Essentials of Rhinology (Hitesh Verma, Alok Thakar)

Essentials of
Rhinology
Hitesh Verma
Alok Thakar
Editors
123
Essentials of Rhinology
Hitesh Verma • Alok Thakar
Editors
Essentials of Rhinology
Editors
Hitesh Verma Alok Thakar
Department of Otorhinolaryngology Department of Otorhinolaryngology
All India Institute of Medical Sciences All India Institute of Medical Science
New Delhi New Delhi
India India
ISBN 978-981-33-6283-3 ISBN 978-981-33-6284-0 (eBook)

https://doi.org/10.1007/978-981-33-6284-0
Jointly published with Byword Books
© The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature
Singapore Pte Ltd. 2021
This work is subject to copyright. All rights are solely and exclusively licensed by the Publisher,
whether the whole or part of the material is concerned, specifically the rights of translation,
reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any
other physical way, and transmission or information storage and retrieval, electronic adaptation,
computer software, or by similar or dissimilar methodology now known or hereafter developed.
The use of general descriptive names, registered names, trademarks, service marks, etc. in this
publication does not imply, even in the absence of a specific statement, that such names are
exempt from the relevant protective laws and regulations and therefore free for general use.
The publishers, the authors, and the editors are safe to assume that the advice and information in
this book are believed to be true and accurate at the date of publication. Neither the publishers
nor the authors or the editors give a warranty, expressed or implied, with respect to the material
contained herein or for any errors or omissions that may have been made. The publishers remain
neutral with regard to jurisdictional claims in published maps and institutional affiliations.
This Springer imprint is published by the registered company Springer Nature Singapore Pte Ltd.
The registered company address is: 152 Beach Road, #21-01/04 Gateway East, Singapore
189721, Singapore
Foreword
Rhinology has been perhaps the most rapidly involving subspecialty in oto-
rhinolaryngology over the last few decades. Essentials of Rhinology is an
up-to-date and excellently illustrated text on the subject which captures the
essence of contemporary rhinology. As a multi-author book, led by the team
of Dr. Hitesh Verma and Dr. Alok Thakar at AIIMS New Delhi, it brings
together the experience of many recognized pioneers and experts from the
Indian subcontinent.
The book expands its scope beyond the conventional by including sections
on rhinological instruments, biofilms, packing materials, surgical cavity man-
agement, open transcranial skull base surgery, and a detailed description of
complications and their management. Authors from allied specialties have
contributed to sections on diagnostic microbiology, intervention radiology,
and nuclear medicine in sino-nasal diseases. Controversies are covered in a
comprehensive and balanced manner.
My congratulations to the editors in compiling this excellent textbook on
the subject. It serves both as a textbook on fundamental aspects of the subject
and as a reference guide for the recent advancements in the field.
Naresh Panda
Department of Otolaryngology
PGIMER
Chandigarh, India
v
Preface
The nose is an amazing organ. It undertakes humidification, filtration, and

heat exchange of inhaled air. It communicates with the four pairs of paranasal
sinuses to enable vocal resonance, allow spacing for the brain and eyes, and
enable protection of these structures from trauma. The exact dynamics relat-
ing to its contribution of inspiratory and expiratory resistance in respiration
and ventilatory physiology and sleep disordered breathing are yet not fully
apparent. Rhinology has benefited enormously from recent improved diag-
nostic tools and refinement of surgical techniques. The field of rhinology has
matured and evolved in the last two decades, but it does seem that there is yet
some way to go for its complete understanding.
This book is an attempt to capture the state of current knowledge in the
subject. It focuses on the basic principles of diagnosis and treatment, and
supplements on these with recent developments. Sections from allied special-
ties including microbiology, nuclear medicine, and interventional radiology
are designed to enable integrated care. Sinusitis, as the most common clinical
entity encountered by the practicing rhinologist, is discussed in detail, and
lessons from the past regarding the practice of non-endoscopic external sinus
procedures in current times are well covered.
We would hope and expect that the book shall provide rhinologists with a
template for contemporary care for their patients and also enable a basic
understanding of principles so as to be able to evaluate and adopt newer
developments as they become available.
New Delhi, India Hitesh Verma

Alok Thakar
vii
Contents
1 Endoscopic Anatomy and Surgery �� 1

Hitesh Verma, Smita Manchanda, Sunil Kumar, Vaibhav Saini,
Debesh Bhoi, Nagesh Tangirala, Abha Kumari,
and Anandita Gupta
2 Rhinoplasty Anatomy and Procedures�� 31
Arvind K. Kairo, Saurav Sarkar, Anindya Nayak,
Prateek Sharma, and Rakesh Kumar
3 Nasal Physiology and Sinusitis�� 49
K. Davraj, Mayank Yadav, Preetam Chappity, Prity Sharma,
Mohnish Grover, Shitanshu Sharma, Tanmaya Kataria,
Kranti Bhawna, Anand Pendakur, Gurbax Singh,
David Victor Kumar Irugu, Anoop Singh, and Nitin Gupta
4 Granulomatous Disease and Faciomaxillary Trauma�� 103
Gaurav Gupta, Pooja D. Nayak, Manju Silu,
Shashank Nath Singh, and Harpreet Kocher
5 Diagnostic Method and Instrumentation in Rhinology�� 121
Gagandeep Singh, Immaculata Xess, Ankur Goyal,
Ashu Seith Bhalla, Shamim Ahmed Shamim,
Hitender Gautam, Zareen Lynrah, Pradip Kumar Tiwari,
Ripu Daman Arora, Nikhil Singh, and Nitin M. Nagarkar
6 Tumours of Nose and Paranasal Sinuses �� 157
Gyan Nayak, Hitesh Verma, Rakesh Kumar, Rupa Mehta,
Nikhil Singh, Kuldeep Thakur, Kapil Sikka, Anchal Kakkar,
and Deepali Jain
7 Extended Procedures �� 203
Pankuri Mittal, Hitesh Verma, Amit Kesari, R. S. Virk,
Kshitiz Charya, Smriti Panda, Alok Thakar,
Rajesh Kumar Meena, Ramesh S. Doddamani, Manish Gupta,
Rohit Verma, Vikas Gupta, Ganakalyan Behera, Amit Shanker,
Namrita Mahmi, M. Ravi Sankar, and Arulalan Mathialagan
ix
x Contents
8 Prevention and Management of Complications�� 277

Anupam Kanodia, Hitesh Verma, Avni Jain,
Gopica Kalsotra, Sheetal Kumari, Sonu Kumari Agrawal,
Hitender Gautam, Darwin Kaushal, Abhishek Gugliani,
and Jaini Lodha
9 Septum, Adenoid, and Epistaxis �� 309
Ravneet Singh, Hitesh Verma, Shashikant Paul,
Sanjeev Bhagat, and Vishal Sharma
10 Radiotherapy, Chemotherapy, and Quality of Life�� 329
Bharti Devnani, Suman Bhasker, Raja Pramanik,
Surya Prakash Vadlamani, and Suresh Mani
About the Editors
Hitesh Verma MBBS (SMS Medical College,

Jaipur), MS (PGIMER), DNB, MBA (IGNOU),
is working as Associate Professor of
Otorhinolaryngology, All India Institute of Medical
Sciences, New Delhi. The focus of his work has
been on rhinology and skull base surgery, sleep sur-
gery, and airway surgeries. Dr. Hitesh’s research
has included three funded research projects and
more than 70 research publications. He has also
received gold medal and Junior Consultant Award
by the Indian Rhinology and Delhi AOI society.
Alok Thakar MBBS (AIIMS), MS (AIIMS), DNB,

DLO (London), FRCS (Edinburgh), is the Professor
and Head of Otorhinolaryngology, All India Institute
of Medical Sciences, New Delhi. He worked as a
Specialist Registrar and a Skull Base Fellow-
Commonwealth Fellow in the UK. Dr. Thakar’s
research includes 11 funded research projects, more
than 250 research publications, with 2200 citations,
and 2 patent applications. He has also received
Shakuntala Amir Chand Award by the ICMR and a
Gold Medal by the NES Society of India.
xi
List of Contributors
Abha Kumari ENT, Command Hospital, Kolkata, West Bengal, India

e-mail: abhak12@gmail.com
Abhishek Gugliani ENT, AIIMS, Jodhpur, Rajasthan, India
e-mail: abhishekgugliani@gmail.com
Amit Kesari Neurootology, SGPGIMS, Lucknow, UP, India
e-mail: amitkeshri2000@yahoo.com
Amit Shanker ENT, Brighton and Sussex University Hospital NHS,
Brighton, UK
e-mail: shankarpgi22@yahoo.com
Anand Pendakur Allergy Asthma ENT Clinic, Bangalore, Karnataka, India
e-mail: pendakur.anand@gmail.com
Anandita Gupta ENT, Army College of Medical Sciences, New Delhi,
India
e-mail: anandita0508@gmail.com
Anchal Kakkar Pathology, AIIMS, New Delhi, India
e-mail: aanchalkakkar@gmail.com
Anindya Nayak ENT, AIIMS, Bhubaneswar, Odisha, India
e-mail: anindaa_nayak30690@yahoo.in
Ankur Goyal Radiology, AIIMS, New Delhi, India
e-mail: ankurgoyalaiims@gmail.com
Alok Thakar Department of ENT, AIIMS, New Delhi, India
e-mail: drathakar@gmail.com
Anoop Singh ENT, AIIMS, New Delhi, India
e-mail: anoop.aiims1@gmail.com
Anupam Kanodia ENT, AIIMS, New Delhi, India
e-mail: kanodiaanupam@gmail.com
Arulalan Mathialagan Neurootology, SGPGIMS, Lucknow, UP, India
e-mail: arulalan87@gmail.com
Arvind K. Kairo ENT, AIIMS, New Delhi, India
e-mail: arvindkairo@yahoo.com
xiii
xiv List of Contributors
Ashu Seith Bhalla Radiology, AIIMS, New Delhi, India

e-mail: ashubhalla1@yahoo.com
Avni Jain ENT, ESIC Medical College Faridabad, Faridabad, Haryana,
India
e-mail: avanijain87@hotmail.com
Bharti Devnani Radiotherapy, AIIMS, New Delhi, India
e-mail: bhartidevnani@gmail.com
Darwin Kaushal ENT, AIIMS, Jodhpur, Rajasthan, India
e-mail: drdarwin.aiims@gmail.com
David Victor Kumar Irugu ENT, AIIMS, New Delhi, India
e-mail: irugudavid72kumar@rediffmail.com
Debesh Bhoi Anaesthesiology, Pain Medicine and Critical Care, AIIMS,
New Delhi, India
e-mail: debeshbhoi@gmail.com
Deepali Jain Pathology, AIIMS, New Delhi, India
e-mail: deepalijain76@gmail.com
Gagandeep Singh Microbiology, AIIMS, New Delhi, India
e-mail: drgagandeep@gmail.com
Ganakalyan Behera ENT, AIIMS, Bhopal, MP, India
e-mail: drganakalyan@gmail.com
Gaurav Gupta ENT, SP Medical College, Bikaner, Rajasthan, India
e-mail: drgauravgupta24@gmail.com
Gopica Kalsotra ENT, GMC, Jammu, India
e-mail: drgopikapgimer@gmail.comm
Gurbax Singh ENT, GGS Medical College and Hospital, Faridkot, Punjab,
India
e-mail: drgurbax@gmail.com
Gyan Nayak ENT, PGIMER, Chandigarh, India
e-mail: gyani.nayak@gmail.com
Harpreet Kocher ENT, Yatharth Superspeciality Hospital, Greater Noida,
UP, India
e-mail: hpskochar@gmail.com
Hitender Gautam Microbiology, AIIMS, New Delhi, India
e-mail: drhitender@gmail.com
Hitesh Verma ENT, AIIMS, New Delhi, India
Department of ENT, AIIMS, New Delhi, India
e-mail: drhitesh10@gmail.com
Immaculata Xess Microbiology, AIIMS, New Delhi, India
e-mail: immaxess@gmail.com
List of Contributors xv
Jaini Lodha ENT, Seven Hills Hospital, Andheri East Mumbai,

Maharashtra, India
e-mail: jainilodha@gmail.com
K. Davraj ENT, KMC, Manipal, Karnataka, India
e-mail: deardrdr@gmail.com
Kapil Sikka ENT, AIIMS, New Delhi, India
e-mail: kapil_sikka@yahoo.com
Kranti Bhawna ENT, AIIMS, Patna, Bihar, India
e-mail: bhavana.kranti@gmail.com
Kshitiz Charya Indus Hospital, Mohali, Punjab, India
e-mail: charaya.k@gmail.com
Kuldeep Thakur ENT, AIIMS, New Delhi, India
e-mail: drkuldeep70@gmail.com
M. Ravi Sankar Neurootology, SGPGIMS, Lucknow, UP, India
e-mail: drravisankarpgi@gmail.com
Manish Gupta ENT, MMIMSR, MMU, Ambala, Haryana, India
e-mail: manishgupta1217@gmail.com
Manju Silu ENT, SP Medical College, Bikaner, Rajasthan, India
e-mail: manjusilu35@gmail.com
Mohnish Grover ENT, SMS Medical College, Jaipur, Rajasthan, India
e-mail: drmohnish.aiims@gmail.com
Mayank Yadav ENT, SHKM GMC, Nalhar, Nuh, Haryana, India
e-mail: drmayankyadav@yahoo.co.in
Nagesh Tangirala Anaesthesiology, Pain Medicine and Critical Care,
AIIMS, New Delhi, India
e-mail: nag947@gmail.com
Namrita Mahmi Department of ENT, AIIMS, New Delhi, India
e-mail: namritamehmi@gmail.com
Nikhil Singh ENT, AIIMS, Raipur, Chhattisgarh, India
e-mail: doc.niks03@gmail.com
Nitin Gupta ENT, GMCH, Chandigarh, India
e-mail: nitinent123@gmail.com
Nitin M. Nagarkar ENT, AIIMS, Raipur, Chhattisgarh, India
e-mail: nmnent63@gmail.com
Pankuri Mittal Department of ENT, AIIMS, New Delhi, India
e-mail: mamc.pankhuri@gmail.com
Pooja D. Nayak ENT, SP Medical College, Bikaner, Rajasthan, India
e-mail: poomahe2007@gmail.com
Pradip Kumar Tiwari ENT, NIGRIMS, Shillong, Meghalaya, India
e-mail: dr.pradiptiwari@gmail.com
xvi List of Contributors
Prateek Sharma ENT, AIIMS, New Delhi, India

e-mail: drprateeksharma.mamc@gmail.com
Preetam Chappity ENT, AIIMS, Bhubaneswar, Odisha, India
e-mail: drcpreetam@aiimsbhubaneswar.edu.in
Prity Sharma ENT, AIIMS, Bhubaneswar, Odisha, India
e-mail: sharmaprity21@gmail.com
R. S. Virk ENT, PGIMER, Chandigarh, India
e-mail: virkdoc@hotmail.com
Raja Pramanik Medical Oncology, Dr.B.R.A-IRCH, AIIMS, New Delhi,
India
e-mail: drrajapramanik@gmail.com
Rajesh Kumar Meena Neurosurgery, AIIMS, New Delhi, India
e-mail: drrajeshmeena165@gmail.com
Rakesh Kumar ENT, AIIMS, New Delhi, India
e-mail: winirk@hotmail.com
Ramesh S. Doddamani Neurosurgery, AIIMS, New Delhi, India
e-mail: drsdramesh@gmail.com
Ravneet Singh ENT, GMCH, Chandigarh, India
e-mail: ravneetrverma@gmail.com
Ripu Daman Arora ENT, AIIMS, Raipur, Chhattisgarh, India
e-mail: neelripu@gmail.com
Rohit Verma ENT, DMC, Ludhiana, Punjab, India
e-mail: rohitaiims@yahoo.co.in
Rupa Mehta ENT, AIIMS, Raipur, Chhattisgarh, India
e-mail: rmehta0409@yahoo.com
Sanjeev Bhagat ENT, Rajindra Hospital Patiala, Patiala, Punjab, India
e-mail: sbent224@gmail.com
Saurav Sarkar ENT, AIIMS, Bhubaneswar, Odisha, India
doc.sauravsarkar@gmail.com
Shamim Ahmed Shamim Nuclear Medicine, AIIMS, New Delhi, India
e-mail: sashamim2002@gmail.com
Shashank Nath Singh ENT, SMS Medical College, Jaipur, Rajasthan, India
e-mail: drshashanknathsingh@gmail.com
Shashikant Paul ENT, JIPMER, Pondicherry, India
e-mail: drshashikantpol@gmail.com
Sheetal Kumari ENT, GMC, Jammu, India
e-mail: gphonshashetal@gmail.com
Shitanshu Sharma ENT, SMS Medical College, Jaipur, Rajasthan, India
e-mail: shsharma811@gmail.com
List of Contributors xvii
Smita Manchanda Radiology, AIIMS, New Delhi, India

e-mail: smitamanchanda@gmail.com
Smriti Panda Department of ENT, AIIMS, New Delhi, India
e-mail: smriti.panda.87@gmail.com
Sonu Kumari Agrawal Microbiology, AIIMS, New Delhi, India
e-mail: drhitender@gmail.com
Suman Bhasker Radiotherapy, AIIMS, New Delhi, India
e-mail: drsumanbhasker@gmail.com
Sunil Kumar ENT, LHMC, New Delhi, India
e-mail: suku321@rediffmail.com
Suresh Mani ENT, CMC, Vellore, Tamil Nadu, India
e-mail: msuresh.doc@gmail.com
Surya Prakash Vadlamani Medical Oncology, Dr.B.R.A-IRCH, AIIMS,
New Delhi, India
e-mail: vadlamanisuryaprakash@gmail.com
Tanmaya Kataria ENT, SMS Medical College, Jaipur, Rajasthan, India
e-mail: tanmayakataria@gmail.com
Vaibhav Saini ENT, AIIMS, Bhatinda, Punjab, India
e-mail: drvaibhavsaini@gmail.com
Vikas Gupta ENT, AIIMS, Bhopal, MP, India
e-mail: vikasmsent@gmail.com
Vishal Sharma ENT, Rajindra Hospital Patiala, Patiala, Punjab, India
e-mail: drvishalsharma2@gmail.com
Zareen Lynrah ENT, NIGRIMS, Shillong, Meghalaya, India
e-mail: zareenalynrah@gmail.com
Endoscopic Anatomy and Surgery
1
Hitesh Verma, Smita Manchanda, Sunil Kumar,
Vaibhav Saini, Debesh Bhoi, Nagesh Tangirala,
Abha Kumari, and Anandita Gupta
Contents
1.1 Part A: Anatomy of Nasal Cavity and Paranasal Sinuses 2
1.1.1 Ethmoid Cells 4
1.1.2 Frontal Sinus 6
1.1.3 Maxillary Sinus 6
1.1.4 Anterior Ethmoid Artery 6
1.1.5 Sphenopalatine Artery 7
1.1.6 Cribriform Plate 7
1.1.7 Sphenoid Sinus 7
1.1.8 Optic Nerve Relationship with Paranasal Sinuses 8
1.2 Part B: Local Anesthesia and Regional Blocks in Nasal Surgery 8
1.3 Part C: General Anesthesia 13
1.3.1 Preoperative Concerns 13
1.3.2 Anesthesia Technique 14
1.3.3 Hypotensive Anesthesia 14
1.3.4 Acute Normovolemic Hemodilution 15
1.3.5 Juvenile Nasopharyngeal Angiofibroma with Intracranial Extension 15
1.3.6 Emergence from Anesthesia 15
1.3.7 Postoperative Concerns 15
1.3.8 Emergency Surgical Intervention 16
D. Bhoi · N. Tangirala
H. Verma (*) Anaesthesiology, Pain Medicine and Critical Care,
ENT, AIIMS, New Delhi, India AIIMS, New Delhi, India
A. Kumari
S. Manchanda ENT, Command Hospital, Kolkata,
Radiology, AIIMS, New Delhi, India West Bengal, India
S. Kumar A. Gupta
ENT, LHMC, New Delhi, India ENT, Army College of Medical Sciences,
V. Saini New Delhi, India
ENT, AIIMS, Bhatinda, Punjab, India
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2021 1
H. Verma, A. Thakar (eds.), Essentials of Rhinology, https://doi.org/10.1007/978-981-33-6284-0_1
2 H. Verma et al.
1.4 Part D: FESS 16

1.4.1 Diagnostic Endoscopy 16
1.4.2 FESS Techniques and Steps 17
1.4.3 NASAL POLYP and FESS 23
1.4.4 AFRS and FESS 23
1.4.5 ESS in Pediatric Age Group 23
1.4.6 Balloon Sinuplasty 24
1.4.7 Conclusion 24
1.5 Part E: Packing Materials for Nose and Paranasal Sinuses 24
1.5.1 ses of Nasal Packing
U 24
1.5.2 Types of Nasal Packing Material 25
1.5.3 Non-Absorbable Nasal Packs 25
1.5.4 Absorbable Nasal Packs 27
References 29
1.1 art A: Anatomy of Nasal

P or split of these processes will present as con-
Cavity and Paranasal Sinuses genital anomalies like cleft lip, cleft palate, cho-
anal atresia, etc. The vestibule is the initial part
The nasal cavity is the initial entry point in the of the nasal cavity which extends from the exter-
airway. It extends from anterior nares to poste- nal opening till the nasal valve. The vestibule is
rior choana. Pneumatized air spaces within facial a line by the skin with vibrissae, sweat, and seba-
bones are known as paranasal sinuses. They con- ceous gland. The nasal cavity proper is the
verse with the nasal cavity at various levels. The remaining part of the nasal cavity which is a line
frontal sinus is the supraorbital airspace within by pseudo-stratified columnar epithelium. The
the frontal bone which comes in the superior anatomy of the nose and paranasal sinuses is
relationship of the nasal cavity and it drains into very complex. The detailed knowledge of ana-
the middle meatus via frontal recess. The maxil- tomical variation is the foremost thing to over-
lary sinus is the airspace inside the maxilla bone come complications of surgery. The lateral nasal
which communicates with the middle meatus via wall contains three to four projections which are
ethmoid infundibulum. Ethmoid air cells are known as turbinates [1].
located within the nasal cavity just below the
skull base from agger nasi cells till anterior wall A. Inferior Turbinate: Inferior turbinate is a
of the sphenoid sinus. The sphenoid sinus is the separate bone with an irregular surface. It is
airspace of the body of the sphenoid and it lies in the largest turbinate of the nasal cavity
the superior relationship of the nasopharynx. (Fig. 1.1).
The nasal placode and mesenchymal processes B. Middle Turbinate
around the primitive mouth develop nose. A 1. In the sagittal plane, it attaches with crib-
primitive nasal cavity develops by fusion of riform plate at the junction of the vertical
maxillary process of the first brachial arch with and horizontal lamina (Fig. 1.1).
the medial nasal process and frontonasal pro- Inadvertent pooling of middle turbinate
cess. Choana is derived by a split of bucconasal can lead to cribriform plate injury and iat-
membrane which separates the primitive oral rogenic CSF leak. The collection of air
cavity from the nasal cavity. The nasal cavity is within the lower free part of the middle
divided into two half by fusion of septum with turbinate is known as concha bullosa
palatine process of both sides. Failure of fusion (Fig. 1.1).
1 Endoscopic Anatomy and Surgery 3
CP
UP
MM
MT
IM
IT
Fig. 1.1 NCCT PNS orbit (Coronal cuts) is showing infe- The central picture is depicting bullosa of MT (white
rior turbinate (IT), inferior meatus (IM) middle turbinate arrow) and the right side picture is showing paradoxical
(MT), middle meatus (MM), and cribriform plate (CP). MT with uncinate process attachment on middle turbinate
2. In frontal and horizontal plane it attached opening. Surgical window to reach the
with lamina papyracea. It is known as floor of the maxillary sinus in endoscopic
ground lamella. Ground lamella divides surgery, in ancient surgery like Proof
ethmoid air cells into anterior and poste- puncture and for inferior meatal antros-
rior ethmoid cells. Lamina papyracea is tomy (2 × 1 cm) is performed at genu
thin at the site of attachment so that unin- because lateral wall bone is thinnest in this
tentional pooling of turbinate can leads to area. The middle meatus is the space pres-
orbital fat prolapse. ent lateral to the middle turbinate. It con-
3. Normally middle turbinate is concave on tains the uncinate process, hiatus
the middle meatus side. Paradoxical turbi- semilunaris, bulla ethmoidalis, and eth-
nate is the convex presentation of middle moid infundibulum (Fig. 1.2). Anterior
turbinate which reduces the volume of ethmoid air cells, maxillary, and frontal
middle meatus (Fig. 1.1). Minimum sinuses drains into middle meatus. Middle
inflammation in the middle meatus can turbinate along with its contents is known
affect the drainage of anterior sinuses as osteomeatal complex (Fig. 1.2).
significantly. Superior meatus is the smallest meatus.
Meatus is the part of the nasal cavity It is located between the middle and supe-
which is present deep and lateral to the tur- rior turbinate and posterior ethmoid cells
binate. Sphenoethmoidal recess and lies within it. Sphenoethmoid recess is the
supreme meatus are present medial to space above and behind the superior
superior turbinate (Fig. 1.7). Inferior meatus. Posterior ethmoid cells and sphe-
meatus is the largest and it is present along noid sinus drains into it.
the entire length of the inferior turbinate. C. Uncinate Process
Nasolacrimal duct opening locates at ante- It is a boomerang shape of two-dimensional
rior third and posterior two-third junction structure. It attaches laterally with the lacrimal
of the inferior turbinate. Genu is the part of bone and inferiorly with the inferior turbinate.
inferior meatus which locates just below Superiorly, the uncinate process has three dif-
and posterior to the nasolacrimal duct ferent kinds of attachments. In 70–80% cases,
4 H. Verma et al.
it attaches with the lamina papyracea and responsible for the upper attacment of the
allows the drainage of the frontal sinus into the uncinate process. Hiatus semilunaris inferior is
middle meatus. Recess terminalis is the blind the space between the free posterior edge of
sac formed by the attachment of the uncinate the uncinate process and bulla ethmoidalis
process with the lamina papyracea. Skull base (Fig. 1.2). It allows the drainage of the eth-
and middle turbinate are two other attachments moid infundibulum into the middle meatus.
and it allows the drainage of the frontal sinus D. Ethmoid Infundibulum
into ethmoid infundibulum (Fig. 1.1). The It is a three dimensional space. It is bounded
presence of the frontoethmoidal cells may be anteriorly by the uncinate process, posteriorly
by the bulla ethmoidalis, medially by the unci-
nate process medial surface (Fig. 1.2). It com-
municates with middle meatus via hiatus
semilunaris inferior. Superiorly, it is either end
as recess terminalis or it continues with frontal
recess, when the uncinate process attaches
with the middle turbinate and the skull base.
1.1.1 Ethmoid Cells
Ethmoid air cells are 3–18 in number. It is broadly

divided into anterior and posterior by the ground
lamella. The anatomical variations are seen more
in and around anterior ethmoid cells.
1. Agger Nasi Cells

(a) Anterior most ethmoidal cells locate over
Fig. 1.2 Osteomeatal Complex. Components of osteo- the lacrimal bone (Fig. 1.3). It lies ante-
meatal unit are maxillary ostium (MO), ethmoidal infun-
dibulum (EI), uncinate process (UP), hiatus semilunaris
rior and superior to the axilla of the mid-
(HS), and bulla ethmoidalis (BE) dle turbinate.
Type 1
Type 3
AN
Fig. 1.3 The NCCT PNS orbit (sagittal cut) is depicting type 1 Frontoethmoidal air cells. The coronal cut is depicting
type 3 frontoethmoidal cell
2. Frontal Cells nate. It extends posteriorly till the anterior

Frontal cells (frontoethmoidal cells, anterior face of the sphenoid sinus. It drains into the
ethmoid cells) are present in a 20–41% popula- nasal cavity by superior meatus or by spheno-
tion (Fig. 1.3). It is classified into four types [2]. ethmoidal recess. Onodi cell is the posterior
(a) Type 1 (most common)—single cell above extension of the posterior ethmoid cell over
the agger nasi cells (Fig. 1.3) the sphenoid sinus. The optic nerve runs very
(b) Type 2- the tier of cells above close to the lateral wall of the Onodi cell.
(c) Type 3 (least common)—large cell pro- Fovea ethmoidalis is the part of skull bone
truding more than 50% within frontal present over ethmoid cells. Fovea ethmoidalis
sinus (Fig. 1.3) is found higher when the ratio of the vertical
(d) Type 4 is found in the frontal sinus. Some height of ethmoid air cells with a vertical
time extended pneumatization of the bulla height of maxillary sinus or orbit is more than
ethmoidalis can presented as isolated cell 50% and when skull base angle with the hori-
in the frontal sinus. Saggital section is the zontal lamina of the cribriform plate is more
useful tool to differentiate both type of cells than 55°. In such cases chances of injury to the
Frontal bullar cell is the single cell above bulla skull base is more at fovea ethmoidalis region.
ethmoidalis and it may extend anteriorly into
frontal sinus. Its infection can affect the drain- Frontal recess is bound anteriorly by the
age of the frontal sinus by narrowing the fron- uncinate process, laterally by lamina papyra-
tal recess area. cea, medially by middle turbinate. The poste-
3. Bulla Ethmoidalis rior boundary is the anterior face of the bulla
It is the largest anterior ethmoid air cells ethmoidalis or lateral sinus in the superior part.
(Fig. 1.2). It drains into the middle meatus. It continues inferiorly with the ethmoid infun-
Well pneumatized bulla ethmoidalis reaches dibulum or the middle meatus, which depends
upto skullbase and ground lamella. Lateral on the superior attachment of the uncinate pro-
sinus (suprabullar cell) is the air space found cess (Fig. 1.4).
above the bulla ethmoidalis when it is not
extent till the skullbase. Retrobullar recess is
the space between the bulla ethmoidalis and
ground lamella. Hiatus semilunaris superior is
the medial communication of the retrobullar
recess with the middle meatus. Torus ethmo-
idalis is the terminology used for nonpneuma-
tized bulla ethmoidalis. Pneu matized bulla
ethmoidalis is three types
(a) Simple bulla-single cavity
(b) Compound bulla—two–three compart-

ments communicated at hiatus
semilunaris
(c) Complex bulla—two–three compartments
communicated at hiatus semilunaris, eth-
moid infundibulum
4. Heller cell
(a) It is an infraorbital anterior ethmoid cell.
It can affect the drainage of the maxillary
Fig. 1.4 Depicting frontal sinus and frontal beak at the
sinus by narrowing its outflow tract. level of the frontal ostium. The frontal sinus is above the
Posterior ethmoid cells are the cells present frontal beak and the frontal sinus drainage pathway
behind the ground lamella of the middle turbi- (FSDP) is below the beak
6 H. Verma et al.
1.1.2 Frontal Sinus rior accessory maxillary sinus ostium are found
at membranous fontanelle. they are visible on
Frontal sinus dimensions are 24 × 20 × 12 mm with endoscopic examination. Accessory ostium is
a volume of 6–7 ml. It develops from the embryonic round and it is present in up to 43% of cases. The
infundibulum at frontal recess superior part during lining epithelium is the pseudo stratified ciliated
the 16th week of intrauterine life. The frontal columnar epithelium and it is known as
sinuses are absent at birth and reach their full size Schneiderian membrane.
by the end of puberty. The anterior edge of the fron-
tal sinus ostia is formed by the frontal beak and the
posterior edge by the skull base. Ostia is the narrow- 1.1.4 Anterior Ethmoid Artery
est part of the frontal outflow tract. Frontal sinus is
an asymmetrically paired sinus with scalloping It is the largest branch of the ophthalmic artery. It
margins which may loss in the frontal sinus chronic runs in the orbit between the superior oblique and
diseases e.g mucocele. The anterior wall is thicker medial rectus muscles. It enters into the nasal
than the posterior wall (Fig. 1.4). cavity via the anterior ethmoid foramen and runs
in the ethmoid roof 1–2 mm behind the anterior
end of bulla ethmoidalis. The anterior ethmoid
1.1.3 Maxillary Sinus foramen is present 24 mm deep to anterior lacri-
mal crest. Anterior ethmoid artery runs out of
Maxillary sinus is also known as the antrum of fovea ethmoidalis in the nasal cavity in 8–10% of
Highmore. It is pyramidal in shape. It is the larg- cases. The radiological sign for the nasal cavity
est paranasal sinus with a volume of approxi- entry point is visible in the form of a point
mately 10 ml. Maxillary sinus ostium is lying (Kennedy nipple) the radiological features for
high in the medial wall which opens into the eth- intranasal course of anterior ethmoid artery are
moid infundibulum (Fig. 1.2). Maxillary sinus Keros 3 cribriform plate, presence of supraorbital
ostium is 2–3 mm oval structure. It is not visible cell or wide antero-posterior width of frontal
on routine nasal endoscopy as the ostium is cov- recess and more than 2 cm length of cribriform
ered by the uncinate process. Anterior and poste- plate (Fig. 1.5).
a b Frontal
recess
Anterior
ethmoid
artery
Fig. 1.5 (a) NCCT PNS orbit is showing bilateral soft tis- operative endoscopic picture is showing the intranasal
sue density in the nose and paranasal sinus. Anterior eth- anterior ethmoid artery
moid artery enter site is depicted by the arrow. (b) Post
1.1.5 Sphenopalatine Artery injury to the cribriform plate is less but the
height if the skull base is less so that the risk of
It is the largest terminal branch of third part of injury is more in fovea ethmoidalis (bone of
maxillary artery and it supplies a major part of skull base over ethmoid air cells). Type 2 is
the nasal cavity and paranasal sinuses. It origi- when the depth of olfactory fossa varies from 4
nates within the pterygopalatine fossa region and to 7 mm. It is the most common keros type.
it enters into the nose via the sphenopalatine Type 3 is when the depth of olfactory fossa is
foramen. Foramen lies just deep to the posterior- more than 8 mm and it is least common. Type 3
most attachment of middle turbinate. The pres- is more associated with skull base injury at the
ence of the anterior bony crest in the middle cribriform plate area. The thickness of the verti-
meatus close to posterior end of middle turbinate cal lamina is 0.2 mm. The thickness reduces
is the landmark for endoscopic surgery (see with increasing height of vertical lamina [3].
Chap. 9). The thickness is 0.05 mm at the entry point of
the anterior ethmoid artery. It is the weakest part
of the vertical lamina [4].
1.1.6 Cribriform Plate
It is made up of the horizontal medial part (lam- 1.1.7 Sphenoid Sinus

ina cribrosa) and vertical lateral part (Fig. 1.6).
Crista galli is the thick upward middle projec- Sphenoid sinus dimension is 22 × 20 × 22 mm.
tion on the lamina cribrosa. Olfactory nerve Sphenoid sinus ostia is present 7 cm from the
comes out via the perforators in the lamina anterior nasal spine at 30° angle. Other land-
cribrosa. Flax cerebri attaches with the crista marks for ostium are 1–1.5 cm above choana and
galli and the olfactory bulb and tract lie above 5 mm from the septum. Pneumatized sphenoid
lamina cribrosa. Keros classification is based on sinus can show bluish hue when the skull base is
the depth of olfactory fossa (height of vertical exposed. The skull base is concave whereas it is
lamina). Type 1 is when the depth of the olfac- convex over sphenoid sinus anterior wall.
tory fossa varies from 1 to 3 mm. In this risk of Conchal, presellar, and sellar are types of pneu-
matization. In the conchal type, the sphenoid
Lateral lamella cribriform plate
sinus is either nonpneumatized or minimally
pneumatized and it is the rarest type of pneumati-
zation. Seller is the most common subtype. The
protrusion of the internal carotid artery (ICA) in
the lateral wall ranges from 8% to 70% in differ-
ent studies (Fig. 1.7). ICA dehiscence ranges
Crista galli from 3% to 30% and it is more common with the
sellar type of pneumatization. Accessory pneu-
matization is more commonly seen in the sellar
type. Optic canal dehiscence is documented from
4% to 30% (Fig. 1.7). The presence of accessory
sphenoid septa ranges from 10% to 80% and it is
more common on the right side. It can inserts on
the carotid canal and optic canal in 6–26% of
Medial lamella cases [5]. Inadvertent injury to accessory septa
cribriform plate
can lead to the internal carotid artery or optic
Fig. 1.6 Crista galli is a thick upward projection on lam- nerve injury so that whenever required, accessory
ina cribrosa. The olfactory fossa is bounded by lateral septum must be drilled.
lamella of cribriform plate laterally, medial lamella of
cribriform plate inferiorly, and crista galli medially
8 H. Verma et al.
Internal carotid artery Type 3 ON ICA
Sphenoid sinus
Fig. 1.7 CT angiography is depicting the relationship of internal carotid artery with sphenoid sinus. The right picture is show-
ing relationship of the internal carotid artery and optic nerve and the optic canal is dehiscent on both sides
classified into four different types. Type 1 is

when no indentation visible in the lateral wall on
SO the sphenoid sinus. Type 2 is when indentation
visible in the lateral wall on the sphenoid sinus.
Type 3 is when the optic canal is within the
SR sphenoid sinus. Type 4 is when the optic canal is
present adjacent to the posterior ethmoid and
sphenoid sinus.
1.2 art B: Local Anesthesia

