERAS), 26, 54, 234
gastrointestinal tract, 232 endometrial cancer, tamoxifen, 326 Entamoeba histolytica, 193
parathyroid glands, 339 endoscopic mucosal resection, gastric enteral nutrition, 54
thyroid, 331 carcinoma, 146 pancreatitis, 204
emergencies, 109–111 endoscopic retrograde preoperative, 8
acute abdomen, 649–652 cholangiopancreatography, short‐gut syndrome, 239
angle closure glaucoma, 754 174 enteric fistula, 240–241
bleeding varices, 221–223 choledocholithiasis, 169 entero‐atmospheric fistula, 241
burns, 448–450 for gallstone pancreatitis, 205 enterocutaneous fistula, 241
confused patients, 740 obstructive jaundice, 645–646 Crohn’s disease, 265
Crohn’s colitis, 265 pancreatitis from, 200 entero‐enteric fistula, 241
diplopia, 760 endoscopic submucosal dissection, enterohepatic circulation, 163–164
epiglottitis, 363 gastric carcinoma, 146 enteroscopy, 38
Fournier’s gangrene, 729 endoscopic surgery, 38 enterovesical fistula, Crohn’s
gastrointestinal bleeding, 138 endoscopic ultrasound disease, 265
hepatocellular carcinoma cholelithiasis, 168 entrapment neuropathies, 513–516,
rupture, 183 chronic pancreatitis, 206 721–722
hernias, 384 dysphagia, 680 common peroneal nerve, 5, 717
hiatus hernias, 117 gastric carcinoma, 145 enzyme‐linked immunosorbent assay,
laparoscopic cholecystectomy, 170 gastrointestinal stromal hydatid disease, 194
leg pain, 722 tumours, 148 enzymes
low back pain, 715, 722, 725 obstructive jaundice, 645 pancreas, 199–200
massive rectal bleeding, 634–635 pancreatic cancer, 211 replacement therapy, 206
meningococcal septicaemia, pancreatic cystic diseases, 217 ependymoma, 498
421–422 endoscopy, 38 spinal cord, 519, 520
metacarpophalangeal joint bleeding varices, 222 epidermal cysts, 397
infections, 417–418 chronic pancreatitis, 206 epidermal growth factor receptors
preoperative management for, 7–8 dysphagia, 680 antibody, colorectal liver
priapism, 572 ear surgery, 361 metastases, 187
spinal cord compression, 517–519 gastric carcinoma, 145 see also HER2
sudden‐onset severe headache, therapeutic, 146 epidermis, 443
745–748 gastro‐oesophageal reflux disease, epididymis
tension pneumothorax, 609 118, 120 appendix of, 727–729
testicular torsion, 573, 727 haematemesis and melaena, cysts, 573–574, 731
thoracic aortic aneurysms, 598 638–639 epididymitis, 574
transplant recipients, 85 massive rectal bleeding, 634, 635 epididymo‐orchitis, 729, 730, 732
ulcerative colitis, 259, 260–261 nasal, 677, 712 epidural abscess, 718
vocal fold paralysis, 364 peptic ulcer disease epidural anaesthesia, on stress
emphysema, signs, 604 bleeding, 137, 138 response, 55
empyema duodenal ulcers, 134 epidural infusions, local
chest, 608 gastric ulcers, 136 anaesthetics, 24
gallbladder, 165 endotracheal intubation, preoperative epigastric hernia, 390–391
empyema necessitans, 607 assessment, 20 epiglottitis, 363, 675
encephalopathy (hepatic), 223 endovaginal ultrasound, 655 episcleritis, 752, 753
TIPS, 221 endovascular coiling, 554 epistaxis, 711–713
endarterectomy, 531 cerebral aneurysm, 506 Epstein–Barr virus, nasopharyngeal
carotid, 539–542 endovascular procedures, 553–562 cancer, 367
end‐ileostomy, 260–261, 265 ASD closure, 597 Erb’s palsy, 512
endoanal ultrasound, 295, 627 cardiac surgery, 588, 601 erectile dysfunction, radical
endobronchial biopsy, 604 cardiac valve surgery, 596 prostatectomy, 579
endocrine disturbance, pituitary peripheral arterial disease, 531 erections, neural control, 571
tumours, 501–503 endovenous laser therapy, 549 erosive oesophagitis, 116
endocrine therapy end‐to‐end anastomoses, bowel eschar, 445
breast carcinoma, 326–327 surgery, 232, 233 escharotomy, 448, 450
oncology, 88 end‐to‐side anastomoses, bowel ethmoid sinus, adenocarcinoma, 363
endocystectomy, hydatid cysts, 195 surgery, 232 ethylene oxide, 36
endografts, 555 enemas, ulcerative colitis, 257 eustachian tube, 359
endoleak, aneurysms, 529, 557, 558 energy requirements, 49, 50, 240 Ewing’s sarcoma, 478–479
778 Index
examination under anaesthesia, face‐lifting surgery, 428 fibrous dysplasia, 475–476

anal, 295 face masks, surgeons, 35 finasteride, 569
excision facet joints, 716 fine‐needle aspiration, neck lumps,
burns, 451–452 dislocations, reduction, 522 669–670
rectal cancer, 278 facial nerve, in parotid gland, fine‐needle aspiration cytology
total mesorectal (TME), 231, 372, 373 breast lumps, 311
275–276, 277, 278 facial paralysis, head injuries, 485 thyroglossal duct cyst, 331–332
vertebrae, 725 faecal incontinence, 295–296, 299, thyroid cysts, 333
excisional biopsy, 89 625–633 thyroid nodules, 332–333
breast lumps, 312 obstetric injury, 626, 631 Finney strictureplasty, 264
neck lumps, 670 prevention, 631 first aid
exomphalos, 391 proctocolectomy, 260 burns, 448
exostoses, 473–474 stomas to prevent, 230, 631 chemical burns, 448
expanded RAS analysis, colorectal treatment, 628–631 spinal injuries, 522
liver metastases, 187 faeces fistulas
expected weight loss electrolytes, 28 anal, 303–305
LAGB, 152 occult blood testing, 281 aorto‐enteric, 529
sleeve gastrectomy, 155 fallopian tubes, torsion, 251 buried mucous, 289
explanatory brochures see patient falls, confused patient, 739 cerebrospinal fluid via, 491
explanatory brochures false aneurysms, 527, 534 Crohn’s disease, 263–265, 266
external anal sphincter, 293, familial adenomatous polyposis diverticular disease, 271
625, 629 (FAP), 281, 282–283, 406 enteric, 240–241
external fixation, fractures, 461 familial hypocalciuric pancreatic (CR‐POPF), 212
external hernias, 381, 382 hypercalcemia, 340 fistulotomy, 304
extra‐adrenal phaeochromocytomas, family history 5α‐reductase inhibitors, 569
345 breast carcinoma, 317 5‐aminosalicylate, 257
extracellular fluid, 27, 32, 686 dysplastic naevi, 400 fixation, fractures, 459, 461
extracolonic cancers, Lynch multinodular goitre, 333 flaps, 423–424, 426
syndrome, 283 fascicles, nerves, 511 V–Y advancement flaps, 427
extracorporeal membrane Fasciola hepatica, 196 flexion–extension views, spine, 723
oxygenation, 599–600 fasciotomy, 535 flexor retinaculum, 514
extracorporeal shock wave fasting, preoperative, 8, 20 flexor sheath infections, 417
therapy, 169 fat(s) flora, skin, 101
extracranial vascular disease, body composition, 52 flucloxacillin, 466, 467
537–543 as energy source, 49, 50 fludrocortisone, septic shock, 60
extradural haematoma, 485–487 fat‐free body hydration, 50 fluid levels, small bowel obstruction,
extraintestinal manifestations, fat‐free mass index, 50 244, 245
inflammatory bowel fat homeostat, 151 fluids
disease, 256 fatigue, postoperative, 52 loss, 28, 32
extraocular muscles, 757, 758 fat wrapping, Crohn’s disease, 261 postoperative management, 25,
surgery, 761 feculent vomiting, 243, 286 27–28, 32
extrasphincteric fistula, 304 felons, 416–417 replacement, 27–28
extravaginal testicular torsion, 727 femoral hernia, 388–389 burns, 449
exudates, pleural effusions, femoral pulse, limb ischaemia, 530 head injuries, 490
607, 608 femoral stretch test, 723 inadequate, 701–702
ex vivo autogenous chondrocyte femoropopliteal bypass, 531 pancreatitis, 204
culture, 478 fever see pyrexia see also volume resuscitation
eye, 749–755 fibroadenoma, breast, 312–313 restriction, 742
anatomy, 749 fibroblast growth factor 23, 341 from wounds, 30, 42
examination, 750–752 fibrocystic change, breast, 314 fluid thrill, 661
infections, 357, 750 fibrolamellar hepatocellular fluid volumes, gastrointestinal
injuries, 353–357 carcinoma, 181 tract, 237
movement testing, 759 fibromatosis fluorescein
primary management, 752–754 head and neck, 371 corneal foreign body, 356
protection, 35 see also desmoid tumours eye examination, 752
see also diplopia fibromuscular dysplasia (FMD), 18
F‐fluorodeoxyglucose see positron
eyelids 538–539 emission tomography
blepharitis, 750, 752, 753 angioplasty, 541 foam enemas, 257
burns, 356 fibrosarcomas, head and neck, 371 folate, sulfasalazine on
injuries, 353 fibrosis, chronic pancreatitis, 205 absorption, 257
Index 779
FOLFIRINOX, pancreatic cancer, galactorrhoea, 314 gastro‐oesophageal reflux disease,

214, 215 gallbladder 115–122
FOLFOX see doublet chemotherapy cancer, 167, 178–180 investigation, 118–120, 681
follicular thyroid carcinoma, 334 from cholelithiasis, 163 on larynx, 363
fine‐needle aspiration radical resection, 180 sleeve gastrectomy, 121, 155
cytology, 333 function, 164 treatment, 120–121
fomites, 415 obstruction, 165 Gd‐EOB‐DTPA, 174–175
foot, diabetes mellitus, 532–533 gallium‐68 DOTA‐TATE, PET, 215 gemcitabine, pancreatic cancer, 215
forceps, 39–40 gallstone pancreatitis, 165–166, gender
foreign bodies 200, 204 abdominal hernias, 382
airway obstruction, 675, 676 treatment, 205 cholelithiasis, 164
cornea, 356–357 gallstones see cholelithiasis colorectal carcinoma, 273
eye, 753 gamma‐glutamyltranspeptidase, 644 gallbladder carcinoma, 178
Fournier’s gangrene, 70, 302, 729 gamma rays, sterilisation, 36 General Medical Council, surgical
fourth cranial nerve, 757 gangrene, 421 risk assessment, 13, 14
palsy, 758, 760 Gardner’s syndrome, 406 germ cell tumours
4:2:1 rule, 449 gas bubbles, pancreatitis, 202 mediastinum, 613
fractional flow reserve, 589 gas gangrene, 421 testes, 583
fractures, 457–462 gastrectomy germinomas, pineal region, 503
analgesia, 740 gastric carcinoma, 146 giant cell arteritis, 538, 747, 760
cervical spine, 521 peptic ulcer disease, 135–136, 137 Glasgow Coma Scale, 489, 737, 738
complications, 461–462 see also sleeve gastrectomy Gleason grading, prostate
dislocations with, 462–463 gastric adenocarcinoma, 143–147 carcinoma, 578
immobilisation, 461 gastric banding, 152–153 glioblastoma multiforme, 494, 495
mandible, 440 complications, 154 gliomas, 493–496
nerve injuries, 513 gastro‐oesophageal reflux brainstem, 498
orbit, 354–355 disease, 121 glomerular filtration rate, chronic
outcomes, 461 gastric dilatation, 28–29 kidney disease, 21
pelvis, 695 gastric disconnection procedure, 639 glomus intravagale, 375
protection while healing, 461 gastric heterotopia, Meckel’s glomus jugulare tumours, 375
rehabilitation, 462 diverticulum, 252 gloves, 102, 103
skull, 485, 491, 740–741 gastric juice, electrolytes, 28 glucocorticoids
spinal cord compression, 522 gastric outlet obstruction, 140 adrenocortical tumours
thoracic spine, 518 gastric tubes producing, 347
free flaps, 423–424 trauma, 438 septic shock, 60
Frey procedure, 207 see also nasogastric tubes glucose, insulin and potassium
Froment’s sign, 516 gastric ulcers, 136–137 (GIK), 8
frusemide, extradural bleeding, 637–638 glue ear, 361
haematoma, 486 perforation, 139 glutamine, 55
fucosyltransferase deficiency, 211 gastrin, Zollinger–Ellison glutaraldehyde, 36
full blood counts, acute abdomen, syndrome, 140 gluteal hernia, 393
651, 653 gastrinoma, 140, 148, 216 glyceryl trinitrate
full‐thickness burns, 445, 446, 451 gastrinoma triangle, 140 anal fissure, 296
full‐thickness skin grafts, 425 gastroenteritis, appendicitis vs, 251 infusions, 599
fulminant colitis, 70 Gastrografin follow‐through, glycogen, 50, 51
functional end‐to‐end 244–245 goitre, 331
anastomoses, 233 gastrointestinal stromal tumours, multinodular, 333–334
functional liver remnant, 173 148, 246 thyrotoxicosis, 335
functional scans, soft tissue sarcoma, gastrointestinal tract golden hour, 434
409–410, 411 bacteria, 654 golimumab, ulcerative colitis, 258
funding, 107 bleeding, 137–138, 221–223, gonioscopy, 754
fundoplication, 121 637–638 Goodsall’s law, 303
fungal infections, extremities, embryology, 232 gout, 476, 721
415–416, 551 endoscopy see endoscopy gowning, 102
funicular inguinal hernia, 385 motility, 617 graciloplasty, electro‐stimulated, 629
physiological changes, grading
gabapentin, 24 237–242 prostate carcinoma, 578
gadolinium‐EOB‐DTPA, 174–175 postoperative function, 28–29 soft tissue sarcomas, 407
gait, 723 resistance to infection, 66 graft analogy, bowel
antalgic, 715, 721 systemic effects of burns, 451 anastomoses, 231
780 Index
graft dysfunction, transplantation, 82 primary survey, 437 Helicobacter pylori

grafts, 423 resuscitation, 437, 438 eradication, 135
arteries, 531 retrobulbar, 353 gastric carcinoma, 143
coronary artery bypass varicose veins, 546 gastric lymphoma, 149
grafting, 590 see also bleeding oesophageal carcinoma, 124
heart valves, 595 haemorrhoidectomy, 298 peptic ulcer disease, 133, 134, 137
for open fractures, 460 haemorrhoids hemiparesis
skin, 425–426 bleeding, 297–298 head injuries, 486, 489
burns, 452–453 Crohn’s disease, 266 meningiomas, 499
see also bypass grafts; endografts; thrombosis, 297 hemithyroidectomy, 335
stent‐grafts haemostasis, 40 heparin
Graves’ disease, 335 after arteriography, 556 deep vein thrombosis, 704
GreenLight photoselective hair, preoperative removal, low‐molecular‐weight heparin, 7, 31
vaporisation of the 46, 101 patients on warfarin, 9
prostate, 569 hand hygiene, 6, 101 postoperative, 26
greenstick fractures, 457 central lines and, 68 prophylactic, 7
Grey Turner’s sign, 201 Hartmann’s procedure, 270, 277, hepatectomy
growth hormone, 502 280, 289–290 colorectal liver metastases,
guarding, appendicitis, 250 Hartmann’s solution, 449 187–189
gunshot wounds, 433 harvest injury, 82 down‐staging for, 187, 189
gynaecomastia, 315 Hashimoto’s thyroiditis, 335–336 hepatocellular carcinoma, 183
histopathology, 333 hydatid cysts, 195
H2 receptor antagonists see histamine hazards, operating rooms, living donors, 76–77
H2 receptor antagonists 36–37, 104 patients with cirrhosis, 225
haemangiomas, 404, 405 headache surveillance after, 189
head and neck, 371 diplopia with, 758 hepatic artery
haematemesis, 137, 637–641 raised ICP, 494 bacterial infections, 191
haematomas subarachnoid haemorrhage, 504 pancreatic cancer, 212
intracranial, 440, 485–488, sudden‐onset severe, 745–748 hepatic venous pressure, 220
505–506, 740 trauma, 739 hepatic venous wedge pressure, 220
neck, 336, 542 head and neck hepatitis B virus, organ donors, 82
osteomyelitis, 465 cancer, 364–367, 369–377 hepatitis C virus
perianal, 296–297 reconstruction, 424 hepatocellular carcinoma, 181
spine, 718 lipomas, 671 organ donors, 82
wounds, 30 head injuries, 483–492 transplantation results, 83
haematuria, 567–568, 693–698 primary survey, 437 hepatobiliary malignancy,
urothelial cancer, 580 secondary survey, 439 classification, 176
haemodilution, 587 see also brain injury hepatocellular carcinoma,
haemodynamic theory, stroke, 537 headlight examination, epistaxis, 712 180–184, 185
haemoglobin, preoperative, 10 healthy patients, preoperative cirrhosis, 225
haemolysis, cholelithiasis, 164 assessment, 5 computed tomography, 174,
Haemophilus influenzae, hearing impairment, 361–362 175–176
meningitis, 507 head injuries, 484–485 magnetic resonance imaging,
haemoptysis, massive, 707–709 heart 175–176
haemorrhage breast carcinoma hepato‐iminodiacetic acid,
after cardiac surgery, 600 radiotherapy, 325 99m
Tc‐labelled, 169
diverticular disease, 271 congenital heart disease, hepatorenal syndrome, 660, 665
endovascular treatment, 560 596–597 HER2 (human epidermal growth
epistaxis, 711–713 valve surgery, 592–596 factor receptor), gastric
fractures, 461 see also ischaemic heart disease; carcinoma, 145
intracranial, 440, 483–484, entries beginning cardiac… HER2‐enriched breast
485–488, 537, 747–748 heart block, 598 carcinoma, 324
subarachnoid, 503–506, VSD repair, 597 herceptin, gastric carcinoma, 147
745–747 heartburn, 117 hereditary diaphyseal aclasis,
massive rectal bleeding, 634–635 heart–lung machine, 587 473–474
oesophageal carcinoma, 125 heart–lung transplantation, 80 hereditary gastric carcinoma, 143
peptic ulcer disease, 137–138 heart transplantation, 600 hereditary syndromes
portal hypertension, 220, results, 84 adrenocortical tumours, 347
221–223 Heineke–Mikulicz colorectal carcinoma, 273,
postoperative, 33 strictureplasty, 264 282–284
Index 781
pancreatic cancer, 209 human papillomavirus hypokalaemia, 33

pancreatic neuroendocrine anal warts, 298 Conn’s syndrome, 347, 348
tumours, 215 upper aerodigestive tract hyponatraemia, 32
hernias, 381–393 cancer, 364 burns in children, 449
of brain, 483–484, 489 hunger, 151 post‐traumatic confusion, 742
intervertebral discs, 519–520, Hutchinson’s melanotic hypoparathyroidism, 342–343
716–717, 718, 724 freckle, 400 thyroidectomy, 336, 342–343
strangulation, 244 hybrid procedures, CABG, 592 hypopharynx, cancer, 365, 366
see also hiatus hernia; inguinal hydatid disease, 193–196 hypopituitarism, 502
hernia; umbilical hernia hydatid of Morgagni (appendix hypoproteinaemia
hernioplasty, 387 testis), 573, 727–729 ascites, 659
herniorrhaphy, 387, 389 hydration, 50 leg swelling, 686–687
Hesselbach’s triangle, 385 hydrocele, 573, 574, 730, 731 hypotension, septic shock, 59, 61, 67
heterotopic transplantation, 80 after inguinal hernia repair, 388 hypothermia, 98
hiatus hernia, 115, 116–117, 118 hydrocephalus, trauma, 484, 740 irrigation of burns, 448
repair, 121 hydrocortisone, 9 hypothermia (therapeutic), 491, 587
hidradenitis suppurativa, 305, septic shock, 60 hypothyroidism, bones, 472
419–420 hydrofluoric acid, antidote, 448 hypoxaemia
high‐dose dexamethasone hydrogen ion, gastric, 28 confusion, 30, 700, 741–742
suppression tests, 348 hydroxyethyl starch, 60 postoperative, 29, 700
highly selective vagotomy, 136 3‐hydroxysteroid dehydrogenase,
high voltage, 445–446 deficiency, 348 ice, not for burns, 448
histamine H2 receptor antagonists hygiene, 6 identification of patient, 5
gastro‐oesophageal reflux hyperacute antibody‐mediated ileal pouch, 259–260
disease, 120 transplant rejection, 82 ileal pouch–anal anastomosis, 283
peptic ulcer disease, 135 hypercalcaemia, 340 ileorectal anastomosis, colectomy
histopathology hyperparathyroidism, 341, 342 with, 260, 265
breast carcinoma, 319–324 parathyroidectomy for, 341 ileostomy, 238, 239, 260
Hashimoto’s thyroiditis, 333 hypercapnia, head injuries, 490 diverticulitis, 270
intraoperative, 107 hyperdynamic vasodilated septic diverting loop ileostomy, 260,
history‐taking shock, 61 270, 271
acute abdomen, 649 hyperextension injuries, cervical end‐ileostomy, 260–261, 265
burns, 450 spine, 521 for faecal incontinence, 631
constipation, 619 hyperkalaemia, 32–33 rectal cancer surgery, 278
faecal incontinence, 626 hypernatraemia, 27, 32 ileum
haematuria, 695 hyperosmolar solutions, bowel electrolytes, 28
large bowel obstruction, 286 preparation, 230 physiology, 238
leg swelling, 687 hyperparathyroidism ileus, 29, 245, 287–289
neck lumps, 667 bones, 341, 472 iliac bifurcation disease, 559
rectal bleeding, 633 primary, 339–341, 343 ilioinguinal nerve, injury, 388
HIV secondary, 341–342, 343 image intensifier systems, 106
organ donors, 82 tertiary, 342 imaging, 106–107
see also AIDS hyperphosphataemia, 341 chest, 603–604
HLA antigens, 81–82 hypertension gastro‐oesophageal reflux disease,
hoarseness, 679 leg ulcers, 689 119–120
holding bays, 104 phaeochromocytomas, perihilar cholangiocarcinoma,
holmium laser enucleation of the 346, 347 175–176
prostate, 569 hypertensive crisis, prevention, 347 see also specific modalities
hormone replacement therapy, breast hyperthyroidism see thyrotoxicosis imatinib, gastrointestinal stromal
carcinoma, 317–318 hypertrophic non‐union, tumours, 148
hospital‐acquired meningitis, fractures, 462 imiquimod, 298
antibiotics, 507 hyperventilation, post‐traumatic immobilisation
hospital‐acquired pneumonia, confusion and, 742 dislocations, 463
69–70 hyphaema, 353, 356 fractures, 461
hospital administration, 107 hypocalcaemia, 336, 341, 343 immune response, transplants, 81–82
hospital admission criteria, head hypochloraemic alkalosis, gastric immunocompromise, burns, 451
injuries, 490 outlet obstruction, 140 immunoelectrophoresis, hydatid
hospitals, trauma care, 432 hypoglycaemia disease, 194
human epidermal growth factor burns in children, 449 immunohistochemistry, breast
receptor see HER2 insulinoma, 215 carcinoma, 322
782 Index
immunomodulators infective endocarditis, 596 internal fixation, fractures, 461

Crohn’s disease, 262, 266 bacteria, 68 internal hernias, 381
ulcerative colitis, 257–258 inferior mesenteric vessels, 219, internal mammary lymph
immunonutrition, 55 231, 278 nodes, 319
immunosuppression, 65 inferior oblique muscle, 757 internal rectal intussusception, 628
bowel surgery, 229 inferior vena cava, deep hypothermic International Society of Urological
cancer from, 83 circulatory arrest to treat, 587 Pathology, prostate carcinoma
emergencies, 85 inflammatory arthritis, 469–471 grading, 578
squamous cell carcinoma, 399 inflammatory bowel disease, interossei, 516
transplantation, 81 255–266 intersphincteric abscess, anal, 301
immunotherapy, melanomas, 402 blood tests, 295 intersphincteric fistula, anal,
impetigo, 418 inflammatory breast carcinoma, 310 303–304
implantable cardioverter inflammatory response, 66 interstitial fluid, 27, 686
defibrillators, 599 inflammatory strictures, diverticular interval appendicectomy, 252
incidentalomas, adrenal, 346, disease, 285 intervertebral disc prolapse,
348–349 infliximab 519–520, 716–717, 718, 724
incisional hernia, 389–390 Crohn’s disease, 263, 266 intestinal failure, 239
incisional SSI, 67 ulcerative colitis, 258 intestinal obstruction, 243–246
incisions, 40 information brochures see patient hernias, 383
bowel surgery, 233 explanatory brochures Meckel’s diverticulum, 252
cardiac valve surgery, 595 informed consent see consent; see also large bowel obstruction
for chest tubes, 606 discussion with patient intestinal transplantation, 84
respiratory disease and, 16 ingrown toenail, 418 intimal dissection, 534
incontinence inguinal hernia, 384–388, 729–730 intra‐abdominal collections, 69, 701
urinary, radical prostatectomy, 579 femoral hernia vs, 388–389 intra‐abdominal pressure, 382–383
see also faecal incontinence surgical risk, 14 intra‐aortic balloon pumps, 599
indeterminate colitis, 255 inguinal ligament, 386, 388 intracellular fluid, 27, 32
indirect inguinal hernias, 384, 385, inguinoscrotal hernia, 385 intracerebral haematoma, 488
386 inhalation injury, 448, 450 intracerebral haemorrhage, 747
indocyanine green retention test, 173 inherited syndromes see hereditary intracerebral shearing, 483
infections syndromes intracranial haemorrhage, 440,
airway obstruction, 675 injection injury, nerves, 513 483–484, 485–488, 537,
arthritis, 468 injection therapy, varicose veins, 747–748
ascites, 662 548–549 subarachnoid, 503–506, 745–747
back pain, 718 inner sphenoidal wing intracranial pressure, 494–495, 498
bones, 465–467 meningiomas, 499 extradural haematoma, 486
cardiac surgery, 600 Inokuchi shunt, 223 management, 491
chest wall, 607 inotropic agents, 60–61, 599 pupils, 489
defined, 59 instruments (surgical), 39–40 sedation on, 739
extremities, 415–422 cleaning, 104–106 subdural haematoma, 487–488
eye, 357, 750 management, 98 intracranial tumours, 493–503
fractures, 461 supply, 106 benign, 499–503
intracranial, 506–508 insulin malignant, 493–499
leg swelling, 687 for hyperkalaemia, 33 intraductal papillary mucinous
leg ulcers, 691 preoperative management, 8, 21 neoplasm (IPMN), pancreas,
liver, 191–198 insulinoma, 215–216 210, 217
lymphoedema, 550 intensive care units, 57 intraductal papilloma, breast, 314
pancreatitis, 200 postoperative care, 104 intraepithelial neoplasia
paranasal sinuses, 362 Intergroup 0116 trial, gastric anus, 298–299
postoperative, 31, 65–73 carcinoma, 147 pancreas, 210
postoperative pyrexia, 701 intermittent claudication, 529, 531, intrahepatic cholangiocarcinoma,
post‐traumatic confusion, 742 532, 559, 715, 717, 721, 724 treatment, 177
preoperative management for, 6 intermittent pneumatic compression, intralesional margins, 411, 412
surgical, 65–73 lymphoedema, 551 intraluminal drainage, abscesses, 656
transplant patients, 82 internal anal sphincter, 293, 625 intramedullary tumours, spinal
wounds see surgical site internal auditory canal, acoustic cord, 519
infections neuromas, 501 intraocular infections, 357
see also sepsis internal carotid arteries, 537 intraocular pressure, 356
infection stones, 566 disease, 538, 539–542 angle closure glaucoma, 754
infective arthritis, chronic, 468 duplex ultrasound, 539 tonometry, 752
Index 783
intraoperative cholangiography, janus kinase inhibitors, ulcerative Kiesselbach’s area, 711