P
and Regional Blocks in
Nasal Surgery
SS
The detailed preoperative evaluation is very

much important to attain the healthiest patient.
Type 4 ON It helps in reducing perioperative morbidity and
OC mortality to a significant extent. The cardiovas-
cular and respiratory system needs more atten-
tion to overcome the possibility of complication
Fig. 1.8 Optic nerve (ON) is visible in lateral relation during surgery under local anesthesia (LA).
with the left side Onodi cell (OC). Sphenoid ostia (SO) is
demarked on the right side which communicates with a Routine laboratory investigations like hemo-
sphenoethmoidal recess (SR) gram, electrolytes, ECG, and chest X-ray are
part of the basic preoperative workup for sur-
gery. Pre-existing acute and chronic medical ill-
1.1.8 O
ptic Nerve Relationship with nesses needs stabilization. Cardiovascular
Paranasal Sinuses illnesses require detail preoperative evaluation
and intraoperative monitoring by the anesthe-
The optic nerve runs in the lateral wall of the tist. Proper consent and good preoperative med-
sphenoid sinus and Onodi cell (Fig. 1.8). It is ication are requiring to obtain excellent
intraoperative patient’s cooperation. Daycare 3. 1 cc of sodium bicarbonate in every 9 ml of

surgery and minor operations can be performed LA would increase potency and reduce the
under local anesthesia and regional block. It is burning sensation
also administered for the procedure in general
anesthesia as part of preoperative preparation to Lignocaine is a heat-stable and autoclavable
get good local vasoconstriction and postopera- local anesthetic drug. The duration of action is 1
tive pain control. The outcome of surgery under h for injectable preparation and it can extend to
local anesthesia is based on detailed knowledge 2–3 h by the accumulation of adrenaline. The
of anatomy and injection techniques. Sensory infiltrative form comes in 0.5–1.5% formulation.
innervations of the nose are supplied by the The dose of lignocaine (0.5%) without adrena-
branches of the trigeminal nerve (V). The exter- line is 3 mg/Kg body weight with maximum safe
nal nose is supplied by branches of the trigemi- administrative dose is 200 mg in healthy adults
nal nerve (supratrochlear, infratrochlear, whereas lignocaine with adrenaline is 7 mg/kg
anterior ethmoid nerve) and maxillary nerve body weight. The maximum dose is 500 mg in
(branches of the infraorbital nerve). The internal healthy adult. 2% viscous, 4% solution, and 10%
nose is supplied by anterior and posterior eth- spray are the lignocaine preparations for topical
moid nerves, sphenopalatine, and greater pala- anesthesia with maximum safe limit is 200 mg.
tine nerve. Local anesthetic drugs act by Mucosal surface anesthesia is required to pre-
reversible blocking or inhibiting conduction at pare the nose prior to the application of injection
nerve endings by blocking the inflow of sodium [6]. The action lasts till 20 min. Bupivacaine is
ions via the nerve membrane. These agents are more potent than lignocaine and it comes only in
applied at mucosa or in the neighborhood of injection form [7]. The dose without adrenaline
peripheral nerve endings. Commonly used drugs (0.5%) is 2 mg/Kg body weight and the maxi-
are lidocaine, prilocaine, bupivacaine, ropiva- mum safe limit is 175 mg/dose whereas with
caine, cocaine, etc. Cocaine is out of use because adrenaline, the dose is 2.5 mg/kg body weight
of its high toxicity profile and addictive poten- and the maximum safe limit is 225 mg/dose. It is
tial. The action of local anesthetic depends on generally used for regional nerve block because
the following parameters. of its long duration of action. Other drugs like
prilocaine and amethocaine are less effective
1. Diffusion, water solubility, and penetration in than lignocaine. For adrenaline, the dose is
tissue, potency, etc. 0.01 mg/kg with maximum safe limit is 0.5 mg
2. Protein binding ability. in healthy adults and 1: 200,000 is required for
3. Ionized drugs are more diffusible at the nerve surgical procedure.
ending and have a faster onset of action. The toxicity profile can vary from redness at
Inflamed tissue has poor drug penetration by the application site to multi-organ failure [8]. An
decreasing local tissue pH. Sodium bicarbon- allergic reaction is relatively rare and the com-
ate increases potency by increasing the pH at mon ones are rashes, bronchospasm, etc. so pre-
the inflamed nerve ending site. operative sensitivity should be done for all cases
4. Local anesthetic drugs can cause vasodilata- planned under LA. The cardiac effect is hypoten-
tion except for cocaine and lignocaine. sion and circulatory collapse. The neurological
Administration of adrenaline reduces drug side effect can be classified into three stages.
absorption and increases the duration of
action. 1. Early stage—local anesthetics can cross the
blood brain barrier. It depresses inhibitory
The amount of doses that need to be adminis- cortical activity and presents with symptoms
tered is depending on listed parameters. of light-headedness, tinnitus, visual changes,
slurred speech, dizziness, etc.
1 . Smallest effective dose 2. Late stage—If proper resuscitative methods
2. Addition of adrenaline are not taken than symptoms like drowsiness,
10 H. Verma et al.
disorientation, seizure, loss of consciousness, soaked in 4% lignocaine solution with

etc. can develop. adrenaline. One pack is kept along the floor
3. Respiratory distress, severe hypoxia occurs if of the nasal cavity. The second is above first
proper resuscitative measures are not taken. one and encroaching in the middle meatus.
Third one is at the frontal recess area for
The therapeutic measures for mild to moder- 10–20 minutes. Periodic suctioning over
ate levels of toxicity are the administration of the throat is required to prevent aspiration
100% oxygenation. Anesthetist and resuscitation during surgery as pharyngeal mucosa gets
cart should be warranted if muscle twitching and anesthetized.
convulsion occur. The commonly used technique (c) For endoscopic surgery—First block is
for the regional block is mentioned below. applied at the uppermost part of the middle
turbinate and at the axilla of the middle
(a) Moffett’s technique—The original Moffett’s turbinate to anasthetise the anterior ethmoid
solution was 2 ml cocaine 8%, 2 ml sodium neurovascular tissue and infraorbital neuro-
bicarbonate 1%, 1 ml 1:1000 adrenaline. vascular tissue. It can be blocked by external
Modified Moffett’s solution is prepared by route as mentioned in nasociliary (anterior
4% xylocaine (6 ml) with 1: 100,000 adrena- ethmoid) block. The second injection is
line. It is poured in each nostril, in drop by applied to block the sphenopalatine neuro-
drop form in a hyperextended position vascular tissue (Fig. 1.10). It is performed
(Proetz position) of the neck. The drops are by administration of drug at the posterior-
dispensing along the superior most part of most part of the middle meatus just infe-
lateral wall of the vestibule to block the sphe- rior to the middle turbinate and above
nopalatine nerve (Fig. 1.9). choana.
(b) For nasal packing—Self-prepared cotton ( d) For rhinoplasty—Local anesthetic is
pledgets or commercially available non- applied at columella over the tip, in between
absorbable packs can be used. They are and around the dome of lower lateral carti-
lage, at the rim of lower lateral cartilage. The
quantity is varying from 0.1 to 0.3 ml with 26
gage needle to prevent distortion of anatomy.
For intercartilaginous incision, LA is injected
at limen nasi in the subperichondrial plane.
For osteotomies, LA is injecting inside and
outside of the frontal process of the maxilla
in the sub-periosteal plane.
Nerve blocks—It is required for the therapeu-

tic purpose only. The various kind of blocks
require for nasal surgeries are mentioned subse-
quently [9].
A. Frontal Nerve Block

It is required for the median forehead flap.
Supraorbital and supratrochlear divisions of
frontal nerve exit through supraorbital fora-
Fig. 1.9 The white line is showing chin and the external men and supply frontal scalp and forehead,
auditory canal is in the same line. The needle is pointed
towards the supero-lateral part of the vestibule (Courtesy—
medial part of the upper eyelid, and root of
Dr. Hitesh Verma, Associate Professor, AIIMS, New the nose. Supraorbital foramen can easily be
Delhi, India) palpated along the medial orbital rim. It is
MT
MT
Nasopharynx
Polypoidal
uncinate IT
process
Fig. 1.10 Both figures are representing the site of local rior turbinate (Courtesy—Dr. Hitesh Verma, Associate
infiltration for the anterior ethmoid and the sphenopala- Professor, AIIMS, New Delhi, India)
tine neurovascular structure. MT middle turbinate, IT infe-
2 cm from the midline in adults. Series of bral fold and the eyebrow. The needle is
injections from central to medial brow block directed forward and medially till it reaches
frontal nerve branches. After the injection, the bony roof of the orbit. At a depth of
firm pressure is applied for better anesthetic 1.5–2 cm, the needle is at the level of the ante-
spread and prevention of ecchymosis. rior ethmoidal foramen. 1–2 ml of local anes-
B. Infraorbital Nerve Block thetic solution is infiltrated (Fig. 1.12).
It can be blocked by two routes: Extraoral and D. Greater Palatine Nerve Block
intraoral Greater palatine nerve supplies the lower part
1. Extraoral route: A longitudinal line is
of the septum and floor of the nasal cavity.
drawn along the pupil, another horizontal Greater palatine foreman is located 1 cm
line along the ala of the nose. At the point medial to second/third molar or 1.4–1.5 cm
of intersection, the needle is advanced in lateral to the maxillary suture line. The needle
lateral-to-medial direction, as the foramen is inserted 0.5–1 cm and 1 cc of local anes-
is directed medially and caudally. thetic is applied (Fig. 1.13).
2. Intraoral approach:-The needle is inserted E. Sphenopalatine Nerve Block
into the canine fossa and the finger is kept Two approaches are recommended: Intraoral
over the infraorbital foramen to assess the and intranasal approach.
proper location of the needle tip. 1–3 mL 1. Intraoral approach: Palpate the greater pal-
of local anesthetic is injected after negative atine foramen intraorally just medial to the
aspiration (Fig. 1.11). second/third molar 5–7 mm anterior to the
C. Nasociliary Nerve (Anterior Ethmoid posterior margin of the hard palate. A nee-
Nerve) Block dle bent 45° and advanced 2 cm in greater
It is blocked at the anterior ethmoidal foramen. palatine foreman and 1–2 ml injected.
A 26 G needle was inserted 1–1.5 cm above 2. Intranasal approach: The nerve is blocked
the medial canthus halfway between the palpe- by injecting anesthetic solution near the
12 H. Verma et al.
Fig. 1.11 Intraoral approach for infraorbital nerve block (Courtesy—Dr. Hitesh Verma, Associate Professor, AIIMS,
New Delhi, India)
Fig. 1.13 The site of local infiltration is corresponding to

the second and third molar for greater palatine nerve block
(Courtesy—Dr. Hitesh Verma, Associate Professor,
AIIMS, New Delhi, India)
sphenopalatine foramen region, near the

posterior attachment of middle turbinate
[10] (Fig. 1.10). Alternatively, cotton
Fig. 1.12 Blue dotted line is marked from the inner can-
thus. 26 G needle is inserted 1 cm above the line
tipped soaked in the local anesthetic solu-
(Courtesy—Dr. Hitesh Verma, Associate Professor, tion can be placed in the region and kept
AIIMS, New Delhi, India) for 5–10 min (Sluder’s) method.
F. Maxillary Nerve Block 1.3 Part C: General Anesthesia

The techniques for maxillary nerve block are
external approcah, high tuberosity approach Endoscopic sinus surgery (ESS) is the primary
and greater palatine canal approach. approach used today for the surgical treatment of
1. External approach—Needle is inserted just most of the rhinological illnesses e.g. chronic
below the zygomatic arch at the midway of sinusitis, nasal polyposis. The surgical manage-
the coronoid and the condylar process of ment of juvenile nasopharyngeal angiofibroma
the mandible. It is inserted at the right (JNA) has also got revolutionized with nasal
angle to the skin till pterygoid plates are endoscopic approaches; however, the extensive
palpable. Local anasthetic is injected after vascularity and vital structures nearby pose sig-
minimal withdrawal of needle. The needle nificant challenges for surgery as well as anesthe-
is pushed anteriorly towards the eye to sia [12]. Preoperative optimization including
reach the pterygopalatine fossa. 5 cc of the angioembolization of feeding vessel in high-
anesthetic drug is injected. grade JNA lessens the perioperative complica-
2. High tuberosity approach—Three centime- tions related to extensive blood loss. General
ter insertion of the needle is done in the anesthesia or TIVA maintaining a lower accept-
upper gingivobuccal sulcus at the level of able blood pressure (hypotensive anesthesia) is
second molar at 45° angle. 2 cc of the drug preferred. The anesthetic techniques should
is needed to block maxillary nerve. For address specific concerns like stable hemody-
posterior superior nerve block, the needle namics during surgery, effective management of
is inserted at 2 cm depth. blood loss, adequate analgesia, and smooth emer-
3. Greater palatine canal approach—The nee- gence. A good perioperative multimodal analge-
dle is inserted till 3 cm depth in the greater sia is associated with better emergence.
palatine canal and 1.5–2 cc drug needs to
be injected (Fig. 1.13).
1.3.1 Preoperative Concerns
Advantages of LA
1. Patient is conscious The possibility of difficult airway should be
2. Maintain airway assessed, which might be because of the distorted
3. Smooth recovery face due to swelling of the cheek, trismus, or
4. Less monitoring, less postoperative care, less inferior displacement of the soft palate by the
expensive bulk of tumor. Specifically in cases of JNA of
5. Less pain medication required higher grade, embolization of the terminal
branches of the internal maxillary artery should
Disadvantages of LA ideally be done 24–48 h before surgery. Adequate
1. Less operable time blood and blood products should be cross-
2. Experience required matched. Premedication is done with anxiolytic
3. Accidental intravenous administration can
(benzodiazepine), the night before and morning
induce generalized toxicity on the day of surgery. Perioperative steroid
administration is done to decrease mucosal
Satisfactory application of the local anesthesia edema and improve endoscopic visibility during
technique is the utmost requirement for the surgi- surgery.
cal execution, patient cooperation [11].
14 H. Verma et al.
1.3.2 Anesthesia Technique explained to the patient in preoperative visit and

informed consent should be taken. Positive end
General anesthesia or Total Intravenous expiratory pressure (PEEP) is avoided. Throat
Anesthesia (TIVA) with oral cuffed endotracheal packing with roller gage is done to reduce the
tube is preferred in such cases. In the case of blood contamination of the airway and at the end
FESS laryngeal mask airways (LMA) have also of surgery, it should be removed after thorough
been used successfully by experienced anesthesi- suctioning. Normothermia is maintained by
ologists. Two large-bore (16 gauze is preferred) infusing warm fluids through the hotline and also
IV cannulas are secured and one is preferentially by the use of warming blankets. The urinary
placed in the lower limb great saphenous vein, as bladder is catheterized, so that hourly urine out-
the site is most easily accessed after positioning put of around 0.5–1 ml/kg can be maintained
and placing the anesthesia workstation at the foot with adequate volume resuscitation. Local anes-
end. Routine American Society of thetic with vasoconstrictor (1:100,000 adrenaline
Anesthesiologist (ASA) standard monitoring or phenylephrine drops) is either instilled topi-
(electrocardiogram, plethysmography, and non- cally or infiltrated. However caution should be
invasive blood pressure) is done. In case of JNA, applied in patients with hypertension, coronary
invasive blood pressure monitoring is done by artery disease as systemic absorption of these
securing radial artery, anterior tibial, or dorsalis drugs causes hypertension, tachycardia, and
pedis artery so that beat to beat blood pressure arrhythmias. Ideally, the dose of phenylephrine
can be monitored, and also serial blood gas sam- should not exceed 4 drops of 0.25% preparation
pling can be done at frequent interval. Peripherally (0.5 mg) in adults or 20 mcg/kg in children upto
inserted central catheter (PICC) is inserted 25 kg of body weight. If hypertension is severe
through the antecubital vein preferably, as the after local vasoconstriction, direct vasodilator or
neck is not accessible. It can be used for central α2—antagonists are administered. Cough and
venous pressure (CVP) monitoring and vasopres- straining during light plane increase the bleeding,
sor administration if needed, as there is the antic- so adequate depth of anesthesia is very essential.
ipation of significant blood loss and hemodynamic Blood loss is managed with crystalloids, colloids,
instability. However in cases with intracranial packed red blood cells, fresh frozen plasma, and
extension, the subclavian vein is chosen for can- platelets.
nulation. Central venous access is often required
for the infusion of irritant medications (concen-
trated potassium chloride) or vasoactive agents, 1.3.3 Hypotensive Anesthesia
certain diagnostic or therapeutic radiologic pro-
cedures, and in any patient for whom peripheral Deliberate decrease of systemic blood pressure
access is not possible. For cases with intracranial below 20% of normal or maintenance of systolic
extension, N2O should be used cautiously or blood pressure 85–90 mmHg with mean arterial
avoided as there is the chance of increase in ICP, blood pressure (MAP) at 60 ± 5 mmHg helps to
although hyperventilation, barbiturates, benzodi- provide a dry surgical field by decreasing the
azepines, or narcotics can attenuate the effects. In oozing and blood loss [9]. This can be achieved
these cases, hypotensive anesthesia is also with reverse Trendelenburg position at 30 degrees
avoided, as it might impair the cerebral perfu- with flexed knees. For maintenance of higher
sion, because of swelling and rise in ICP. The air- minimum alveolar concentration, (MAC) isoflu-
way is secured with cuffed endotracheal tube rane or other inhalational agent is required. Total
(South Pole Ring Adair Elwin or Armored tube) intravenous anesthesia is possible with propofol
preferred over standard tube after muscle relax- and fentanyl or remifentanil with the added
ant [13]. advantage of decrease of sympathetic response
Patients with difficult airways require video during intubation or surgical stimulation.
laryngoscope or fiberoptic bronchoscope inter- α-agonists such as clonidine and dexmedetomi-
vention for securing the airway. These should be dine infusion decreases the central sympathetic
outflow, thereby helps to induce controlled hypo- (ICP). The extensiveness of the surgery with
tension. It also decreases the requirement of massive blood loss, postoperative mechanical
anesthetic agent. Nitroglycerine and sodium ventilation with intensive care unit (ICU) stay
nitroprusside infusion, by vasodilatation reduce should be explained in informed consent.
the peripheral vascular resistance. Beta-blockers
like esmolol, labetalol, or metoprolol, and cal-
cium channel blockers also help to maintain 1.3.6 Emergence from Anesthesia
hypotension. Magnesium sulfate infusion also
helps to induce hypotension and helps to reduce Smooth recovery of anesthesia is warranted to
blood loss, however, it might prolong the anes- prevent any straining and bleeding. The throat
thesia emergence time [14]. pack is removed after suctioning of the oral cavity
and it is better to do under either direct laryngo-
scope or video laryngoscope. Postnasal space
1.3.4 Acute Normovolemic should be carefully evaluated to remove any blood
Hemodilution clots. Administration of esmolol or lignocaine
prevents extubation response. Decompression of
It can be used as a technique for blood conserva- the stomach with an orogastric tube should be
tion strategies. After induction of anesthesia, performed prior to extubation to remove the blood
blood is withdrawn upto a limit of 7 g% hemo- clots, which is a predisposing factor for postop-
globin, and subsequently, crystalloids and col- erative nausea and vomiting. In cases with mas-
loids are infused to maintain the blood volume. sive blood loss or high-grade JNA with intracranial
Intraoperative red blood cell salvage is not done extension, patients are kept intubated and mechan-
as there is chance of contamination by nasal flora. ically ventilated to avoid any rise of ICP by hyper-
Blood loss is carefully estimated by counting the carbia. Dexamethasone is administered 0.1 mg/kg
number of gauze pieces used and from the suc- to decrease airway edema by surgical trauma.
tion bottle. End tidal CO2 is maintained to pre- Extubation should be done in controlled environ-
vent any hypercarbia or hypocapnia. ment with adequate hemostasis, stable coagula-
Normothermia is maintained for the proper function status, and hemodynamics [16].
tioning of platelets and coagulation factors.
1.3.7 Postoperative Concerns

1.3.5 Juvenile Nasopharyngeal
Angiofibroma Patients should be kept in closed observation
with Intracranial Extension with monitoring of vitals. Postoperative hemo-
gram should be done to ensure adequate replace-
Patients with Radkowski Grade III tumors are ment of blood loss.
usually require combined approach with the neu- For Nausea and Vomiting:
rosurgery team. Intraoperative blood loss is an
predicting factor for better Glasgow Outcome • The presence of blood in the stomach, inflam-
scale, so these cases should be planned with mul- mation of the uvula and throat and the
tidisciplinary approach involving the neurosur- occasional use of opioids for pain control is
geon, intervention radiologist, and contributing factors. Intraoperatively ondan-
anesthesiologist, so that there will be minimal setron and dexamethasone are administrated
blood loss and stable hemodynamics periopera- as a prophylactic measure.
tively [12, 15]. Such cases are kept intubated and
put on mechanical ventilatory support to main- Postoperative Pain:
tain the end tidal carbon dioxide (EtCO2), as
hypercarbia can cause cerebral vasodilatation • The expected postoperative pain from FESS
and subsequent rise in intracranial pressure may range from mild to moderate and is due to
16 H. Verma et al.
surgical trauma as well as nasal packing. Oral tion by restoring physiologic sinus ventilation
acetaminophen and an NSAID/cyclo-and drainage. A proper diagnosis of the condition
oxygenase 2 inhibitor usually provide safe and by thorough history, clinical examination,
effective analgesia. Encourage the patient to Endoscopy, imaging is necessary. Correct knowl-
breathe through the mouth due to the presence edge of the endoscopic anatomy, its variations,
of nasal packing. The patient should have and steps of surgery aids in the successful out-
counseled in the preoperative visit. come of the surgery. With advances in better
understanding of disease and the introduction of
newer antibiotics along with better endoscopes,
1.3.8 Emergency Surgical the treatment of CRS has greatly revolutionized.
Intervention Among the various options available for surgery
it may range from Mini FESS, i.e., middle meatal
Sometimes there is postoperative orbital hema- antrostomy and anterior ethmoidectomy to full
toma or might be progressive deterioration of FESS with the opening of frontal, sphenoid, and
vision warranting a relook for hemostasis. In complete ethmoidectomy. More recent advances
such situation airway is secured by rapid sequence have come like balloon sinus dilatation to the use
intubation with anticipation of blood in the oral of high-powered drills and computer navigation
cavity and difficult mask ventilation. The wide system. The use of the appropriate surgical tech-
bored suction catheter should be kept ready dur- nique will depend on proper evaluation of dis-
ing securing of airway. Invasive monitoring is ease, its extent, and the expertise available. Here
continued in the perioperative period. Arterial in this chapter, we would briefly discuss the steps
blood gas analysis should be done to know the of FESS, with emphasis on various techniques,
current hematocrit, lactate levels, and electro- complications, and recent advances.
lytes. Sometimes patients with JNA present with
epistaxis in the causality, which might be resis-
tant to traditional compression or vasoconstrictor 1.4.1 Diagnostic Endoscopy
drops. Such cases need emergency embolization
and subsequent diagnostic procedures, so that A careful diagnostic endoscopy is the key for
excision can be planned. In such cases with epi- successful diagnosis and planning for surgery. It
staxis, the airway is secured by rapid sequence is of two types anterior to posterior
induction followed by intubation with cuffed (Messerklinger technique) and posterior to ante-
endotracheal tube. rior (Wigand technique). In anterior to posterior,
it consists of three passes. In first Pass, The 0°
endoscope (or 30° endoscope) passes along the
1.4 Part D: FESS floor of the nasal cavity between the inferior tur-
binate and septum. The structures studied are
Chronic rhinosinusitis is defined as inflammation nasal septum, inferior turbinate and inferior
of the nose and paranasal sinuses which gener- meatus, nasal cavity anterior and inferior to the
ally lasts for more than 3 months. It is character- middle turbinate, posterior choana, posterior wall
ized by two or more symptoms, one of which is and roof of the nasopharynx, eustachian tube,
either nasal discharge or blockage/obstruction/ fossa of Rosenmueller, and nasolacrimal duct. In
congestion along with the presence or absence of second Pass, The scope passes medial to the mid-
either facial pain or reduction of the sense of dle turbinate. Structures studied are the space
smell. Treatment of CRS mostly involves medi- medial to middle turbinate, anterior face of sphe-
cal therapy with surgery reserved for those cases noid sinus, sphenoid ostium, superior turbinate
where symptoms persist in spite of adequate and meatus, sphenoethmoidal recess. In third
medical therapy. Functional Endoscopic Sinus Pass, it is done to examine the contents of the
Surgery (FESS) aims to restore mucociliary func- middle meatus (Fig. 1.14). The scope is gently
Fig. 1.14 Diagnostic nasal endoscopy is showing right is visible after removal of polyps (Courtesy—Dr. Hitesh
polypoidal uncinate process with polyp in middle meatus Verma, Associate Professor, AIIMS, New Delhi, India)
passed into the middle meatus, the adjacent lat- 1. Traditional Method/Anterior to Posterior
eral nasal wall. The structures studied are middle It was first described by Messerklinger. It
turbinate, uncinate process, ethmoid bulla, starts with identification of the anterior attach-
ground lamella, and any variations or pathologi- ment of the uncinate. It is first incised off the
cal process [17]. Wigand approach (posterior to lateral wall using sickle knife/freer’s elevator,
anterior) is the diagnostic technique in revision then incision is extended to release it from its
surgery. It starts from choana then the identifica- anterior attachment to the lacrimal bone
tion of sphenoid ostia and follows skull base in (Fig. 1.15). It can be dangerous by injuring to
retrograde fashion. lamina papyracea resulting in prolapse of
orbital fat. To overcome complications of
orbital injury in lateralized/contracted UP in
1.4.2 FESS Techniques and Steps traditional method and NLD injury in swing
door approach, two more approaches are
The classification of ESS based on the extent of futher introduced.
surgery (Japanese Rhinologic Society, 2013) (a) Uncinectomy Through the Anterior Nasal
Fontanelle
• Type I removal of the ostiomeatal complex; Anterior fontanelle is membranous struc-
• Type II single-sinus procedure ture located between the lower and mid-
• Type III polysinus procedure dle concha. It separates the maxillary
• Type IV pansinus procedure sinus and the nasal cavity only by the
• Type V the extended procedure beyond the mucosa. This approach allows complica-
sinus wall tion free maxillary sinus exposure in
selected cases.
Uncinectomy is the first step in FESS. The (b) Uncinectomy Through Posterior Fontanelle
technique of doing uncinectomy by various The posterior fontanelle is located between
methods depends on surgeons' training and per- the tails of the middle and inferior turbi-
sonal preference [18]. nate, behind the hiatus semilunaris, and
18 H. Verma et al.
Fig. 1.15 Freer’s elevator is used for antero-posterior uncinectomy. Ethmoid infundibulum is opened and fungal muck
is visible through maxillary sinus ostia (Courtesy—Dr. Hitesh Verma, Associate Professor, AIIMS, New Delhi, India)
under the ethmoid bulla. It is mainly com- Maxillary sinusotomy is of four types
posed of soft tissue as a part of the medial (Fig. 1.17):
wall of the maxillary sinus. It is identified,
as an iatrogenic opening. The wide antros- 1. Infundibulotomy (uncinectomy): Removal of
tomy is performed by combining uncinec- the uncinate process, preserving the mucosa
tomy and removal of medilal wall of of the natural maxillary ostium. The superior
maxillary sinus. attachment of the uncinate can be left intact.
2 . Swing Door Technique (retrograde 2. Type I—Enlarging the natural maxillary

uncinectomy) ostium posteriorly by less than 1 cm.
Retrograde uncinectomy is initiated by identi- 3. Type II—Antrostomy is opened 2 cm posteri-
fying the posterior edge of uncinate process orly and inferiorly.
(Fig. 1.16). The retrograde uncinate window is 4. Type III—Antrostomy is opened up to the
made with small backbiting forceps. The unci- posterior wall of maxillary antrum. anteriorly
nate process is removed inferiorly. The unci- to the lacrimal sac, and inferiorly to the base
nate is swung forward using the ball probe and of the inferior turbinate.
then removed with blakesley forceps. The
advantage is less risk of injury to orbit but it The natural ostium of bulla ethmoidalis lies
can damage nasolacrimal duct when it runs in postero-medial to the anterior face. It can be
the free medial wall of the maxilla. located using ball probe or curette. Anterior eth-
moidectomy is initiated at antero-inferior part
Middle meatal antrostomy is performed by the of bulla to avoid orbital and anterior ethmoid
identification of maxillary sinus ostium, at the artery injury [20]. Bullectomy can be done by
same level of inferior edge of the middle turbi- placing J curette in retrobullar recess followed
nate. The opening is widened posteriorly and by anterior fracture of bulla (Fig. 1.18). Anterior
inferiorly by removing mucosa [19]. If accessory ethmoid artery generally runs intracranially but
ostia have previously been identified, surgical in 10% of cases, it can be found in suprabullar
window and accessory ostium should be inter- recess so one has to be careful using micro-
connected to avoid a subsequent recirculation debrider to avoid injury to artery (Fig. 1.5). The
phenomenon. anterior ethmoid artery is 1–2 mm posterior to
a b
MT
Uncinate
process
c d
Uncinate
flap
Fig. 1.16 (a) and (b) is showing site of lower cut in pos- needed. (d) is showing uncinate flap generated after both
terior to anterior technique. (c) is showing site of upper cuts (Courtesy—Dr. Hitesh Verma, Associate Professor,
cut which can be vary in the relationship of exposure AIIMS, New Delhi, India)
the superior limit of the anterior wall of the The preservation of vertical sagittal and hori-
bulla ethmoidalis. The distance between the zontal lateral attachment is required to maintain
artery and the middle turbinate axilla is the stability of middle turbinate. Few situations
17–20 mm. Mini-ESS is performed by uncinec- where partial or total resection of the middle
tomy and opening of the bulla with preservation turbinate is necessary are
of 3 or 4 mm of the anterior and inferior edge of
the bulla. If a posterior ethmoidectomy is • Concha Bullosa
required. Complete anterior ethmoidectomy • Polypoidal middle turbinate
should be done. • Lateralized Atrophic Middle Turbinate
For post ethmoidectomy, ground lamella is • Lateral displacement of the middle turbinate
perforated in infero-medial quadrant (Fig. 1.19). with narrowing of the frontal recess to create
It minimizes the risk of injury to the skull base or the wide exposure in extended endoscopic
lamina papyracea. appraoches
20 H. Verma et al.
a b
Type 1
c d
Maxillary
sinus
Type 2
Fig. 1.17 (a) is representing view after complete unci- the maxillary sinus after type 3 enlargement (Courtesy—
nectomy. (b) is showing visibility of maxillary sinus after Dr. Hitesh Verma, Associate Professor, AIIMS, New
type 1 enlargement. Figure (d) is showing inside view of Delhi, India)
The detail study of preopertive radiology refactory anterior ethmoid disease. Inferior
helps in mapping the anatomy of posterior eth- uncinectomy and anterior ethmoidectomy is
moid sinus, presence of Onodi cell, and course of performed to clear the frontal recess.
optic nerve. Clearance of disease in the ostiomeatal com-
Surgery of Frontal Sinus—Three distinct phi- plex allows resolution of disease in the fron-
losophies for surgical management of chronic tal sinus and frontal recess.
rhinosinusitis affecting the frontal sinus and fron- 2. Frontal sinusitis is formed due to frontal

tal recess is proposed by P J Wormald [21]. recess involvement. Complete uncinectomy,
anterior ethmoidectomy with removal of agar
1. Minimal Invasive Sinus Technique (MIST)— nasi and frontoethmoid cells is performed to
Frontal sinusitis is developed secondary to clear the outflow tract of frontal sinus.
a b
Fig. 1.18 The instrument is indicating site of entry in bulla ethmoidalis. J curette is placed in retrobullar recess for
postero-anterior bullectomy (Courtesy—Dr. Hitesh Verma, Associate Professor, AIIMS, New Delhi, India)
1. HRCT (nose and paranasal sinuses)- 1 mm cuts

are prepared to assess the antero-posterior (AP)
diameter of frontal recess, type of frontoeth-
Lamina moidal cells, degree of pneumatization frontal
papyrecea sinus. Bony remodeling and scarring of frontal
Ground
lamella outflow tract in revision surgery needs mapping
and scarring created by previous surgery in
Middle frontal recess. Two-dimensional CT Scans in
turbinate coronal, parasagittal, and axial planes are used
to create a three-dimensional picture of the
anatomy of the frontal recess.
2. Angled endoscopes are required to see the
frontal sinus.
3. Axillary flap technique—It starts by removal
of the anterior wall of the agger nasi cell. The
flap is created by making incision 8 mm above
the axilla of middle turbinate and brings 8 mm
Fig. 1.19 The suction tip is indicating site of entry in forward, turned down vertically 1–1.5 cm, and
posterior ethmoid after anterior ethmoidectomy in the left turned back under the axilla on to the roof of
nasal cavity (Courtesy—Dr. Hitesh Verma, Associate
Professor, AIIMS, New Delhi, India)
the middle turbinate. The mucosal flap is
based medially on middle turbinate and is
replaced at the end of the procedure to cover
3. Complete exteriorization of cells of osteome- the raw exposed bone to prevent granulation
atal complex with wide frontal sinusotomy is and fibrosis formation. Direct examination of
indicated in refractory frontal sinusitis. frontal sinus is possible after the removal of
frontal beak.
Instruments and techniques require viewing of 4. Frontal sinus mini-trephination (mentioned in
frontal Sinus are listed here. the chapter on frontal sinus).
22 H. Verma et al.
5. Computer-aided surgery (CAS, or image

guidance surgery), radiological probing (C
arm) are helpful in localizing frontal sinus in Frontal sinus
difficult cases.
1. Extensive nasal polyposis