645, 646 colitis, 258 Klatskin tumour see perihilar
intraoperative endoscopy, massive Japanese Society of Biliary Surgery, cholangiocarcinoma
rectal bleeding, 635 gallbladder carcinoma Klotho deficiency, 341
intraoperative histopathology, 107 staging, 179 Klumpke’s paralysis, 512
intraoperative radiology, Japan Integrated Staging score, knots, 41
106–107 hepatocellular carcinoma, 182 KRAS mutations
intravaginal testicular torsion, 727 jaundice, 643–647 colorectal liver metastases, 187
intravenous access, 22–23, 43 see also obstructive jaundice pancreatic cancer, 209, 210
intravenous fluids, 27, 32 jejunum Krukenberg tumours, 275
see also parenteral nutrition electrolytes, 28 kwashiorkor, 50, 52, 659
intravenous pyelography, CT, 696 physiology, 238
intussusception, 252 joints, 476–478 lactate
internal rectal, 628 fractures, 462 large bowel obstruction,
invasion pain and swelling, 467, 721 286–287
breast carcinoma, 318 see also arthritides septic shock, 59
hepatocellular carcinoma, 182 J‐pouch, proctocolectomy, 259 D‐lactic acidosis, 240
melanomas, Clark’s levels, 401 jugulodigastric lymph node, 667 laminectomy, 725
invasive ductal carcinoma, breast, junctional naevi, 399 laparoscopic surgery, 39
320–321 juvenile angiofibroma, 363 adjustable gastric banding,
invasive lobular carcinoma, breast, juvenile naevi, 400 152–153
321–322, 323 juvenile nasopharyngeal complications, 154
involucra, 465 angiofibroma, 711 gastro‐oesophageal reflux
iodine‐based antiseptics, 36, 102 juvenile polyposis syndrome, 284 disease, 121
ion‐exchange resins, 33 adrenalectomy, 349
iridotomy, 754 Kanavel’s signs, 417 appendicectomy, 251
iron Karydakis procedure, 306 bowel surgery, 233
oral, 10 keel repair, epigastric hernia, 390 colorectal carcinoma, 276
studies for large bowel keratinocytes, 443 cholecystectomy, 169–170
obstruction, 287 keratitis, 752, 753 burden of disease, 170
irreducibility, hernias, 383 keratoacanthoma, 398 patients with cirrhosis, 224
irrigation keratosis surgical risk, 14
burns, 448 actinic, 398 gallbladder carcinoma, 180
chemical burns, 448 seborrhoeic, 397 gastric carcinoma, 146
colorectal, on‐table, 271 ketamine, 24 hepatectomy, 188
eye injuries, 354 keto‐adaptation, 51 hernia repair, 387
open fractures, 460 Ki67, breast carcinoma, 323–324 incisional hernia repair, 390
wounds, 67 kidney oesophagectomy, 127–129
irritable bowel syndrome, 622 abscesses, 570 laparoscopy
ischaemia anatomy, 565 gallbladder carcinoma, 179
fractures, 462 causes of haematuria, 693 gastric carcinoma, 145
small bowel, 243, 246–247 resections see nephrectomy lavage, diverticulitis, 270
see also acute limb ischaemia; trauma, 695 peritoneal metastases, 189
chronic limb ischaemia tumours, 694 ruptured hepatocellular
ischaemic colitis, 247 see also chronic kidney disease; carcinoma, 183
ischaemic heart disease entries beginning renal… ultrasound, choledocholithiasis,
surgical risk assessment, 16 kidney stones, 565–567 169
see also angina; myocardial computed tomography, laparotomy, 110–111
infarction 566, 697 large bowel obstruction,
ischaemic priapism, 572 Crohn’s disease, 262 285–292
ischiorectal abscess, 301 haematuria, 694–695 history‐taking, 286
islet cell transplantation, 84 short‐gut syndrome, 240 investigation, 286–287
iso‐osmolar solutions, bowel kidney transplantation treatment, 287–290
preparation, 230 living donors, 76 large cell carcinoma, lung, 610
ISUP (International Society of positions of organs, 85 laryngeal nerve palsy, 130
Urological Pathology), results, 83 larynx
prostate carcinoma skin cancer, 399 cancer, treatment, 366
grading, 578 surgery, 80 gastro‐oesophageal reflux disease
Ivor Lewis oesophagectomy, tertiary hyperparathyroidism, 342 on, 363
127, 128 waiting patients, 80 Lasègue’s stretch test, 723
784 Index
laser treatment, 37 non‐functional PNET luminal A breast carcinoma, 323

benign prostatic hyperplasia, 569 metastases, 216 luminal B breast carcinoma, 324
endovenous therapy, 549 resection see hepatectomy lumps
head and neck cancer, 366 venous outflow obstruction, breast, 309–312
iridotomy, 754 659, 664 inguinal hernia, 386
oesophageal carcinoma, 130 see also under metastases neck, 667–673
lateral cutaneous nerve of the liver disease perianal, 294, 298–299
thigh, 516 ascites, 663 see also masses
lavage preoperative management, 9–10 Lund and Browder chart, 446
colon, 289 recurrence, 83 lung carcinoma, 609–612
gas gangrene, 421 signs, 661 brain metastases, 497
laparoscopic, diverticulitis, 270 surgical risk, 16 lung disease see respiratory disease
laxatives, 621 see also cirrhosis lung metastases, soft tissue sarcoma,
left gastric‐caval shunt, 223 liver failure, 220 407, 409
left gastric vein, 219 treatment, 75 lung transplantation, 84
left gastroepiploic vein, 219 liver fluke disease, 196 lung trauma, 440
left hemicolectomy, 277 liver function tests, 644 lymphangiography, 551, 688
left‐sided obstruction, colon, 289 preoperative, 173 lymphangiomas, head and neck, 371
left ventricle, aneurysms, 591 liver transplantation lymphangitis, 419, 420
leg pain, 715–726 for hepatocellular carcinoma, 182 lymphatic mapping, melanomas, 401
leg swelling, 685–692, 703–704 living donors, 76 lymphatics, 549
leiomyomas, oesophagus, 123 neuroendocrine tumours, 216 breast, 309
lentigo maligna, 400 portal hypertension, 223 cellulitis, 419, 420
lesser sac, abscesses, 654 results, 83 leak into peritoneum, 660–661
leucocytosis, appendicitis, 250 surgery, 80 nuclear scintigraphy, 551
LeVeen shunt, 664–665 living donors, 76–77 oesophageal carcinoma
Lewis antigen negativity, pancreatic for hepatocellular carcinoma, 182 metastases, 125
cancer, 211 results, 83 scrotum, 573
Lhermitte’s sign, 517 lobectomy, 611 testes, 583
lichen sclerosis, 572 lobular carcinoma in situ, breast, 315 lymph nodes
lifestyle change, gastro‐oesophageal local anaesthetics, infusion, 24 breast, 310
reflux disease, 120 long saphenous vein breast carcinoma, 319, 325
LIFT procedure, 305 stripping, 548 gallbladder carcinoma, 179
ligation, 40 system, 545 gastric carcinoma, 144–145
lower limb veins, 548 long‐term central venous lymphoedema, 551
sphenopalatine artery, 712 catheters, 43 melanomas, 401, 667
like with like concept, plastic loop stomas, 238, 260 mesenteric, adenitis, 251
surgery, 424 see also diverting loop colostomy; resection, 90–91
limb ischaemia see acute limb diverting loop ileostomy breast carcinoma, 325
ischaemia; chronic limb Looser’s zones, 471 gastric carcinoma, 144–145
ischaemia loperamide, short‐gut syndrome, 240 oesophageal carcinoma, 127
limb perfusion, chemotherapy, Lord’s procedure, 631 squamous cell carcinoma, 671, 672
melanomas, 401 loss of heterozygosity, pancreatic thyroid carcinoma, 334
limb swelling, 685–692, 703–704 cancer, 209 upper aerodigestive tract cancer, 364
linea alba, epigastric hernia, 390 low back pain, 715–726 see also cervical lymph nodes
linear staplers, 233 low‐dose dexamethasone suppression lymphocele, 81
lip, squamous cell carcinoma, 369 test, 348 lymphocytic thyroiditis see
lipase, pancreatitis, 203, 653 lower oesophageal sphincter, Hashimoto’s thyroiditis
lipomas, 403, 404 115–116 lymphoedema, 549–552, 685–686,
head and neck, 371, 671 lower urinary tract symptoms 687, 688
soft tissue sarcomas vs, 407 (LUTS), 694, 695 lymphoedema praecox, 550
liposarcoma, head and neck, 371 low‐molecular‐weight heparin, 7, 31 lymphoedema tarda, 550
Listeria spp., meningitis, 507 low voltage, 445 lymphoma
lithium, hyperparathyroidism, 340 Ludwig’s angina, 675, 676 gastric, 149
lithotripsy, 169 lumbar canal stenosis, surgery, 725 head and neck, 371
Little’s area, 711 lumbar hernias, 392–393 mediastinum, 613
Littré’s hernia, 381 lumbar puncture pancreas, 216
liver, 182 subarachnoid haemorrhage, 746 small bowel, 245
imaging, 174–176 see also cerebrospinal fluid thyroid, 334, 335
infections, 191–198 lumbosacral nerve roots, 716 Lynch syndrome, 283
Index 785
Maastricht categories, circulatory mannitol, extradural mediastinoscopy, 604–605