2. Revision surgery
3. Distorted endoscopic anatomy
4. Extended endoscopic or open procedures Lamina
payrecea
Endoscopic management of frontal sinus dis- Lamina
eases is classified by Draf into three types [22]. papyrecea
• Type-1 is Simple Drainage (DRAF1)—It is

characterized by complete removal of the
anterior ethmoid cells and uncinate process
and obstructive frontal cells inferior to frontal
ostium. The indication is limited frontal sinus- Fig. 1.20 The postoperative cavity after DRAF 3 proce-
itis with intractable ethmoid sinusitis. dure (Courtesy—Dr. Hitesh Verma, Associate Professor,
• Type-2 Extended Drainage (DRAF 2)—It is
subdivided into type IIa and IIb approaches. In
type 2a, complete removal of the floor of fron-
tal sinus from lamina papyracea to middle tur- Sphenoid ostia
binate is performed. In type 2b, frontal sinus
floor is removed from the lamina papyracea till
the nasal septum. The indications are compli-
cated frontal sinusitis, muco or pyocele, and
benign tumour extending into the frontal sinus.
• Type-3 Endonasal median Drainage (DRAF
Septum
3)—Entire floor of both side of frontal sinus is
removed. The limit is from one side lamina
papyracea to the other side (Fig. 1.20). The Retracted
middle and
indications are revision surgery, intractable superior
frontal sinusitis and polyposis in ciliary dys- turbinate
function syndromes (Kartagener’s syndrome,
mucoviscidosis, etc.) and benign and malig-
nant tumour.
Fig. 1.21 The figure is depicting sphenoid ostia in the

Sphenoid sinus is the posterior-most sinus and
left nasal cavity after lateralization of middle and superior
the landmarks for sphenoid sinus ostium and turbinate (Courtesy—Dr. Hitesh Verma, Associate
sphenoid sinus are (Fig. 1.21): Professor, AIIMS, New Delhi, India)
1. Ten–fifteen millimetre above the upper end of

bony posterior choanae. 3. Seven centimeter from anterior nasal spine at
2. Maxillary ridge is an imaginary line between 30° angle superiorly.
the medial and inferior wall of the orbit and it 4. Four–five millimetre lateral to septum.
extends backwards from the upper border of 5. Sphenoid sinus floor is not visible whereas
the maxillary ostium. Sphenoid sinus is lying posterior ethmoid sinus floor is always in
below it and ethmoid cell above it. view.
The sphenoid sinus can be accessed by landmarks. The location of these instruments is
medial route (medila to middle turbinate) and tracked by the machine with fitted navigation
lateral route (lateral to middle turbinate) after probe. The machine displayed images in all
ethmoidectomy transethmoid approach. In planes corresponding to the pateints anatomy
intermediate approach, the lower half of supe- prepared from prefeeded radiology (CT and/or
rior turbinate is removed to get access in the MRI) in the system. The Indications are
sinus. The sinus ostium is lies half the distance
between the superior and inferior border on the 1 . Revision sinus surgery
anterior wall of the sphenoid. Sinus ostium is 2. Distorted surgical anatomy
gently widened in infero-medial direction in 3. Extensive nasal polyposis
the intial step of widening to examine the 4. Pathology involving the skull base
spehnoid sinus lateral wall structures and to
prevent inadvertent injury to perisinus struc-
tures. Posterior nasal branch of sphenopalatine 1.4.3 NASAL POLYP and FESS
artery may injure during inferior widening
which can be prevented by pushing mucosa • Functional endoscopic sinus suergery (FESS)
inferiorly before removing the bony wall. is indicated for complicated sinusitis and
Caution to be taken for the posterior attachment chronic sinusitis with or without nasal polypo-
of intersphenoid septa and accessory septa. sis, failed maximum medical management.
Natural dehiscence of the optic nerve and inter- FESS aims to improve sinus ventilation and
nal carotid artery is always keep in mind while drainage as well as removing polyps. The
removing disease and violating septas. Onodi extent of surgery varies with the extent of dis-
cell is the posterior extension of posterior eth- ease, the surgeon’s individual practice, and
moid cells over the sphenoid sinus and the optic available technology.
nerve may be seen in its lateral wall [23]. Onodi
cell is present above the imaginory line passes
from the roof of maxillary sinus. 1.4.4 AFRS and FESS
Robot-Assisted Surgery (RAS) • Surgery is usually the first-line treatment for

The robotic guidance system facilitates manipu- the management of AFRS. The goal of surgery
lation in the surgical field and full visualization is wide opened sinus ostium with complete
of the face of the anterior skull base. It is hands- removal of fungal muck and allergic mucin.
free semi-automated endoscope guidance for
advanced applications in surgery of the paranasal
sinuses and the anterior skull base [24]. The lit- 1.4.5 ESS in Pediatric Age Group
erature is emerging on it.
The Role of ESS is limited in pediatric chronic
Simulation/Three-Dimensional Tracking rhinosinusitis. It should be considered after a
It has been used for surgical training but the lack period of medical management (and/or adenoid-
of practicality and haptic feedback limits wide- ectomy) and after exclusion of underlying pathol-
spread use. Three-dimensional printing has revo- ogies. If required, ESS should be limited to up to
lutionized simulation, providing high-resolution disease extent.
models for patient-specific anatomy [25]. Absolute indications for ESS in children
Navigation and Image-Guided Surgery • Complicated sinusitis

The system uses computerized tracking devices • Nasal polyposis
to monitor the position of endoscopic instru- • Mucocoeles or mucopyocoeles
ments in conjuction to the patient’s anatomical • Fungal rhinosinusitis
24 H. Verma et al.
1.4.6 Balloon Sinuplasty minimize complications and in patient admission.

Nasal bleeds can be either anterior or posterior.
Balloon Sinuplasty technology uses a flexible, Mostly anterior bleeds can be managed with cau-
balloon catheter to open up the blocked sinus terization of the bleeding point after identification
ostium, by inflation with a calibrated pressure using either a headlight or an endoscope.
gauge. When the sinus balloon is inflated opti- Cauterization can be done either using silver
mally, it gently restructures the sinus ostium by nitrate (chemical cautery) or bipolar diathermy
inducing micro-fractures and bony displacement (electrical cautery). Traditionally nasal packing
around the occluded ostium, thus circumferen- has been used in the emergency setting for control
tially widening the walls of the ostium, while of bleeding, though with the availability of endo-
maintaining the integrity of the sinus mucosal scopes which allows better visualization of bleed-
lining around the ostium. The indication is ing point, it is less preferred. Hemostatic nasal
chronic sinusitis limited mostly to ostial obstruc- packing is rarely required for anterior bleeds
tion of the frontal, maxillary, and sphenoidal unless the bleeding and coagulation profile of the
sinuses, with near-normal middle meatal integ- patient is deranged [27]. Whereas the source of
rity [26]. The advantages are posterior nasal bleeds is not easily identifiable in
an emergency setting and may require nasal pack-
1. Preservation of the normal anatomy of the ing for emergent control of bleeding. Packing of
vital ostiomeatal complex, while precisely the nose and para nasal sinuses may also be
focusing on the occluded sinus ostium and the required in postoperative setting. Availability of
diseased sinus cavity beyond it. various packing materials has made nasal packing
2. Reduction in the invasiveness of the interven- less traumatic and unpleasant. Also use of some
tion, hospital stay, recovery time, postopera- newer materials prevents nasal synechiae, hence
tive debridement, postoperative medications, preferred in the postoperative setting [28]. Other
and office follow-up visits. conditions requiring nasal packing include endo-
scopic sinus surgery, septal surgery, turbinate
reduction, and reduction of nasal fractures. Though
1.4.7 Conclusion significant hemorrhage post-surgery is rare, small
quantity of blood oozing out from the surgical site
• Endoscopic sinus surgery is a remarkably safe can cause significant anxiety to the patient.
and effective procedure. The knowledge of The aim of this chapter is to introduce the
three-dimensional anatomies of sinuses, ana- reader to various such materials available and
tomical landmarks, and its variations is essen- guide them about their utility and usage.
tial for the successful outcome.
1.5.1 Uses of Nasal Packing

1.5 art E: Packing Materials
P
for Nose and Paranasal • Provision of hemostasis in cases of nasal sur-
Sinuses gery or epistaxis
• Intranasal support to bony or cartilaginous
Nasal mucosa has a rich vascular supply deriving dorsum, nasal septum, middle turbinate, or
branches both from the internal and external mucosal surfaces
carotid artery system. Epistaxis is one of the com- • Prevention of mucosal adhesions
monest presentations in the accident and emer- • Induces hemostasis
gency room. It is seen in all age groups including • Tamponade effect
the elderly patients who often have other co-mor- • Provision of moist environment for mucosal
bid conditions. A non-specialist may be required healing
to do the initial management, therefore a stepwise • Steroid or antibiotic impregnation may
algorithm should be available in emergency to achieve better surgical outcomes
Fig. 1.22 Anterior and

posterior nasal pack
preparation
Figure 1.22 shows the preparation required for

placing ribbon gauze in the anterior nasal cavity.
Posterior nasal packs are prepared using roller
gauze to which tapes (or threads) are attached.
Two rubber catheters are inserted through the
right and left nasal cavities. The tapes on the pos-
terior nasal pack are tied to the loose end of the
rubber catheter. The pack is then pulled through
the oropharynx in the posterior nasal cavity by
withdrawing the rubber catheters through the
nasal cavities. The tapes are then tied to each
other over the columella over a small strip of
gauze piece placed in between to prevent pres-
sure necrosis. Though uncomfortable and
requires experience for placement, it achieves
good control of posterior epistaxis (Fig. 1.23).
Fig. 1.23 Posterior nasal pack
In unexperienced hands, it can cause more
traumas to the delicate nasal mucosa and aggra-
vate bleeding especially in patients with coagu-
1.5.2 T
ypes of Nasal Packing lopathy. Choice of packing material used depends
Material upon the inherent practice of the surgeon, cost,
and availability. Both absorbable and non-
Traditional nasal packing is prepared from ribbon absorbable materials are available.
gauge. The anterior and posterior nasal packs are
prepared differently for control of bleeding.
Anterior packing consists of ribbon gauze of 1.5.3 Non-Absorbable Nasal Packs
around a meter length soaked in antibiotic oint-
ment or bismuth iodine paraffin paste (BIPP) and Hydroxylated Polyvinyl Acetate Packs
placed in the nasal cavity in layers. (PVA) Commonly used is Merocel which is
26 H. Verma et al.
Fig. 1.24 Polyvinyl
acetate nasal pack
(Merocel)
available both with and without an external

polyethylene coating (Fig. 1.24). Other PVA
packs are Netcell packs. These compressed,
dehydrated sponges are undergo expansion due
to in situ rehydration with blood and nasal flu-
ids and achieve hemostasis through tampon-
ade. Increased localization of clotting factors
is achieved which facilitates coagulation.
Merocel packs laminated with polyethylene
film are less adhesive to the surrounding nasal
mucosa and thus less traumatic and painful
during removal [29].
Rapid Rhino Device Nasal device consisting of

inflatable polyvinylchloride nasal balloon with a
carboxymethyl cellulose (CMC) infused hemo-
static exterior to which an inflatable pilot cuff is
attached (Fig. 1.25). Moist CMC forms a hydro-
colloid gel and upon inflation with air conforms
itself to the nasal cavity. It facilitates coagulation
and provides a moist environment for the healing
of traumatized nasal tissues. The pilot cuff is
Fig. 1.25 Rapid Rhino device for bilateral nasal packing
used to maintain a steady intranasal pressure to
achieve compression for hemostasis and intrana-
sal separation of tissues. It provides high volume
and low-pressure tamponade on the nasal mucosa. Pain and bleeding during removal are minimized
Device models both with and without airway are as hydrocolloid gel formed on the exterior makes
available for control of unilateral and bilateral only gentle contact with the nasal tissues without
epistaxis and vary from 4.5 cm to 9 cm in length. any adherence.
Algosteril It is a calcium alginate nasal pack

that has both hemostatic and wound healing
properties. It absorbs sodium ions within the
nasal cavity and transforms into a hydrophilic
sodium alginate gel which allows mucosal heal-
ing without adhering to it. It provides moist envi-
ronment which facilitates epithelial regeneration.
The calcium ions are discharged locally and
facilitate the coagulation process. It also stimu-
lates local platelet aggregation. Though it can be
left in situ, removal becomes difficult due to frag-
mentation of the pack if kept beyond 24–48 h.
Petroleum Jelly Impregnated Gauze

Strips These can cause hemostasis, however,
pressure necrosis of mucosa, granuloma forma-
tion, bleeding upon removal have been reported.
Balloon Catheter Device It is specially

designed device made of medical-grade silicone
for control of anterior and posterior bleeding.
The smaller balloon is inflated for control of pos-
Fig. 1.26 Foley’s catheter inflated with saline used for
terior epistaxis and the larger balloon for anterior tamponade effect in the posterior choana
epistaxis. Normal saline is preferred for inflation
of balloon as air leaks out through the silicon ferred in an emergency setting. Benefits other
bulb thereby releasing the tamponade effect. The than hemostasis include—prevention of forma-
volume of normal saline used for inflation tion of septal hematoma, synechiae, stabilization
depends upon the pressure required for the tam- of septal cartilage, and middle turbinate [30].
ponade of vessels. An integrated airway in the
device provides a channel for breathing making Disadvantages of Non-Absorbable Packs Use
them more acceptable to the patient. A Foley’s of these packs requires in patient admission and
catheter of size 12 F or 14 F can be used for pos- antibiotic cover. Considerable pain, nasal block-
terior epistaxis control when such specialized ade, and sleep disturbance occurs when these
devices are not available (Fig. 1.26). Overinflation packs are in situ. Discomfort and bleeding during
of posteriorly placed balloon can cause inferior removal are often reported. Other problems
displacement of soft palate resulting in gagging encountered are—damage to the nasal mucosa,
and problems with deglutition. Mucosal necrosis allergic reaction, and sinus infection. Toxic shock
is more common as compression is over a larger syndrome has also been reported when these
surface area rather than direct compression of packs are used without the antibiotic cover.
bleeding vessels. All patients with posterior
packs require in patient admission for observa-
tion as posterior pack displacement can cause
fatal airway obstruction, adequate pain relief, and 1.5.4 Absorbable Nasal Packs
monitoring of oxygenation. Broad-spectrum anti-
biotic cover to prevent toxic shock syndrome and Hyaluronic Acid (HA) Products (Merogel) It
rhinosinusitis should also be started. is a polymer consisting of esterified hyaluronic
acid. Upon hydration, it transforms into a gel-like
Advantages of Non-Absorbable Packs state within 24–48 h, provides hemostasis, keeps
Insertion requires minimal training and thus pre- the mucosal surfaces apart, and provides a moist
28 H. Verma et al.
environment for healing [31, 32]. It is available

both as a nasal foam stent and injectable nasal gel.
A hybrid product consisting of HA (20%) and
collagen (80%) also available. It has been found
to induce osteoneogenesis in animal models
which may not be a favored outcome in operated
nasal cavities. Hyaluronan hydrogel is a recently
available agent in this group and has shown better
epithelialization in postoperative setting.
Collagen Derived Products These are derived

from bovine or porcine collagen. They expand
upon contact with blood to provide tamponade
Fig. 1.27 Gelfoam, a sponge form of gelatin
effect and activate coagulation cascade. They are
available as:
thane. It keeps the edematous mucosal surfaces
(a) Gelatin film. apart during the initial healing phase thus pre-
(b) Gelfoam which is its sponge form (Fig. 1.27). venting adhesion formation and provides ade-
(c) FloSeal—It is a viscous gel prepared by com- quate structural support. It starts to dissolve
bining gelatin granules with human thrombin within days and can be suctioned from the nasal
just prior to use and applied topically with an cavity after a few days [35].
applicator. Easy bedside preparation, good Polyethylene Glycol—It is a Thermo-
hemostasis, less chances of re-bleeding, no sensitive product. It forms a hydrogel barrier
requirement of antibiotic cover or hospital in the operated nasal cavity which lasts for a
admission, and better acceptance by the week and prevents adhesion formation.
patients favor its use over standard nasal pack- 2. Natural Biopolymers
ing in emergency setting. Due to incorpora- Carboxymethyl Cellulose (CMC) Nasal
tion into the healing mucosa, adhesion Dressings. Various CMC based products
formation has been noted with its use [33]. available are
(a) Rapid Rhino Nasastent—5 cm intrana-
sal splint which can be cut to the desired
Fibrin Glue It is a surgical sealant consisting of size and placed in the nasal cavity.
pooled human origin coagulation products. It is (b) Rapid Rhino Sinu-Knit—a mesh-like
prepared by combining thrombin (bovine origin) fabric of CMC (Fig. 1.28).
reconstituted with calcium chloride and fibrino- (c) Injectable Stammberger Sinu Foam—
gen (lyophilized pooled human concentrate). It dry CMC fiber within a syringe which
activates the coagulation cascade and attaches after contact with sterile water forms
firmly to nasal tissues providing hemostasis. It viscous foam that can be inserted into
causes minimal inflammation, granulation tissue the nose.
formation, and crusting [34]. Upon hydration with sterile water CMC turns
into a hydrocolloidal gel which eventually
Biopolymers Synthetic and Natural Biopolymers drains out via the natural drainage pathway
Are Available: within ten days or can be removed with suction
aspiration. The dense gel provides a moist
1. Synthetic Biopolymers hydrocolloid physical barrier which prevents
Nasopore—These are biodegradable, biologi- postoperative bleeding and adhesions.
cally inert fragmenting foam made of polyure- Antibiotic ointments or any other liquids such
thane that absorbs water and blood. Hemostasis as saline should be avoided as the gel formation
is due to the compressive properties of polyure- and hemostatic properties get inhibited [36].
Due to fragmentation, these absorbable nasal

packs are easily removed using suction aspiration
after 7–10 days thus cause less irritation of the
inflamed nasal mucosa. Retention beyond 10
days may increase the chances of synechiae for-
mation as the fragmented parts may get incorpo-
rated into the healing mucosa and facilitate
epithelialization between the middle turbinate
and lateral nasal wall [31]. Other benefits of
absorbable packs include—increased patient
comfort due to lack of feeling of nasal pressure,
nasal blockade and headache, better mucosal
healing. As formal removal is not required pain,
discomfort, and bleeding associated with removal
of non-absorbable packs are avoided.
References
1. Stemmberger H, Kennedy DW. Paranasal sinuses:
anatomic terminology and nomenclature. Ann Otol
Rhinol Laryngol. 1995;104:7–16.
Fig. 1.28 Rapid Rhino Sinu-Knit—a mesh-like fabric of 2. Bent JP, Cuilty-Siller C, Kuhn FA. The frontal cell
CMC as a cause of frontal sinus obstruction. Am J Rhinol.
1994;8:185–91.
3. Gera R, Mozzanica F, Karligkiotis A, Preti A, Bandi
Oxidized Regenerated Cellulose It promotes F, Gallo S, Schindler A, Bulgheroni C, Ottaviani F,
platelet aggregation. It is preferably used for Castelnuovo P. Lateral lamella of the cribriform plate,
hemostasis in deeper regions of the nasal cavity a keystone landmark: proposal for a novel classifica-
tion system. Rhinology. 2018;56(1):65–72.
which are difficult to access for direct vessel con- 4. Kainz J, Stammberger H. The roof of the anterior eth-
trol. It creates an acidic environment which moid; a place of least resistance in the skull base. Am
causes platelet activation and prevents bacterial J Rhinol. 1989;4:191–9.
growth. Resorption is prolonged and favors the 5. Elwany S, Yacout YM, Talaat M, EI-Nahaas M,
Gunied A. Surgical anatomy of the sphenoid sinus. J
formation of granulation tissue and adhesions. Laryngol. 1983;97:227–41.
6. Wei S, Yu-Han Z, Wei-Wei J, Hai Y. The effects of
Microporous Polysaccharide Beads These are intravenous lidocaine on wound pain and gastrointes-
derived from purified potato starch. These are tinal function recovery after laparoscopic colorectal
surgery. Int Wound J. 2020;17(2):351–62. https://doi.
available as an injectable powder consisting of org/10.1111/iwj.13279.
spheres ranging from 10 to 200 μm. Due to poros- 7. Yilmaz AH, Ziypak E, Ziypak T, Aksoy M, Adanur S,
ity it extracts the fluid from the blood and Kocakgol H, Demirdogen SO, Polat O. Comparison of
increases the local concentration of platelets and the effect of lidocaine versus a lidocaine-bupivacaine
combination in a periprostatic nerve block undergo-
coagulation factors. ing transrectal ultrasound-guided prostate biopsy: a
double-blind randomized controlled trial. Curr Urol.
Chitostan It is a hemostatic agent that is de- 2016;9(3):153–8.
acetylised polysaccharide derived from shellfish 8. McAlvin JB, Reznor G, Shankarappa SA, Stefanescu
CF, Kohane DS. Local toxicity from local anes-
chitin. It is known to possess anti-fungal and thetic polymeric microparticles. Anesth Analg.
anti-bacterial properties. It prevents adhesion for- 2013;116(4):794–803.
mation by inhibiting fibroblast growth. It is avail- 9. Moskovitz JB, Sabatino F. Regional nerve
able as aerosol and gel form. blocks of the face. Emerg Med Clin North Am.
2013;31(2):517–27.
30 H. Verma et al.
10. DeMaria S Jr, Govindaraj S, Chinosorvatana N,

Otorhinolaryngol Head Neck Surg. 2015;14:Doc08.
Kang S, Levine AI. Bilateral sphenopalatine gan- https://doi.org/10.3205/cto000123.
glion blockade improves postoperative analgesia 24. Friedrich DT, Sommer F, Scheithauer MO. An inno-
after endoscopic sinus surgery. Am J Rhinol Allergy. vate robotic endoscope guidance system for t ransnasal
2012;26(1):e23–7. sinus and skull base surgery: proof of concept. J
11. Beeson WH. The nasal septum. Otolarvngol Oin
Neurol Surg B. 2017;78:466–72.
North Atli. 1997;20:743–67. 25. Barber SR, Jain S, Son YJ. Virtual Functional

12. Ahmad R, Ishlah W, Azilah N, Rahman JA. Surgical Endoscopic Sinus Surgery Simulation with 3D-Printed
management of juvenile nasopharyngeal angiofi- Models for Mixed-Reality Nasal Endoscopy.
broma without angiographic embolization. Asian J Otolaryngol Head Neck Surg. 2018;159(5):933–7.
Surg. 2008;31(4):174–8. 26. Zalzal HG, Makary CA, Ramadan HH. Long-term
13. Simpson P. Perioperative blood loss and its reduc- effectiveness of balloon catheter sinuplasty in pedi-
tion: the role of the anaesthetist. Br J Anaesth. atric chronic maxillary sinusitis. Ear Nose Throat J.
1992;69(5):498–507. 2019;98(4):207–11.
14. Petrozza PH. Induced hypotension. Int Anesthesiol 27. Melis A, Karligkiotis A, Bozzo C, Machouchas N,
Clin. 1990;28(4):223–9. Volpi L, Castiglia P, et al. Comparison of three dif-
15. Khanna P, Br R, Resident S, Sinha R. Anaesthetic ferent polyvinyl alcohol packs following func-
management of endoscopic resection of juvenile tional endoscopic sinus surgery. Laryngoscope.
nasopharyngeal angiofibroma: our experience and a 2015;125:1067–71.
review of the literature. South Afr J Anaesth Analg. 28. Douglas R, Wormald PJ. Update on epistaxis. Curr
2013;19(6):314–20. Opin Otolaryngol Head Neck Surg. 2007;15:180–3.
16. Bennett J, Haynes S, Torella F, Grainger H,
29. Wang YP, Wang MC, Chen YC, Leu YS, Lin HC,
McCollum C. Acute normovolemic hemodilution in Lee KS. The effects of Vaseline gauze strip, Merocel,
moderate blood loss surgery: a randomized controlled and Nasopore on the formation of synechiae and
trial. Transfusion. 2006;46(7):1097–103. https://doi. excessive granulation tissue in the middle meatus
org/10.1111/j.1537-2995.2006.00857.x. and the incidence of major postoperative bleeding
17.
Kim DH, Seo Y, Kim KM, Lee S, Hwang after endoscopic sinus surgery. J Chin Med Assoc.
SH. Usefulness of nasal endoscopy for diagnosing 2011;74:16–21.
patients with chronic rhinosinusitis: a meta-analysis. 30. Verim A, Seneldir L, Naiboglu B, Karaca CT, Kulekci
Am J Rhinol Allergy. 2020;34(2):306–14. https://doi. S, Toros SZ, et al. Role of nasal packing in surgical
org/10.1177/1945892419892157. outcome for chronic rhinosinusitis with polyposis.
18. Puranik V, El-Sheikha A. Uncinectomy: Stammberger Laryngoscope. 2014;124:1529–35.
or swing-door technique? Eur Arch Otorhinolaryngol. 31. Massey CJ, Singh A. Advances in absorbable bioma-
2007;264(10):1151–5. terials and nasal packing. Otolaryngol Clin N Am.
19. Kim HJ, Ahn JC, Hong SN, et al. Posterior fontanelle 2017;50(3):545–63.
approach for uncinectomy and middle meatal antros- 32. Valentine R, Wormald PJ, Sindwani R. Advances

tomy in endoscopic sinus surgery. Laryngoscope. in absorbable biomaterials and nasal packing.
2016;126:1311–4. Otolaryngol Clin N Am. 2009;42(5):813–28.
20.
Schaefer SD, Li JC, Chan EK, Wu ZB, 33. Chandra RK, Conley DB, Kern RC. The effect of
Branovan DI. Combined anterior-to-posterior FloSeal on mucosal healing after endoscopic sinus
and posterior- to-
anterior approach to parana- surgery: a comparison with thrombin-soaked gelatin
sal sinus surgery: an update. Laryngoscope. foam. Am J Rhinol. 2003;17(1):51–5.
2006;116(4):509–13. 34. Iqbal IZ, Jones GH, Dawe N, Mamais C, Smith ME,
21. Wormald PJ. Three dimensional building block
Williams RJ, et al. Intranasal packs and haemostatic
approach to understanding the anatomy of the frontal agents for management of adult epistaxis: systematic
recess and frontal sinus. Oper Tech Otolaryngol Head review. J Laryngol Otol. 2017;131:1065–92.
Neck Surg. 2006;17:2–5. 35.
Weber RK. Nasal packing and stenting.
22. Weber R, Draf W, Kratzsch B, Hosemann W, Schaefer Laryngorhinootologie. 2009;88(Suppl 1):139–55.
SD. Modern concepts of frontal sinus surgery. 36. Kastl KJ, Betz CS, Siedek V, Leunig A. Effect of car-
Laryngoscope. 2001;111(1):137–46. boxymethylcellulose nasal packing on wound heal-
23. Weber RK, Hosemann W. Comprehensive review on ing after functional endoscopic sinus surgery. Am J
endonasal endoscopic sinus surgery. GMS Curr Top Rhinol Allergy. 2009;23:80–4.
Rhinoplasty Anatomy
and Procedures 2
Arvind K. Kairo, Saurav Sarkar, Anindya Nayak,
Prateek Sharma, and Rakesh Kumar
Contents
2.1 art A: External Nasal Anatomy, Aesthetics and Photography
P 31
2.1.1 Photography and Analysis 34
2.2 Part B: Open and Close Rhinoplasty and Tip Plasty 39
2.2.1 I ntroduction 39
2.2.2 Approaches 39
2.2.3 Tip Defining Procedures 40
2.2.4 Management of the Overprojecting Tip 41
2.2.5 The Under-Projected Nasal Tip 41
2.2.6 The Broad Nasal Tip 42
2.2.7 Complications 42
2.3 art C: Nasal Dorsum Correction and Material for Rhinoplasty
P 42
2.3.1 Post-Operative Management 44
2.3.2 Materials for Reconstruction in Rhinoplasty 45
References 47
2.1 art A: External Nasal

P
Anatomy, Aesthetics
and Photography
The external nose is pyramidal in shape. The root

is continuing with the forehead and the apex is
formed by a nasal tip. The nasal dorsum is part of
the nose located in between the root and nasal tip.
Dorsum elevation is slightly behind the line from
nasion to tip defining point in female whereas in
the male it is at the line. Nasal ala is the lower lat-
A. K. Kairo · P. Sharma · R. Kumar (*)
ENT, AIIMS, New Delhi, India eral surface of the external nose which is formed
e-mail: winirk@hotmail.com by alar cartilage and supportive tissue. Dome is the
S. Sarkar · A. Nayak anterior projecting segment of lower lateral carti-
ENT, AIIMS, Bhubaneswar, Odisha, India lage and anatomically, it is formed by the junction
32 A. K. Kairo et al.
Fig. 2.1 The chart is EXTERNAL NASAL ANATOMY

showing various parts
involve in the built-up of
the nose Externalnasalanatomy
Skin Frame Work Support tissues
cartilages bones muscles ligaments
of middle and lateral crural of lower lateral carti- two-third part of the nose and adherent and
lage [1, 2]. External nasal soft tissue anatomy can thicker over the lower one-third part, thinnest at
be divided into parts for easy understanding, i.e. the junction of upper one-third and lower two-
skin, framework and supporting tissues (Fig. 2.1). third. Thinner skin makes underlying anatomy
Skin is separated from underlying bone and more visible thus more precision is required in
cartilage by four layer of tissue; the external most such patients. Postoperative results of the rhino-
is the superficial fatty layer follow by the fibro- plasty surgery also depend on the thickness of the
muscular layer and deep fatty layer. Periosteum/ skin. When the patient has thick skin, slight
perichondrium is the last layer that separates the imperfection can be hidden beneath the thick
skin from underlying bone/cartilage. The surgical skin whereas thinner skin can show slight uneven-
plane is created deep to the perichondrium as ness but results are not that much visible as visi-
blood supply for nasal framework runs in the deep ble in thin skin (Fig. 2.2).
fatty layer. The soft triangle is part of the nostril
apex where outer dermis is in direct contact with Support Tissues
the inner dermis without any deep tissue. Bony Overlying skin is attached to underlying bone
framework is the upper framework and it is formed and cartilage by different ligaments and other
by contribution of the nasal bone, frontal process soft tissues like fat and muscle. If ligaments are
of maxilla, and part of the frontal bone. The ante- severed during surgery, it should be mended at
rior nasal spine is a projection formed at the ante- the end of the surgery. If the surgeon forgets this
rior most part of the intermaxillary suture line. step then the stability of the dorsum will be com-
Cartilaginous framework is formed by two alar promised. Other soft tissue is subcutaneous fat,
and one septal cartilage. Septal cartilage is hooked dermo-cartilaginous ligament (ligament of
in the midline by the maxillary crest. Nasal valve Pitanguy) and muscles. Eight nasal muscles have
(10°–15°) is formed by anterior most end of the been described. Out of these, only two muscles,
inferior turbinate, alar nasi (junction of upper and procerus and nasalis, are in a position to impact
lower cartilage) and septum. In this chapter, surgi- the nasal profile.
cally relevant and concise anatomy is given along
with how to document and analyse the pre and Blood Supply
postoperative changes. Dorsum of the nose is very vascular especially in
Skin: For aesthetics, it is divided into subunits. the central part where there is rich anastomosis of
These subunits are dorsum, lateral walls, tip and bilateral blood supplies. Unlike the major part of
the alar region. Scar of any subunit should see as the face, it gets supplies from both external and
part of that subunit and should be dealt with internal carotid artery. The blood supply is from
accordingly. The thickness of the skin over the anterior ethmoids, dorsal nasal, columellar
nasal dorsum is not even and its thickness keeps branches from superior labial and dorsal nasal
changing. It is mobile and thinner in the upper artery from the angular artery. Columellar
2 Rhinoplasty Anatomy and Procedures 33
Fig. 2.2 The clinical a b

photograph is showing
the thin (a) and thick (b)
skin types of patients.
Figure (b) is showing
wide nose in the middle
and lower third whereas
(a) it is in the normal
range. (Courtesy—Dr.
Hitesh Verma, Associate
Professor, AIIMS, New
Delhi, India)
branches and dorsal nasal arteries are anastomo- cess of the maxilla (Fig. 2.3). Nasion is a mid-
sis to form arcades over the dorsum of the nose. line point over the frontonasal suture line just
These arcades get damaged by excessive removal superior to the root of the nose. Rhinion is the
of soft tissue from dorsum. anterior tip at the end of the nasal bone suture
line. Bony vault is narrowest and thickest at the
Nerve Supply intercanthal level. It requires osteotomies for
Nerve supply follows the embryological origin of correction.
the area. The major part of the dorsum is supplied
2
Middle one-third (Upper Cartilaginous
by first branch of the trigeminal nerve (ophthal- Vault)—Upper lateral cartilage is the main con-
mic) for sensory innervation. Some part of the tent in the middle vault. An area of tight syn-
lateral wall and the inner lining second branch of chondrosis between the bony and upper
the trigeminal nerve (mandibular). For motor cartilaginous vault along with its attachment to
innervation, the facial nerve is a supplier. Dorsal the dorsal septum is known as key stone area
nasal skin up to the tip is derived from branches (Fig. 2.3). Overlap of lower lateral cartilage
of the trigeminal nerve (from branches of the with upper lateral cartilage is known as the
supratrochlear and anterior ethmoidal nerve, scroll area (Fig. 2.3). Attachment of upper lat-
branch of the ophthalmic nerve). The infraorbital eral cartilage with the dorsal septum forms the
nerve may also contribute branches to the lateral internal nasal valve, which can be improved by
nasal walls, columella and vestibule. For endona- using spreader graft.
sal mucosa—branches come from sphenopala- 3
Lower one-third (Lower Cartilaginous
tine ganglion. Vault)—It is comprised of alar cartilage which
is divided into three parts as medial, intermedi-
Frame Work ate and lateral crural (Fig. 2.3). It is an essen-
The external nasal framework is divided into tial part of the tip and its projection. Tip
three nasal vaults [1, 2]. support is assessed by Tip recoil phenomenon.
Tardy described nasal tip support mechanisms
1 Upper one-third (Bony Vault)—It is formed by in major and minor groups
paired nasal bone and part of the frontal pro- (a) Major Tip Support
Fig. 2.3 The line Frontal bone

diagram is depicting the
nasal framework and
facial division in both Nasal bone
planes (vertical and
horizontal) Keystone area
Upper
Lateral
Cartilage
Sesomoid Scroll area
Cartilage
fatty
Alar Cartilage
Fibro
e
maxilla tissu
Septal Cartilage
(i) Size, shape and resilience of the Anatomically middle crus is further divided into
lower lateral cartilages domel and lobular segment. Domel segment is thin,
(ii) Attachment of the medial crural foot- delicate and narrowest part of the entire alar arch.
plate to the caudal septum Convex, box and concave are the type of domel seg-
(iii) Scrolled attachment of the cephalic ment shape. Angulations, the position with other
margins of the lower lateral cartilages dome and thickness of overlying skin affect the
to the caudal margin of the upper lat- shape of the nasal tip [1]. Nasal supports are essen-
eral cartilages tial in maintaining the normal nasal airway, as
( b) Minor Tip Support excessive resection of intermediate crura for pinch-
(i) Dorsal septum ing effect leads to nasal airway obstruction.
(ii) Interdomal ligaments
(iii) Membranous septum
(iv) Anterior nasal spine 2.1.1 Photography and Analysis
(v) Attachment of the lower lateral carti-
lages to the skin–soft tissue envelope Photographs are important for pre-operative anal-
(vi) Lateral crural attachment to the pyri- ysis, documentation and for comparing postopera-
form aperture tive results. Photographs should cover the full face
(hairs to chin). Recently, computer software’s are
Nostril is divided into three types (cheek, labial available for rhinoplasty. They are useful for plan-
and tube) based on the relationship of nostril floor ning surgery, for explanation purposes and postop-
with ala base. Medial crus of further divided into erative outcome assessment (Table 2.1).
columellar and foot segment. The width of the colu-
mella is affected by the intrinsic shape of cartilage, 1. Ratios—Facial ratios can be defined to assess
amount of soft tissue and posterior caudal edge of harmony in facial features. Following are few
septal cartilage (Fig. 2.4). Asymmetric parallel, of common ratios
flare and straight symmetry are paring patterns of (a) Rule of fifths—face can be divided verti-
the medial and middle crux. Columella skin flap cally into five equal parts equal to the size
must rise in full depth to maintain the symmetry of of length from medial cantus to lateral
the medial crux at the end of the operation. cantus (Fig. 2.5).
Fig. 2.4 Caudal septal

deviation and
asymmetry in the
curvature of ala affects
the width of columella
(Courtesy—Dr. David
Victor Kumar Irugu,
Associate Professor,
AIIMS, New Delhi)
Table 2.1 Computer software’s for aesthetic assessment for rhinoplasty [3]
Computer softwares Pros Cons
www.facetouchup.com Online Cannot calculate different angles
Cosmetic digital image editing Software
Also on Android
Free
Adobe Photoshop Software Proportionate measurement angular relationship Require more skills to use
Easily available
Alter image Cosmetic digital image editing software Expensive
Dental simulation also present
Mirror suite Cosmetic digital image editing software Expensive
Easy to measure distances, angles, proportions
Colour and orientation can be matched
3D version is also available
(b) Rule of thirds—face can be divided hori- mella to line between the base of the colu-
zontally into three equal parts equal to the mella to mentum in lateral view. In the
size of length from glabella to nasal tip male, it is 90o–95o and in the female
(Fig. 2.5). 95o–110o.
(c) Golden ratio—Fibonacci ratio or ‘divine (b) Nasomental angle—it is angle in between
proportion’—Consider a line is divided lines from nasal dorsum to tip and from
into two parts (A and B) where A is tip to pogonion. It is in between 120o–130o.
smaller than B. The golden ratio (ɸ) is (c) Nasofacial angle—it is in between lines
when A/B = (A + B)/A = 1.618. If nose from nasal dorsum and nasion to pogo-
width is 1 than length is 1.618. nion. It is around 30o–35o.
2 . Angles ( d) Naso-frontal angle (Fig. 2.6)—it is the
(a) Nasolabial angle (Fig. 2.6)—it is the intersection of tip nasion and glabella and
angle between a line running from colu- it is around 130o.
Fig. 2.5 It is showing

both vertical and
horizontal rule for
aesthetic division of face
3. Nasal Tip—The points that need to be evalu- deviation of the bony and cartilaginous compo-
ated are tip rotation, projection (Fig. 2.6). nent of the nasal framework. Brow-tip aesthetic
Aesthetically, the face can divide into two line, alar shape, lobular bulbosity, nostril size and
equal half from the midline. In normal condi- shape are also evaluated in frontal view. Bifidality
tions, the width of the nasal dorsum is half of of the nasal tip is observed in this plane.
the width of intercanthal distance. The width 2. Right and left lateral view (profile view)
of the nasal ala is approximately equal to the (Figs. 2.6 and 2.7)—The assessment is done in
width of the eyebrow free medial border. relationship to the Frankfurt plane. The projec-
Nasal projection is 50–60% of nasal length tion of nasal dorsum, tip, chin with nasal length
as per the rule of 3–4–5. It is also calculated and height of radix are assessed in this plane.
by the division of line from the nasal tip from Nasal tip rotation, break and columella show
ala groove by an imaginary line from the are observed in this plane. Naso-frontal, naso-
upper lip and anterior part is around 50–60% labial angles, etc. are calculated in this plane.
in normal individual (Fig. 2.7). 3. Right and left lateral-Oblique view (three

quarter view)—Brow-tip aesthetic line and
Standard photographic views are [4] soft tissue facets are assessed in this view.
4. Base view—It is for calculation of the shape
1. Frontal view—It is for the assessment of facial of crura’s of lower cartilage, tri-angularity,
and nasal symmetry (Figs. 2.2 and 2.4). It is use- columella to lobular ratio. The shape of the
ful to assess the width, symmetry and midline nasal base is equilateral triangle ideally with
a b
Nasofrontal angle
Naso labial angle
Fig. 2.6 The line diagram is representing nasolabial lateral view (Courtesy—Dr. Hitesh Verma, Associate
angle and naso-frontal angle. Naso-frontal angle is almost Professor, AIIMS, New Delhi, India)
180° with tip ptosis and less tip projection is visible in
the lobular, intermediate and basal part of col-

umella as three equal segments. Nostril is 2/3
of the height of the nose in basal view. Normal
columella to lobular ratio is 2:1. Nostril shape
and position, septum position, length of
medial crura and basal width are also checked
Nasion in this plane. Nostrils are oval shape, elon-
gated and commonly oriented 30–45° towards
the midline (Fig. 2.8).
Goode Ratio
5. Smiling view—Upper lip height, upper labial
Tip
defining point for crease, nasal tip projection and nasal length
Tip Projection are assessed in this plane. Depressor septi nasi
muscle is responsible for smiling face defor-
mity [5].
6. Skyline view (helicopter view) and Bird eye
frontal view with chin up 45° are other views
Poganion recommended by some author for routine
practice and they are providing special details
such as
Fig. 2.7 Nasal projection is 50–60% of the length of the
nose from nasion to tip defining point. Black line is the
imaginary line that bisects the nasal projection line. The Setup for Taking Photograph [6]
anterior part of line should be 50–60% Digital cameras come in two categories; fixed
lens (smartphone) and interchangeable lens
camera (DSLR and mirrorless interchangeable
a b
Fig. 2.8 Basal view is providing detail of nostril types, of nostril, thin cartilage and wide arch with normal colu-
shape of crura, nostril height, etc. Figure (a) is showing mella (Courtesy—Dr. David Victor Kumar Irugu,
cheek type of nostril, thick alar cartilage, narrow arch with Associate Professor, AIIMS, New Delhi)
thick basal part of columella and (b) is showing tube type
Synchronized studio flashes Synchronized studio flashes
2 meters
45°
12 to 18 inches
A solid cloth background
Fig. 2.9 The diagram is representing ideal setup for photography
lens). An interchangeable lens is recommended removed with hair retracted to improve the vis-
for photography because of flexibility with gaze ibility of the forehead and ear. Pre and post-
at focal length, focus and resolution. The focal operative photography should be performed in
length of the camera lens should be 85–105 mm the same clothes and cloth should have a bland
and the aperture in lens varies from f/9 to f/11. neck line. Solid coloured back drop preferably
Two synchronized studio flashes are placed on light blue as it is kind to all skin tones with good
either side of the camera with 45° horizontal disparity and less glare. The patient needs to sit
angle between the patient-camera axis with on the stool with a rough position of an eye
flashlight. The makeup and jewellery should be within the camera (Fig. 2.9).
2.2 art B: Open and Close

P approach is more preferred as it provides direct
Rhinoplasty and Tip Plasty visualization, allows working from both hands,
provide accurate assesssment and precise rectifi-
2.2.1 Introduction cation of deformity [7]. Practically, all deformity
of the external nasal framework is managed by
Rhinoplasty is a commonly done procedure the open approach but more specific indications
worldwide mostly for aesthetic and in some are nasal cartilages correction, difficult anatomy,
cases for functional benefit. The anatomy of post-traumatic cases, revision surgery and com-
the tip cartilages is complex. The nasal tip municated fracture of the bony framework. In the
comprises the columella, lobule and ala. Lower open approach, mid-columellar stair step incision
lateral cartilage is U shaped stracture and it has is extends on both sides along the caudal border
two processes: the medial and lateral crura. of intermediate and lateral crus of lower lateral
The medial crura and overlying skin and sub- cartilage (marginal incision). The flap is raised in
cutaneous tissue form the columella. The key subperichondrial avascular plane and dissection
support mechanism of the tip comprises the is extend over the lower and upper lateral carti-
size, shape and strength of the lower lateral lage up to caudal aspect of nasal bones where dis-
cartilages, the connection of the feet of the section is extended further in the subperiosteal
medial crura to the caudal edge of the septum, plane till radix. The tissue handling should be
and the connection of the upper lateral carti- mapped according to deformity. The disadvan-
lages to the lower lateral cartilages at the scroll tages are prolonged surgical time, need additional
region. Surgical strategies should keep in mind support for the cartilaginous framework, prolong
the size, shape, position and orientation of postoperative edema and external scar. In the
each crus including their relationships with the close approach, indications are limited for cor-
ipsilateral and c ontralateral crura of both lower rection of isolated deformity of nasal tip and
lateral cartilage rings. It is important to be pre- nasal dorsum. Infra cartilaginous, intercartilagi-
cise as every step has the potential for unin- nous and trans-cartilaginous approaches are
tended as well as intended change. The most types of incision used to expose the deformies
common problems are due to an under or over- and rest of the flap elevation is done in subperi-
projected tip. In this chapter, the methods used chondrial and subperiosteal plane. In the newer
most widely have been described. The three semiopen approach, the marginal incision is
basic surgical approaches are described in the made and the rest of the procedure is done under
literature. The approach may be selected after skin. Surgical approaches to the nasal tip are of
taking into consideration the desired outcome three types. Non-delivery and delivery approaches
and patient characteristics. At the end of each are come under close technique.
surgery, the result should be a normal stable
nose. 1. Non-Delivery Approaches:
(a) Cartilage-splitting approach
(b) Retrograde approach
2.2.2 Approaches (i) Delivery approach
(ii) External rhinoplasty
Rhinoplasty is the problem-oriented practice
with combination of reduction, rearrangement 1. Non-Delivery Approach: The non-delivery
and amplification of tissue. Surgical treatment approach is useful in cases where small vol-
needs to be tailored according to deformity. ume reduction of the lateral crus is required
Rhinoplasty surgeries are broadly classified and when the slight cephalic rotation of the tip
under the external and endonasal approach. The is required. It is of further two types. In
choice of surgical approach is based on training cartilage-splitting technique is the least trau-
and surgeon experience. In general, the open matic of the commonly used rhinoplasty tech-
a b
Frontal bone
Frontal bone
Nasal bone
Nasal bone
Keystone area
Orbit
Keystone area
Orbit
Upper
Lateral Upper
Cartilage Lateral
Cartilage
Sesomoid
Scroll area Sesomoid
Cartilage
Scroll area
fatty Alar Cartilage Cartilage
maxilla Fibro
tissu
e
fatty
Alar Cartilage
Septal Cartilage
maxilla Fibro
e
tissu
Septal Cartilage
Fig. 2.10 The diagram is showing the site of the intercartilaginous incision (red line). (b) is showing the placement of
the tip delivery incisions (Courtesy—Dr. Arvind Kairo, Associate Professor, ENT, AIIMS, New Delhi)
nique. A single incision is made at the position till the nasal dorsum is exposed. Medial crura
that overlies the cartilaginous part. Cephalic can be separated to expose the caudal end and
strip of cartilage with or without underlying dorsal area of the nasal septum.
skin can be removed. In this, an intercartilagi-
nous incision is made followed by retrograde
dissection over the lateral crus at the non- 2.2.3 Tip Defining Procedures
vestibular side, eversion of the lateral crus and
resection of the planned cephalic portion of Under-projected nasal tip can correct by various
the cartilage (Fig. 2.10a). techniques. The choice of approach can be sim-
2. Tip delivery is indicated when the tip is bifid, ple removal of the cephalic strip of lower lateral
cephalically rotation and over-projected. It cartilage, vertical division + / − strip excision of
delivers the alar cartilages with the underlying lower lateral cartilage, tip suturing and tip graft-
skin and mucosa as a ‘bucket handle’ [7]. The ing alone or in combination [7].
incisions are made along the caudal margin
and cephalic margin of the alar cartilage 1. Strip excision/division of cartilage: Tip is nar-
(Fig. 2.10b). The overlying soft tissue and rowed by trimming the cephalic part of lower
skin are dissected off the alar cartilage leaving lateral cartilage (Fig. 2.12). Lateral part of the
the cartilage attached to its underlying skin lower lateral cartilage is left intact to maintain
and mucosa. the integrity of the nasal valve. Cephalic edge
3. External rhinoplasty is described by Gillie and of the lower lateral cartilage can be approached
popularized by Rethi [8]. Inverted V shaped by a cartilage-splitting incision, tip delivery
incision is joined with bilateral rim incision to approach, or via the external rhinoplasty
prepare of the columella skin flap (Fig. 2.11a). approach. Approximately 10 mm of lower lat-
Incision should not disturb the underlying car- eral cartilage should be left in situ to avoid
tilage of the medial crura (Fig. 2.11b), to pre- buckling of the cartilage.
vent postoperative skin necrosis and visibility 2. Tip suturing techniques. Cephalic trimming
of scar [7]. Skin flap is elevated and dissected reduces straight of the nasal value area. Tip
Fig. 2.11 Showing a b
elevation of the flap by
external rhinoplasty
approach (Courtesy—
Dr. David Victor Kumar
Irugu, Associate
Professor, AIIMS,
New Delhi)
(Goldman). Tip delivery approach followed by ver-

tical division of the alar domes approximately
1 mm lateral to the highest point of the dome. The
cartilage and its underlying mucosa are incised.
The intermediate crura are rotated anteriorly and
sutured with the medial crura. The classic Goldman
procedure can result in irregularities of the tip,
lower nasal third pinching, alar notching and a
Fig. 2.12 It is showing the technique of excision of a pointed ‘tent pole’ nasal tip which was addressed
cephalic strip of cartilage by Adamson et al. [10] They described by the
placement of vertical incision medial to the high
point of the dome and overlapping of the lower lat-
suturing technique is free of such complica- eral cartilage as a method of avoiding these compli-
tions and it is reversible. Interdomal sutures cations. Third technique is by interrupted strip with
are used to narrow the nasal cartilages. It is cartilage excision. Excising a vertical strip of carti-
indicated when support graft is needed for tip lage from the medial [11] or lateral crura or a com-
preparation, to strengthen the medial crura bination can result in better cephalic rotation of the
and for tip projection (Fig. 2.13). tip. Lateral segment excision is preferred because
the cartilage excision is covered by thicker seba-
ceous skin. Goldman tip suturing & Adamson
2.2.4 Management modification are the techniques to prepare single
of the Overprojecting Tip tip in bifid nasal tip conditions [12].
The causes of tip over-projection are alar cartilage

development, nasal spine overdevelopment, caudal 2.2.5 The Under-Projected Nasal Tip
septal deviation, overdeveloped quadrangular carti-
lage, elongated columella and iatrogenic over-pro- The nasal tip may appear under-projected because
jection [9]. It can be done by applying complete of disproportionately small alar cartilages or
transfixion incision. This helps in the separation of because the middle and or upper third of the nose
the membranous septum from the medial crural is disproportionately large [7] Methods to
footplates. It allows the alar cartilages to be reposi- increase tip projection are the Goldman tip tech-
tioned in relation to the nasal septum [7]. It can also nique, onlay graft (Fig. 2.13), lateral crural steal
be done by the vertical dome division technique and shield graft. For onlay graft, conchal carti-
Fig. 2.13 Left ala is lower than right ala. Cartilage piece ala before separating both ala’s. Suture needs to be passed
is placed over the left dome and in between both sides of in the same fashion with other ala and supporting cartilage
medial crura. The suture is passed from the right side of to prepare tip (Courtesy—Dr. David Victor Kumar Irugu,
right side medial ala where it was approximate with other Associate Professor, AIIMS, New Delhi)
lage and septal cartilage grafts are generally used. may be related to scar tissue or to excessive
The disadvantages of this method are that it lower lateral cartilage excision and subse-
thickens the tip of the nose. In the lateral crural quent loss tip support.
steal technique, alar cartilages are dissected off (b) Retracted ala: This is due to excessive lower
the underlying vestibular skin in the intermediate lateral cartilage and/or vestibular skin exci-
crural area and the alar cartilages may be deliv- sion causing retraction of the alar cartilages.
ered. The lateral crura are then advanced to the (c) Alar asymmetry is caused by unequal alar
medial crura and sutured with permanent sutures. cartilage remnants.
Shield graft is useful in short columella and weak (d) Retracted columella: This may be related to
lower lateral cartilages (Fig. 2.13). either excessive resection of the caudal edge
of the septum or medial crura.
(e) Bossae: weakening and subsequent bending
2.2.6 The Broad Nasal Tip of the alar cartilage.
It is seen in thick skin people or in the abnormal These complications are often managed with
shape of alar, septal cartilages. Nasal tip can be an open rhinoplasty approach for accurate diag-
narrowed and a more triangular base be obtained nosis and it can be resolved by local grafts.
by either using a Goldman tip technique or
sutures to create a narrow tip.
2.3 art C: Nasal Dorsum
P
Correction and Material
2.2.7 Complications for Rhinoplasty
Patient dissatisfaction is the most common com- The external nasal scaffold extends from the root
plication of rhinoplasty [7]. This can be managed of the nose till the nasal tip is known as the nasal
by accurate pre-operative assessment, realistic dorsum. The bony nasal dorsum is formed by
expectations and better communication. nasal bone and the frontal process of the maxilla
Haemorrhage and infection are other complica- and nasal part of the frontal bone. The cartilagi-
tions. Deformities relating to the nasal tip are: nous part is formed by upper lateral cartilage.
Deformity of nasal dorsum is described as hump
(a) Pollybeak deformity: This produces loss of (over-projected), saddle (under-projected),
tip definition with supratip fullness. This twisted, C and S shaped which can involve bony
1. Lateral Osteotomy—It is done to narrow or

straighten the bony nasal dorsum. It can be
done with two techniques:

(a) Linear or single cut—It is performed
intranasally. It starts from the lateral
attachment of an inferior turbinate. Using
an osteotome, the linear bony cut is made
along nasofacial groove. Based on the site
of the starting point, it is further of three
types.
(i) High-low-high technique–Taking
the nasofacial groove as a reference,
Fig. 2.14 The diagram is representing the site of medial
the osteotomy is done above the
and lateral osteotomies and how it should run to join each nasofacial groove (high). Incision is
other extending along the nasofacial
groove (low) thereby leaving a small
and cartilaginous part alone or in combination. triangle of bone with the ligamental
The causative factors are broadly classified into attachments, and is then merged with
congenital, traumatic and iatrogenic. Nasal dor- the medial osteotomy by curving it
sum deformities correction is possible with both anteriorly (high).
endonasal and external approaches. The choice (ii) Low-low-high technique—Taking
of approach is based on the deformity and the the nasofacial groove as the refer-
surgeon’s preference. The first surgical step to ence, the lateral osteotomy is started
correct the hump is the separation of upper lateral in the nasofacial groove and contin-
cartilage from septum after exposure. Septum ued upward (low-low) to merge with
proper is reduced in incremental fashion follow the medial osteotomy by curving it
by bony hump correction and final modification anteriorly (high). The problem with
is performed by grafting, suturing or by osteoto- this type of osteotomy is the collapse
mies alone or in combination. In saddle nose, the of the internal nasal valve due to the
nasal dorsum is under-projected so grafts are lack of preservation of the suspen-
needed to augment it. Various grafts and materi- sory ligament attachment triangle of
als are used to augment saddle nose deformity. bone.
Twisted, c and s shaped nasal dorsum require (iii)
Low-low-low technique—It is
osteotomies to correct deformity [12]. Following started in the nasofacial groove and
osteotomies, the nasal dorsum can be narrowed extended upwards till the medial
or broadened and straightened. Osteotomies are canthus where it is joined to the
extended from the piriform aperture upwards into transverse osteotomy [13].
the nasal process of the frontal bone (Fig. 2.14). A small triangle of bone at the
They can be done either with linear or percutane- piriform aperture is left intact to pre-
ous techniques using osteotomes. There are many serve the lateral attachments of the
types of osteotomies including lateral, medial, suspensory ligaments. The bony cut
transverse and intermediate. Materials for the is extended along the nasofacial
reconstruction of the nose can be autologous, groove till the medial canthus where
homologous or allografts. In this section, we are it can be joined with transverse oste-
discussing osteotomies, post-operative manage- otomy. Alternatively, it can be curved
ment, grafting materials and commonly used anteriorly from the level of inferior
grafts. orbital margin to meet medial oste-
otomy. It is important to stay close to leading to nasal obstruction. A rare but

the maxilla while making the bony dreaded complication might be CSF leak if
cut, otherwise it can lead to a step the osteotomy extends too far superiorly.
deformity. If it is carried higher into 3. Transverse Osteotomy—Small cutaneous
the thicker bone of the naso-frontal puncture is created with a 2-mm osteotome
suture a rocker deformity may result. midway between the nasal dorsum and the
(b) Percutaneous—it is also called perforat- medial canthal region. Care should be taken to
ing technique, as serial perforations are remain below the naso-frontal suture line, oth-
made along the route of osteotomy, erwise it may cause injury to the cribriform
through percutaneous stab incisions at plate, leading to CSF leak.
nasofacial junction. Then the osteotomy 4 . Intermediate Osteotomy—This type of oste-
is completed using digital pressure over otomy is done in only select cases. When
nasal bone. This technique preserves the done, it should be done as the first osteotomy,
bridges of the periosteum, which prevent as it is not possible to perform intermediate
inward fall of the fractured fragment and osteotomy in a free nasal bone. It can also be
prevent nasal collapse. This is the pre- done by endonasal or percutaneous route. For
ferred technique in revision surgeries and endonasal route, intercartilaginous incision is
difficult cases. made.
Complications-osteotomies are associ- Indications
ated with the risk of inadvertent injury to (a) To narrow the extremely wide nose that
the surrounding structures like the eye- has a good height (bilateral osteotomy).
ball, medial canthal ligament. There can (b) To correct the deviated nose with one
be bleeding from small arteries, but it is sidewall much longer than the other.
rare. Improper technique may lead to step (c)
To straighten a markedly convex nasal
deformity or rocker deformity as bone.
explained above. There may be residual
scar or keloid formation in the percutane-
ous technique. 2.3.1 Post-Operative Management
2. Medial Osteotomy—It is done to mobilize
the lateral nasal wall (along with lateral oste- Systemic review proposed use of intraoperative
otomy) [14]. It naturally occurs after hump hypotensive anaesthesia, steroid, head end eleva-
removal. After medial osteotomy, upper lat- tion can reduce post-operative pain and edema
eral cartilage moves along with the lateral significantly [15]. Direct lateral nasal compres-
nasal wall, owing to its fixed attachment to sion for 5 min reduces post-operative edema sig-
the inner surface of the nasal wall. So care nificantly. Other post-operative management are
should be taken while narrowing the nasal
dorsum, as it can lead to internal nasal valve (a) Nasal packing—It is done to stop bleeding,
collapse. adhesion, septal hematoma formation (if sep-
Technique—It is done between the nasal toplasty is concurrently done), but few arti-
bone and septum, from the inferior piriform cles contradict the above statement [16, 17].
aperture margin to meet transverse/lateral It also stabilizes nasal bones from internal
osteotomy superiorly at the level of the medial collapse. This should not be too tight and it
canthus. can be removed after 24–48 h.
Complications—There can be injury to the (b) Steri-strips and external nasal splint—
upper lateral cartilages, which may lead to Steri-strips are applied to prevent or decrease
inverted V deformity. There may be irregular post-operative edema by its compressive
surface after hump removal. Medial osteot- effect and it also helps in psychological moti-
omy can cause internal nasal valve collapse, vation with partially visible post-operative
appearance. External nasal splint protects the characteristics like non-immunogenic, non-
loose nasal bone fragments from external carcinogenic, no foreign body reaction, not inter-
pressure [18]. fering with healing, must match the surrounding
(c) Cold application—Post-operative pain, tissue, non-absorbable, available in adequate
edema and ecchymosis are common after quantity, easy to manipulate into the desired
surgery. This can be minimized with the cold shape, low cost. Grafts can be autologous, homol-
application as it reduces inflammation and ogous or xenologous/semi-synthetic. It can be
metabolism by induced vasoconstriction. It porous or non-porous. Porous material with pore
also increases than pain threshold and size of 10–50 μm cannot be penetrated by macro-
reduces nerve impulse but Meta-analysis phages, thus it is more prone to bacterial infec-
failed to show a statically significant tion. If the pore size is more than macrophage
difference. penetration and tissue in growth is good, there-
(d) Medications—Pain is the main post- fore less chances of infection. Materials with par-
operative complaint and it generally lasts ticle size between 20 and 60 μm have least
for a few days at a mild to a moderate level chances of shredding of particles, which can be
after rhinoplasty. It is more with a costal phagocytosed by macrophages and may lead to
cartilage graft where it can last from weeks chronic inflammatory reactions [19].
to a month. Muscle sparing technique and Autografts—They can be cartilaginous or
preservation of the inner laminar arch bony. Cartilage gives better matching with sur-
reduces the need for analgesics. Long- rounding structure as it is soft and easy to reshape.
standing local anaesthetic should be applied Cartilage is very close to the ideal graft defini-
at the donor site to block intercostals nerves. tion. It can be harvested from nasal septum, con-
Post-operative antibiotics may require till chal or costal cartilage. Small deficit is managed
the nasal pack removed. by septal and conchal cartilage graft whereas
(e) Head end elevation—It is to prevent/ large deficit is managed by costal cartilages.
decrease post-op edema. It should be done in Right side costal cartilage graft is preferred over
the initial post-operative period. left to prevent injury to pericardium and post-
(f) Donor site management for costal carti- operative misunderstanding of donor site pain
lage graft—The dead space should be oblit- from angina. The graft is generally harvested
erated completely and dressing should be in from middle (sixth–eighth) ribs and sixth costal
place for the next 3 days to prevent post- cartilage shows more similarity with nasal dor-
operative hematoma formation. X-ray chest sum in term of depth and width. Conchal and sep-
is recommended on the first post-operative tal cartilage graft harvesting is associated with no
day to look for pneumothorax. or minimal morbidity. Pain, scar, risk of pneumo-
(g) Follow up—Regular follow up should be thorax and relatively prolong surgery time with
done to ensure proper healing and post-op hospital stay are the morbidities associated with
changes. costal cartilage graft. Costal cartilage has more
(h) Photography—Post-op photography should warping and reabsorption chances than other car-
be done in similar background and angles for tilage grafts. Warping can be minimized by com-
proper post-operative comparison. plete removal of perichondrium and by delaying
the insertion of graft by 30 min. Bone on other
hand gives a hard un-natural feel in rhinoplasty
2.3.2 Materials for Reconstruction and it can be harvest from iliac crest, ribs or split
in Rhinoplasty calvarium. Moreover, it has more donor site mor-
bidity, difficult fabrication of dorsal L strut and it
There has been a long search for the ideal recon- appear as more rigid, abnormal at the reconstruc-
struction material for rhinoplasty, but it is yet to tion site. Absorption rate of split calvarium is less
be found. An ideal material should have some than iliac crest bone. Post auricular fibro-
connective tissue and mastoid fascia graft are of connective tissue which increases the
used to correct minute residual deformities. Soft acceptability of implant at donor site. It is
tissue graft is also useful to correct soft tissue more user-friendly material with less extru-
loss [20, 21]. sion rate but the cost is high.
Homografts—Usually not used because of • Hydroxyapatite material is resembled more
fear of transmission of slow viruses. Irradiated with human bones. Its graft form coarse,
homologous costal cartilage is used in literature highly fragile, poor moldable feature whereas
and it has no chance of virus transmission with granular form is more user-friendly with good
excellent tolerance to tissue and infection. It take-up rate.
reduces the operative time, need for auto graft • Proplast and Teflon—it produces significant
but it stability of graft is questionable. In some inflammatory reaction. It is not in use because
series, it is around 70–100%. Acellular allo- of its high collapsibility and fragmentation
genic cadaveric dermis (alloderm) is used to rate with shearing power.
augment tapered soft tissue encase but it has • Supramid is the polyamide mesh and it is not
high absorption rate [20–22]. in use because of high chances of graft
Alloplastic materials—the most accepted absorption.
indication for alloplastic material is lack of suf- • Polyethylene tetraphthalate mesh is easy mold-
ficient autograft. It is applicable at stationary ana- able and stable graft material. It is less in use
tomical areas such as nasal dorsum as extrusion due to high infection and graft failure rates.
chances high at the mobile area. Scarred, thin
scaffold with under-tension allograft has got high Commonly used terminology for grafting
chances of extrusion. materials is listed below.
• Gortex—Polytetrafluoroethylene (PTFE) is • Spreader graft—Autologous cartilage is

being marketed under the trade name of gor- placed between the nasal septum and upper
tex. It has good tissue compatibility, the feel of lateral cartilage. Dimensions can vary from
soft tissue and is supplied in sheets of different patient to patient. Commonly used dimen-
thickness that can be custom cut and layered. sions are length 10–15 mm, height approx.
The material can be re-sterilized if not used. 2 mm and width 1–2 mm. It is used commonly
There is little foreign body reaction or rejec- to increase the valve area. It can also be used
tion, it is not prone to migration and the infec- as a stent for correcting mid-third C shaped
tion rate is low. It appears that Gortex is deformity of cartilage, by placing it only on
becoming the synthetic implant of choice for the concave side of septum.
the nasal dorsum [8]. • Batten graft—A small piece of cartilage is
• Silastic—It is firm, slippery, non-porous and placed in the lateral nasal wall, just superior to
easily sculptural. Medical-grade silicon is the posterior part of lower lateral cartilage. It
called silastic. It has been used extensively in is used to provide strength to collapsible nasal
the past. It is non-immunogenic, does not ala.
react with the tissue. Its stability is based on • Shield graft—It is used to increase tip projec-
the formation of peri-implant capsule. It is not tion, done by placing a small piece of cartilage
used commonly now because of its high extru- over the domes of lower lateral cartilage
sion rate, migration, resorption of the underly- (Fig. 2.13).
ing bone, changes colour of overlying skin, • Caudal extension graft—It is used to increase
etc. tip support and projection.
• Medpor is linear high-density polyethylene • Turkish delight—0.5–1 mm cartilage pieces
with interconnection pore size of 160–320 μm are wrapped in temporalis fascia or surgicel. It
which makes it flexible. Pore allows in growth can be moulded and digitally corrected in the
first 2–3 weeks thus it reduces the chances of 10. Adamson PA, McGraw-Wail BL, Morrow TA,

Constantinides MS. Vertical dome division in open
post-operative malposition. It has less chances rhinoplasty. Arch Otolaryngol Head Neck Surg.
of warping as graft is not compressed or 1994;120:373–80.
battered. 11. Momeni A, Gruber RP. Primary open rhinoplasty.