death, 77–78 haematoma, 486 mediastinotomy, anterior, 605
machine perfusion, organs for manometric dilatation, mediastinum
transplant, 79 oesophagus, 682 ectopic parathyroid glands, 339
MAGIC trial, gastric carcinoma, manometry infections, cardiac surgery, 600
146–147 anorectal, 294, 621, 628 thoracoscopy, 39
magnesium, ICF and ECF, 27 oesophagus, 118–119 tumours, 613–614
magnetic anal sphincter, 629 Mantoux test, chronic infective medical castration, 580
magnetic resonance arthritis, 468 medical oncology, 88
cholangiopancreatography, marasmus, 50, 51 medical students, 100–101
175, 645 Marfan’s syndrome, 597 medullary thyroid carcinoma,
choledocholithiasis, 169 marginal margins, 411–412 334, 335
pancreatic cancer, 211 marginal vessels, colon, 231 medulloblastoma, 498
magnetic resonance imaging margins of surgical excision, 90, 399, megacolon, 256
bone sarcomas, 478 401, 411–412 colectomy, 260–261
breast, 311 Marjolin’s ulcer, 689–690 megaloblastic anaemia, 10
cervical myelopathy, 521 marking of patient, 5 Meig’s syndrome, 660
colorectal carcinoma, 275 Martorell’s ulcers, 689 melaena, 137, 634, 637–641
fractures, 459 massage, leg swelling, 688 melanoma antigens, 401
haematuria, 696 masses melanomas, 400–402
head and neck cancer, 365 parotid, 373 head and neck, 371, 377
intracranial tumours, 495 right iliac fossa, 252 lymph nodes, 401, 667
liver abscess, 192 small renal, 581–582 MELD score, 75, 79–80, 173, 181,
liver tumours, 174–176 see also lumps 223–224
meningiomas, 500 massive haemoptysis, 707–709 meningiomas, 499–500
osteomyelitis, 466 massive rectal bleeding, 634–635 spinal cord compression, 519, 520
pancreatic cancer, 211 mastalgia, 312 meningismus, 504
post‐traumatic confusion mastectomy meningitis, 506–507, 748
and, 741 prophylactic, 318 after head injuries, 741
prostate, 578 total, 324 post‐traumatic confusion, 742
schwannomas, 405 mastoid air cells, 359 meningococcus see Neisseria
soft tissue tumours, 403, 409 mastoidectomy, 360–361 meningitidis
spinal cord compression, 518, 519 material risks, 3 mental illness, preoperative
main duct IPMN, pancreas, 217 maxillary sinus, squamous cell management, 11
maintenance fluids, burns in carcinoma, 363 meralgia paresthetica, 516, 717,
children, 449 Maydl’s hernia, 381 721–722
major histocompatibility antigens, Mayo repair, epigastric hernia, 6‐mercaptopurine, 257–258, 262
81–82 390–391 mesalazine, 257
major trauma services, 432 May–Thurner syndrome, 560 mesentery
malabsorption Maze procedure, 594 adenitis, 251
bariatric surgery, 152 McBurney’s point, 250 angiography, 635
pancreatitis, 206 McCune–Albright syndrome, 475 Crohn’s disease, 261
Malgaigne’s bulge, 386 Mckeown’s oesophagectomy, infarction, 653
malignant fibrous histiocytoma, 407 127, 128 mesh
head and neck, 371, 376 mebendazole, hydatid cysts, 195 hernioplasty, 387
malignant pleomorphic mebrofenin, technetium‐labelled, 173 incisional hernia repair, 390
adenoma, 374 mechanical back pain, 716 stomal hernia repair, 392
Mallory–Weiss tear, 638 mechanical calf compression meshing, skin grafts, 453
malnutrition, 50–51 devices, 7 mesorectum, 231
enteric fistula, 241 mechanical valves, cardiac, 594–595 see also total mesorectal excision
Roux‐en‐Y gastric bypass, 157 mechanical ventilation, 26, 29, 62 metabolic acidosis, small bowel
sleeve gastrectomy, 155 hospital‐acquired pneumonia from, ischaemia, 246
MALT lymphoma, 149 69–70 metabolic screening, kidney
malunion, fractures, 462 Meckel’s diverticulum, 252 stones, 566
mammary duct ectasia, 314 Littré’s hernia, 381 metabolic stress, 53–54
mammography, 310–311, 323 Meckel’s scan, 252 see also catabolism
screening, 318 medialisation, vocal folds, 364 metacarpophalangeal joint,
mandible median nerve, carpal tunnel infections, 417–418
fracture, 440 syndrome, 514–515 metachronous colorectal liver
radiotherapy on, 366 median sternotomy, 607 metastases, 184
786 Index
metachronous tumours, Milan criteria, HCC, 182 motility studies, oesophagus, 681
oesophagus, 123 milia, 397 motor function, spinal examination,
metaiodobenzylguanidine, nuclear milrinone, 599 722–723
scintigraphy, 347 mineralocorticoids, tumours moulds, yeasts vs, 415
metanephrines, 346–347 producing, 347 mTOR inhibitors, 81
metastases minimally invasive surgery, 39 mucinous cystic neoplasm (MCN),
adrenal glands, 348 gastric carcinoma, 146 pancreas, 210, 217
ascites, 660, 663 parathyroidectomy, 340, 343 mucoepidermoid carcinoma, 374
bone, 479–480 rectal cancer, 276 mucus, anal leakage, 294
brain, 496–497 see also endovascular procedures multidetector computed tomography
breast carcinoma, 319, 327 minor traumatic brain injuries, 735 large bowel obstruction, 287
chest wall, 607 Mirizzi syndrome, 178 pancreatic cancer, 211
colorectal carcinoma, 275, 281 mismatch repair genes, 273, 283 multidisciplinary care, 87–89
liver, 176, 184–189, 281 mitral valve, 592 burns, 453–454
gastric carcinoma, 145 mechanical valves, 595 multidisciplinary meetings, 90, 126
gastrointestinal stromal surgery, 591, 593–594 multifilament sutures, 41
tumours, 148 mitral valve clips, 596 multinodular goitre, 333–334
head and neck, 369 Mittelschmerz, 251 multiple endocrine neoplasia
liver, 184–189 mixed salivary tumour, 373, 374 gastric neuroendocrine tumours, 148
colorectal carcinoma, 176, MMR genes, 273, 283 gastrinoma, 216
184–189, 281 mobilisation hyperparathyroidism, 340
computed tomography, 174, 176 colorectal, 232 medullary thyroid carcinoma, 334
magnetic resonance imaging, postoperative, 26 phaeochromocytoma, 345
175, 176 model for end‐stage liver disease multiple organ dysfunction
non‐colorectal, 189 score, 75, 79–80, 173, 181, syndrome, 61
neck, 366–367, 369, 376–377, 223–224 multiple suture closure devices,
667, 669, 671, 672 modified Marshall scoring system, arteriography, 556
non‐functional PNETs, 216 organ failure, 203 Murphy’s sign, 165
oesophageal carcinoma, 125 modified Nigro protocol, 299 muscles
pancreas, 216–217 modified radical mastoidectomy, 361 diverticulosis, 267
parotid gland, 374 molecular signatures, colorectal liver examination, 723
pleural effusions, 608 metastases, 187 nutritional assessment, 53
prostate carcinoma, 577 molecular therapy, gastric strain, 716
sacrum, 719 carcinoma, 147 trauma, 440
small bowel obstruction, 245 monitoring music, 104
soft tissue sarcoma, 407, 409 acute abdomen, 651 MUTYH‐associated polyposis, 283
spinal cord compression, 517, intracranial pressure, 491 mycobacteria, chronic infective
518, 519 intraoperative, 23, 98 arthritis, 468
testicular cancer, 583 postoperative, 25 mycophenolate mofetil, 81
metastatic brain abscesses, 507 trauma, 438–439 mydriasis, traumatic, 356
methotrexate, Crohn’s disease, 262–263 monocular diplopia, 757–758, 760 myelography, 723–724
meticillin‐resistant S. aureus, 416 monofilament sutures, 41 myelomalacia, 521
metronidazole, amoebic liver monopolar diathermy, 100 myelopathy
abscess, 193 Montreal System, ulcerative cervical, 520–521, 721
microchimerism, 82 colitis, 256 thoracic, 721
microdiscectomy, 724–725 morbidity, surgical procedures, 14 mylohyoid muscle, 372
microlithiasis, 164 morphine, 24 myocardial infarction, 589
micropapillary thyroid carcinoma, mortality surgery for complications, 591
334, 335 abdominal aortic aneurysms, 528 myositis ossificans, 409
microsatellite instability, colorectal cardiac surgery, 596, 600 myotomy, oesophagus, 682
carcinoma, 273 emergency surgery, 110, 111 myringoplasty, 360, 361
microvascular cranial nerve enterocutaneous fistula, 241 myringotomy, 361
palsy, 760 large bowel obstruction, 292 myxoma, 406
microvascular invasion, HCC, 182 obesity, 151 myxomatous degeneration, heart
microwave ablation (MWA), surgical procedures, 14, 15, 21–22 valves, 592, 594
HCC, 182 trauma, 433, 434
mid‐dermal burns, 445 waiting lists for transplantation, nab‐paclitaxel, pancreatic cancer, 215
middle ear cleft, 359 79–80 naevi, 399–400
mid‐inguinal point, 386 Morton’s neuralgia, 717, 721–722 junctional naevi, 399
midstream urine, 696 motility, gastrointestinal tract, 617 strawberry naevi, 404
Index 787
naevoid BCC syndrome, 398 nerves, anatomy, 511 North American Symptomatic
narcotics see opioids nerve sheath tumours, 404 Carotid Endarterectomy
nasal cavity see also neurofibromas; Trial, 539
blood supply, 711 schwannomas nose see nasal cavity; rhinology
polyps, 362 neurapraxia, 512 notes (operative), 104, 105
tumours, 363, 367 neuroendocrine tumours nuclear scintigraphy
nasal packs head and neck, 370 bone sarcomas, 478, 479
airway obstruction, 676, 677 pancreas, 215–216 dyschondroplasia, 473
for epistaxis, 712 small bowel, 245–246 fractures, 457
nasendoscopy, 677, 712 stomach, 148–149 gastro‐oesophageal reflux
NASHA injection (sphincter neurofibromas, 404 disease, 120
augmentation), 629 head and neck, 371, 376 liver function assessment, 173
nasogastric tubes, 29 see also schwannomas lymphatics, 551
acute abdomen, 651 neurofibromatosis, 404 massive rectal bleeding, 635
large bowel obstruction, 287–289 neurogenic claudication, 717, 721, 724 Meckel’s scan, 252
small bowel obstruction, 245 neurogenic tumours, metaiodobenzylguanidine, 347
spinal injuries, 522 mediastinum, 613 oesophageal transit studies, 680
trauma, 438 neurological examination osteomyelitis, 466
nasopharyngeal tubes, 677 head injuries, 489 septic arthritis, 467
nasopharynx, carcinoma, 367 spine, 722–723 thallium‐201 scans, 410
nasotracheal tubes, 677 neurolysis, 724–725 see also positron emission
nausea, postoperative, 21, 34 neuromas, 511 tomography; single photon
neck neuromodulation, faecal emission computed tomography
dissection, 364, 366–367, 672 incontinence, 629–630 nucleic acid testing, organ donors, 82
haematomas, 336, 542 neuropathic joint, 476 nutrition, 49–56
metastases, 369, 376–377 neuropathies absorption, 237–238
swellings, 667–673 diabetes mellitus, 533 burns, 451
necrotising fasciitis, 70–71, entrapment, 513–516, 721–722 pancreatitis, 54, 204
420–421, 729 neurotmesis, 511 perioperative, 54–55
necrotising pancreatitis, 199, 202 nifedipine, anal fissure, 296 preoperative management, 7, 8,
needle holders, 40 Nigro protocol, modified, 299 52–54
needlestick injuries, avoidance, 37 nipple short‐gut syndrome, 239, 240
negative pressure wound therapy, 47, breast reduction surgery, 427 see also malnutrition; parenteral
48, 68 discharge, 313–314 nutrition
see also suction drains Paget’s disease, 310 Nutritional Risk Screening, 53
Neisseria meningitidis, 422 nitinol stents, tissue aortic valves nystagmus, posterior fossa
meningitis, 507 on, 596 tumours, 498
septicaemia, 421–422 nitroprusside, 599
neoadjuvant therapy, 88 nocturia, 570 obesity, 151–159
bladder carcinoma, 581 nodular adrenal hyperplasia, 348 breast carcinoma, 317
breast carcinoma, 326 nodular melanoma, 401 cholelithiasis, 164
gastric carcinoma, 146–147 nodules gastro‐oesophageal reflux
oesophageal carcinoma, 126 thyroid, 332–333, 669, 670 disease, 116
pancreatic cancer, 214–215 vocal, 363 oesophageal carcinoma, 123
rectal cancer, 278, 280 non‐absorbable sutures, 40 pancreatic cancer, 209
soft tissue sarcoma, restaging, 411 non‐alcoholic fatty liver disease, patient positioning, 97
neostigmine, 291 transplantation results, 83 objective assessment, surgical risk, 14
neovascularisation, varicose vein non‐functional PNETs, 216 obstetric injury, 626, 631
surgery, 549 non‐muscle‐invasive bladder obstruction
nephrectomy cancer, 581 bladder outlet, 568
living donors, 76 non‐proliferative breast conditions, colon see large bowel obstruction
partial, 583 314–315 gallbladder, 165
radical, 583 non‐selective shunts, portal hernias, 383
nephron‐sparing surgery, 583 hypertension, 222–223 hiatus hernia, 117
nephrotic syndrome, 686 non‐steroidal anti‐inflammatory laparoscopic adjustable gastric
nephroureterectomy, 580–581 drugs, 24 banding, 154
nerve injuries gastric ulcers, 137, 638 small bowel see under small bowel
acute, 511–513 on stress response, 55 stomach outlet, 140
common peroneal nerve, 5 non‐union, fractures, 462 venous outflow, liver, 659, 664
nerve roots see spinal nerve roots normal saline, 60 see also intestinal obstruction
788 Index
obstructive jaundice, 643–647 oncology osteomas, head and neck, 371

choledocholithiasis, 166, 168, follow‐up, 91 osteomyelitis, 465–467
645–646 surgical, 87–92 back pain, 718
preoperative management, 9–10 oncotic gradient, 686 vertebrae, 520
obstructive sleep apnoea, 363 on‐table large bowel irrigation, 271 osteoporosis, 475
bariatric surgery on, 152 onychocryptosis, 418 short‐gut syndrome, 240
preoperative management, 9 onychomycosis, 416 vertebral collapse, 725
obturator hernia, 393 open drainage, 42 osteosarcoma, 478–479
occupational safety, operating rooms, open fractures, 457, 460–461 head and neck, 371
36–37, 104 skull, 491 osteotomy, 469
octreotide, short‐gut syndrome, 240 open reduction otitis media
oculomotor nerve see third cranial dislocations, 463 brain abscesses, 508
nerve fractures, 459 chronic, 359–361
odynophagia, 365 open surgery, 38–39 otology, 359–362
oedema open wounds, 47–48 tumours, 362
cerebral, 449 operating rooms, 35, 93–108 otorhinolaryngology, 359–368
leg, 686–689 equipment management, 97 otosclerosis, 361
lymphoedema vs, 550–551 hazards, 36–37, 104 ovary
posterior reversible inner sanctum, 94–104 cysts, torsion, 251
encephalopathy outer networks, 104–107 function suppression, 326–327
syndrome, 747 see also angiography suites Krukenberg tumours, 275
oesophagectomy operative risk, classification, 4–5 polycystic ovarian syndrome,
carcinoma, 127–130 ophthalmology see eye bariatric surgery on, 152
complications, 129–130 ophthalmopathy, 335 overweight, defined, 151
surgical risk, 14 see also proptosis oxygen saturation
oesophagitis, 116 opioids, 24 intraoperative, 23
oesophago‐gastric junction, gastric post‐traumatic confusion, 738, postoperative, 29
carcinoma, 143–144 739–740 preoperative, 20
oesophagoscopy, 680 short‐gut syndrome, 240 oxygen therapy, intraoperative, 23
oesophagus, 115, 124 optic nerve, meningiomas oxysterol 7α‐hydroxylase, 163
bleeding, 637 compressing, 499
dysphagia, 679–683 oral contraceptive pill, breast pacemakers, 598–599
ectopic parathyroid glands, 339 carcinoma, 318 paclitaxel‐coated balloon
foreign body, 676 oral rehydration solution, short‐gut angioplasty, 531
lower sphincter, 115–116 syndrome, 240 Paget–Schroetter disease, 560
manometry, 118–119 orbit, blow‐out fracture, 354–355 Paget’s disease (bone), 474–475
motility studies, 681 orchidopexy, 732 Paget’s disease (nipple), 310
transit studies, 680 orchiectomy, 573 pain
tumours, 123–131 radical, 583 abdominal wall, 111
dysphagia, 682 organ donation, 76–79 acute abdomen, 649
prognosis, 130 organ failure, 61 appendicitis, 249
staging, 125–126 modified Marshall scoring biliary colic, 165
surgery, 127–130 system, 203 bone sarcomas, 478
treatment, 126–130 pancreatitis, 200, 201 carpal tunnel syndrome, 514–515
twenty‐four‐hour pH transplantation for, 75 chest, 589
monitoring, 120 organisational hazards, 36–37 postoperative, 700–701
varices, 220, 221–223, 637 organ preservation fluids, 78–79 chronic infective arthritis, 468
see also Barrett’s oesophagus organ/space SSIs, 67, 69 compartment syndrome, 462
offloading, diabetic foot, 533 orthotopic transplantation, 80 conjunctivitis, 750
off‐pump coronary surgery, 591 ossicles critical limb ischaemia, 530
Ogilvie’s syndrome, 290–291 hearing impairment, 361 degenerative arthritis, 468
olfactory groove meningioma, 499 reconstruction, 361 diffuse oesophageal spasm, 682
olfactory neuroblastoma, 370 ossification, soft tissue sarcomas, 408 duodenal ulcers, 134
oligodendroglioma, 496 osteoarthritis, 468–469, 470 inguinal hernia, 386
oliguria, postoperative, 32, 701–702 osteochondritis dissecans, 477–478 after inguinal hernia repair, 388
Ollier’s disease, 473 osteochondroma, 473–474 intermittent claudication, 529
omega‐3 fatty acids, 55 osteodystrophy, renal, 341 joints, 467, 721
omentum, patch repair with, 139 osteogenesis imperfecta, 472–473 large bowel obstruction, 286
omphalocele, 391 osteomalacia, 471 leg pain, 715–726
oncological resection, colon, 289 short‐gut syndrome, 240 low back pain, 715–726
Index 789
mastalgia, 312 pantaloon hernia, 385 pathological fractures, 457