Aesthet Surg J. 2016;36(9):983–92.
12.
Bloom J, Immerman S, Constantinides
M. Osteotomies in the crooked nose. Facial Plast
References Surg. 2011;27(05):456–66.
13. Cerkes N. The crooked nose: principles of treatment.
1. Suhk J, Park J, Nguyen AH. Nasal analysis and Aesthet Surg J. 2011;31(2):241–57.
anatomy: anthropometric proportional assessment in 14. Lykoudis EG, Peristeri DV, Lykoudis GE, Oikonomou
Asians-aesthetic balance from forehead to chin, part GA. Medial osteoectomy as a routine procedure in
I. Semin Plast Surg. 2015;29(4):219–25. rhinoplasty: six-year experience with an innovative
2. Farkas LG, Katic MJ, Forrest CR, et al. International technique. Aesthet Plast Surg. 2018;42(1):256–63.
anthropometric study of facial morphology in 15. Adrian AO, Zachary F, Andrew RK, et al. Interventions
various ethnic groups/races. J Craniofac Surg. to decrease postoperative edema and ecchymosis after
2005;16(4):615–46. rhinoplasty: a systematic review of the literature.
3. Pawar SS, Garcia GJM, Rhee JS. Advances in tech- Plastic Reconstr Surg. 2016;137(5):1448–62.
nology for functional rhinoplasty. Facial Plast Surg 16. Repanos C, McDonald SE, Sadr AH. A survey of
Clin. 2017;25(2):263–70. postoperative nasal packing among UK ENT sur-
4. Tardy ME Jr, dayan S, Hecht D. Preoperative rhi- geons. Eur Arch Otorhinolaryngol. 2009;266:1575–7.
noplasty: evaluation and analysis. Otolaryngol Clin 17. Lee HS, Yoon HY, Kim IH, et al. The effectiveness
North Am. 2002;35(1):1–27. of postoperative intervention in patients after rhino-
5. Kalantar-Hormozi A, Beiraghi-Toosi A. Smile plasty: a meta-analysis. Eur Arch Otorhinolaryngol.
analysis in rhinoplasty: a randomized study for 2017;274:2685–94.
comparing resection and transposition of the 18. Farahvash MR, Khorasani G, Mahdiani Y, Taheri

depressor septi nasi muscle. Plast Reconstr Surg. AR. The effect of steri-strip dressing on patients’ sat-
2014;133(2):261–8. isfaction and reduction of ecchymosis in lower eyelid,
6. Swamy RS, Sykes JM, Most SP. Principles of photog- malar and cheek following rhinoplasty. World J Plast
raphy in rhinoplasty for the digital photographer. Clin Surg. 2016;5:51–7.
Plast Surg. 2010;37(2):213–21. 19. Gendeh BS, Mallina S. Graft selection in rino-

7. Stearns M. The nasal tip and nasolabial angle. In: plasty: indications and limitations. Med J Malaysia.
Gleeson M, editor. Scott Brown’s otorhinolaryngol- 2008;63(1):35–8.
ogy, head and neck surgery, vol. 3. 7th ed. London: 20. Cingi C, Bayar Muluk N, Winkler A, Thomas JR. Nasal
Hodder Arnold; 2008. p. 2995–3005. tip grafts. J Craniofac Surg. 2018;29(7):1914–21.
8. Rethi A. Raccourcissement du nez trop long. Revue 21. Dresner HS, Hilger PA. An overview of nasal dorsal
Chirurgerie Plastique. 1934;2:85. augmentation. Semin Plast Surg. 2008;22(2):65–73.
9. Cingi C, et al. Nasal tip sutures: tech- 22. Murakami CS, Cook TA, Guida R. Nasal reconstruc-
niques and indications. Am J Rhinol Allergy. tion with articulated irradiated rib cartilage. Arch
2015;29(6):205–2011. Otolaryngol Head Neck Surg. 1991;117(3):327–30.
Nasal Physiology and Sinusitis
3
K. Davraj, Mayank Yadav, Preetam Chappity,
Prity Sharma, Mohnish Grover, Shitanshu Sharma,
Tanmaya Kataria, Kranti Bhawna, Anand Pendakur,
Gurbax Singh, David Victor Kumar Irugu,
Anoop Singh, and Nitin Gupta
Contents
3.1 Part A: Physiology of Nose and Paranasal Sinuses 50
3.1.2 Nasal Secretions and Mucociliary Drainage 51
3.1.3 Nasal Breathing 52
3.2 Part B: Olfactory Nerve and Olfactory Dysfunctions 54
3.2.1 natomy of Olfactory Nerve
A 54
3.2.2 Blood Supply of Olfactory Nerve 56
3.2.3 Smell Disorders 56
3.2.4 Management of Smell Disorders 56
3.2.5 Bioelectronic Nose 57
3.2.6 Applications of Bioelectronic Nose 57
3.3 Part C—Acute and Chronic Rhinosinusitis 58
3.3.1 ummary
S 58
3.3.2 Introduction 58
3.3.3 Pathophysiology 58
3.3.4 Diagnostic Work Up 59
3.3.5 Radiological Staging 60
3.3.6 Differential Diagnosis 61
3.3.8 Treatment 62
3.3.9 Surgery 62
K. Davraj
A. Pendakur
ENT, KMC, Manipal, Karnataka, India
Allergy Asthma ENT Clinic,
M. Yadav Bangalore, Karnataka, India
ENT, SHKM GMC, Nalhar, Nuh, Haryana, India
G. Singh
P. Chappity · P. Sharma ENT, GGS Medical College and Hospital,
ENT, AIIMS, Bhubaneswar, Odisha, India Faridkot, Punjab, India
M. Grover · S. Sharma · T. Kataria D. V. K. Irugu (*) · A. Singh
ENT, SMS Medical College, ENT, AIIMS, New Delhi, India
Jaipur, Rajasthan, India e-mail: irugudavid72kumar@rediffmail.com
K. Bhawna N. Gupta
ENT, AIIMS, Patna, Bihar, India ENT, GMCH, Chandigarh, India
50 K. Davraj et al.
3.4 Part D: Frontal Sinusitis 62

3.4.1 ummary
S 62
3.4.4 Preoperative Workup 63
3.5 Part E: Complications of Sinusitis 67
3.5.1 ummary
S 67
3.5.3 Conclusion 71
3.6 Part F: Allergic Rhinitis 72
3.6.2 Clinical Manifestations and Differential Diagnosis 73
3.6.3 Cascading Inflammation of AR Causing Complications and Comorbidities 74
3.6.4 Management of AR: Therapeutic Options 76
3.6.5 Leukotriene Receptor Antagonists 78
3.6.6 Difficult-to-Treat AR 81
3.6.7 Allergen Immunotherapy (AIT) 82
3.6.8 Allergens and Non-Allergic Triggers 85
3.6.9 SLIT as Food Allergen Immunotherapy 85
3.6.10 Allergen Avoidance, Complimentary Lifestyle, and Prevention 85
3.7 Part G: Vasomotor Rhinitis 87
3.7.2 Pathogenesis 87
3.7.3 Clinical Features 87
3.7.4 Diagnosis 87
3.7.5 Treatment 88
3.8 art H: Non-Invasive Fungal Sinusitis
P 91
3.9 Part I: Invasive Fungal Sinusitis 94
3.9.1 linical Presentations
C 95
3.9.2 Diagnosis 95
3.9.3 Imaging 96
3.9.4 Pathology 96
3.9.5 Treatment 97
3.9.6 Outcome and Follow-Up 97
References 98
3.1 art A: Physiology of Nose

P ciliated epithelium, with microvilli on the sur-
and Paranasal Sinuses face. Mucus secretion produced by submucosal
seromucinous glands and mucosal goblet cells is
3.1.1 Introduction important for optimal functioning of the nose and
paranasal sinuses. Around 0.5 to 2 L of mucus is
Nose and paranasal sinuses play a significant role produced every day in an individual and coordi-
in humidifying and filtering the inspired air, as nated ciliary beat propels the mucus from each
well as contributes critically to the function of sinus in peculiar fashion to the nasal cavity and
olfaction. These functions can get affected by then to the pharynx.
many anatomical changes, physiological process, The nasal cycle is nothing but alternate con-
inflammatory conditions, and drugs. Most of the gestion and decongestion of the nasal turbinate
nasal cavity is lined by pseudostratified columnar mucosa, probably to warm and humidify the
3 Nasal Physiology and Sinusitis 51
inspired air. It can be appreciated in children as rior vestibular part having stratified squamous
young as 3 years, would be present in a majority lining with sebaceous glands and vibrissa,
of the adults, lasts around 2–4 h, and can persist while the rest of the nasal cavity except the
even after cessation of nasal airflow. In physio- olfactory region having pseudostratified
logical conditions, nasal breathing is dependent columnar ciliated epithelium, with microvilli
vastly on the nasal cycle. The objective assess- on the surface [3]. Submucosal lamina propria
ment of nasal airway and breathing can be done contains the mucosal glands and the neuro-
by tests like acoustic rhinometry, rhinosteriome- vascular tissues which are involved in pecu-
try, and rhinomanometry. The present clinical liar autonomic and inflammatory responses of
indications for these objective tests of nasal the nasal cavity.
breathing include assessment of dynamic intrana-
sal pressure changes and the site(s) of obstruction 3.1.2.2 Contents of Nasal Secretions
in obstructive sleep apnea, for choosing the Approximately 0.5–2 L of mucus is produced
appropriate patients for surgery, and for compar- every day in an individual, 95% of which is
ing the improvement in nasal breathing after sur- water, and rest of it contains peptides like glyco-
gery or medical therapy. proteins, lactoferrin, lysozyme, immunoglobu-
The nose is a physiological conduit through lins, surfactants, and antitrypsin along with
which the air is inspired and expired to the human some salts, and debris [3]. Nasal mucus consists
body, whereas the paranasal sinuses are air-filled of two layers, a continuous inner “sol” phase of
pockets in the skull, communicating with the lower viscosity surrounding the shafts of cilia;
nasal cavities. Together they are involved in and a discontinuous outer “gel” phase of higher
humidifying and warming the inspired air, filter- viscosity, which rides along the tips of the
ing the inspired air, regulation of intranasal pres- extended cilia [2, 3].
sure, increasing surface area for olfaction,
lightening the skull weight, resonance to voice, 3.1.2.3 Mucociliary Drainage Pattern
and absorbing shock during trauma preventing Around 50–200 cilia per epithelial cell, each
injury to brain and orbit. Anatomical variations of measuring 5–7 μm in length and 0.2–0.3 μm in
nose and sinuses, inflammatory diseases like rhi- diameter, clear the mucus blanket of 10–15 μm
nosinusitis, systemic diseases like diabetes [1], thickness [2], by beating in a coordinated and
drugs, and trauma can all influence these physio- rhythmic manner [3]. The average basal ciliary
logical functions. Nasal cycle is characterized by beat frequency in humans is 9–15 Hz and the
alternate nasal obstruction. It is because of resultant dynamic range of mucus velocity is
changes in venous sinusoid blood volume. It lasts about 3–25 mm/min [3]. Ciliary beat to propel
for 4–12 h. The autonomic nervous system con- the mucus is coordinated and peculiarly ori-
trols the changes. ented in the nasal cavity and each sinus as
shown in Fig. 3.1. The mucociliary flow from
the anterior sinuses is drained to posterior
3.1.2 Nasal Secretions nasopharynx passing anteriorly and inferiorly
and Mucociliary Drainage to the eustachian tube orifice, and from the
posterior sinuses to the posterior nasopharynx
Nasal secretions are important to carry out most passing posteriorly and superiorly to the eusta-
of the listed functions of the nose and are pro- chian tube orifice [3].
duced by submucosal seromucous glands and
mucosal goblet cells [2].
3.1.2.4 Tests for Mucociliary Clearance
3.1.2.1 Nasal Mucosal Lining Dysfunctional mucociliary clearance is central
The distribution of glands and epithelium var- pathology in hereditary conditions like cystic
ies at different regions of nasal cavity, ante- fibrosis and primary ciliary dyskinesia includ-
52 K. Davraj et al.
a b
Fig. 3.1 Diagrammatic representation of sinonasal eral wall to frontal ostium in medial aspect of floor) and
mucociliary clearance pattern. (a) Whorl pattern in the (b) Stellate pattern in maxillary sinus (from floor to max-
frontal sinus (from the medial wall through roof and lat- illary ostium located in superior part of medial wall)
ing Kartagener syndrome. In addition, muco- 3.1.3.1 Measurement of Nasal

ciliary clearance can get affected by commoner Breathing
inflammatory diseases like chronic rhinosi- Detailed history taking and thorough clinical
nusitis, by physiological stimuli like de-hydra- examination of the nose including diagnostic nasal
tion and hormonal changes, and by endoscopy are essential in the evaluation of nasal
pharmacological agents like anti-cholinergics breathing abnormalities. These will not only be
and antihistamines. Saccharin test is a simple helpful in identifying the possible cause for nasal
clinical test to measure mucociliary clearance, obstruction but also would enable the subjective
and in some cases, the movement of anteriorly quantification of the severity of the obstruction
placed radiolabeled dye can be detected by and thus may aid in treatment planning and prog-
serial imaging. nostication in a majority of the patients. Though
the objective assessment of nasal airway may be
necessary often in clinical practice, the utility of
3.1.3 Nasal Breathing these objective tests listed in Fig. 3.2. It is limited
to research and trials at present.
The extent and quality of nasal breathing is
physiologically dependent on multiple factors • Present clinical indications for these objective
including race, built, etc. but can also be influ- tests of nasal breathing include
enced by local anatomical variations like sep- –– To know the dynamic intranasal pressures
tal deviation, and by the local physiological changes and the site(s) of obstruction in
phenomenon in the nasal cavity like nasal obstructive sleep apnea, to aid treatment
cycle. Nasal cycle is nothing but alternate con- planning [5].
gestion and decongestion of the nasal turbi- –– For choosing the appropriate patients for
nate mucosa, probably to warm and humidify surgery, and for comparing the improvement
the inspired air. It can be appreciated in chil- in nasal breathing after surgery or medical
dren as young as 3 years, would be present in therapy [6, 7].
a majority of the adults, lasts around 2–4 h, –– To demonstrate the non-restriction of the
and can persist even after cessation of nasal nasal airway in atrophic rhinitis or func-
airflow [4]. tional cases.
OBJECTIVE ASSESSMENT OF NASAL FUNTIONS
For intransal dimensions For nasal airflow and For nasal mucosal For olfaction For ciliary function
and cross sectional area transuasal pressure blood flow
Computer tomography Nasal peak flowmeter Doopler Electro–olfactogram Saccharin test

(+/– computational fluid dynamics) (rate of airflow) velocimetry
Chemosomatosensory– Rhinoscintigraphy
Magnetic resonance imaging Nasal spirometer
evoked potentials
(volume of airflow)
Rhinostereometry Gamma scintigraphy

Rhinomanometry
(airflow and pressure)
Acoustic rhinometry
Fig. 3.2 Schematic diagram showing the objective tests for nasal functions
3.1.3.2 Important Objective Tests

of Nasal Breathing
• Test Conditions: This needs to be done in a
quiet, comfortable environment on a calm
patient who has not taken any drug or tobacco
or coffee before the test.
• Acoustic Rhinometry: Here an acoustic
click is presented to each nostril separately,
both before and after decongestion, and the
distortions in the reflected sound wave are
recorded as a computer-generated graph.
Using this, the cross-sectional areas at vari-
ous levels of the nose and the overall volume
of each nasal cavity can be estimated sepa-
rately. The first minimal cross-sectional area
(CSA1) recorded corresponds to the nasal
valve, and the CSA2 corresponds to the infe-
rior turbinate [8].
• Rhinostereometry: For studying the changes
in the nasal mucosal congestion using a micro-
scope, mainly for the demonstration of the Fig. 3.3 The clinical photograph is showing anterior rhi-
nomanometry (Courtesy—Dr. Hitesh Verma, Associate
nasal cycle and for studying the effects of
drugs on nasal blood flow.
• Rhinomanometry: It measures the transnasal
pressure and airflow characteristics simultane- opposite nostril (anterior-rhinomanometry),
ously. The transnasal pressure of one side of or at the oropharynx transorally (posterior-
nasal cavity can be measured as the difference rhinomanometry). Air can be pumped through
of pressure between the front of the nose and the nose (passive-rhinomanometry), or the
behind the nose. The posterior nasal pressure patient’s respiratory flow (active-
sensor can be kept at the posterior nose (per- rhinomanometry) can be used for measure-
nasal/postnasal-rhinomanometry), on the ments (Fig. 3.3).
54 K. Davraj et al.
3.1.3.3 References Values for Normal investigation is required for intracranial lesions.

Adults Treatment policy ranges from conservative to
The nasal volume (Vol) and the minimal cross- surgical, depending on the findings. Recent
sectional area (MCA) varies significantly between advances in bio-inspired electronics have resulted
races, and the Vol and MCA of Caucasians in the in the development of potential artificial sensory
non-decongested state are 0.69 cm2 and 4.67 cm3, systems. The first artificial olfactory system was
respectively [9]. The normal means of total nasal built by Persaud and Dodd in 1982, by using a
resistance in the non-decongested nose is around microsensor gas array based on metal-oxide
0.24 Pa/cm3/s in adult men about 0.24 Pa/cm3/s in structure. The current definition of “Electronic
adult women [10]. nose” was given by Gardner in 1988. Recently
many artificial olfactory sensors, based on bio-
materials like mammalian cells or olfactory
3.2 art B: Olfactory Nerve
P receptors have been developed to improve the
and Olfactory Dysfunctions specificity of the sensors for odorants in the elec-
tronic nose and the new concept is now referred
Olfactory nerve is the special visceral afferent to as “Bioelectronic nose.”
(SVA) nerve carrying the sense of smell or olfac-
tion. Olfaction is an ancient, evolutionarily con-
served chemosensory system. Nerves related to 3.2.1 Anatomy of Olfactory Nerve
olfaction and taste is the only sensory nerves that
lack decussation. Nerve endings are present in Olfactory nerve is the only cranial nerve that lacks
the superior part of olfactory cleft and adjacent the pre-cortical connection to the thalamus [11].
nasal mucosa. The olfactory nerve enters the Olfactory epithelium, in the postero-superior por-
brain via cribriform plate and end in the olfactory tion of each nasal cavity, consists of somas of bipo-
bulb. Olfactory tract is formed by the efferent lar olfactory neurons, six to ten million in the nasal
fiber of olfactory bulb. Olfactory tract connects mucosa (on an area of 2.5 cm2 in each nasal cavity
primarily and secondarily with several cortical [12]. These bipolar neurons are considered first
structures. Smell disorders may be caused by an order neurons in the olfactory pathway. Odoriferous
impaired nasal airway or by lesions in the olfac- particles come in contact with dendrites of these
tory system, leading to reduced or distorted smell bipolar neurons which are projecting on the olfac-
perception. Olfactory dysfunction may be the tory epithelial surface. Odorant molecules bind to
first presenting symptom of Alzheimer’s or G-protein coupled receptors on the dendrites of the
Parkinson’s disease. Drugs that can cause olfac- olfactory neurons. Basal projections of these neu-
tory and gustatory dysfunction are macrolides, rons ascend as unmyelinated axons which traverse
terbinafine, fluoroquinolones. Chemical sub- through the cribriform plate in form of small nerve
stances causing olfactory dysfunction include— bundles (Fila olfactoria), there are 15–20 such bun-
acrylates, benzene, solvents, formaldehyde, dles on each side, each forming olfactory nerves
cadmium, nickel dust. In head injury, occipital that passes through the cribriform plate surrounded
blows tend to produce more frequent and more by a meningeal covering (arachnoid). These Fila
severe olfactory damage than frontal blows olfactoria penetrate the cranial cavity, pass through
because of coup-contra-coup injury. Olfactory the subarachnoid space, immediately enter the ven-
epithelium has a great potential for regeneration tral surface of olfactory bulbs, and synapse here
due to its stem cell reservoir. Axel and Buck with second order bulbar neurons. Olfactory bulb-
received 2004 Nobel Prize in physiology or med- acts as a relay station for the impulses passing
icine for their discoveries of odorant receptors between the olfactory mucosa and upper olfactory
and the organization of the olfactory system. centers. It is bilateral and elliptical, ventro-dorsally
Nasal endoscopy is the initial investigation of oriented structure with 11–15 mm length and
choice to see nasal pathology. Radiological 4–5 mm thickness, the medial edge is convex and
the lateral edge is flat. The dorsal surface is in con- Olfactory tract- it is a 28–30 mm long, thin, tri-
tact with orbital and rectus gyri (inferior surface of angular, myelinated nervous projection with
frontal lobes), with a double layer of arachnoid approximately 5 mm thickness anteriorly which
separating them. The ventral surface of olfactory narrows down posteriorly upto 2 mm thickness. It
bulb overlies posterior 1/3 of the cribriform plate originates in the anterior cranial fossa and ends in
which is also the horizontal plate of the ethmoid the middle fossa, giving rise to olfactory trigone.
bone. It is divided medially by crista galli, which is During its course, the olfactory tract passes over
a vertical bony prominence in the anterior part of the optic nerves, which in turn pass over the oculo-
ethmoid. There are two grooves on each side of motor nerves. Olfactory tract lacks Schwann cells
crista galli, which harbor olfactory tracts and are (similar to olfactory bulb). Each olfactory tract is
known as “olfactory ethmoidal canals.” Cribriform traverse posteriorly to end into olfactory trigone
plate has 18–22 foramina on each side through which is located above the anterior clinoid pro-
which the Fila olfactoria pass into the cranial cavity cess. This olfactory trigone is basically a widening
and synapse with the olfactory bulb. The micro- of the olfactory tract that eventually becomes tri-
scopic laminar structure of the olfactory bulb con- angular, it divides and gives rise to two main olfac-
sists of seven layers. The glomerular stratum, tory striata (medial and lateral) and a small central
consisting of glomeruli of dendritic projections, is Olfactory stria, these striata eventually relay to
the second layer among the 7 layers of the olfactory higher brain regions. Primary olfactory cortex,
bulb and it contains the second-order neurons anterior olfactory nucleus, olfactory tubercle,
which synapse with fila olfactoria. This is the first amygdaloid complex are the important central cor-
relay of olfactory sensory information. The most tical structures related to olfaction (Fig. 3.4).
important second-order neurons in the olfactory Hippocampus, hypothalamus, thalamus, orbito-
pathway are Mitral cells, Tufted cells, and peri- frontal cortex, cerebellum are the secondary cen-
glomerular cells. Each glomerulus and all the neutral olfactory structures. The axons of the three
rons synapsing in it are considered the basic olfactory striata (medial, lateral, and central) are
functional unit of odor perception. The axonal pro- distributed to central olfactory areas. The interac-
jections of the Mitral and Tufted cells form bundles tions of medial olfactory stria axons are primarily
that traverse the olfactory bulb and pass dorsally, responsible for the autonomic responses associ-
merging together to form secondary olfactory pro- ated with the sense of smell, e.g., salivation in
jection or olfactory tract. response to odor of food or increased gastric juice
1.
2.
7.
3.
8. 4.
9.
5.
10.
6.
11.
Fig. 3.4 Schematic diagram of basal view of the brain stria, 5. Insular cortex, 6. Primary olfactory cortex, 7.
showing the ventral aspect of the frontal lobes with olfac- Medial olfactory stria, 8. Olfactory tubercle, 9.
tory centers and pathways. 1. Olfactory bulb, 2. Olfactory Amygdaloid complex, 10. Hippocampal formation, 11.
tract, 3. Anterior olfactory nucleus, 4. Lateral olfactory Entorhinal cortex
56 K. Davraj et al.
secretion and increased intestinal peristalsis in • Phantosmia—perception of a non-existing

response to the smell of food. The lateral olfactory odor (i.e., smell hallucination).
stria has the maximum number of fibers in the • Hyperosmia—increased olfactory acuity
olfactory tract, so it is the stria with the greatest (heightened sense of smell), usually caused by
functional transcendence. The area of the brain a lower threshold for odor.
which is specialized in the interpretation of the • Conductive smell loss—is due to impaired
olfactory sensory stimuli is the primary olfactory transport of odorant molecules to olfactory
cortex, which is located near the uncus, in the tem- epithelia.
poral lobe and it includes—The pyriform (peri- • Sensorineural smell loss—is due to
amigdaline) and prepyriform areas. impaired receptor function, processing, or
neurotransmission.
3.2.2 B
lood Supply of Olfactory 3.2.3.1 Epidemiology
Nerve The prevalence increases with age and males are
more commonly affected than females. Risk fac-
The entire course of the olfactory tract and olfac- tors are increasing age, male gender, smoking,
tory bulb is supplied by the olfactory artery which stroke, epilepsy, nasal congestion, URTIs, nasal
is either a direct branch of the anterior cerebral polyps. The most common etiology for smell loss
artery or a collateral branch of the medial fronto- is aging. Other three major etiological factors for
basal artery, which in turn is a branch of the ante- smell loss are—URTIs, sinonasal disease, and
rior cerebral artery [13]. The blood supply of head trauma (Table 3.1).
olfactory nerve also includes anterior and posterior
orbital arteries also known as anterior and poste-
rior ethmoidal arteries or accessory o lfactory arter- 3.2.4 Management of Smell
ies. Other less significant arteries are Frontopolar Disorders
artery, the recurrent artery of Heubner.
3.2.4.1 Investigations
1. Diagnostic nasal endoscopy—It is to exclude
3.2.3 Smell Disorders potential causes of conductive olfactory loss,
e.g., rhinitis, nasal polyps, tumors, etc.
• Hyposmia—partial loss of smell perception. 2. Radiological imaging—MRI is the investiga-
• Anosmia—complete loss of smell tion of choice if the nasal cavity is normal. It
perception. provides better soft tissue detail for intracra-
• Parosmia/Cacosmia/Troposmia—the dis- nial pathology. It can also detect reduced
torted perception of an existing odor, when a olfactory bulb volume in congenital smell loss
person perceives even pleasant odors to be or parosmia.
foul smelling, as similar to feces, burning, rot- 3. Olfactory tests—Olfactory tests are listed
ten, or chemical odor. below.
Table 3.1 Illustrating the etiological factor and possible causes

Aging URTI Sinonasal disease Head trauma
Presumed Functional decrement in Viral damage of Nasal obstruction caused Cribriform plate
cause quality and quantity of olfactory by hypertrophic mucosa injury and shearing
olfactory receptors; epithelium and and nasal polyps, cosal of olfactory
ossification of cribriform neurons. inflammation. filaments.
plate foramina.
Common >65 years 40–60 years 20–60 years 20–50 years
age group
(a) UPSIT (University of Pennsylvania Smell than topical steroid therapy alone, in decreasing
Identification Test)—This forced choice polyp size and improving olfaction [14]. In nasal
standardized test uses 40 microencapsu- polyposis, surgery is reserved for cases not
lated odorants which are released on responding to optimal medical therapy and can
scratching using pencil on the standard- improve olfaction even in some of the refractory
ized odor impregnated test booklets. cases. Surgical resection of olfactory neurons
Patients are asked to identify the odor may lead to olfactory reinnervation from the
from 4 choices provided for each odor. basal stem cells, leading to recovery of smell.
Hence scoring is done out of a total score
of 40.
(b) Smell diskettes test—It is a questionnaire- 3.2.5 Bioelectronic Nose
based test with illustration.
(c) Cross-Cultural Smell Identification Test Bioelectronic nose mimics the olfactory function
(CC-SIT)—It is 12 item cross-culture of the natural nose by converting chemical sig-
smell identification test and it is relatively nals into electrical signals using novel forms of
quick than UPSIT. It is prepared with transducers. In the human nose, odorants are first
familiar odorant of different countries. recognized by olfactory receptors; nearly 400
(d) Sniffin’ sticks test—It is semi-objective different olfactory receptors binds with specific
test. Olfaction is assessed by calculating odor molecules. A key challenge for mimicking
the mean of three subfactor threshold, the olfactory system is the development of
identification, and discrimination. appropriate transducers to modify odor mole-
4 . Electrophysiologic testing of olfactory disor- cules into electrical signals. Advancements in
ders usually includes the recording of olfac- nanomaterials, such as CNTs, grapheme, and
tory event-related potentials. In response to conducting polymers, have enabled hybridiza-
odorant induced stimulation, the olfactory tion of olfactory receptors via nanoelectronics
receptor neurons oscillate and the slow nega- interface formation. The bioelectronic nose con-
tive DC voltage changes recorded from the sists of primary perception elements and second-
olfactory mucosa are termed ary transducers and amplifiers, inspired by
Electrolfactograms (EOGs) and are regarded biological chemoreceptors and nerve systems.
as compound receptor potentials of olfactory So combining biological receptors with novel
receptor neurons in the olfactory epithelium. forms of transducers, such as microelectrode
This diagnostic tool presents the final method arrays (MEAs), electrochemical and optical
to confirm anosmia, but it is more used for devices, and nanomaterial-based field effect
research purposes. transistors (FETs) effectively convert external
chemical signals into electrical signals. Optical
3.2.4.2 Treatment Options transduction techniques, including fluorescence
It depends upon the etiological factors; lifestyle and calcium imaging, offer accurate and objec-
modifications are breathing exercise and regular tive cue of smells with visualized binding pat-
nasal douches, etc. Oral steroids may help in terns. Combined with electronic sensors, such
regaining of smell in idiopathic cases. Counseling optical transduction methods can improve the
is necessary in cases of parosmia and phantos- performance of the bioelectronic nose.
mia. Psychiatric or neurological treatment (e.g.,
antidepressants or antiepileptic drugs) may be
required in some patients. In cases of chronic rhi- 3.2.6 Applications
nosinusitis with nasal polyposis, the highest level of Bioelectronic Nose
of evidence exists in support of use of glucocorti-
coids. Initial oral steroid therapy followed by 1. In medical diagnosis: By detecting Volatile
topical steroid therapy seems to be more effective organic compounds (VOCs) released from the
58 K. Davraj et al.
body during infections, intoxication, meta- conservative management and cases with
bolic diseases, or cancers [15]. complications.
2. In food quality control: It is quick and accu-
rate method to detect microbial spoilage of
food materials [16]. It is also useful to monitor 3.3.2 Introduction
the maturity of fruits so that fruits can be har-
vested at the best possible time and for the Rhinosinusitis is by far the most common para-
determination of quality and identity of nasal sinus disease. As the name suggests, it is
cheese. the inflammation of the nasal and sinus mucosa.
3 . In environmental monitoring: The bioelec- Acute rhinosinusitis (ARS) prevalence rates
tronic nose provides cheap, improved, and vary from 6 to 15% with a prevalence of recur-
reliable method for rapid, accurate detection rent ARS estimated at 0.035% [17] Chronic rhi-
and quantification of environmental chemical nosinusitis (CRS) represents a significant
pollutants. disease burden worldwide, affecting at least
4 . In smell visualization: It is based on the bio- 11% of the population which creates substantial
electronic nose which expects to enable anos- economic burden to healthcare systems and to
mic patients to perceive smells that have not the economy, by loss of productivity in the
been sensed before. workplace [18]. Rhinosinusitis is primarily clas-
sified based on the duration of signs and symp-
toms (Table 3.2).
3.3 art C—Acute and Chronic
P CRS is further classified into those cases with
Rhinosinusitis polyps and those without polyps based on endo-
scopic findings. A proportion of patients with
3.3.1 Summary polyps also fall into a unique subset, character-
ized by coexistent asthma and aspirin sensitivity
Rhinosinusitis is by far the most common para- known as Samter’s triad or aspirin-exacerbated
nasal sinus disease encountered by rhinologists respiratory disease (AERD) [19].
worldwide. The etiopathogenesis of acute rhi-
nosinusitis is mostly attributed to infectious eti-
ology, whereas chronic rhinosinusitis arises 3.3.3 Pathophysiology
from inflammatory processes triggered by vari-
ous agents. The diagnosis of this condition is Acute rhinosinusitis (ARS) can be viral or bacte-
given by various criteria. The European position rial, with viral etiology being the most common
paper on rhinosinusitis and nasal polyps (EPOS (>95%) [20]. Predisposing factors to ARS include
2012) defined rhinosinusitis as a diagnosis made sinus-related anatomical factors (e.g., Haller/
on clinical grounds based on the presence of
characteristic symptoms, combined with objec- Table 3.2 Rhinosinusitis is classified on the basis of
tive evidence of mucosal inflammation. duration of symptoms
Evidence-based review and EPOS 2012 have Type of
recommended against routine use of antibiotics rhinosinusitis Duration of inflammation
in rhinosinusitis. Steroid nasal sprays are the Acute Up to 4 weeks
Chronic >12 weeks
gold standard for the medical management of
Sub-acute 4–12 weeks
CRS. It decreases mucosal inflammation and
Recurrent ARS >4 episodes per year without
causes partial polyp resolution. FESS evidence of CRS
(Functional endoscopic sinus surgery) is quite Each episode lasts 7–10 days
often required for management of CRS and very Acute on CRS The inflammation never touch
occasionally in ARS, in cases not responding to baseline
infra-orbital ethmoid cells, concha bullosa), infiltration. It appears to be associated with a

allergy, smoking, poor mental health, typical T-helper 2 cell (TH2) skewed eosino-
Immunodeficiency, ciliary disorders, etc. The philic inflammation, with high interleukin (IL-
most commonly implicated viruses in ARS 5) and eosinophil cationic protein (ECP)
include rhinoviruses (50%), influenza and para- concentrations in the polyps. CRS without pol-
influenza viruses, adenovirus, respiratory syncy- yposis is characterized by fibrosis, basement
tial virus, and enterovirus [21]. If bacteria do membrane thickening, goblet cell hyperplasia,
become implicated, the organisms most com- subepithelial edema, and mononuclear cell
monly seen are S. pneumoniae (27%), H. influen- infiltration. It exhibits a T-helper 1 cell (TH1)
zae (44%), M. catarrhalis (14%) with other milieu, with increased levels of interferon-
organisms sometimes seen including S. pyogenes gamma (IFN-γ) in inflammed sinus mucosa and
and S. aureus [22]. ARS is bacterial (ABRS) if at low ECP/myeloperoxidase ratios [23].
least three of the symptoms co-exist: Diagnostic criteria: There are two most com-
monly used diagnostic criteria.
1 . Discolored discharge (unilateral Rhinosinusitis Task Force of the American
predominance) Academy of Otolaryngology–Head and Neck
2. Severe local pain (unilateral predominance) Surgery classification of rhinosinusitis (1997)
3. Fever (>38 °C) [24] (Table 3.3).
4. Elevated ESR/CRP (Erythrocyte sedimenta- Diagnosis requires the presence of either two
tion rate/C—Reactive protein) major factors, or one major and two minor fac-
5. “Double-sickening”—Deterioration of symp- tors. The European position paper on rhinosinus-
toms after the initial milder phase of illness itis and nasal polyps (EPOS 2012) defined
rhinosinusitis as a diagnosis made on clinical
Pathophysiological mechanisms relating to grounds based on the presence of characteristic
viral agents include cell invasion of the respiratory symptoms, combined with objective evidence of
epithelium leading to inflammatory changes mucosal inflammation (Table 3.4) [17].
including mechanical changes, epithelial damage, Chronic rhinosinusitis (CRS) is divided
and activation of humoral and cellular defenses. In broadly into two subtypes, with nasal polyposis
bacterial cases, this is largely a super-infection fol- (CRSwNP) and CRS without polyposis
lowing an initial viral insult where epithelial dis- (CRSsNP). Phenotype and endotype classifica-
ruption has already occurred and there has been an tion for CRS is also proposed in view of the num-
associated decrease in ciliated cells and increase in ber of subtypes of CRS.
goblet cells which eventually cause sinus ostial
obstruction. The accumulating mucus causes an
initial increase in the intra-sinus pressure followed 3.3.4 Diagnostic Work Up
quickly by negative pressure due to the lack of
ventilation. This then sets up a vicious cycle of fur- Rigid nasal endoscopy and CT scanning of the
ther congestion, mucus retention; impaired gas sinuses are at the present time the gold standard
exchange, and pH balance and largely prevents investigations for CRS (Fig. 3.5). Endoscopy
clearance of inflammatory products and debris allows the clinician to assess the nose for the
leading to an ideal medium for bacteria to flourish. presence of polyps, mucopus discharge, or mid-
The patients who do not respond to therapy might dle meatal edema. The endoscope can be also
have the pathophysiology of biofilms, superanti- used to accurately sample any mucopus for
gens, or persistent osteitis. microbiological analysis [25]. CT scanning is
Chronic Rhinosinusitis (CRS) with polypo- considered mandatory for all cases requiring sur-
sis is characterized by an intense edematous gical intervention or with complications/impend-
stroma in the sinonasal epithelium, with albu- ing complications [26]. The other tests of
min deposition, pseudocyst formation, and sub- significance are used to enumerate the cause or
epithelial/perivascular inflammatory cell exclude an differential diagnosis [27]:
60 K. Davraj et al.
Table 3.4 Clinical definition of Rhinosinusitis

Symptoms should be correlated by either
Diagnostic criteria for rhinosinusitis endoscopic and/or radiological findings
Primary symptoms (requires at least one to be present, but if both Nasal blockage/obstruction/congestion
are present it is sufficient to make the diagnosis on the basis of Nasal discharge (anterior/posterior)
symptoms)
Additional symptoms (may also be present and at least one is Facial pain/pressure
needed if only one of the primary symptoms is present) Olfactory dysfunction
Hyposmia/anosmia
Duration >10 days, <3 months = acute
>3 months = chronic
Endoscopy (any of these) Nasal polyps
Mucopurulent discharge
(middle meatus)
Edema/mucosal obstruction
in middle meatus
CT scan findings Mucosal changes within the ostiomeatal
(as well as or instead of endoscopic findings) complex and/or sinuses
1. Allergy testing—skin prick testing or IgE lev- Table 3.3 Symptoms and signs of rhinosinusitis
els (specific and total) Major symptoms/signs
2. Nasal brushings for cytology Facial pain/pressure
3. Nasal biopsy for the exclusion of neoplasia, to Facial congestion/fullness
look for granulomas/vasculitis, or to examine Nasal obstruction/blockage
Nasal discharge/purulence, discolored posterior
for evidence of eosinophilia, fungal hyphae, drainage
ciliary disorders, etc. Hyposmia/anosmia
4. Blood tests—full blood count (serum eosino- Purulence on nasal examination
philia), ANCA (Wegener’s granulomatosis), Fever (acute rhinosinusitis only)
ACE (sarcoidosis) Minor symptoms/signs
5. Olfactory testing: Psychophysical (threshold Headache
(quantitative) and discrimination/identifica- Fever (nonacute rhinosinusitis)
tion (qualitative)), Olfactory event-related Halitosis
Fatigue
potentials (OERPs) (objective)
Dental pain
6. Physiological testing
Cough
(a) Peak inspiratory nasal flow Ear pain/pressure/fullness
(b) Rhinomanometry
(c) Acoustic rhinometry
(d) Mucociliary clearance (saccharin test)
7. Ciliary function testing is a widely used method for documentation and
(a) Ciliary beat frequency comparison (Table 3.5).
(b) Ciliary beat pattern analysis For each sinus, score 0 means no opacifica-
(c) Electron microscopy tion, score 1 means partial and 2 means complete
opacification whereas for ostiomeatal complex,
the score is either 0 (not obstructed) or 2
3.3.5 Radiological Staging (obstructed). Each side is graded separately. A
combined score of up to 24 is possible. In case of
The common staging used for scoring of radio- an aplastic or absent frontal sinus, a score of 0 is
logical findings is Lund-Mackay score [28]. This awarded.
Fig. 3.5 CT scan depicting CRS involving soft tissue

density in the bilateral maxillary sinus Fig. 3.6 The presence of fungal Muck with allergic mucin
in the sinus differentiates CRS from allergic fungal rhinosi-
nusitis which is an important differential diagnosis
Table 3.5 Lund-Mackay score
Score:
• 0 (no abnormality)
• 1 (partial opacification) or
• 2 (complete opacification)
3.3.6 Differential Diagnosis
Rhinosinusitis needs to be evaluated closely as

many other conditions mimic rhinosinusitis.
Appropriate history, endoscopy, and radiologi-
cal evaluation are useful to rule out other dif-
ferential diagnosis. Common diseases like
fungal rhinosinusitis, benign nasal, and para-
nasal tumors, intermediate grade tumors like Fig. 3.7 The figure is showing left side preseptal celluli-
inverted papilloma, and malignancy need to be tis secondary to sinusitis (Courtesy—Dr. Hitesh Verma,
ruled out in cases not responding to treatment Associate Professor, AIIMS, New Delhi, India)
(Fig. 3.6).
and thus needs early drainage and debridement.
Ethmoid sinusitis can lead to orbital cellulitis and
3.3.7 Complications sphenoid sinusitis can lead to cavernous sinus
thrombosis. Hematogenous spread can lead to
Acute rhinosinusitis can cause complications due brain abscess, meningitis, and toxic shock syn-
to local spread, like the erosion of lamina papyra- drome. CRS is usually associated with mucocele
cea or through preformed foramina’s (Fig. 3.7). or pyocele formation and in case of acute exacer-
Pott’s puffy tumor or frontal subperiosteal bation can lead to different varieties of acute
abscess can lead to intracranial complications complications.
62 K. Davraj et al.
3.3.8 Treatment risk of systemic side effects. As allergy can be asso-

ciated, anti-histaminics and lifestyle modification
3.3.8.1 Antibiotics plays a major role in minimizing the predisposing
As most cases are viral in origin, antibiotics are inflammation and recurrence of symptoms.
usually not required. Only superadded bacterial
infection dictates the use of antibiotics. Due to
the varied bacterial infection in ARS and CRS, 3.3.9 Surgery
the antibiotic cover is different from CRS requir-
ing long-term antibiotics. Ideally treatment FESS (Functional endoscopic sinus surgery) is
should be culture directed and re-evaluation is quite often required for management of CRS and
required for a possibility of change in antibiotics very occasionally in ARS. The role of surgery is to
if there is no response to treatment within 72 h. clear the sinus opening of any obstruction and
allow the delivery of medications. Utmost care is
3.3.8.2 Nasal Sprays and Irrigation taken to preserve the normal ciliated columnar epi-
Steroid nasal sprays are the gold standard for thelium. The surgery is usually indicated in cases
the medical management of CRS [29]. It not responding to long-term medical management
decreases mucosal inflammation and causes or in cases of impending complication [32].
partial polyp resolution. Saline and hypertonic
saline nasal irrigation keeps the mucosa moist,
improves naso-ciliary clearance, and prevents 3.4 Part D: Frontal Sinusitis
crust formation [30].
3.4.1 Summary
3.3.8.3 Oral Steroids
and Anti-Histaminics The frontal sinus is one of the most complex para-
The oral steroid is immensely effective in reducing nasal sinuses. The frontal sinus is paired sinus and is
inflammation and sometimes leads to near com- separated by an intersinus septum that can vary
plete resolution of polyposis (Fig. 3.8) [31]. In in location. The frontal sinus outflow tract (FSOT)
comparison to nasal steroid spray, it runs a higher is described as an hourglass. Management of frontal
Fig. 3.8 Pansinusitis is completely resolved by oral steroid treatment (Courtesy—Dr. Hitesh Verma, Associate
sinus pathologies has evolved from open approaches age pathway. It is essential to clear the outflow
to endoscopic approaches in the past few decades. tract in case of any pathology obstructing the
The introduction of various classification systems drainage pathway without causing iatrogenic ste-
like Bent and Kuhn system, Wormald classification, nosis. Outflow tract (FSOT) is described as an
and the latest International frontal sinus anatomy hourglass. Identification of this drainage pathway
classification system for frontal cells has helped in helps in directing a surgeon to dissect in a way
the surgical management of the sinus. Surgical deci- that minimizes mucosal trauma. It appears by the
sion making with respect to the ideal approach to age of 4 years and expands in adolescence. In
the frontal sinus, can be a challenge. Hence, a thor- radiological studies, it appears by the age of
ough understanding of the available surgical tech- 8 years. It gains its maximum size by 19 years of
niques and the specific circumstances in which each age. Frontal sinus is a paired asymmetric structure
is most effective is critical. with intersinus septum that can vary in location.
Frontal recess is a three-dimensional space
(Fig. 3.9). Anteriorly, it lined by agger nasi (AN)
3.4.2 Introduction (Fig. 3.10a), frontoethmoidal cell (FEC) and the
frontal process of maxilla, frontal beak (FB), pos-
The frontal sinus is one of the most complexes of teriorly by the upward continuation of the anterior
all paranasal sinuses because of its complex drain- face of the bulla (Fig. 3.10b), laterally by lamina
papyracea (Fig. 3.10c) and medially by upper
attachment of middle turbinate (Fig. 3.10d).
FL
FS 3.4.3 Pathophysiology
Mucociliary transport in the frontal sinus is an

active inwardly directed one. Secretions climb
along the intersinus septum, then pass along the
FB
roof and then along the floor drain out in
FSOT. All of the secretions is not drained out of
FEC
the ostium at once and some of it recirculate back
BE into the sinus for another trip. This results in
AN
whorl like mucociliary clearance from the sinus.
MT
3.4.4 Preoperative Workup

Fig. 3.9 The figure is showing the relationship of the
frontal sinus and frontal recess with the surrounding Non-Contrast Computed Tomography scan is the
structure major backbone of the diagnostic workup.
a b c d
Fig. 3.10 The figure is showing the boundary of frontal recess

64 K. Davraj et al.
Parasagittal view helps in identifying the com- 3.4.4.1 Surgical Approaches

plex cells within the frontal sinus and the outflow The conservative management of acute frontal
tract. Structures to look for sinusitis is documented in the previous part.
Factors which should be considered while deal-
1. Uncinate process—the site of its superior
ing with frontal sinus pathology are listed in
attachment impacts on the drainage of frontal Table 3.7.
sinus. Draf classified frontal sinus surgery into four
2. Frontal cells—they are present in 20% of
types [35]:
patients. Bent and Kuhn divided these into
four types [33]: 1. Draf I—Anterior ethmoidectomy, including

(a) Type I—single cell above agger nasi the frontal recess but sparing the frontal sinus
(b) Type II—Multiple cells above agger nasi infundibulum and ostia.
(c) Type III—Cell extends into frontal sinus 2.
Draf IIa—Anterior ethmoidectomy +
(d) Type IV—Isolated frontal cell Resection of frontal sinus floor from lamina
papyracea laterally to middle turbinate
Recently PJ Wormald proposed International medially.
Frontal Sinus Anatomy Classification [34] 3.
Draf IIb—Anterior ethmoidectomy +
(Table 3.6). Removal of frontal sinus floor from lamina
Magnetic resonance imaging (MRI) is indi- papyracea laterally to nasal deptum.
cated in doubtful diagnosis as it provides better 4. Draf III (Endoscopic Modified Lothrop

soft tissue detail. Tumors show enhancement in Procedure)—resection of the anterior superior
T1 sequence with contrast while fluids do not. aspect of the nasal septum as well as the infe-
Mucus and secretions enhance on T2 weighted rior portion of the frontal intersinus septum in
scans and it is particularly useful for predicting addition to bilateral type IIb procedures.
dural involvement: Recently, International classification of f rontal
Table 3.6 International frontal sinus anatomy classification

Cell type Cell name Definition
Anterior cells Agger nasi cell Cell that sits either anterior to the origin of the middle turbinate or sits
(push the drainage directly above the most anterior insertion of the middle turbinate into
pathway of the the lateral nasal wall.
frontal sinus Supra agger cell Anterior-lateral ethmoidal cell, located above the agger nasi cell (not
medial, posterior, pneumatizing into the frontal sinus).
or Supra agger frontal Anterior-lateral ethmoidal cell that extends into the frontal sinus. A
posteromedially) cell small SAFC will only extend into the floor of the frontal sinus, whereas
a large SAFC may extend significantly into the frontal sinus and may
even reach the roof of the frontal sinus.
Posterior cells Supra-bulla cell Cell above the bulla ethmoidalis that does not enter the frontal sinus
(push the drainage Supra-bulla frontal Cell that originates in the supra-bulla region and pneumatizes along the
pathway cell skull base into the posterior region of the frontal sinus. The skull base
anteriorly) forms the posterior wall of the cell.
Supraorbital An anterior ethmoid cell that pneumatizes around, anterior to, or posterior
ethmoid cell to the anterior ethmoidal artery over the roof of the orbit. It often forms
part of the posterior wall of an extensively pneumatized frontal sinus and
may only be separated from the frontal sinus by a bony septation.
Medial cells (push Frontal septal cell Medially based cell of the anterior ethmoid or the inferior frontal sinus,
the drainage attached to or located in the interfrontal sinus septum, associated with
pathway laterally) the medial aspect of the frontal sinus outflow tract, pushing the drainage
pathway laterally and frequently posteriorly.
Table 3.7 The factors related to patient, anatomy, and pathology of frontal sinus are listed in the consideration column.
The surgical plan is listed in the surgical options column
Considerations Surgical options
Patient 1. Limited disease Simple FESS with minimal manipulation
2. Compliance issues and significant comorbidities. of the frontal recess.
Asthma and aspirin sensitivity Comprehensive clearance of frontal
recess.
If recurrence see below
Anatomy Preserved landmarks, minimum previous surgery, no Draf type I procedure
complex cells
Poor landmarks, osteoneogenesis, multiple revision Draf type (modified endoscopic lothrop)
procedures, thick frontal beak, complex frontal cells
Pathology Chronic frontal sinusitis with or without polyps, No Draf type I procedure
previous surgery.
Recurrent disease, ASA with polyp, Eosinophilic mucin Draf type (modified endoscopic lothrop)
CRS, tumors, Lateral mucoceles. Recalcitrant.
Complicated frontal sinusitis with the erosion of posterior Draf type III or an osteoplastic flap
table, anterior table osteitis, lateral extending tutors approach.
Combined approach.
Table 3.8 International classification of frontal sinus surgery

No exploration No disease
Balloon sinuplasty May have a role in certain situations with limited disease.
Draf type I Removing cells within the frontal recess, following FESS
Draf type IIa and b Remove cells extending into the frontal sinus and resect bone between the
lamina papyracea and middle turbinate (a) or nasal septum (b)
Draf type III, modified endoscopic Resection of the floor of the frontal sinus, superior nasal septum, and
lothrop (MEL), frontal sinus drillout intersinus septum
Osteoplastic flap + MEL Above and below approach
Osteoplastic flap with obliteration Removal of all mucosa within the sinus and obliteration with fat
Reidel’s Procedure Removal of the anterior table of the frontal sinus
Cranialization Removal of the sinus mucosa and the posterior table.
sinus surgery is proposed on the basis of struc- sible via a MEL alone or with the aid of an
tures removed (Table 3.8) [36]. It also incor- external trephine.
porated recent modifications in treatment 3. The junction of the anterior and posterior wall
policy. in the most lateral part of the frontal sinus may
be too narrow to admit a drill. Similarly,
The considerations for endoscopic manage- supraorbital ethmoid cells may limit lateral
ment of frontal sinus tumors are: access for tumor removal.
4. In general, tumors arising from the anterior
1. Lesions not extending beyond a sagittal plane wall of the frontal sinus are difficult to access
through the lamina papyracea are accessible endoscopically. Those arising low down may
endoscopically. Lesions extending beyond be accessible via a MEL.
this may be accessible depending on the 5. A narrow anterior-posterior dimension of the
anterior-posterior dimension of the floor of floor of the frontal sinus (<10 mm) can limit
the frontal sinus and the intercanthal endoscopic access and favor open or com-
distance. bined approaches.
2. Tumors arising from the medial quarter of the 6. Superior reach within the sinus may not be
orbital plate of the frontal sinus may be acces- possible in well-pneumatized sinuses.
66 K. Davraj et al.
between nasion and medial canthus. Periosteum

is incised and elevated and medial canthal liga-
ment detached and tagged. The lacrimal sac is
lifted up from the fossa. Frontoethmoidal suture
line is exposed and anterior ethmoidal artery is
identified and ligated. Artery forms the superior
limit of dissection. Bone of lacrimal fossa and
lamina papyracea is perforated as per the
requirement for ethmoidectomy. Frontal sinus
is accessible by removal of the floor and ante-
rior wall of the frontal sinus.
Indications are:
(a) Chronic frontal sinusitis
(b) Drainage of orbital abscess
(c) Drainage of orbital hematoma
(d)
Orbital decompression of endocrine
Fig. 3.11 Red lines are dividing the frontal sinus into
three parts exophthalmos
(e) Removal of tumor from frontal and eth-
moid sinuses
7. Lesions originating in the lower third of the
posterior wall of the frontal sinus are usually Complications
accessible via an endoscopic approach (a) Injury to the lacrimal sac
(Fig. 3.11). (b) Orbital hematomas
(c) Closure of the nasofrontal duct by pro-
3.4.4.2 Open Approaches lapsed of orbital fat, or by fibrosis and
1. Frontal sinus trephination is performed by the osteoneogenesis
creation of window in anterior wall. It starts (d) Failure to reattach the medial canthal liga-
with 1–1.5 cm incision slightly anterior or at ment can result in pseudohypertelorism
the medial eyebrow. Periosteum over anterior 3.
Osteoplastic Flap with and Without
wall of frontal sinus is incised and elevated. Obliteration
Small window made using a burr at the junc- The procedure starts with the creation of accu-
tion of floor and the anterior wall of the sinus. rate template of the frontal sinus by using
Sinus is irrigated with or without drain place- 6-feet Caldwell view plain radiograph. Outline
ment. Irrigation with color dye can aid the sur- of frontal sinus is marked after the creation of
geon in detecting the sinus outflow tract flap by Gull wing incision/bi-coronal incision.
endoscopically. (Mini trephination). Periosteum is incised along the template’s
Indications are: periphery and along the intersinus septum.
(a) Acute frontal sinusitis not responding to Bone flap is elevated obliquely for easy repo-
conservative management sition postoperatively. Incision is extending
(b) Chronic frontal sinusitis till the orbital rim for the easy lift of bone.
(c) Depressed fracture of anterior wall of Pericranium can be left attached at the lower
frontal sinus part of bone flap for subsequent vascularity.
(d) Biopsy of frontal sinus lesion Interfrontal sinus septa can be easily braked
(e) As an adjuvant to endoscopic approach to by osteotome or by drill. Contents of the sinus
localize frontal sinus especially in revi- are removed. Cavity can be either obliterated
sion surgery with fat or is left unobliterated depending
2. External frontoethmoidectomy starts with c
upon the indication of surgery.
shape incision which is placed at mid point in Indications
(a) Chronic frontal sinusitis ment can lead to permanent sequalae and even
(b) Mucoceles lead to mortality.
(c) Tumors Due to the close proximity of sinuses to the orbit
(d) Fractures and the brain, management often warrants com-
(e) Correction of pneumatoceles bined efforts of ENT surgeons, Ophthalmologists,
and Neurosurgeons.
Complications:
(a) Fracture of the bone flap, accidental intra-
cranial entry 3.5.2 Introduction
(b) Paresthesia and anesthesia on forehead
(c) Postoperative mucoceles Complications of sinusitis can be both benign
Management of frontal sinus pathologies and potentially fatal. The incidence of complica-
requires a thorough understanding of the tions has come down drastically due to the timely
anatomy of the sinus and its outflow tract. use of appropriate antibiotics. Generally, compli-
Each case of frontal sinus pathology is cations of sinusitis can be divided into three cat-
unique and so requires an individualized egories [37–39]
approach for management. Though endo-
scopic approaches form the mainstay of (a) Local (Osseous) (5–10%).
frontal sinus surgery, open approaches have (b) Orbital (60–75%).
a role as an adjuvant to the endoscopic (c) Intracranial (15–20%).
approach. (d) Other rare complications of cranial nerve

palsy and optic neuropathy.
3.5 art E: Complications

P The proximity of orbit and brain to all the
of Sinusitis paranasal sinuses makes these structures prone to
develop complications.
3.5.1 Summary
(a) Local/Osseous/Benign Complications
Sinusitis under routine circumstances does not (5–10%)
cause serious problems and can be often man- These complications are usually the least
aged conservatively. Once complications arise dangerous among all and can be managed
it can take serious turn if not managed appro- without much morbidity to the patient
priately well within time. Complications can be (Table 3.9). They can range from
benign/localized around the sinuses or it can be (i) Mucocele (Fig. 3.12)
potentially serious or even fatal if it involves (ii) Pott’s puffy tumor (Frontal sinusitis
vital structures like orbit, cavernous sinus, and with acute osteomyelitis)
the intracranial compartment. Orbital compli- (iii) Facial cellulitis (Fig. 3.13)
cations are the most common and comprise (iv) Facial abscess
around 60–75% of the total whereas local osse- (b) Orbital Complications (60–75%) [40]
ous complications and intracranial complica- Orbital complications are the most common
tions account for about 5–10% and 15–20% complications of sinusitis (Table 3.10). The
respectively. The proximity of orbit and brain proximity of the eye to all the paranasal
to all the paranasal sinuses makes these struc- sinuses makes the orbit prone for infections
tures prone to develop complications. Early and serious complications associated with
stage of complications can be well managed sinusitis. The only soft tissue barrier is the
conservatively using appropriate antibiotics but periorbital septum. The superior and infe-
as severity increases, surgical management rior ophthalmic veins are valve less and
becomes the treatment of choice. Delayed treat- infection from the sinuses can spread to the
68 K. Davraj et al.
Table 3.9 It is showing local complication list, clinical features, and management
Complications Clinical features Management
Mucocele Can present as swelling in and around the eye (ethmoid and Endoscopic clearance or external
frontal mucocele) or just some pressure symptoms or approach
orbital symptoms (sphenoid mucocele)
Pott’s puffy Frontal sinusitis with acute osteomyelitis. Subperiosteal Managed by combined
tumor pus collection in the frontal sinus leads to puffy fluctuance. neurosurgical and ENT team.
• Patient presents with fever, headache, neurological
findings, periorbital/frontal swelling, nasal congestion,
and rhinorrhea.
• May be associated with other abscess like pericranial,
periorbital, epidural, subdural, and intracranial abscess if
not managed adequately.
• Fronto- cutaneous fistula as a late complication.
• CT Scan imaging modality of choice.
Facial cellulitis These complications are local complications associated Managed by aggressive antimicrobial
and abscess with acute sinusitis especially of the ethmoids and therapy followed by surgery to clear
maxillary sinusitis. the pus and open the sinuses.
Fig. 3.12 Left side frontal mucocele. The left eyeball is pushed inferomedially and radiology is correlating with clini-
cal photograph (Courtesy—Dr. Hitesh Verma, Associate Professor, AIIMS, New Delhi, India)
orbit very rapidly. They are given as

Chandler’s criteria [42]
(i) Preseptal cellulitis (Fig. 3.13)
(ii) Orbital cellulitis (Fig. 3.14)
(iii) Subperiosteal abscess (Fig. 3.15)
(iv) Orbital abscess
(v) Cavernous sinus thrombosis (Fig. 3.16)
(c) Intracranial Complications (15–20%)