obturator hernia, 393 papillary thyroid carcinoma, patient explanatory brochures, 4, 94–97
Paget’s disease, 474 334–335 see also consent; discussion with
pancreatitis, 204, 206 thyroglossal duct cyst vs, 331 patient
perforated ulcer, 138 papilloedema, 495 patient safety, 5, 36–37
perianal, 293, 296–297 papilloma (intraductal), breast, 314 pectus carinatum, 607
postoperative, 23–24, 25 papillomatosis, 314 pectus excavatum, 607
preoperative planning for, 21 paracentesis, 220, 664 pelvic appendicitis, 250
renal colic, 566 paracetamol, 23–24 pelvic floor retraining, 621
scrotum, 727–733 paracolic gutters, 139, 654 pelvic inflammatory disease, 251
small bowel ischaemia, 246 paradoxical aciduria, 140 pelvic venous insufficiency, 546, 547
small bowel obstruction, 243 paragangliomas, 345–347 pelvis
Spigelian hernia, 392 head and neck, 370, 374–375 abscesses, 655
spinal cord compression, 517 paralytic ileus, 29, 245, 287–289 drainage, 656
testes, 573 paranasal sinuses chronic pain, 570
paired exchange, living donors, 76 infections, 362 fractures, 695
palatal incompetence, 679 tumours, 363, 367 penetrating injuries, 433
palliative care, 88–89 paraneoplastic syndromes cardiac arrest, 438
oesophageal carcinoma, 130, 682 lung carcinoma, 610 head, 483
pancreatic cancer, 214 renal cell carcinoma, 582 to staff, 37, 104
chemotherapy, 215 para‐oesophageal hernia, 117 penicillin, cellulitis, 551
palliative surgery, 91 paraparesis, 517 penis, 571–572
pancreatic cancer, 214 paraphimosis, 572 cancer, 583–584
rectal cancer, 280 paraplegia, spinal stroke, 718 peptic ulcer disease, 133–141
stomas, 230 parasagittal meningiomas, 499 acute abdomen, 652, 653
pallor, anaemia, 10 parasitic infections, liver, 193–197 bleeding, 637–638
pampiniform plexus, 573 parastomal hernias, 392 complications, 137–140
varicoceles, 574 parathyroidectomy, 341, 342, 343 percussion
Pancoast’s syndrome, 610 minimally invasive, 340, 343 ascites, 661–662
pancreas parathyroid glands, 339–344 tympanitic, 286
carcinoma, 209–215 autotransplantation, 342–343 percutaneous balloon valvuloplasty,
cystic diseases, 217 localisation, 340–341 593
fistula (CR‐POPF), 212 thyroidectomy, 336, 337 percutaneous coronary intervention,
function testing, 206 tumours, 370 589
metastases to, 216–217 parathyroid hormone, 339 percutaneous drainage
neuroendocrine tumours, 215–216 hyperparathyroidism, 341 abscesses
secretion of electrolytes, 28 levels, 340 abdominal, 655–656
surgical risk assessment, 13 para‐umbilical hernia, 391 diverticulitis, 269–270
transplantation parenteral nutrition, 54–55 hydatid cysts, 195
positions of organs, 85 cholelithiasis, 164 percutaneous endovascular
results, 84 preoperative, 8 procedures see endovascular
surgery, 80 short‐gut syndrome, 239, 240 procedures
pancreatectomy, 207 Parinaud’s syndrome, 503 percutaneous transhepatic
pancreatitis, 199–208, 653 Paris classification, early gastric cholangiography, 174, 646
ascites, 661 cancer, 145 perforating injury, eye, 354
autoimmune, 645 Parkland formula, 449 perforating veins, 545–546
cholelithiasis, 165–166, 170 Park’s operation, 629 ligation, 548
complications, 200–201, 204 paronychia, 417 oedema, 687
investigation, 201–204 parotid gland tumours, 372, perforation
nutrition, 54, 204 373–374 acute colonic pseudo‐obstruction,
pancreatic cancer, 209 benign, 669 290
positron emission tomography, 211 malignant, 374 appendicitis, 249
treatment, 204–205 partial nephrectomy, 583 caecum, 251
pancreatoduodenectomy, 178, partial shunts, portal colorectal carcinoma, 277, 289
207, 213 hypertension, 223 diverticulitis, 269, 271
pancreatic cancer, 212 partial‐thickness burns, 444–445, free gas, 654
surgical risk, 13, 14 446, 447 large bowel obstruction, 285
pancreatosplenectomy (radical passive incontinence, faecal, 625 pain, 649
anterior modular), 212 patch repair, duodenal ulcers, 139 peptic ulcer, 138–139
panniculus adiposus, 443 patent ductus arteriosus, 596–597 tympanic membrane, 360, 361
790 Index
performance improvement, trauma pituitary apoplexy, 502, 747–748 chest, 604

care, 440 pituitary tumours, 501–503 colorectal carcinoma, 275
perianal disorders, 293–300 plasma renin and aldosterone liver metastases, 176, 185
abscess, 301 ratio, 348 gallium‐68 DOTA‐TATE, 215
constipation, 619 plasma water, 27 gastric carcinoma and, 145
Crohn’s disease, 261, plaster of Paris casts, 461 head and neck cancer, 365
265–266, 303 plastic surgery, 423–428 lung carcinoma, 610–611
examination, 295 pleomorphic adenoma, 373, 374 pancreatic cancer, 211
haematomas, 296–297 pleural effusions, 607–608 pancreatic neuroendocrine
investigation, 295–296 aspiration, 605 tumours, 215
sepsis, 301–306 signs, 604 soft tissue sarcomas, 410
periductal mastitis, 314 pleurodesis, 608 POSSUM (risk scoring system), 15
perihilar cholangiocarcinoma plunging ranula, 669, 671 post‐anal repair, 629
imaging, 175–176 pneumatic compression, posterior arch vein, 545
treatment, 178 lymphoedema, 551 posterior fossa tumours
perineum, examination, 627 pneumaturia, 271 children, 497–498
peripheral vascular disease, 529–534 pneumocephalus, 740–741 meningiomas, 499–500
endovascular procedures, 557–560 pneumonectomy, 611 posterior reversible encephalopathy
peritoneovenous shunts, 664–665 pneumonia, hospital‐acquired, 69–70 syndrome, 747
peritoneum pneumothorax, 440, 608–609 posterior tibial nerve
chronic inflammation, 660 signs, 604 stimulation, 630
gastric carcinoma spread, 145 see also tension pneumothorax posterior triangle, lymph nodes, 667
leaks into, 660–661 point‐of‐care testing, 107 post‐ICU syndrome, 57
metastases, laparoscopy, 189 polyamide, sutures, 41 postoperative complications,
peritonitis, 652–654 Pólya’s gastrectomy, 135 699–705
appendicitis, 250 polycystic ovarian syndrome, airway obstruction, 676
ascites, 662, 664 bariatric surgery on, 152 ascites, 661
diverticulitis, 269, 270 polyethylene glycol, 230 fatigue, 52
large bowel obstruction, 286 polyglactin, sutures, 41 infections, 65–73, 701
signs, 138, 652 polyglycolic acid, sutures, 41 nausea and vomiting (PONV),
spontaneous bacterial, 219 polymorphonuclear leukocytes, 66 21, 34
peritonsillar abscesses, 363 polypeptide response, pancreas, 206 pancreatic fistula (CR‐POPF), 212
petechial haemorrhages, head polypropylene, sutures, 41 renal failure, 16
injuries, 735, 741 polyps respiratory disease, 29
Peutz–Jeghers syndrome, 284 colorectal, 281–284 postoperative management, 25–34
Peyronie’s disease, 572 nasal, 362 bowel surgery, 233–234
phaeochromocytomas, 345–347 vocal folds, 363 cardiac valve surgery, 596
pharyngo‐oesophageal polytetrafluoroethylene, sutures, 41 nutrition, 54
dysphagia, 681 polyunsaturated fatty acids, 55 orders, 104
phimosis, 572 polyvinyl alcohol pain, 23–24, 25
phlegmon microspherules, 554 transplantation, 80–81
appendiceal, 252 popliteal artery ward care, 106
Crohn’s disease, 262 aneurysms, 527, 528 wounds, 47–48
phosphates pulse, 530 post‐traumatic amnesia, 735
hyperparathyroidism, 341 popliteal vein, 545 post‐traumatic confusion, 735–743
ICF and ECF, 27 porta hepatis, imaging, 176 post‐traumatic dermoid cysts, 397
phyllodes tumour, 313 portal hypertension, 219–223 posturing, head injuries, 489
physiotherapy ascites, 659 potassium, 27
dislocations, 463 surgical procedures, 222 dietary requirements, 50
low back pain, 724 portal vein, 219 gastric outlet obstruction, 140
see also rehabilitation bacteraemia, 191 hyperkalaemia, 32–33
pigmented lesions, skin, 399–402 embolisation, 173 intravenous, 33
pigmented villonodular pancreatic cancer, 212 in secretions, 28
synovitis, 477 portosystemic anastomoses, 219, see also hypokalaemia
Pilates, 724 219–220, 664 pouchitis, 260
pilocytic astrocytoma, 494 Portsmouth P‐POSSUM (risk scoring pre‐admission clinics, 15–16
pilonidal sinus, 305–306 system), 15 pre‐Cushing’s syndrome, 347
pineal region tumours, 503, 504 positioning of patient, 37, 97 prednisolone
piriformis syndrome, 717, 721–722 occupational safety, 104 Crohn’s disease, 262
pitting oedema, 688 positron emission tomography ulcerative colitis, 257
Index 791
pregabalin, 24 prolactinoma, 502 pulmonary embolism, 32, 700–701

pregnancy prolapse, rectal, 299, 633 pulmonary function tests, 16, 603
appendicitis, 250–251 proliferative breast conditions, pulmonary hydatidosis, 194
asymptomatic bacteriuria, 571 314–315 pulmonary hypertension, inotropic
cholelithiasis, 164 proptosis, 353 agents, 599
varicose veins, 546 sinusitis, 362 pulse oximeters, 23
pre‐hospital management, trauma, see also ophthalmopathy pulses, limb ischaemia, 530
431–432, 488 prostate pupils, 353
pre‐immune suppression screen, 258 anatomy, 565 diplopia, 758–759
preoperative management, 3–11, see also benign prostatic extradural haematoma, 486
94–97 hyperplasia intracranial pressure, 489
acute surgery, 7–8 prostate carcinoma, 577–580 pyelonephritis, 570
allergies, 8 bone metastases, 479, 577 pyeloscopy, 698
anaemia, 10, 21 haematuria, 694 pylorus‐preserving
anaesthesia, 19–22 prostatectomy, 569 pancreatoduodenectomy, 212
anticoagulants, 9 radical, 579 pyramid, thyroid, 331
bowel surgery, 229 prostate‐specific antigen, 89, pyrexia
assessment, 4–5 568, 577 head injuries, 490
bowel surgery, 229–230 5α‐reductase inhibitors on, 569 postoperative, 31, 234, 701
cardiovascular disease, 8–9, 20–21 prostatitis, 570 pyuria, appendicitis, 250
cerebrovascular disease, 9 prostheses
corticosteroids, 9 auditory, 361 quinsy, 363
diabetes mellitus, 8, 21 heart valves, 594–596
discussion with patient, 3–4, intervertebral cages, 725 R0 resection, pancreatic cancer, 214
25, 94 joints, 469 radial neck dissection, 366–367
hair removal, 101 protective clothing, 35, 101, 104 radial scars, breast, 315
kidney function, 10 protein radiation protection, 104, 107
liver disease, 9–10, 224 body composition, 50, 52 angiography, 553
liver function assessment, 173 catabolism, 51–52 radical anterior modular
nutrition, 7, 8, 52–54 dietary requirements, 49, 50, 240 pancreatosplenectomy
phaeochromocytomas, 347 protein–energy malnutrition, 50 (RAMPS), 212
proctocolectomy, 259 proton pump inhibitors, 120 radical cystectomy, 581
psychological aspects, 11, 94 on gastrin levels, 140 radical nephrectomy, 583
respiratory disease, 9 on Helicobacter pylori radical orchiectomy, 583
transplant patients, 85 detection, 134 radical prostatectomy, 579
wound management, 45–46 peptic ulcer disease, 135, 137 radicular pain, 716
prescribed medications, PRSS1 gene, 200 radioactive iodine,
preoperative, 20 prucalopride, 621 thyrotoxicosis, 335
preservation fluids, 78–79 pseudoaneurysms, 527, 534 radiofrequency ablation (RFA)
pressure points, positioning of pseudocapsule, soft tissue hepatocellular carcinoma, 182
patient, 97 sarcoma, 407 varicose veins, 549
priapism, 572 pseudocyst, pancreatitis, 201, radiofrequency therapy, anal
primary haemorrhage, 33 205–206 canal, 631
primary sclerosing cholangitis, pseudogout, 476 radiography
perihilar cholangiocarcinoma pseudomembranous colitis, 70 acute abdomen, 651, 653
and, 178 pseudomeningocele, 513 arthritis, 469
primary survey pseudo‐obstruction, 29, 290–291 dislocations, 462–463
burns, 448–449 pseudopapillary neoplasms, head injuries, 490
trauma, 435, 436–437 pancreas, 217 hyperparathyroidism, 472
Primovist, 174–175 psoas sign, 250 large bowel obstruction, 287
processus vaginalis, 384, 385, 387 psychosocial support neck lumps, 670
proctectomy, patients with critical illness, 62 osteomyelitis, 466
cirrhosis, 225 oncology, 88, 91 perforated ulcer, 139
proctitis puborectalis, 625 pleural effusions, 608
ulcerative colitis, 256 pudendal nerves rickets, 471
treatment, 257 function testing, 295–296 small bowel ischaemia, 246–247
proctocolectomy, 259–260, 265 latency time, 628 small bowel obstruction, 244, 245
restorative, 283 pulmonary angiography, CT, soft tissue sarcomas, 408
proctography, 295, 620–621, 628 700–701 spine, 723
proctoscopy, 633 pulmonary autograft procedure, 595 trauma, 435
792 Index
radioisotopes see nuclear prolapse, 299, 633 resection rectopexy, 299

scintigraphy stapled transanal resection, 622 resonium ion‐exchange resins, 33
radiotherapy, 87–88 villous adenoma, 281 respiratory disease
bone sarcomas, 478 recurrence gastro‐oesophageal reflux
brain metastases, 497 breast carcinoma, 327 disease, 116
breast carcinoma, 324, 325 colorectal carcinoma, operative risk, 5, 16
cystitis from, 694 275–276, 281 postoperative complications, 29
gastric carcinoma, with inguinal hernia, 387 postoperative management, 26–27
chemotherapy, 147 liver disease, 83 preoperative assessment, 20
gliomas, 496 peptic ulcer disease, 135 preoperative management, 9
head and neck cancer, 366 soft tissue sarcoma, 407 respiratory infections
lung carcinoma, 611–612 spontaneous pneumothorax, 609 hospital‐acquired, 69–70
melanomas, 401–402 varicose veins, 549 resistance to, 65
oesophageal carcinoma, 130 volvulus, 290 respiratory muscle strength, 53
pancreatic cancer, 215 recurrent corneal erosion restaging
prostate carcinoma, 579 syndrome, 750 soft tissue sarcoma, 411
for skin cancer, 372 recurrent laryngeal nerve, 337, 339, see also down‐staging
soft tissue sarcomas, 412 363–364 restorative proctocolectomy,
for spinal cord compression, 519 oesophagectomy, 130 259–260, 283
rapid urease test, 134 palsy, 336, 363–364, 676 rest pain, 530
RAS‐mutant colorectal liver recurrent urinary tract restraint, confused patient, 739
metastases, treatment, 187 infections, 570 resuscitation
rat’s tail appearance, red cells, transfusion, 10 acute abdomen, 651, 653
schwannomas, 405 red eye, 749–755 burns, 449
Raynaud’s syndrome, 534 reduction haemorrhage, 438
reactionary bleeding, 33 dislocations, 463 preoperative, 7
rebound tenderness, 250 fractures, 459 trauma, 435, 436–437, 737
receiver–stimulators, cochlear for spinal cord compression, 522 see also volume resuscitation
implants, 362 reduction surgery, breast, 427 retention sutures, 42, 47
recipient selection, transplantation, referred pain retractors, 40
79–80 to leg, 717, 722 use of, 100
reconstruction to scrotum, 731 patients with cirrhosis, 224
breast, 324–325, 424 regeneration, nerves, 511 retrobulbar haemorrhage, 353
head and neck cancer, 366, 424 regional trauma services, 432 retrocaecal appendix, 250
ossicles, 361 regorafenib, GISTs, 148 retrograde amnesia, 484
plastic surgery, 427 regurgitation, gastro‐oesophageal retrograde pyelography, 696
reconstructive ladder, plastic reflux disease, 118 retrograde urethrography,
surgery, 424 rehabilitation 569–570, 696
recording (operative), 104, 105 fractures, 462 retroperitoneal metastases, testicular
recovery rooms, 104 head injuries, 491 cancer, 583
rectal bleeding, 137, 293–294, see also physiotherapy retroperitoneoscopic
633–635 rejection, transplants, 81–82 adrenalectomy, 349
rectal examination renal cell carcinoma, 581–583 revascularisation, small bowel
for bleeding, 633 renal colic, 566 ischaemia, 247
constipation, 619 renal failure reversible cerebral vasoconstriction
low back pain, 723 ascites, 662–663, 665 syndrome, 746–747
rectoanal inhibitory reflex, 293, 628 leg swelling, 686 reversible posterior
rectum, 231, 294 postoperative, 16, 32 leucoencephalopathy
anastomoses, 232 see also chronic kidney disease syndrome, 747
balloon expulsion test, 621 renal injury, anaemia of, 10 Revised Atlanta Classification,
cancer, 275 renal osteodystrophy, 341 pancreatitis, 201
chemotherapy, 280 renal veins, 565 rhabdomyosarcomas
familial adenomatous renin epistaxis, 711
polyposis, 283 excess, 660 head and neck, 371, 376
large bowel obstruction, 289 levels, 348 rheumatic fever, heart valves, 592
minimally invasive surgery, 276 reperfusion syndrome, 535 rheumatoid arthritis, 470
surgery, 231, 277–278, 279, 280 reports (operative), 104, 105 rhinology, 362–363
compliance, 628 research, oncology, 91 tumours, 363, 367
dyssynergia, 620 resectability, colorectal liver rhinorrhoea, 362
function, 617 metastases, 186–187 cerebrospinal fluid, 362, 491
Index 793
Richter’s hernia, 381, 382 saliva hepatocellular carcinoma, 181

rickets, 471 cortisol, 348 prostate carcinoma, 577
right gastric vein, 219 electrolytes, 28 screening profiles, healthy patients, 5
right gastroepiploic vein, 219 secretion rate, 237 scrotum, 727, 728
right hemicolectomy, 276, 289 salivary glands, tumours, 370, anatomy, 572
caecal volvulus, 290 372–374 hernia repair complications, 387
right iliac fossa saphenofemoral junction, 545 inguinal hernia into, 385
masses, 252 saphenofemoral ligation, 548 lymphatics, 573
pain, 649 saphenopopliteal ligation, 548 pain, 727–733
right paracolic gutter syndrome, 139 sarcomas scrubbing, 35–36, 102
rigidity, appendicitis, 250 bone, 478–479 scrub nurses, 98
ringworm, 416 head and neck, 371 sebaceous cysts, 397
risk groups, prostate carcinoma, 578 see also soft tissue sarcomas seborrhoeic keratosis, 397
risks sarcopenia, 50 SECCA therapy, anal canal, 631
assessment, 4–5, 13–17, 21–22 satellite lesions, soft tissue secondary bleeding, 33
material, 3 sarcoma, 407 secondary brain injury, 737
rivaroxaban, 9 Saturday night palsy, 513 secondary survey
robotic surgery, 39 scalds, 443 burns, 450
colorectal liver metastases, 188 scalp injury, 491 head injuries, 439
gallbladder carcinoma, 180 SCAR (mnemonic), 94 trauma, 438
gastric carcinoma, 146 scarring, burns, 451 second primary, breast
oesophagectomy, 127–129 schistosomiasis, 662 carcinoma, 327
radical prostatectomy, 579 schwannomas, 404, 405 sedation
rodent ulcer, 398 acoustic, 500–501 for postoperative confusion,
Rome IV consensus, head and neck, 371, 375–376 31, 700
constipation, 617 spinal cord compression, 519 for post‐traumatic confusion,
Ross procedure, 595 see also neurofibromas 738, 739
rotation flaps, 426 sciatica, 715, 717, 719, 724 seizures
Roux‐en‐Y gastric bypass, sciatic hernias, 393 brain abscesses, 508
155–158 sciatic nerve, examination, 723 dislocations, 462
gastro‐oesophageal reflux scintigraphy see nuclear scintigraphy; Seldinger technique, 555, 556
disease, 121 positron emission selective internal radiation therapy
Rovsing’s sign, 250 tomography; single photon (SIRT), HCC, 183
rubber band ligation, emission computed selective shunts, portal hypertension,
haemorrhoids, 297 tomography 222–223
rule of nines, 444, 445 scissors, 100 self‐expanding stents, 555
rupture sclera, injuries, 353 semilunar line, 392
aneurysms, 527, 528, 529 scleritis, 752, 753 sensation, spinal cord lesions, 723
abdominal aorta, 653 scleroderma, 682 sensorineural hearing loss, 361
cerebral, 503–506 scolicidal agents, 195 sentinel headache, 504
thoracic aorta, 598 scoring systems sentinel node biopsy, breast
choroidal, 356 Child–Pugh score, 173, 181, carcinoma, 325
eye globe, 354 223–224 sepsis, 57–60, 66
hepatocellular carcinoma, 183 colorectal liver metastases, 186 confusion, 700
hydatid cysts, 194 faecal incontinence, 626–627 diabetic foot, 533
liver abscess, 192 Japan Integrated Staging kidney stones, 567
myocardial infarction, 591 score, 182 on metabolism, 51–52
varicose veins, 546 MELD score, 75, 79–80, 173, 181, perianal disorders, 301–306
Rutherford classification 223–224 post‐traumatic confusion, 739, 742
acute limb ischaemia, 559 organ dysfunction, 61 septic arthritis, 721
chronic limb ischaemia, 557, 558 pancreatitis, 203 acute, 467–468
SOFA score, 59 septic shock, 58–61, 67, 701, 703
S‐1 (chemotherapy drug), 147 surgical risk assessment, 14–15, septum, nasal, 362
sacral nerve stimulation, 299, 622, 21–22 sequential organ failure assessment
629–630, 631 SYNTAX score, 589 score, 59, 61
sacral sparing, 723 scout nurses, 98 sequestra, 465, 467
sacroiliitis, 721 screening for cancer, 89 serology
saddle area numbness, 722 breast carcinoma, 318 amoebic liver abscess, 193
safety (patient safety), 5, 36–37 colorectal carcinoma, 281 Helicobacter pylori, 134
saline (normal), 60 gastric carcinoma, 145 hydatid disease, 194
794 Index
seromas, 30 skin, 443 hypernatraemia, 27, 32