[43–46]
Intracranial infection due to sinusitis occurs
either due to direct extension of infection or
through hematogenous spread. Direct exten-
sion occurs due to either sinus wall erosion or
through fracture lines or neurovascular foram- Fig. 3.13 Right side preseptal cellulitis with facial
ina. Hematogenous spread on the other hand is cellulitis
Table 3.10 It is showing the type of orbital complications, Symptomatology, and treatment
Orbital
compli
cations Symptomatology Treatment [41]
Preseptal • Eyelid edema and erythema • Immediate i.v antibiotics, warm compress, and
cellulitis • Extraocular movement intact head elevation
• Normal vision • Facilitate sinus drainage using nasal
• May have eyelid abscess decongestants, mucolytics, and saline nasal
• CT Scan: Diffuse thickness and edema of douching.
lids and conjunctiva
• Least severe, most frequent
Orbital • Post septal infection • Immediate i.v antibiotics, warm compress, and
cellulitis • Eyelid edema/erythema head elevation
• Proptosis and chemosis • Facilitate sinus drainage using nasal decongestants,
• Impaired Extra ocular movt. mucolytics, and saline nasal douching
• No discrete abscess • Surgical intervention to facilitate sinus drainage if
• Visual acuity intact symptoms worsen in 48 h.
• CT shows low attenuation adjacent to • This could be done either endoscopic or external
lamina papyracea approach
Subperi • Pus formation between periorbita and lamina • Medical and surgical management
osteal papyracea • Look for worsening of visual acuity and EOM
abscess • Displace orbital contents downward and movements
laterally • Surgical drainage by doing external
• Proptosis, chemosis, ophthalmoplegia ethmoidectomy (Lynch Operation). Remove
• Risk for residual visual sequelae lamina papyracea
• May rupture through septum and present in • Endoscopic approach for medially placed
eyelids abscesses
• CT Scan: Rim enhancing hypodensity with • Transcaruncular approach
mass effect adjacent to lamina papyracea (transconjunctival incision extend medially around
lacrimal carbuncle)
Orbital • Pus formation within orbital tissues • Drain sinuses and abscess
abscess • Severe exophthalmos and chemosis • Incise periorbita and drain the intraconal abscess
• Ophthalmoplegia • Similar approaches as with subperiosteal
• Visual impairment • Abscess (Lynch incision, Endoscopic for medial
• Risk for irreversible blindness extent)
• Can spontaneously drain through eyelid
Cavernous • Orbital pain • Condition is very serious and warrants immediate
sinus • Proptosis and chemosis attention
thrombosis • Ophthalmoplegia • I.V Antibiotics which cross blood-brain barrier in
• Symptoms in contralateral eye high doses
• Associated with sepsis and meningismus • Surgical drainage of sinuses
• Radiology: Poor venous enhancement on • Mortality can be as high as 30%
CT. Better visualized on MRI • Anticoagulant use to stop further propagation of
clot is controversial.
through the diploic skull veins or through ves- (i) Meningitis

sels in the ethmoid bone. Thrombophlebitis (ii) Epidural abscess
originating in the mucosal veins progressively (iii) Subdural abscess
involves the emissary veins of the skull, the (iv) Intracerebral abscess
dural venous sinuses, the subdural veins, and, (v) Cavernous sinus, venous sinus
finally, the cerebral veins. By this mode, the thrombosis
subdural space may be selectively infected Intracranial involvement usually presents with
without contamination of the intermediary common symptomatology of fever, headache,
structure; a subdural empyema can exist with- nausea, and vomiting, seizures, altered senso-
out evidence of extradural infection or osteo- rium, hemiparesis, visual disturbance, and
myelitis. Intracranial infections are (Table 3.11) meningismus.
70 K. Davraj et al.
Fig. 3.14 NCCT PNS orbit is showing left side orbital

cellulitis Fig. 3.15 NCCT PNS orbit is showing right side subperi-
osteal abscess (Courtesy—Dr. Hitesh Verma, Associate
Fig. 3.16 Left cavernous sinus thrombosis (chemosis with dilated fixed pupil and restriction of extraocular move-
ments) (Courtesy—Dr. Hitesh Verma, Associate Professor, AIIMS, New Delhi, India)
Table 3.11 It is showing the type of intracranial complications, clinical features, and management
Intracranial
complications Symptomatology Treatment
Meningitis • Most intracranial common complication • Initially treated with antibiotics that
• Headache penetrates blood-brain barrier
• Meningismus • Followed by surgical drainage of the
• Fever sinus
• Cranial nerve palsies
• Kernig’s and Brudzinski sign (neck rigidity)
• Usually due to involvement of sphenoid and
ethmoid sinus
Epidural • Second most common complication • Good antibiotic coverage for long
abscess • Fever, headache, nausea and vomiting, duration (may range for 4–6 weeks)
papilledema, hemiparesis, seizures • Neurosurgical intervention for drainage
• Usual sinus involved: Frontal of abscess
• CT: Crescent hypodensity • Followed by ENT intervention of frontal
sinus drainage (trephine, cranialization)
or drainage of other involved sinuses.
Subdural • Third most common complication. Condition of • Aggressive medical therapy
Abscess the patient deteriorates very rapidly leading to • Antibiotics
high mortality rates of residual neurological • Anticonvulsants
sequeal. • Hyperventilation, mannitol, steroids
• Headaches • Drain sinuses and abscess
• Fever • Medical therapy possible if <1.5 cm
• Nausea, vomiting • Craniotomy or stereotactic burr hole
• Hemiparesis • Endoscopic or external sinus drainage
• Lethargy, coma
Intracerebral • Least common complication • Aggressive medical therapy
abscess • Generally due to frontal sinus involvement • Antibiotics
followed by ethmoid and sphenoid sinus • Anticonvulsants
• Headache • Hyperventilation, mannitol, Steroids
• Altered sensorium • Drain sinuses and abscess
• Focal neurological deficit • Medical therapy possible if abscess
• Fever <2.5 cm
• Seizure, meningismus, papilledema • Excision or aspiration
• 60% chance of neurological sequeal and high • Diagnostic aspiration if <2.5 cm or
mortality (20–30%) cerebritis
• Stereotactic-guided aspiration
• Endoscopic or external sinus drainage
Venous Sinus • Retrograde thrombophlebitis from the frontal • Antibiotics, steroids, anticonvulsants
thrombosis sinus may lead to thrombosis of the superior • Anticoagulation
sagittal sinus. • Drain source of infection the sinuses
• Can be associated with other intracranial
abscesses
• MRI: Decreased cavernous carotid artery flow
void
• Mortality rate is high
3.5.3 Conclusion imal but if not addressed on time, may become

potentially fatal. If these complications worsen
Complications of sinusitis have come down dras- further immediate surgical attention using endo-
tically due to timely intervention with adequate scopic or external approach has helped reducing
antibiotics. Complications of sinusitis can be min- the mortality following these complications.
72 K. Davraj et al.
3.6 Part F: Allergic Rhinitis Chirurgical Society on 16 March 1819 “Case of a

periodical affection of the eyes and chest,” the
3.6.1 Introduction first recorded description of what he later called
“catarrhus aestivus” or summer catarrh, and
Allergy is a common disease the Indian incidence which soon became known as hay fever [47, 48].
of which is 25–30%. In some countries, the inci- IgE-mediated allergy is a very common dis-
dence is as high as 40% of the general population, ease affecting a significant component of the gen-
especially in young children. Though it can affects eral population. Children and adults in productive
person of any age, it is generally a disease of the age are the common sufferers. Irrespective of the
young. Children and adults of productive age are race and geographic distribution, the incidence of
the common sufferers. Allergy is quite secular in allergy is very high. Allergy cuts across the entire
affecting people of any race and of any geographi- system of human organism and can affect any
cal region. Women and men are both affected by organ or any tissue but it generally affects the
allergies. Barring cardiovascular diseases and dia- skin and mucous membrane of respiratory sys-
betes mellitus which are common ailments of older tem and that of the gastrointestinal system.
people, allergy is by far the commonest non-infec- Among different clinical manifestations of
tive disease especially of the young. It is IgE- allergy, allergy affecting the respiratory system is
mediated signifying that the affected person the most common ailment. Nose being the main
produces IgE class of antibodies in excess to the door to the respiratory system bears the brunt of
normal range of it. The antibodies will be specific allergic insult. In other words, allergy affecting
to the causative allergen. An individual with such a the nose or AR happens to be the most common
status is referred to be an atopic person. Allergy manifestation of allergy. Russel Settipane reports
cuts across the entire system of human organism that 42% of Americans suffer from AR. AR has
and can affect any part of the body but it generally an estimated worldwide prevalence of 10–25%
affects the skin, and the mucous membrane of and is one of the most common diseases in child-
respiratory system and gastrointestinal system. hood with a prevalence reaching up to 40% in
When it affects the skin, common clinical condi- some regions [49, 50]. In the year 2000, more
tions that manifest are Urticaria, Angioedema, and than US$ 6 billion were spent on prescription
Atopic Dermatitis. When it affects the respiratory medications for this condition [50, 51]. An esti-
system, it causes Rhinitis, Conjunctivitis, Sinusitis, mated 14.1 million visits to a physician office are
Serous Otitis Media, and Asthma. Nose being the attributed to AR in the USA each year [52].
main door to the respiratory system bears the brunt When the disease is persistent and when the
of allergic onslaught and so Allergic rhinitis is the symptoms are also of moderate or of severe
most common manifestation of atopic allergy. degree, there will be a significant impact on the
Allergic Rhinitis (AR) is the most common quality of life of the sufferer. Normal daily activi-
manifestation of atopic allergy. When the disease ties get hindered. Work and School activities are
is persistent and when the symptoms are moder- affected. Sleeplessness and tiredness result in
ate and or severe, AR causes a considerable mor- lowering of learning and cognitive functions. All
bidity in the patient, especially when the patient these may result in an embarrassing situation for
is a young child or an adult of productive age. AR a growing child.
can affect all the vital functions of the nose. AR AR is unfortunately undertreated and is
must be diagnosed clinically and specifically. ignored to a large extent causing the disease to
Patients of AR must be treated adequately to pro- cascade to neighboring tissues like conjunctiva,
vide relief of suffering, to prevent the develop- paranasal sinuses, middle ear, and then to the
ment of complications, to reduce the suffering lower airways. AR is caused by many aeroaller-
due to comorbidities and to prevent gens like tree, weed, and grass pollen; cat, dog,
poly-sensitization. house dust mite (HDM), and molds. HDM is the
John Bostock discovered AR when he pre- most common indoor allergen causing perennial
sented an interesting case to the Medical and AR [47, 53].
Symptoms of AR appear on exposure to the • Slight to moderate difficulty in hearing due to

causative allergens and triggers. Attempt must be inflammation spreading to the Eustachian tube
made to avoid exposure to the causative allergens. and sometimes into the middle ear
However, objective evidence of raised serum spe- • Heaviness in the Head due to sinuses getting
cific IgE (ssIgE) to an inhalant aeroallergen is blocked
essential before a patient spends time and money • Lack of Concentration
for extensive allergen avoidance measures. In UK • Lack of Interest in Normal Social Activity
general practice, diagnosis by history alone resulted • Mouth Breathing due to Nasal Obstruction
in false-positive identification of allergen triggers of • Anosmia due to Inflammation affecting the
32% for cat allergy, 48% for grass pollen, 75% for Olfactory Nerve Endings
HDM, 54% for tree pollen, and 27% for dog when
compared with formal allergy assessment including The complexity of symptoms could be a com-
skin prick test (SPT). There is no value in extensive bination of several of these symptoms and can
HDM avoidance or removal of a family pet if the vary differently in different cases.
sufferer is non-atopic and has no relevant allergic
sensitivities [54]. Thus, objective assessment of IgE I. Sneezing in AR is the most common symp-
sensitivity improves accuracy in identifying aller- tom. Sneezing can vary from one or two to as
genic triggers and accurate diagnosis [55]. many as hundreds in a day. There are a few
Furthermore, once ssIgE to an inhalant aller- conditions mimicking AR. Every case of
gen is detected, the test must be interpreted cor- sneezing need not be of AR. Acute infective
rectly, and the clinician must distinguish between rhinitis, which is due to rhinovirus infection,
sensitization and allergy. At least 15% of people would be of very recent origin. Accompanying
with a positive skin test do not develop symptoms symptoms of infection like fever, malaise,
on exposure to the relevant allergen, so the clini- and signs of infective inflammation of the
cal history must be consistent with skin tests to mucosa will be present. Eosinophilic non-
confirm a clinically relevant sensitivity. For exam- allergic rhinitis and Nasal mastocytosis are
ple, if a patient has year-round symptoms, severe two other conditions simulating AR but are
rhinosinusitis, and nasal polyps, an isolated posi- non-atopic. The incidence of these two con-
tive skin test to birch pollen is almost certainly ditions has not been documented in India. A
irrelevant. However, they have a high negative revision documentation of history and
predictive value, and therefore a patient with a absence of positive correlating skin prick test
negative skin prick test or no evidence of raised will assist the diagnosis of these two condi-
ssIgE is likely to be genuinely non-allergic. tions. Cytology of nasal secretions will
reveal the preponderance of eosinophils in
eosinophilic non-allergic rhinitis and of mast
3.6.2 Clinical Manifestations cells in nasal mastocytosis.
and Differential Diagnosis II. Rhinorrhea in AR can be mild to very severe
and in severe cases, it can cause general
Following are the main or primary symptoms of weakness with lack of interest in either stud-
AR: ies or at professional and social activities.
The discharge, unless complicated by an
• Sneezing infection, is thin and watery. Vasomotor
• Rhinorrhea Rhinitis (VMR) is the only other condition
• Nasal Obstruction that mimics AR and is not uncommon in
young women. In VMR, Rhinorrhea and
Following are the associated symptoms of AR: Obstruction are commonly present, and
sneezing is generally absent. Trivial stimuli
• Pruritus like spicy food, odors, changes in temperature
• Nasal Intonation and humidity, sexual arousal, defecation, etc.
74 K. Davraj et al.
may act as triggers to produce the symptoms. obstruction. Polyps can cause unilateral and
Similar symptoms may be produced in some bilateral obstruction. Sometimes they are con-
cases due to other systemic drugs like some comitantly present with AR. Ethmoid polyps are
antihypertensive and hormonal medication. commonly associated with AR. A foreign body
The absence of supportive information on and a tumor are other causes of unilateral obstruc-
nasal cytology and SPT for allergy will help tion. Bilateral obstruction may be due to Rhinitis
the diagnosis. Very rarely though, VMR may Medicamentosa, which results due to the misuse
be present concomitantly with AR when it is of locally applied alpha-adrenergic drugs. History
quite a challenge for the patient and to the of obstruction in elderly patients must make the
doctor treating the case. Cerebrospinal fluid clinician to suspect atrophic rhinitis. Examination
(CSF) rhinorrhea is a rare condition that can will reveal atrophic changes of the turbinates
be mistaken for the rhinorrhea of AR. History with crusts. These days it is not uncommon to
of trauma and injury to the skull must make encounter atrophic rhinitis among youngsters
a clinician to suspect CSF rhinorrhea. Do also, especially after surgical procedures in the
consider a congenital defect as a point of dif- nose.
ferential diagnosis in a very young child for Pruritus in AR is a common symptom. Itching
CSF rhinorrhea. of the eyes and in inner canthi with increased
III. Nasal obstruction is the third major com- tears, itching in the nose and sometimes in the
plaint in AR. A Large number of patients ears may be present. Itching of the palate is not
find it difficult to cope up with this com- uncommon and can be intense. It can be so
plaint when its severity is moderate or more intense in some patients that they try to scratch
than moderate degree. Children find it very the palatal region with a spoon attempting to
difficult to cope up with the nasal obstruc- obtain relief of itching.
tion. It is due to the swollen mucosa, which Nasal intonation is another associated symp-
is the result of the late phase of allergic tom commonly present when the obstruction is
inflammation. There is a play of chemical profound either because of allergic inflamma-
mediators during the late phase. In addition tion or when complicated by the presence of
to Histamine which is a pleiotropic media- polyps.
tor, cysteinyl leukotrienes, prostaglandins
and Kinins are the other mediators that
cause the late phase. Obstruction is usually 3.6.3 C
ascading Inflammation of AR
unilateral and shifts from one side of the Causing Complications
nose to the other every 4–6 h depending on and Comorbidities
the secretory activity of the nose. In some
cases, the obstruction can become bilateral It is quite common in many cases for AR to be
and almost complete when the sufferer will concomitant with conjunctivitis. Eyes are
be in a miserable condition. If there is a mar- exposed to the airborne allergens as much as the
ginally deflected septum also, the obstruc- nose is. Anatomically the nose is better protected
tion could be more on that side of the nose. than the eyes. From another point of view, eyes
Complete nasal obstruction results in the have their lids to close and protect themselves
patient to become a mouth breather and if which the poor nose does not possess. Though
not treated early and adequately, it can affect there is a difference in their structure and their
the normal contour of a growing child’s physiology, they are neighbors to contend with.
face. They are in close proximity and they are inter-
nally connected to each other through the naso-
Unilateral obstruction can be due to a deviated lacrimal duct on either side. Tears are constantly
nasal septum. Very rarely a “S” shaped crooked produced in the eyes to irrigate and keep the eyes
deflection of the septum can cause bilateral moist.
Allergic inflammation when present, cascades clinical marker of disease severity [32]. This
between the nose and the eyes conveniently to complication of AR needs a quick and detailed
each other through the connecting nasolacrimal attention since the loss of olfaction will lead to
duct. That is how many cases of AR are cases of several obstacles in a growing child’s develop-
Allergic Rhinoconjunctivitis. ment. Loss of smell causes loss of perceiving the
Paranasal sinuses are in close proximity to the aroma of food which in turn results in loss of
nose. Mucous membrane in the nose and that in appetite and further non-secretion of saliva and
the paranasal sinuses is the same. In other words, other enzymes, leading to difficulty in digesting
there is a continuity of the same mucosa from the food. It may further result in nutritional defi-
nose into the paranasal sinuses. Secretion from ciency which will stunt the growth of the affected
the sinuses gets drained into the nasal chambers child.
through the ostium of each sinus. Even when the When allergy cascades downwards, it affects
sinuses are not inflamed with allergy, inflamma- the pharynx causing pharyngitis with symptoms
tion of AR may and can occlude the ostium of of the sore throat sometimes associated with
these sinuses causing retention of fluid in the slight difficulty in swallowing and a constant
sinuses. Retention causes heaviness in the head. urge to clear the throat.
The heaviness or fullness in the head may result Further down when it affects the larynx, it
in an unpleasant status and it leads to lack of con- causes laryngitis with loss of range of voice,
centration in studies and at work. Cavities as they hoarseness of voice, and loss of timbre of voice.
are, the sinuses normally lighten the weight of As it cascades further downwards, it causes
the skull being borne by the neck. Sinuses also comorbidity in the trachea causing tracheitis or
provide resonance to the voice. When they are cough variant asthma with dry cough, sometimes
blocked, both of these are affected. Further, the a very annoying difficulty to the patient espe-
allergic inflammation can spread to the sinuses cially at nights.
causing sinusitis. Bronchial asthma is the resultant condition
Inflammation of AR can spread to the middle when allergy invades the lower airways. Episodes
ear through the eustachian tubes causing aller- of cough, tightness of chest, wheeze, and breath-
gic otitis media with effusion or Glue Ear. This lessness which can be of varying degree are the
is especially possible when AR is inadequately symptoms. Significant limitation to the life of a
treated or when it is ignored. There will be loss patient happens when the disease is persistent
of hearing in speech frequency. Loss of hearing and when the symptoms are moderate or more
can be mild to moderate. The affected person than moderate.
will have a feeling of fullness in the affected ear. When these conditions persists, they become
Tinnitus can be present. When a young child comorbidities. These are actually complications
develops glue ear, it can lead to a very bad dis- of AR especially when it is neglected or if AR is
ability for the child not developing proper not treated adequately. Conjunctivitis, Sinusitis,
speech and developing improper intellectual and Asthma could be comorbidities right from
growth. It is important to identify and diagnose the onset of AR in a few cases. Further Inquiry,
this condition as early as possible. Reparative Classification of the Disease and Clinical
measures must be instituted quickly and Findings on examination (Fig. 3.17):
aggressively. Even before you examine a patient of sus-
Anosmia is possible to occur when AR is ill- pected AR, history would be quite revealing in
treated or inadequately treated. It is clearly most of the cases. Depending on the episodes and
related to the disease duration and severity. severity of the symptoms, a patient can be classi-
Persistent inflammation and its effect on the fied into one of the four groups. This guidance is
umbrella of innumerable nerve endings of the very helpful in making a strategy for treatment.
olfactory nerve cause this damage. Loss of smell Anterior rhinoscopy will reveal pale, swol-
can be considered in children, as in adults, to be a len mucosa with rugosity and it will be boggy
76 K. Davraj et al.
Intermittent symptoms Persistent symptoms
< 4 days/ week or < 4 per episode ≥ 4 days/ week &≥ 4 weeks/ episode
Mild symptoms Moderate to severe symptoms (one or more points valid)
• Normal sleep • Disturbed sleep

• Normal working & normal school activity • Working & school activity at problem
• Normal daily activity • Impairment of daily activity
• No disturbing symptom • Disturbing symptom
Fig. 3.17 Classification of the Disease on the basis of duration and interference in daily activities [56]
both over the septum and the turbinates. Clear The existence of an entity called local allergic
transudate will be present in uncomplicated rhinitis (LAR) with nasal production of specific
cases. The diagnostic endoscopic examination IgE (sIgE) antibodies in the absence of atopy, in
will confirm the picture of AR as also of any over 40% of non-allergic rhinitis (NAR) patients
other comorbidity like a deflected septum and a has been reported [57]. Evidence for this entity is
complication like polyps, adhesions, syn- supported by the clinical symptoms, the local
echiae, perforations, atrophic changes; and production of sIgE, and a leukocyte-lymphocyte
presence of a tumor or a foreign body. It will inflammatory pattern, with an increase in the
also provide a picture of the nasopharynx and nasal fluids of eosinophils, mast cells, and T lym-
condition of the ostia of paranasal sinuses, phocytes during natural exposure to aeroaller-
especially of the maxillary sinus. A telescope gens, as well as a positive immediate and dual
of 0o or a 30o and with a wide-angle profile pro- response to a nasal allergen provocation test
vides adequate endoscopic examination. (NAPT) with local production of tryptase and
When necessary, the nasal secretion can be eosinophil cationic protein and an increase of
examined for the type of cells present. To get a nasal sIgE to inhalant allergens [37]. Over recent
good columnar epithelial cell sampling, a small years, increasing evidence has shown that an
sterile cotton-tipped applicator can be passed important number of patients previously diag-
under the interior turbinate and gently rubbed nosed with NAR or idiopathic rhinitis develop a
along the floor of the nose and is then rolled local allergy with nasal production of sIgE and a
onto a clean glass slide. The procedure is done positive response to a NAPT [57]. This entity has
under direct vision. It may either be fixed with been suggested to be entopy or LAR. These
spray-fix for a later study or can be stained with patients could also progress over time to AR [57].
Gram’s stain or Papanicolaou stain immediately
for the study. Epithelial cells, granulocytes, and
mononuclear cells are looked for, and presence 3.6.4 Management of AR:
of bacteria is also observed. These cytograms Therapeutic Options (Fig. 3.18)
can be of substantial help in diagnosing AR or to
rule it out. Unless the disease is mild, AR must not be taken
Nasal obstruction can be measured using a for granted. It must be treated adequately. Patient
Rhino-manometer. It provides a measure of the must be convinced of the need to treat the inflam-
nasal airway resistance present in a given case at matory disease properly.
a given time. The procedure uses a pneumotach- Allergen avoidance is easy said than done.
ograph to measure the flow of air through the Once the causative allergens are found and if
nose. avoidance is possible, it is the best course of
Fig. 3.18 ARIA
Guidelines
Allergen avidance
indicated when
possible
immunotherapy
pharmacotherapy
effectiveness
safety
ARIA specialist
effectiveness prescription may
easily
guideline
alter the natural
administered course of the
disease
Patient education
always indicated
Table 3.12 Effect of treatment on symptoms [58]

Sneezing Rhinorrhea Obstruction Itching Eye symptoms
H 1-antihistamincs
• Oral ++ ++ + +++ ++
• Intranasal ++ ++ + ++ 0
• intra-ocular 0 0 0 0 +++
Corticosteroid
• Intranasal +++ +++ +++ ++ ++
• Oral +++ +++ +++ +++ +++
Chromones
• Intranasal + + + + 0
• Intra-ocular 0 0 0 0 ++
Decongestants
• Intranasal 0 0 +++ 0 0
• Oral 0 0 + 0 0
Anti-cholinergics 0 ++ 0 0 0
Anti-leukotrienes 0 ++ + 0 ++
action. For pet allergens and for some food aller- symptoms. First Generation antihistamines have
gens, avoidance can practically be the complete been discarded because of the profound drowsi-
solution. ness they cause. New generation antihistamines
A variety of molecules are available to treat provide good relief and can relieve comorbid
and address different symptoms of AR. Depending symptoms also. Good compliance is possible
on the severity of symptoms and morbidity, the because of once-a-day dosage. Several of these
medication must be chosen (Table 3.12). molecules do not cause drowsiness. There is an
When AR is mild, H1 blocker, an antihista- array of new generation molecules that have
mine of the new generation can address all the superior therapeutic exertion and a good safety
78 K. Davraj et al.
profile. Such oral H1 blockers are Cetirizine, macrophage migration, reverse the effect of the
Levocetirizine, Loratadine, Desloratadine, early and late phase of inflammation, and inhibit
Fexofenadine, Rupatadine, Ebastine, hyper-reactivity. INS relieves all symptoms of
Olopatadine, and Bilastine. Azelastine and AR, including nasal blockage, and meta-analysis
Olopatadine are available as locally applied anti- shows that INS is more effective than antihista-
histamines also. The onset of action is rapid and mines [53]. They act by suppressing inflamma-
the therapeutic effect is limited to the tissue. They tion in the nasal mucosa leading to a reduction or
are of choice in very mild cases of AR and aller- resolution of symptoms. There is some worry
gic conjunctivitis and as add-on therapy to INS in over the long-term effects of using steroids but
persistent cases of AR and allergic conjunctivitis Fluticasone furoate, Fluticasone propionate,
when it is necessary. Budesonide, and Mometasone have little sys-
Decongestants are sometimes necessary when temic absorption. Mometasone which is a sus-
there is significant nasal obstruction. Local pension is the only molecule recommended to be
decongestants must not be administered for more safe even for a child of 2 years and above. No
than 7–10 days for fear of rhinitis medicamen- significant difference in the number of symptom-
tosa. Systemic decongestants like pseudoephed- free days or quality of life has been reported
rine may be administered for a short duration but between the three drugs [59].
with caution, especially in those patients with Once the disease is persistent and is not mild
hypertension and anxiety neurosis. anymore, allergic inflammation must be
Mast cell stabilizers have a limited role. If the addressed continuously and with adequate dose
patient is younger than 2 years, a mast cell stabi- of INS. If persistent AR is inadequately treated,
lizer like Sodium cromoglycate will be a very the cascade of inflammation does damage the
safe option to be applied locally in the eyes, nose, anatomical structure of nasal mucosa and the tur-
and even as an inhaler. Compliance is a chal- binates. Like inadequately treated persistent
lenge. If VMR is suspected as a concomitant asthma can cause re-modulation of lower airway
partner of disease, addition of anti-cholinergic smooth muscle, re-modulation of the upper respi-
drops instilled intranasally may help. ratory area is quite possible. This is an important
Among the four main symptoms of AR sneez- aspect of the management of chronic AR. If a
ing, rhinorrhea and pruritus are caused by the patient is vehemently opposing INS, the
early phase of allergic inflammation in which his- Leukotriene modifier will be the next best option
tamine is the main chemical mediator and that is and it must be given regularly, for adequate
why a H1 blocker may address these symptoms. period of time, and in adequate dose. Both fluti-
Nasal obstruction is caused by the late phase of casone furoate and mometasone have been shown
inflammation wherein a host of mediators play to reduce symptoms of allergic conjunctivitis as
their role in causing the symptom. Only an anti- well as those of allergic rhinitis [60, 61]. The
inflammatory molecule like a corticosteroid can onset of action is variable among the steroid
address these symptoms. Though oral steroids preparations (Table 3.13) [62]. Mometasone has
are rarely required and if at all for a very short the highest binding ability but flunisolide has
duration, intranasal steroids (INS) are the main- maximum bioavailability (Figs. 3.19, 3.20, and
stay of management of such condition. They pro- 3.21) [63–65].
vide effective treatment for AR and are the
first-line therapy for adults in moderate-to-severe
cases or in individuals who are still symptomatic 3.6.5 Leukotriene Receptor
despite the regular use of antihistamines [53]. Antagonists
INS has the capability to inhibit histamine
release, reduce mucus production, exert anti- Leukotriene receptor antagonists (LTRA) block
edematous and vasoconstrictor activity, inhibit the effects of cysteinyl leukotrienes which are
important pro-inflammatory mediators of nasal may be beneficial. If the nostrils are completely
allergic reactions and whose release locally blocked and if INS cannot simply enter the nasal
induces nasal obstruction. Although some effi- cavities, INS sprays will not be effective of
cacy with LTRAs has been shown in AR, the course, and therefore oral steroids may be co-
spectrum of individual responsiveness remains prescribed along with an INS [53]. It is advisable
variable and the combination of an antihistamine to prescribe a good steroid molecule like
and an LTRA is no more effective than an INS Prednisolone or Methylprednisolone in adequate
alone. However, it is worthwhile considering the dose and for a reasonably good period of time
prescription of an LTRA in patients with difficult like 5–7 days.
AR and concurrent asthma, in addition to treat- Even when symptoms are well under control,
ment with antihistamines and topical nasal ste- the inflammation of AR needs to be addressed on
roids [53]. a continuous basis to prevent damage to the
Systemic corticosteroids are rarely indicated mucosa and to prevent further remodeling [28]. If
in the management of AR. However, there are a patient on INS is stable and symptom free, an
occasions when a short course of oral steroids attempt to reduce the daily dose may be made but
the INS needs to be continued to address the
“minimum persistent inflammation.” Medication-
Table 3.13 Intranasal steroids—onset of action sparing effect can only be achieved by allergen
Medication Onset of action immunotherapy (AIT).
Beclomethasone dipropionate Within 3 days With INS and complementary measures, you
Budesonide Within 24 h may secure satisfactory results and the patient
Flunisolide 4–7 days expectantly becomes symptom free. It means you
Fluticasone furoate Within 12 h have successfully obtained good control of the
Triamcinolone acetonide 24 h
disease. All the more the allergic inflammation
1400
1200
1000
800
600
400
200
0
Mometasone Fluticasone Budesonide Trimsinolone Dexamethasone
Fig. 3.19 Binding ability of steroids

80 K. Davraj et al.
25.00%
Series 1
20.00%
15.00%
10.00%
5.00%
0.00%
Fluticasone Fluticasone Mometasone Budesonide Flunisolide
furoate propionate furoate
Fig. 3.20 Bioavailability of steroids
Fig. 3.21 The treatment

guideline according to
the severity of symptoms Treatment of allergic rhinitis (ARIA)
(ARIA Guidelines) Allergic Rhintis & its impact on Asthma
Moderate Moderate
Mild Severe Mild Severe
ntermittent Intermittent Persistent Persistent
Intra-nasal steroid/ Local chromone
Oral or local non sedative H1–blocker

Intranasal decongestant (7–10 days) or oral decongesteant
Allergen and irritant avoidance
Immunotherapy
persists and prevails because the causative aller- does persist. It is like a cauldron when it has been
gens and other triggers do persist. Even when a controlled. When the inflammation is raked up, it
patient is symptom free with adequate treatment is like an inferno. That is why INS needs to be
do understand that the minimum inflammation continued to address the inflammation. INS is
both a reliever and a preventer. Every possible benefit. Proper documentation of causative aller-
allergic attack must be prevented to further pre- gens is necessary to institute immunotherapy.
vent re-modulation of the internal structure of the The gold standard for the specific diagnosis of
nose. allergy is SPT. Results of SPT will be the founda-
tion for a successful AIT.
Spreading inflammatory cascade can involve
3.6.6 Difficult-to-Treat AR several tissues and cause complications that will
become permanent comorbid conditions [70].
When a patient is still symptomatic despite treat- That is why AR must be adequately treated and
ment with oral antihistamines and INS, the first properly monitored. There is enough evidence to
stage is to check adherence and correct technique demonstrate that upper and lower airways are
[53]. Clinical practice suggests that most patients connected both anatomically and physiologi-
who have found INS unhelpful have not persisted cally. In fact, they are simply upper and lower
with treatment for an adequate period [11]. segments or components of one airway. That is
Patients should be advised that the onset of action why AR needs to be treated properly to prevent
of INS takes some time and that they should be the onset of complications in the adjacent area
used regularly for a minimum of 2 weeks before and lower down in the airway, especially in the
considering them unsuccessful [66]. Patients bronchi causing the onset of asthma. There is evi-
with seasonal AR should commence therapy 2 dence of the existence of inflammation in the
weeks before the pollen season as this improves mucosal layers of lower airways in patients of
efficacy [53, 67] To maximize the response to AR without any symptoms of asthma. In cases of
treatment, patients using INS should be given AR with very mild asthma, adequate dose of INS
clear instructions on this aspect. They must also provides relief of nasal symptoms as well as
be advised to direct the nasal spray laterally those of asthma. In patients with AR, intranasal
(rather than medially towards the nasal septum) procedures to create roominess must be consid-
towards the lowest and anterior most part of infe- ered very carefully. Creating roominess by an
rior turbinate of that side and not to sniff for at inadvertent procedure without proper control of
least 10 min after spraying. All these measures allergy may encourage the entry of allergens and
will increase the benefit. Tipping the head back other triggers into the lower airways causing the
and sniffing hard decreases treatment efficacy. onset of asthma. It will become a complication,
The spray will run down the nasopharynx and an iatrogenic surgeon-induced asthma. Surgery is
patients should be advised not to do this. To max- never an option of management for allergy.
imize effect patients may well be advised to Some cases of AR or asthma will have comor-
douche with saline prior to using their nasal bid symptoms in distant regions like the skin. AR
spray. Saline douching clears mucus and mucus or asthma can have atopic dermatitis as a comor-
plugs if any, from the nasal cavity permitting bidity. In such a case, as you learn the details of
local absorption of the INS, thereby increasing its the case, you find a strong case of allergy being
effectiveness. The use of saline douching has the underlying disease. Treatment must include
demonstrable benefits in symptom reduction in medication and other complimentary measures
children and adults with seasonal rhinitis as well for both conditions. Patient must be convinced of
as in chronic rhinosinusitis [68, 69]. the need for an approach to include proper inclu-
Depending on the severity of disease, the sive medication and necessary changes in
medication must be designed. As the patient lifestyle.
secures benefit, step down of medication may be Some cases of AR may have to be considered
achieved. However, when there are episodes of for treatment with Biological such as omali-
flare up, step up of medication needs to be done. zumab. Though uncommon, rarely you encounter
Once the disease is persistent, AIT must be con- a case of AR where your patient is not getting
sidered especially if the patient desires a curative stable and is not comfortable. If the patient can
82 K. Davraj et al.
afford, it may be worth its while to treat such a • AIT is capable of impeding the onset of
patient with biologicals. Patient may get excel- asthma in cases of allergic rhinitis.
lent benefits especially if there are comorbid • AIT can impede poly-sensitization.
symptoms and the relief may be for all comor- • AIT is capable of providing medication-
bidities. You may be able to shorten the course of sparing effect.
therapy with biologicals with the introduction of • There is enough evidence that the benefit of
allergen immunotherapy. AIT continues to be present for a long tenure
Management must be holistic and integrated. even after concluding the therapy.
Patient must be convinced of the condition being • AIT has the capacity to provide long-term
a non-infectious disease, that it needs to be protective benefit against the development of
addressed as one does for hypertension and or for various other allergic conditions.
diabetes, that the treatment with medicines pro-
vides control of disease but does not cure it, that AIT is the administration of gradually increas-
the doctor and medication are a good part of ing quantities of an allergen vaccine to an allergic
treatment but are not the only one and, that the subject, reaching a dose that is effective in ame-
patient has to comply with the continuation of liorating the symptoms associated with subse-
treatment and complementary measures for their quent exposure to the causative allergens [71].
own wellbeing. Good Rapport with the patient is For an effective AIT, a proper specific diagno-
necessary for a good prognosis. Periodic check- sis must be established. History and clinical
up for a good examination of the nose and to examination are crucial but it is erroneous to
assess the treatment is mandatory. Once a patient make a specific diagnosis based on history alone.
has AR, he will continue to have it unless inter- Causative allergens have to be determined by
vention with SPT is done to document the caus- conducting specific allergy detection tests and
ative allergens and specific AIT is instituted as a correlated with the clinical manifestations.
curative procedure. Regular physical activity, Skin Prick Tests (SPT) can provide evidence
adoption of healthy measures, and good nutrition of causative allergens and will demonstrate the
will complement the management. Rewards to presence of allergen-specific IgE (Fig. 3.22).
the patient and to the doctor will definitely arrive. Serum specific IgE (ssIgE) estimation can pro-
vide a quantitative evidence of the antigen-
specific antibodies in the blood circulation of an
3.6.7 Allergen Immunotherapy allergic individual. Advantage of ssIgE estima-
(AIT) tion is that one blood sample is enough for the
assay. Availability of normal skin is not a require-
Allergen Avoidance and Allergen Immunotherapy ment. There need not be a curfew on immunosup-
(AIT) are the only treatments that modify the pressive drugs when the test is conducted. The
course of an allergic disease either by preventing result of ssIgE may be negative but the patient
the development of new sensitivities or by alter- may have potential allergy. A positive result is an
ing the natural history of disease or disease pro- excellent evidence of specific allergen sensitivity.
gression [71]. SPT done with good quality allergens is the best
AIT provides a window of opportunity for diagnostic option. SPT offers both qualitative and
multiple benefits. Following are the benefits of quantitative measures of an allergen activity. It is
AIT: fairly simple, safe, cost-effective, and reliable.
SPT is hardly an invasive procedure.
• AIT is the only available curative tool. Subcutaneous AIT (SCIT) or Sublingual AIT
• AIT can alter the course of allergic disease for (SLIT) (Fig. 3.23) as a choice is left to the clini-
good. cian and the patient considering various angles of
• AIT is capable of changing the Th2 status therapy and tenure. Possibility of systemic reac-
(allergic) to Th1 status (normal). tions and anaphylaxis that is a major concern in
SPT: Prick through the Drop at 45 to the Skin