seronegative arthritis, 470 as barrier to infection, 65 restriction, 663
serous cystadenoma, pancreas, 217 benign tumours, 397–398, retention, 659–660
serous fluid, from wounds, 30 399–400 in secretions, 28
serrated polyposis syndrome, 284 cancer, 398–399 see also hyponatraemia
serum to ascites albumin head and neck, 369–372 sodium bicarbonate, 33
gradient, 662 transplantation patients, 83 sodium chloride (0.9%), 60
sessile serrated adenomas, 281 flora, 101 SOFA score, 59, 61
99m
Tc‐sestamibi, SPECT, 340 grafts, 425–426 soft tissue sarcomas, 406–413
setons, anal fistula, 304 burns, 452–453 head and neck, 371, 376
severe sepsis, 51, 58, 59, 66 pigmented lesions, 399–402 soft tissue tumours, 403–413
sex steroid‐producing tumours, 348 preparation for surgery, 35–36, solid pseudopapillary neoplasms,
sexually transmitted infections, 46–47, 102 pancreas, 217
epididymo‐orchitis, 729, 732 suturing, 40 solitary pulmonary nodule, 612–613
sharps, 37, 98, 104 skinfolds, 52 see also coin lesions
shearing, intracerebral, 483 skin substitutes, 453 soluble fibre supplements, 621
shifting dullness, 661–662 skin tags, anal, 298 somatic back pain, 716
shingles, tofacitinib and, 258 skull sorafenib, hepatocellular
shock, 437–438 fractures, 485, 491, 740–741 carcinoma, 183
burns, 451 hyperostosis, meningiomas, 500 spatiotemporal plots, oesophageal
cardiogenic, 591 sleeve gastrectomy, 153–155 manometry, 119
postoperative, 703 complications, 156 spectrophotometry, subarachnoid
septic, 58–61, 67, 701, 703 gastro‐oesophageal reflux disease, haemorrhage, 746
short gastric vein, 219 121, 155 speech processors, 362
short‐gut syndrome, 238–240 sliding hiatus hernia, 117 spermatic cord, 573, 727
short saphenous vein, system, 545 sliding inguinal hernia, 386 spermatocele, 573–574
shunts slow transit constipation, sperm granuloma, 731
ascites, 664–665 619–620, 621 sphenopalatine artery, endoscopic
cerebrospinal fluid, 498 small bowel ligation, 712
portal hypertension, 220–223 cancer, 245–246 sphincter(s), spinal cord
shunt surgery, portal Crohn’s disease, 261–265 compression, 517
hypertension, 222 ischaemia, 243, 246–247 sphincter complex (anal), 293, 625
side‐branch IPMN, pancreas, 217 obstruction, 243–246 abscesses, 301
side‐to‐side anastomoses, bowel Meckel’s diverticulum, 252 augmentation, 629
surgery, 232 physiological changes, 237–240 fistula, 303–304
Siewert classification, oesophageal surgery, 229 repair, 629
carcinoma, 124–125 small‐cell carcinoma replacement, 629
sigmoid colon anaplastic high‐grade sphincter of Oddi, pancreatitis, 205
cancer surgery, 277 neuroendocrine tumours, sphincterotomy, anal, 296
diverticulosis, 267 148–149 Spigelian hernia, 392
volvulus, 285, 290 lung, 610 spinal accessory nerve
sigmoidoscopy small renal masses, 581–582 lymph nodes, 667
faecal incontinence, 627 smoke inhalation, 448, 450 neck dissection, 364
flexible, 633 smoking spinal cord compression,
rigid, 295, 633 diabetic foot, 533 516–523, 725
Sigura procedure, 223 neck lumps, 668 spinal cord injury, 490
silk, sutures, 41 operative risk, 5, 9, 20 cholelithiasis, 165
silver‐impregnated dressings, 451 pancreatic cancer, 209 primary survey, 435
single nucleotide polymorphisms, preoperative cessation, 97 spinal cord lesions, sensation, 723
breast carcinoma, 318 SNAP (mnemonic), enteric spinal nerve roots, 716
single photon emission computed fistula, 241 avulsion, 513
tomography snare polypectomy, 282 cervical, 375
99m
Tc‐sestamibi, 340 Snellen chart, 353–354, 751 compression, 716
spine, 724 SNPs (single nucleotide spinal shock, 521
sinusitis, 362 polymorphisms), breast spine
Sister Mary Joseph nodule, 661 carcinoma, 318 anatomy, 715–716
Sitzmark test, 619–620 sodium, 27 dislocations, 522
6‐mercaptopurine, 257–258, 262 dietary requirements, 50 examination, 722–723
sixth cranial nerve, 757 gastric outlet obstruction, 140 haematomas, 718
palsy, 495, 758, 760 gastrointestinal tract, 237 SPECT, 724
Index 795
trauma, 718, 719 steel, sutures, 41 stress ulcers, 133–134

cervical spine, 435, 490, stellate cells, pancreas, 205 strictureplasty, Crohn’s disease,
521, 522 stent‐grafts 263, 264
thoracolumbar spine, 521, 522 aneurysms, 529 strictures
Spitz naevus, 400 see also covered stents large bowel obstruction, 285, 290
splenectomy, gastric carcinoma stenting urethra, 569–570, 695
and, 144 angioplasty, 531, 554–555 stridor, 676–677
splenic flexure, ischaemic colitis, 247 biliary tract, distal tumours, 646 stripping, long saphenous vein, 548
splenic vein, 219 carotid arteries, 541 stroke, 537–543
splenomegaly, portal colon, 289, 290 cardiac surgery, 600
hypertension, 220 coronary arteries, 589 dysphagia, 681
splinting, cellulitis, 419 coronary artery bypass from head injuries, 741
split liver transplantation, results, 83 grafting, 592 preoperative management, 9
split‐thickness skin grafts, 425 endografts, 555 spinal, 718
burns, 452–453 oesophageal carcinoma, 130 see also cerebrovascular disease
spontaneous bacterial peritonitis, 219 stereotactic radiosurgery struvite stones, 566
spontaneous pneumothorax, 609 acoustic neuromas, 501 Stupp protocol, 496
sports injuries, concussion, 484 brain metastases, 497 subacute thyroiditis, 335, 336
spot salivary cortisol, 348 sterility, 35–36, 94, 101–104, 106 subarachnoid haemorrhage,
squamous cell carcinoma loss of, 100 503–506, 745–747
anus, 298–299 sternomastoid muscle, neck subclavian steal, 538
ear, 362 lumps, 668 subclinical Cushing’s syndrome, 347
leg ulcers, 689–690 sternotomy, median, 607 subconjunctival haemorrhage,
lung, 610 sternum, infections, cardiac 752, 753
lymph nodes, 667, 671, 672 surgery, 600 subcuticular sutures, 40
maxillary sinus, 363 stockings see compression stockings; subdural effusion, meningitis, 507
oesophagus, 123, 124 elastic stockings subdural haematoma, 487–488
skin, 369–372, 398–399 stomach subjective assessment, surgical
upper aerodigestive tract, 364–367, bleeding, 637–638 risk, 14
369, 377 carcinoma, 136, 137, 143–147 sublingual glands, 372
stabilisation, open fractures, 460 diffuse large B‐cell lymphoma, 149 tumours, 374
stab wounds, 433 dilatation, 28–29 subluxations, 462–463
staghorn calculi, 567 fluid secretion, 237 submandibular glands, 372
staging of cancer, 89–90 outlet obstruction, 140 swellings, 669
bladder carcinoma, 581 resistance to infection, 66 tumours, 374
breast carcinoma, 319, 320, 321 use in oesophagectomy, 127–128 subperiosteal abscesses, 465
cholangiocarcinoma, 177 see also entries beginning gastric… subphrenic abscess, 655, 655
colorectal carcinoma, 90, stomas, 238 subspecialty training, emergencies
185–186, 274 bowel surgery, 229–230 and, 110
gallbladder carcinoma, 179 colostomy, 238, 271, 289, 631 subtotal cholecystectomy, 224, 225
gastric carcinoma, 143–145 for faecal incontinence, 631 subtotal colectomy, 260–261, 265
hepatocellular carcinoma, 181–182 hernias, 392 subtotal parathyroidectomy,
lung carcinoma, 611 proctocolectomy, 259–260 342, 343
oesophageal carcinoma, 125–126 see also ileostomy sucralfate, 135
pancreatic cancer, 212 stones see cholelithiasis; kidney suction, 100
prostate carcinoma, 578 stones suction drains, 42, 68
renal cell carcinoma, 582 stony dullness, 662 see also negative pressure wound
soft tissue sarcoma, 411 straight leg raising, 723 therapy
upper aerodigestive tract cancer, strain, muscles, 716 sudden‐onset severe headache,
364–365 strangulation, hernia, 244 745–748
Staphylococcus aureus strawberry naevi, 404 sulfapyridine, 257
colonisation, 101 Streptococcus (spp.), 416 sulfasalazine, 257
liver abscess, 192 Streptococcus milleris, brain sump drains, 28
resistance to antibiotics, 416 abscesses, 508 sunitinib, gastrointestinal stromal
stapled transanal rectal resection Streptococcus pneumoniae, tumours, 148
(STARR), 622 meningitis, 507 superficial burns, 444
staples, 42 streptokinase, 416 superficial dermal burns, 444,
bowel anastomoses, 233, 279 stress fractures, 457 446, 447
static cold storage, 79 stress tests, ischaemic heart superficial femoral artery, chronic
Stauffer’s syndrome, 582 disease, 589 limb ischaemia, 530
796 Index
superficial parotidectomy, 373 systemic inflammatory response thiopurine S‐methyltransferase,

superficial spreading melanoma, syndrome, 51, 58, 59, 257–258
400–401 67, 701 third cranial nerve, 757
superficial veins, 545 burns, 451 palsy, 746, 758, 759–760
superior laryngeal nerve, 337 pancreatitis, 200, 203 third space fluid loss, 702
palsy, 336 third ventricle, colloid cyst, 501
superior mesenteric artery TACE (transarterial thoracic aortic aneurysms
embolism, 246 chemoembolisation), endovascular management,
pancreatic cancer, 212 HCC, 183 556–558
superior mesenteric vein, 219 tacrolimus, 81 surgery, 597–598
pancreatic cancer, 212 Takayasu’s arteritis, 538 thoracic duct, oesophagectomy, 130
superior oblique muscle, 757 tamoxifen thoracic outlet syndrome, 534
supernumerary parathyroid breast carcinoma, 326 thoracic surgery, 603–614
glands, 339 adverse effects, 327 minimally invasive, 39
suppositories, ulcerative chemoprevention, 318 thoracolumbar spine, trauma,
colitis, 257 tamponade, 591 521, 522
suppurative peritonitis, 654 tamsulosin, 568–569 thoracoscopic oesophagectomy,
supraclavicular fossa, metastasis, 667 tangential excision, burns, 451–452 127–129
supraglottic tumours, 675 tardy ulnar palsy, 515 thoracoscopic surgery, video‐assisted,
suprasellar meningiomas, 499 target sign, schwannomas, 405 605
suprasphincteric abscess, 301 tarsal eversion, 356 thoracotomy, 605, 606–607
suprasphincteric fistula, anal, 304 tarsal tunnel syndrome, 717, three‐point fixation, fractures, 459
surface area see total body 721–722 thrombocytopenia, portal
surface area tarsorrhaphy, 356 hypertension, 220
surgeons, 98–99 T cells, 82 thromboembolectomy, 559
face masks, 35 teaching, in operating rooms, 94 thromboembolism
trauma care, 433 team time‐out, 99 cardiac valve surgery, 596
surgical nurses, 98 organ procurement operations, 79 see also venous thromboembolism
surgical risk, assessment, 13–17 teamwork thrombolysis, catheter‐directed, 559
surgical site infections (SSI), 45, 48, burns, 453–454 thrombolytic therapy, 534
67–68 operations, 93–94 thrombophlebitis, 43, 546
prevention, 101 tear drop fracture, cervical thrombosis
risk classification, 6 spine, 521 acute limb ischaemia, 533
surveillance technicians, operating rooms, 97 aneurysms, 527
active, prostate carcinoma, 579 temperature, spinal injuries, 522 deep vein thrombosis, 6–7, 31–32,
arterial surgery, 531–532 temporal arteritis (giant cell arteritis), 546, 689, 703–704
after hepatectomy, 189 538, 747, 760 haemorrhoids, 297
inflammatory bowel disease, 255 temporal lobe herniation, small bowel ischaemia, 246
survivorship, 88, 91 483–484, 489 thunderclap headache, 745
sutureless rapid deployment aortic tenderness, appendicitis, 249–250 thymectomy, 342, 343
tissue valves, 595 tendon–bone test, 52 thymoma, 613
sutures, 40–42, 47 tendon sheath infections, 417 thyroglossal cysts, 331–332,
bowel anastomoses, 233 10% tumour, 346 669, 671
cutting, 100 tension pneumothorax, 609 thyroid, 331–337
removal, 42 incisions, 606 adenomas, 370
techniques, 42, 425 tertiary intention, wound healing, 47 anatomy, 337
swinging light reflex, 759 tertiary survey, trauma, 439–440 nodules, 332–333, 669, 670
synchronous colorectal liver testes toxic adenoma, 332–333
metastases, 184 anatomy, 572–573 thyroid carcinoma, 334–335, 370
resection, 189 infarction, 387 Bethesda classification, 332
synchronous tumours, inguinal hernia repair fine‐needle aspiration
oesophagus, 123 complications, 388 cytology, 333
synovectomy, 471 torsion, 573, 727, 729, 732 thyroglossal duct cyst vs, 331
synovial chondromatosis, 477 trauma, 731 thyroidectomy, 334, 335, 336
synovial sarcoma, 407 tumours, 583, 730 airway obstruction, 676
synovial sheath infections, 417 testicular appendages, torsion, hypoparathyroidism, 336,
synovitis, pigmented 727–729 342–343
villonodular, 477 thallium‐201 scans, 410 parathyroid glands, 337
SYNTAX score, 589 thermal injuries, eye, 356 vocal folds, 364
syringomyelia, 721 thiopurines, ulcerative colitis, 258 thyroid function tests, 332, 335
Index 797
thyroiditis, 335–336 trachoma, 357 dermoid cysts, 397

subacute, 335, 336 traction, 461 haematuria, 695
see also Hashimoto’s thyroiditis for spinal cord compression, 522 management, 431–441, 439
thyrotoxicosis, 335 tramadol, 24 definitive care, 434, 439
bones, 471–472 transanal local excision, rectal initial assessment, 433–439
subclinical, 332 cancer, 278 tertiary survey, 439–440
time‐out procedures, 99 transarterial chemoembolisation on metabolism, 51–52
organ procurement operations, 79 (TACE), HCC, 183 mydriasis, 356
tinea pedis, 415–416, 551, 688 transection, arteries, 534 outcomes, 440
Tinel sign, 515 transfer dysphagia, 681 spine, 521–523, 718, 719
tissue banking, 91 transhiatal oesophagectomy, 127 system planning, 431–433
tissue valves, cardiac, 595, 596 transient ischaemic attacks, 537, 540 testes, 731
TNM staging, 90 transient lower oesophageal sphincter vascular, 534–535
bladder carcinoma, 581 relaxations, 115–116 see also head injuries
breast carcinoma, 319, 320, 321 transitional cell carcinoma (urothelial trauma registries, 440
colorectal carcinoma, cancer), 580–581, 695 trauma units, 109
185–186, 274 transition zone, anal canal, 293 triage, pre‐hospital, 431–432
gallbladder carcinoma, 179 transjugular intrahepatic triangle of Grynfeltt–Lesshaft,
gastric carcinoma, 144, 145 portosystemic shunts, 392–393
lung carcinoma, 611 220–221 triangle of Petit, 392
oesophageal carcinoma, 125–126 for ascites, 664 tricuspid valve surgery, 596
pancreatic cancer, 212 liver transplantation and, 223 trigone, 565
prostate carcinoma, 578 transoesophageal triple‐negative/basal‐like breast
renal cell carcinoma, 582 echocardiography, 593 carcinoma, 324
tofacitinib, ulcerative colitis, 258 transplantation, 75–86 triplet chemotherapy, colorectal liver
ToGA trial, 147 cardiac, 600 metastases, 187
Tokyo guidelines complications, 81–83 triple test, breast lumps, 309
acute cholangitis, 167 surgical problems, 84–85 truncal vagotomy, 136
acute cholecystitis, 165, 166 disease recurrence, 83 trusses, 383
tomosynthesis, mammography, kidney see kidney transplantation trypsinogen see cationic trypsinogen
310–311 liver see liver transplantation gene
tonometry, 752 postoperative management, 80–81 TSH receptors, multinodular
tonsillectomy, airway recipient assessment, 75 goitre, 333
obstruction, 676 recipient selection, 79–80 tubed pedicles, 426
tonsils, 363 results, 83–84 tubercle of Zuckerkandl, 331
tumours, 377 sources of organs, 76–79 tuberculosis, chronic infective
TOPGEAR trial, gastric surgery, 80 arthritis, 468
carcinoma, 147 transposition of muscle, anal tuberous sclerosis, 582
tophi, 476 sphincter, 629 tubular adenoma, colorectal, 281
torsion transrectal ultrasound, 578 tumescence fluid, endovenous laser
fallopian tubes, 251 trans‐sphincteric fistula, anal, 304 therapy, 549
testes, 573, 727, 729, 732 transudates tumour suppressor genes
testicular appendages, 727–729 ascites, 659 intracranial tumours, 493
total artificial hearts, 599 pleural effusions, 607–608 pancreatic cancer, 209
total body surface area, 444 transurethral resection of bladder tunica vaginalis, 573
children, 446 tumour, 581 Turcot’s syndrome, 283
total mastectomy, 324 transurethral resection of the 24‐hour pH monitoring, oesophagus,
total mesorectal excision (TME), prostate, 569 119, 120
231, 275–276, 277, 278 transurethral resection 24‐hour urine collection
total parenteral nutrition see syndrome, 569 calcium, 340
parenteral nutrition transversalis fascia, 384, 385, 388 cortisol, 348
tourniquets, 37 transverse colon, cancer surgery, kidney stones, 566
toxic adenoma, thyroid, 332–333 276–277 two‐field dissection, oesophageal
toxic colitis, 256 transverse colostomy and carcinoma, 127
toxic megacolon, 256 drainage, 271 tympanic membrane, 359
colectomy, 260–261 transverse myelopathy, 521 cholesteatoma, 360–361
toxic nodular goitre, 335 trastuzumab, gastric carcinoma, 147 glomus jugulare tumours, 375
TP53 gene, intracranial tumours, 493 trauma perforation, 360, 361
trachea, obstruction, 676 airway obstruction, 676 tympanitic percussion, 286
tracheostomy, 606, 677 confusion, 735–743 tyrosine kinase inhibitors, GIST, 148
798 Index
ulcerative colitis, 255–261 ureters varus deformity, degenerative

Crohn’s disease vs, 255, 265 anatomy, 565 arthritis, 469
surgery, 259–261 Crohn’s disease, 262 vascular pedicles, colon, 231
ulcers urethra vas deferens, 573
Bairnsdale ulcer, 420 anatomy, 565 inguinal hernia repair
gastro‐oesophageal reflux strictures, 569–570, 695 complications, 388
disease, 117 urethroplasty, 570 vasomotor rhinitis, 362
leg, 685, 689–692 urge incontinence, faecal, 625 vasopressors, septic shock,
neuropathic, 533 urgent surgery see emergencies 58–60, 61
rodent ulcer, 398 uric acid, stones, 566 vasospasm
varicose veins, 546–547 urinary catheters cerebral, 505
see also peptic ulcer disease burn patients, 449 upper extremity ischaemia, 534
ulnar nerve trauma, 438 vedolizumab
entrapment at elbow, 515–516 urinary incontinence, radical Crohn’s disease, 263
pressure on, 97 prostatectomy, 579 ulcerative colitis, 258
ultrasound urinary retention, 32 veins, 545–546
abdominal abscess, 655 blood clots, 568 endovascular therapy, 560
abdominal aortic aneurysms, 528 hernia repair, 387 see also varicose veins
angiography, 553–554 spinal cord compression, 517 venepuncture, 42–43
appendicitis, 250 urinary tract venography, 688
ascites, 663 anatomy, 565 venous insufficiency, 687, 688–689,
benign prostatic hyperplasia, 568 endoscopy, 38 690, 691
biliary tract, 644–645 lower urinary tract symptoms leg pain, 721
breast, 311 (LUTS), 694, 695 lymphoedema vs oedema, 550
choledocholithiasis, 169 urinary tract infections, 570–571 pelvic, 546, 547
cholelithiasis, 168 appendicitis vs, 251 venous sinusoids, 545
endoanal, 295, 627 catheter‐associated, 70 venous thromboembolism, 6–7, 26,
endobronchial biopsy, 604 haematuria, 694 31–32
haematuria, 696 stones and, 566, 567 deep vein thrombosis, 6–7, 31–32,
kidney stones, 566 urine 546, 689, 703–704
limb ischaemia, 530 appendicitis, 250 ventilator‐associated pneumonia,
liver, 174 leak into peritoneum, 661 69–70
neck lumps, 670 output, burns, 449 ventricular assist devices, 599
parathyroid glands, 341 tests, haematuria, 696 ventricular escape rhythm, 598
prostate, 568, 578 urolithiasis see kidney stones ventricular septal defect, 597
scrotum, 732 urothelial cancer, 580–581, 695 ventriculoperitoneal shunts, 498
soft tissue tumours, 403 ursodeoxycholic acid, 169 ventriculostomy, subarachnoid
thyroid, 332 ustekinumab, Crohn’s disease, 263 haemorrhage, 746
see also duplex ultrasound; uveitis, 752–754 vertebrae
endoscopic ultrasound collapse, 718, 725
umbilical hernia, 224 vacuum‐assisted dressings, for open excision, 725
children, 391 fractures, 460 osteomyelitis, 520
umbilical veins, 219–220 vagotomy, 135, 136 trauma, 719
undifferentiated pleomorphic vagus nerve, glomus intravagale, 375 vertebral arteries, 537
sarcoma, 407 valgus deformity, 469 dissection, 741
union, fractures, 461, 462 valves, veins, 546 vertebrobasilar disease, 538
Universal Precautions, 36, 37 valve surgery, cardiac, 592–596 vertigo, cholesteatoma, 360
unstable angina, 589 valvuloplasty, percutaneous video‐assisted thoracoscopic
upper aerodigestive tract balloon, 593 surgery, 605
tumours, 370 vancomycin, 461 vigorous achalasia, 682
soft tissue sarcomas, 376 meningitis, 507 villous adenoma, colorectal, 281
squamous cell carcinoma, variable‐rate infusion, insulin, 8 viral infections
364–367, 369, 377 varices conjunctivitis, 750, 752
upper extremity ischaemia, 534 oesophagus, 220, 221–223, 637 transplant patients, 82
upper tract urothelial cancer, 580–581 treatment, 639 Virchow’s node, 661
urea breath test, 134 varicoceles, 574, 731, 732 Virchow’s triad, 704
urease, 566 varicose veins, 545–549 virtual colonoscopy, 633
see also rapid urease test leg ulcers and, 691 visual acuity, 353–354, 750–751
ureteric colic, appendicitis vs, 251 multiple extractions, 548 visual failure, pituitary
ureteroscopy, 698 oedema, 687 tumours, 501
Index 799
vocal folds walled‐off necrosis, pancreatitis, World Health Organization

airway obstruction, 675–676 201, 202 classification of brain tumours,
benign lesions, 363 ward care, operations, 106 493–494
cancer, 365 warfarin classification of hydatid cysts, 194
paralysis, 363–364, 675–676 cardiac valve surgery, 596 Classification of Tumours of Soft
voice preoperative management, 9 Tissue and Bone, 407
thyroidectomy on, 336 reversal, 9 wounds
see also vocal folds warm ischaemia, 78, 82 breakdown, 68
volume depletion, 27, 32 Warren shunt, 223 classification, 46, 67
volume resuscitation Warthin’s tumour, 373–374 closure, 40–42, 47, 424–426
burns, 449 warts, anal, 298 burns, 451–453
paracentesis, 664 watchful waiting, prostate open fractures, 460
septic shock, 59, 60–61 carcinoma, 579 scalp, 491
volume symptoms, gastro‐ water discharge, 702
oesophageal reflux body content, 27 failure, 29–30, 702
disease, 118 overload, 742 follow‐up, 48
volvulus, 285, 290 retention, 659–660 infections see surgical site
vomiting short‐gut syndrome, 240 infections
acute abdomen, 650 wedge fractures, cervical spine, 521 management, 45–48
large bowel obstruction, 286 weight loss, malnutrition, 50 Wuchereria bancrofti, 550
postoperative, 21, 34 weight loss (intentional), 151
small bowel obstruction, 243 LAGB, 152, 153 xanthochromia, cerebrospinal
von Hippel–Lindau syndrome, sleeve gastrectomy, 155 fluid, 504
345, 582 Wexner incontinence scale, 626–627 xenografts, heart valves, 595
von Willebrand’s disease, Whipple’s procedure see X‐rays see radiography
epistaxis, 711 pancreatoduodenectomy
V–Y advancement flaps, 427 Whipple’s triad, 215 yeasts, moulds vs, 415
white cell count, acute abdomen,
waiting list mortality, 651, 652 Zollinger–Ellison syndrome, 133,
transplantation, 79–80 whitlow, 417 140–141, 216
Waldeyer’s ring, 363 wood‐dust, 367 zymogens, 200

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Textbook of Surgery

Contributors, viii 16 Peptic ulcer disease, 133

32 Large bowel obstruction, 285 Section 11 Orthopaedic Surgery

Homayoun Zargar and Anthony J. Costello

67 Obstructive jaundice, 643 76 Massive haemoptysis, 707

Alexios A. Adamides Andrew Bui

Ahmad Aly Adele Burgess

Christine Chen Andrew Danks

Peter F. Choong Anthony Dat

Christopher Christophi AM Stephen A. Deane AM

Scott K. D’Amours Jonathan Foo

Michael J. Grigg Andrew H. Kaye AM

Ian Hastie John Laidlaw

Rodney T. Judson Mehrdad Nikfarjam

Stephen O’Leary Jeffrey V. Rosenfeld AC, OBE

Kurvi Patwala Hani Saeed

Marcos V. Perini Gurfateh Singh Sandhu

Jeffrey J. Presneill Shomik Sengupta

Kenny Rao Rose Shakerian

Fairleigh Reeves Susan Shedda

Head, Department of Cardiothoracic Surgery, Ioana Tichil

act of placing a signature on a form. That signature

Usually associated with minimal blood loss. Evaluation of the elderly

Once in hospital, and particularly once under

can, when used appropriately, significantly reduce

Table 1.1 Risks of postoperative surgical site infection.

Wound infection rate (%)

Without prophylactic With prophylactic

Clean No contamination; gastrointestinal, 1–5 0–1

Table 1.2 Prevention of deep vein thrombosis.

Operative risk factors

Pre‐existing medical comorbidities Diabetes mellitus

Patients with obstructive jaundice (see through such physiological mechanisms as

Woodhead K, Fudge L (eds) Manual of Perioperative Care:

All surgical patients must be in a relaxed state of MCQs

3 Which of the following constitutes the legal standard

For most surgical procedures the benefits of per-

complications and other risks of surgery or inter-

Table 2.1 Overview of the morbidity and mortality of common surgical procedures.

Surgical procedure Morbidity (%) Mortality (%)

Inguinal hernia repair 8–32 0–0.5

There are a number of common comorbidities Neurological risk assessment

Renal risk assessment

anaesthetists but also general practitioners, general

Box 3.1 Factors associated with Box 3.2 Preoperative fasting

Breathing (lung disease)

Table 3.1 American Society of Anesthesiologists Physical Score (ASA‐PS).

ASA‐PS class Definition Examples

ASA I Healthy Healthy, non‐smoking, minimal alcohol use

assessment, patients should be allocated a score using

anaesthetist by the end of the procedure. In check-

Mobilisation Prophylaxis against venous

hyperinflation (inhalation spirometry and physio-

Fluid balance Sodium 135 10

Table 4.2 Approximate electrolyte concentrations.

Sodium Potassium Chloride Bicarbonate Hydrogen

decompression of the stomach. Unfortunately, frequency in the patient undergoing an emergency

Between days 2 and 5

Vomiting the dissection is difficult and the appendix is

seroma formation; and (iv) providing wound sur

which is reflected in an increased risk of SSI follow

ysfunction. Septic shock is defined as sepsis with