SPT Elevate Slightly Allowing the Entry of Allergen
Bolus of Allergen Instilled on the Skin into Stratum Corneum Epithelium
SPT: Significantly +ve Reaction

Large Wheal, Large Erythema with Pseudopodia
Sensitivity Confirmed
Fig. 3.22 Skin prick test
SCIT, is eliminated in SLIT. Proper diagnosis, safety are a major concern in SCIT. For food
good quality allergens, compatible and proper allergy and at present SCIT is not the accepted
combination of allergens, and compliance are option. Considering all these difficulties, SLIT
crucial to successful treatment by AIT. appears to be a safe and viable option. Much
With evidence of SLIT providing excellent higher dose and concentration need to be achieved
therapeutic benefit to patients of AR and allergic in SLIT for it to become success. Proper combi-
asthma and especially with its safety profile, it nation of allergens in the SLIT vaccine is neces-
has emerged and has become the option of choice sary. Treatment happens in the comforts of the
for AIT. SCIT has to be administered by a medi- patient’s home. It is the biggest benefit. This
cal professional. In the initial and build-up phase, itself must not become a hindrance to the mainte-
injections are quite frequent. If the scheduled gap nance of treatment. SLIT works on trust. Patient
between injections is prolonged for any reason and the family must be made to understand this
and if the following higher dose is administered, fundamental aspect. Patient must also be made to
there is a risk of a systemic reaction especially if understand that SLIT contains the same allergens
the sensitivity is high. The danger of anaphylaxis to which the patient is allergic and that it is
is a possibility. For AIT to become effective, the directed to shift the patient’s status of allergy to
effort is necessary to reach the highest possible normalcy, and that it does not directly relieve the
concentration and dose. So, compliance and symptoms like the medication does.
84 K. Davraj et al.
Fig. 3.23 SLIT Prescription form by author’s clinic
The process of AIT commences from the very matitis is so severe that it affects the social and
first dose but it generally takes some time for its professional life of a patient, even if the reason-
beneficial effect to reflect on the symptoms. able benefit can be obtained, AIT will be great.
Allergic Rhinitis, Allergic Conjunctivitis, Selected cases of migraine and Meniere’s disease
Allergic Asthma, Sting Reactions are the classi- especially with comorbid allergy conditions,
cal indications for AIT. AIT may be a good option would be worth the while candidates for AIT.
in some selected cases of drug allergy. The beneficial effect of AIT will not be appre-
Anaphylaxis and angioedema are conditions ciable if it is administered in cases of mild allergy
where AIT if possible, would be a boon to the conditions. When the disease is persistent and
patient and may actually be a life-saving tool. when the symptoms are moderate or moderate-
AIT has been approved as a major option of man- severe, AIT would be a great option in addition to
agement for Atopic Dermatitis. When atopic der- medical management.
Successful AIT will initiate a marked enhance- ize on the tolerogenic antigen-presenting cells in
ment of protective blocking IgG antibodies. AIT the oral mucosa [4, 5]. It is further thought that
will blunt the serum concentration of specific IgE SLIT efficacy can be enhanced by exposure to
antibodies. There will be a down-regulation of the food protein in its intact form before possible
inflammatory cell recruitment, activation, and epitopes are broken down through gastric diges-
mediator release. These will modify the tion [74, 75].
T-Lymphocyte response to the benefit of the Both in adults and children, a judicious com-
patient. Th2 response will get down-regulated bination of AIT, medical management, and cor-
resulting in enhanced Th1 response [72] rection of allergen-rich environment have become
Poly-sensitization is a common feature in the hallmark of providing the complete solution
patients [73]. Poly-sensitization happens over a to the persistent suffering of allergy patients.
course of period. Poly-sensitization can be pre- Wherever necessary, an effort must be made to
vented by the institution of AIT early. Children change the existing lifestyle to suit the prevailing
are the best candidates. Re-modulation of the air- condition to achieve the best results. With better
ways that happens due to persistent allergic understanding, better techniques, quality training
inflammation is prevented with effective and of specialist doctors, proper guidance by experi-
early AIT. AIT also makes it cost-effective in the enced allergy specialists, and better quality of
long run. allergens, AIT can only become a more powerful
and sustaining tool and the option of manage-
ment of allergic diseases.
3.6.8 Allergens and Non-Allergic
Triggers
3.6.10 Allergen Avoidance,
Allergens have to be differentiated from non- Complimentary Lifestyle,
allergic triggers. A clear distinction is necessary. and Prevention
Non-allergic triggers must never be included in
prescriptions for immunotherapy. Infect they 3.6.10.1 Allergen Avoidance:
should not even be included in the tests for Food allergens if documented by diagnostic tests,
allergy. Many of them are inanimate subjects. the best course of action is to eliminate the particu-
They do not contain any allergen themselves. lar food from the diet. If the allergy is severe and
Various dusts other than house dust, smokes, causes anaphylaxis or anaphylaxis type of reac-
fumes, perfumes, dhoop, incense, plastic, paper, tion, extreme precaution is necessary. One must
cement, gravel, nylon, and polyester are such have very quick access to adrenaline injection.
substances. AIT is such a case may be a life-saving effort.
Allergens are substances that initiate and Pet allergy if detected, donating the pet may
cause an allergic reaction in an individual who be the best option of the management. If this is
has developed specific IgE antibodies to those not acceptable to the patient, AIT would be the
substances. They are protein in nature. They can next option.
be broadly classified into three main groups. Pollen allergy if present, during the pollen
They are Injectants or Ingestants or Inhalants. season patient must avoid being outdoors unnec-
essarily and especially in early mornings and
later in the evenings. While going out, wearing a
3.6.9 S
LIT as Food Allergen face mask may provide protection. Such a patient
Immunotherapy must keep the windows of their bedroom closed
at night and early morning when it would be
With SLIT, the food protein is delivered sublin- blossoming time of the plants.
gually in a liquid form and then usually held for Fungal spores if are the causative allergens,
2 min and swallowed. SLIT is thought to capital- all places in the house must be checked for
86 K. Davraj et al.
seepage and fungus infested corners and crev- greens, fresh seasonal and dry fruits if included into
ices. Correction measures and waterproofing of our diet, nutrition will be balanced and that itself will
seepage areas will help. The indoor environment act as highly organic medicine to preserve good
must be kept well ventilated and clean. health and to protect ourselves from the disease.
HDM and insect allergy are very common. Some amount of physical activity regularly will
Repeated and vigorous dust and insect control- make our life robust to ward off allergy. One must
ling measures will help to a good extent both for also try to relax for some time every day.
the mites and for the insects. Minimum things
must be in the bedroom especially. Corners, 3.6.10.3 Prevention of Allergy:
Crevices must be made rid of collected dust. Universal understanding and gigantic efforts are
Wardrobes and cupboards must be dust free. necessary to stop the usage of harmful chemi-
Curtains and carpets to be examined and if neces- cals in agriculture and horticulture. Pollution of
sary, to be done away with. Maximum attention ambient air, water, and soil must be controlled
must be on the mattress and pillows. Dead or by people and governing bodies. These appear
alive parts of mites and their tiny little fecal pel- to be the major triggers all over the world. There
lets are the deadly allergens. Human skin scales is evidence that antibiotic administration to a
are the main food for the HDM. Throwing the pregnant woman will enhance the chance of the
pillow and mattress to hot sunlight and beating child to become an asthmatic. Antibiotics must
them up nicely will help. If the vacuum cleaner is be administered only when it is absolutely nec-
available, it must be generously and repeatedly essary for a pregnant woman. Breastfeeding the
used on the mattress and pillows. Synthetic cas- infant is very important to ward off many pos-
ings for the mattress and pillow are available. sible diseases. A person having an allergic dis-
They are helpful too. Linen must be changed fre- ease must marry a person who does not have an
quently and they must be soaked in very hot allergy so that the possibility of their child being
water for half hour at least before washing a non-allergic child is very high. Intranasal sur-
because dust mite allergen is heat labile. If the gery must be avoided to a great extent in a
washing machine has heat control, linen can patient of AR. Surgery is not a treatment for
alternatively be washed with a minimum of 60 allergy. It can trigger the onset of asthma in a
degrees Celsius temperature. patient of AR. Platt-A Mills’ hygiene hypothe-
sis supports children growing up with pets and
3.6.10.2 Complimentary Lifestyle farm animals. Farm animals like cow release a
We are subjected to various chemicals in the food and very low-grade endotoxin. When a growing
beverages we consume. There is also a play of syn- child is exposed to these farm animals, low-
thetic colors, food additives, and preservatives in grade infections happen but the immune system
most of the available out of the shelf packaged food. responds positively providing an umbrella of
We must be protective of not getting exposed to these protection. This will provide a protection to the
items to whatever extent we can. Many of these items child from developing allergy. Bactericidal and
though not allergens are capable of being triggers. so-called Germ-check ingredients being used in
Injurious data on long-term usage is not completely toothpaste, soaps, handwash, detergents, floor
available. Preprocessed food is not health friendly. cleaning solutions, and sprays could contain
We may be subjected to harmful effects of these pesticides like Triclosan and Triclocarban.
many known and unknown ingredients. Deficiency These will kill and eliminate microbiomes and
of Vitamin-D and Vitamin-B12 predispose us to be will render the homes sterile. An infant or a
vulnerable to many diseases including allergy. young child growing in a sterile house has a
Abundant sun energy is available. We must get our- very high possibility of developing allergy and
selves exposed to sunlight for Vitamin-D. Our nutri- asthma. We need clean homes, not sterile homes.
tion must contain adequate amount of protein. It is impossible to eliminate allergy but efforts
Sprouts, whole grains, legumes, seafood, poultry, can be made to control the disease and to enforce
certain benign things to prevent the onset of 3.7.3 Clinical Features

allergy in the coming generation.
The predisposing factors are the changes in the
environmental humidity, temperature, smoke,
3.7 Part G: Vasomotor Rhinitis etc. the symptoms are persistent throughout the
year. Sneezing after getting up from bed, exces-
3.7.1 Introduction sive rhinorrhea, and nasal obstruction more on
the dependent side are the usual symptoms. Ear
Vasomotor rhinitis (VMR) or idiopathic rhinitis and throat symptoms are absent in intrinsic rhini-
is one of the most prevalent forms of non-allergic tis. Mucosal congestion with enlarged turbinates
rhinitis. It is usually seen around 30–60 years. with smooth to modulated appearance is the stan-
with female predominance. Being more common dard findings on rhinoscopy (Fig. 3.24), whereas
in the female it is suggested that female hor- patients with predominantly excessive rhinorrhea
mones might play some role, but there is no have often distinctive appearance. Postnasal drip
research explaining this possibility. However as is another common symptom of VMR. Other less
VMR may be caused by shifts in temperature and common symptoms of VMR are sneezing, nasal
humidity, patients may experience seasonal pruritis, and eye irritation [81].
symptoms during spring and fall. Thus, seasonal
VMR can easily be confused with Seasonal
Allergic Rhinitis (SAR) [76–78]. The precipitat- 3.7.4 Diagnosis
ing factors are environmental conditions, such as
strong smells, exposure to cold air, changes in The diagnosis of VMR is based on the patient’s
temperature, humidity, barometric pressure, history and their precipitating factors. Its diagno-
strong emotions, ingesting alcoholic beverages, sis is through the exclusion of other causes.
and changes in hormone levels [77]. Patients usually should have normal serum IgE
levels, no eosinophil in nasal smear and negative
skin testing or radioallergosorbent tests (RAST)
3.7.2 Pathogenesis or nasal provocation test [82].
The exact underlying mechanisms causing VMR

are not well understood. However, the most com-
mon theory explaining it, thought to be nonspe-
cific nasal hyper-reactivity to non-immunologic
stimuli on exposure. Other reasons are dysfunc-
tion of nociceptive, autonomic system alone, or
both. Another concept also says the role of
capsaicin-sensitive nociceptors in the nasal
mucosa. Hyperactive parasympathetic innerva-
tions/hypoactive sympathetic innervations explain
an autonomic imbalance towards an excess in
parasympathetic innervations, some studies sup-
port that vasomotor rhinitis is more likely a result
of a hypoactive sympathetic nervous system.
Autonomic imbalance in favor of parasympa-
thetic innervations results in nasal edema from
vasodilatation of the nasal vasculature. Functional
abnormality of sensory afferent nerves and/or
C-fiber stimulation has also been suggested as Fig. 3.24 Enlarged inferior turbinate with smooth to
possible causes of vasomotor rhinitis [79, 80]. modulated appearance
88 K. Davraj et al.
3.7.5 Treatment it is probably due to as an anti-

inflammatory and neuro-inflammatory
1. Avoidance: The home environment must be blocker.
modified to avoid factors that initiate or exac- (c) Decongestants
erbate the rhinitis, like Control of humidity Both oral and topical decongestants effec-
and temperature can lessen nasal instability or tively treat congestion regardless of
vasomotor hyperactivity. underlying cause of VMR. However topi-
2. Exercise: It can help reduce nasal obstruction cal medications cannot be used prolong
by stimulating sympathetic nerve discharge, because continual use for more than
which produces vasoconstriction and lasts for 3—10 days leads to rhinitis
15–30 min. medicamentosa.
3. Medications: First-line of treatment in vaso- ( d) Anti-Cholinergics
motor rhinitis is medical therapy in the form Ipratropium bromide is a potent intranasal
of topical therapy. In mild disease, one med- anti-cholinergic with utility in the treat-
ication should be started along with the ment of rhinorrhea in VMR but it is spe-
option to add a second if symptoms are not cifically treated rhinorrhea and does little
controlled by a single agent whereas in help to improve congestion.
moderate disease, two agents can be started (e) Miscellaneous
simultaneously. In severe cases, an oral Topical saline spray or saline irrigation
medication either a decongestant or anti- devices are help in the reduction of post-
cholinergic, depending on the predominat- nasal drip, sneezing, and congestion.
ing symptom can be added to the topical
therapies. Another therapy for VMR is topical capsaicin
(a) Nasal Corticosteroids intranasally which helps by acting on neural
By contrast, clinical experience suggests fibers in the nose and thus reducing nasal hyper-
that all nasal corticosteroids have some reactivity [83]. Algorithm for medical manage-
effectiveness in treating VMR. ment is mentioned in (Table 3.14).
(b) Antihistamines
It is predictable that first-generation anti- 4. Surgical Treatment
histamines might reduce rhinorrhea If Inferior turbinates are persistently hyper-
through anti-cholinergic actions however trophic after 3 months of medical manage-
by enlarging oral antihistamines are gen- ment then it needs to be reduced to relieve
erally ineffective in reducing congestion nasal obstruction. Various methods of reduc-
in VMR. The combination of an antihista- tion are:
mine and a decongestant might help (a) Lateralization of the inferior turbi-
reduce the congestion in VMR. nate but it is not considered sufficient as
The role of intranasal antihistamines— a stand-alone procedure for the manage-
Azelastine’s efficacy in VMR is not due to ment of significant turbinate hypertro-
histamine receptor blockade but instead, phy [84].
Table 3.14 Algorithm for the medical treatment of vasomotor rhinitis

Clinical
presentation Rhinorrhea predominant Congestion predominant Mixed congestion rhinorrhea
Mild Ipratropium (IB) topical antihistamine TAH or nasal corticosteroids (NCCS)
(TAH)
Moderate IB+ NCCS or TAH TAH + NCCS TAH + NCCS
Severe IB+ NCCS or TAH+ oral TAH + NCCS+ oral TAH + NCCS+ oral decongestant and
anti-cholinergic decongestant anti-cholinergic
(b) Submucosal electrocautery technique (e) Ultrasonic bone aspirator to remove

involves the use of a single needle elec- inferior turbinate bone is the recent
trode or bipolar forceps with needle tips advancement. This device uses ultra-
[85, 86]. Mucosal injury can lead to sonic waves to emulsify bone, with con-
recurrent epistaxis and prolong crusting current irrigation and microsuction of
over mucosa with high risk of synechiae bone particles producing a clean surgical
formation. field; this reportedly enables removal of
(c) Submucosal radiofrequency coblation the inferior turbinate bone without ther-
technique differs from the electrocau- mal or mechanical injury to the sur-
tery technique in that it produces signifi- rounding soft tissue or mucosa.
cantly lower heat than that with (f) Mucosal sacrificing techniques
electrocautery. Mucosal injury and epi- Cryosurgery to the surface of interior
staxis are less common than other treat- turbinates reduces the population of
ment methods. The wand tip is coated in mucus glands. Scarring produced can
saline gel or another conductive media improve the airway but the effect is short
and activated at the head of the turbinate lived.
to produce a devascularized zone. The Partial turbinectomy removes a
wand is then inserted through this zone small portion (1.5–2.0 cm) of full-
and advanced toward the tail of the turbi- thickness tissue at the head of the infe-
nate submucosally. It is then activated rior turbinate in the region of the internal
for a short period (e.g., 10 s), and then nasal valve.
partly withdrawn and activated again Laser for inferior turbinate reduc-
[87]. tion has been used for simple tissue
(d) Powered submucosal turbinate reduc- ablation to laser mucotomy (excision of
tion is used to reduce the amount of sub- superficial mucosa), to partial or total
mucosal erectile tissue, while leaving the turbinectomy with the laser used as a
overlying epithelium unharmed. With cutting instrument.
the recent advent of a smaller (2.0– Total resection or “radical” turbi-
2.9 mm), specifically designed inferior nectomy involves the complete resec-
turbinate microdebrider blade, with an tion of the inferior turbinate using heavy
incorporated tip elevator, this procedure scissors to detach it directly at its site of
has been made easier. The tip of the spe- attachment to the lateral nasal wall. This
cialized microdebrider blade, or a scal- technique can reduce the nasal resistance
pel, is then used to perform a stab up to 50% but eventually fell out of favor
incision in the head of the inferior turbi- with many surgeons owing to concerns
nate. The microdebrider blade is then for severe long-term complications such
advanced (with the cutting surface fac- as atrophic rhinitis and ozaena [88].
ing laterally) and used to create a submu- (g) Vidian neurectomy It has been pro-
cosal pocket on the infero-medial surface posed only for non-allergic rhinitis
of the turbinate bone, using the flat tip as refractory to maximal medical treatment.
an elevator. Care must be taken to avoid However, the evidence base for its bene-
flap perforation, while targeting the ante- fit remains controversial. Despite its
rior and infero-medial submucosal soft original popularity, vidian neurectomy
tissue that contributes most significantly was almost completely abandoned
to nasal airflow obstruction. Submucosal because of its complications and the lack
resection can be carried all the way to of long-term effectiveness. The results
the tail of the turbinate posteriorly. showed poor long-term outcomes with
90 K. Davraj et al.
the return of symptoms within a 2-year the approach to the sphenopalatine

period after surgery. Malcomson in 1957 foramen. Then Probe is advanced
firstly suggested that the vidian nerve into pterygopalatine fossa via sphe-
had a predominantly parasympathetic nopalatine foramen in postero-
effect. He also suggested that it could lateral direction till the lateral end
offer relief in patients with vasomotor of vidian canal opening. Inadvertent
rhinitis (in patients with rhinorrhea pre- trauma to the sphenopalatine artery
dominantly) who are not responding to and resultant bleeding remained a
medical management. Sectioning of key issue.
greater superficial petrosal nerve as a (v) Endoscopic vidian neurectomy
treatment for vasomotor rhinitis was first (EVN) was described by Robinson
proposed by Zeilgelmann in 1934 which and Wormald. Improved endo-
was further suggested by Murray scopic visualization and a better
Falconer in 1954. The different surgical understanding of the anatomy have
techniques are described below. significantly improved the ability of
(i) Golding–Wood’s transantral the surgeon to locate and precisely
approach has the disadvantage of resect the vidian nerve. It is well
being relatively destructive proce- tolerated, safe, and effective in a
dure and various complications like majority of patients. It has two sub-
Severe bleeding from the spheno- types, i.e., type 1 or intrasphenoidal
palatine artery and its branches, approach consists of unroofing the
Numbness of the cheek and palate, superior aspect of the bony vidian
ophthalmoplegia, and even blind- canal in the floor of the sphenoid
ness can occur. sinus followed by isolating and
(ii) Trans-septal vidian neurectomy then dividing the nerve. This
is a method in which trans-septal approach can only be used for those
access is used to elevate flap over well-pneumatized sphenoid sinuses
anterior and inferior wall of sphe- in which the vidian canal is thin and
noid body and is followed by the isolated from the surrounding bone
Identification of sphenopalatine of the sinus floor and walls. In type
foramen and pterygoid canal. Then 2 or transsphenoidal approach, the
Diathermy probe was passed into bone of the anterior wall of the
the pterygoid canal and vidian sphenoid is removed, and this bony
nerve was coagulated. removal is carried out laterally to
(iii) Transpalatal vidian neurectomy the sphenoid process of the palatine
is less popular as it is associated bone. The sphenoid process is
with significant postoperative mor- resected until the vidian canal can
bidity and the risk of oronasal or be identified or a curved probe can
oroantral fistula. be inserted and used to “hook” the
(iv) Transnasal vidian neurectomy is vidian nerve. Once isolated, the
primarily performed via a trans- nerve is then cut.
septal approach and it is a direct (vi) Endoscopic Posterior Nasal
approach along the lateral wall of Neurectomy (EPNN) was emerged
the nasal cavity. It had the advan- to avoid the postoperative compli-
tage of providing a less invasive, cation of xerophthalmia and palatal
more rapid, and direct method than numbness, because the posterior
conventional techniques but still nasal nerve is not located as closely
required a rather blind dissection in to the maxillary nerve as is the
v idian nerve. In this selective and Pathophysiology of the non-invasive spectrum of

distal resection of the posterior fungal rhinosinusitis is still speculative and enig-
nasal nerve (the ramus emanating matic. The fungal ball affects single sinus and
from pterygopalatine ganglion endoscopic removal of disease is typically curative.
especially innervating nasal Allergic Fungal Rhinosinusitis is characterized by
mucosa) was divided. Two separate typical imaging and histopathological features and
techniques for EPNN have been is notorious for recurrence despite of surgical
described. The first, referred to as removal. Fungal rhinosinusitis (FRS) is defined as
the transturbinate approach, is typi- the inflammation of nasal and paranasal sinus
cally performed in combination mucosa associated with fungal elements. Based on
with submucosal resection (SMR) varying clinical presentation, pathophysiology, and
of the inferior turbinate. From inci- histological appearance, FRS has been categorized
sion in turbinate, the mucosa of the into various subgroups [90, 91]. It can be acute
middle meatus/lateral nasal wall is (symptoms for 90 days), indolent condition [92].
elevated and the periosteum cut and As per the recommendations of the international
elevated until the sphenopalatine society for human and animal mycology group,
foramen (SPF) is visualized. The FRS is broadly classified into two categories based
nerve identified as the posterior on the tissue invasion by the fungi as follows
nasal nerve courses from the SPF [91–93]:
toward the inferior turbinate is iso-
lated and cut. Second technique 1. Non-Invasive fungal sinusitis (NIFS)
uses a transnasal approach similar (A) Saprophytic infections
to that described for transnasal (B) Fungal Ball (mycetoma)
endoscopic sphenopalatine artery (C) Allergic fungal Sinusitis (AFS)
ligation and begins with a vertical 2. Invasive fungal sinusitis (IFS)
incision made in the middle meatus (A) Acute Fulminant
roughly 5 mm anterior to the lateral (B) Chronic invasive
attachment of the middle turbinate. (C) Chronic granulomatous
A mucoperiosteal flap is elevated
posteriorly to the crista ethmoidalis (A) Saprophytic Non-invasive Fungal
until the SPF is identified. The pos- Sinusitis (SNIFS)
terior nasal nerve is identified along It is a recently proposed group in NIFS asso-
with the sphenopalatine artery ciated with impaired drainage of the parana-
(SPA) which was cut [89]. sal sinuses causing colonization of the
Overall, the literature has shown that the endo- fungus. Fungal colonization of the sinonasal
scopic approach is associated with less morbidity tract in this condition occurs following a sur-
than the traditional approaches. gical procedure or trauma leading to inflam-
mation and ulceration/crusting of the
sinonasal mucosa. The fungal deposits are
3.8 art H: Non-Invasive Fungal
P restricted to the surface of the mucosa with-
Sinusitis out tissue invasion. The patients are typi-
cally asymptomatic and the fungal deposits
3.8.1 Introduction are observed as incidental findings during
unrelated procedures. This form is the least
The non-invasive fungal rhinosinusitis spectrum described in the literature and removal of the
includes saprophytic infection, fungal ball, allergic crust is the treatment for the saprophytic
fungal rhinosinusitis. This spectrum of rhinosinus- infection.
itis tends to affect immunocompetent individuals. (B) Fungal Ball [92–94]:
92 K. Davraj et al.
It is an entangled mass of fungi involving 3. The mixed theory combines the above
single paranasal sinus subsite usually associ- two and considers both the above factors
ated with minimal mucosal inflammation. It to be contributory to the disease
is usually seen in immunocompetent indi- manifestation.
viduals with the age range being 14–87 years Non-contrast Computer tomography of
with a predilection for females (~57–64% of paranasal sinuses is the investigation of
the patients). According to the above men- choice. Typically imaging shows single
tioned FRS guidelines, the fungal ball is an sinus involvement. Expansion of the
appropriate term for this clinical entity involved sinus is not expected with a fungal
rather than mycetoma or aspergilloma. It can ball, and the opacification of the involved
present as unilateral nasal blockage or facial sinus with patchy areas of high density hav-
heaviness. The incidence of sinus involve- ing fine, round to linear matrix calcifications
ment in the descending order is: maxillary are observed. Histologically, it is character-
sinus (78–84%) followed by sphenoid sinus ized by the mass of fungal elements embed-
(15–40%) and the ethmoid sinus (1–15%), ded in a fibrous necrotic matrix with minimal
however, it can involve multiple sinuses mucosal inflammatory reaction. There is no
also. Pathophysiology is still unclear, how- tissue invasion or granulomatous reaction in
ever, it most likely starts with fungal spores the surrounding tissue. The most commonly
gaining access into the paranasal sinuses isolated pathogen on culture is Aspergillus
spontaneously (in the geographic regions of species. Prior to surgery, the risk factors for
heavy antigen exposure) or getting inocu- the development of fungal ball, like previous
lated by surgery/trauma. The spores may sinonasal surgery, dental procedures, or any
then grow on obtaining a favorable environ- traumatic incidents, should be sought.
ment. There are three theories mentioned in Surgical excision with adequate sinus aera-
the literature regarding its development: air- tion is the treatment of choice.
borne, odontogenic, and mixed. ( C) Allergic Fungal Rhinosinusitis (AFRS)
1. Airborne theory: The fungal spores pres- [92, 94–96]:
ent in the air gain access into the sinuses The term was coined by Robson et al. Even
through natural sinus ostia and multiply. though inhabitation of the sinuses by the
These spores can become pathogenic on fungal elements is common and occurs early
being exposed to the favorable anaerobic on in life, only few individuals go on to
environment in the sinuses. The septal develop AFRS. This entity is seen in immu-
deviation and turbinate hypertrophy are nocompetent, atopic patients; more com-
possible contributing factors causing sta- monly in warm and humid climates such as
sis of secretions by osteomeatal obstruc- in the southern and southeastern the USA,
tion leading to the development of India, and the Middle East. The affected
hypoxic environment with lowering of sinuses contain inspissated, thick clay-like
the pH inside the sinuses, creating a (also described as peanut butter jelly like)
favorable atmosphere for the prolifera- fungal muck with mucin varying in color
tion of fungi. from yellow, green, brown to grayish
2. The odontogenic pathway refers to an iat- (Fig. 3.6). Microscopic examination of the
rogenic affection, where the fungal col- eosinophilic mucin shows thick mucus from
ony is inoculated in the maxillary sinus sinus mucosa admixed with dead epithelial
owing to an oroantral communication cells, eosinophils, eosinophil degradation
secondary to dental extraction, periodon- products like Charcot–Leyden crystals, and
tal lesions, or endodontic treatment. other inflammatory cells arranged in a lay-
ered pattern with occasional fungal hyphae.
The preferred terminology for the tenacious 2. Either (a) Methenamine silver stain of allergic
fungal mucin is “Eosinophilic mucin” rather mucin is positive for fungi (without any fun-
than allergic mucin because of the contro- gal elements inside mucosa) or (b) fungal cul-
versies surrounding the allergic etiology of ture is positive (with or without a positive
the disease. Fungal hyphae can be seen on silver stain); 3) sinus mucosal H&E stain is
Hematoxylin and Eosin (H&E) stain, but are characteristic for AFS and indistinguishable
best highlighted by histochemical stains from the mucosal infiltrate in asthmatic bron-
such as silver stains or Periodic Acid Schiff chial mucosa; and.
(PAS). There is geographical variation in the 3. Other histopathological fungal disorders are
fungi isolated on culture from the AFRS excluded.
patients. Most commonly grown organisms
are either Dematiaceous fungi (Alternaria, Bent and Kuhn [97] have described major
Bipolaris, Curvularia, Drechslera, (five) and minor (six) criteria for the diagnosis of
Exserohilum, etc.) or Aspergillus sp. depend- AFS in adults.
ing on geographical location. In India and Major Criteria:
Saudi Arabia, Aspergillus flavus is the com-
monest fungal organism cultured; while in 1 . Type I (IgE-mediated) hypersensitivity
the USA, Dematiaceous fungi can be cul- 2. Nasal polyposis
tured in 70–90% of cases. The pathogenesis 3. Characteristic CT scan findings showing

of this disease remains unclear. It is believed patchy hyperdensities involving sinuses
to be the result of host reaction to fungal pro- 4. Allergic mucin, and
teins instead of actual fungal infection/inva- 5. Positive fungal smear
sion of the tissues. Traditionally, AFRS has
been considered to be a Type I hypersensitiv- Minor Criteria:
ity reaction to fungal antigens. In fact, one of
the widely used diagnostic criteria for AFRS, 1. Concomitant Asthma
the Bent and Kuhn criteria, includes type 1 2. Unilateral disease predominance
hypersensitivity as a major criterion. 3. Radiographic (CT scan) bone erosion
However, not all patients with the pathologic 4. Positive fungal culture
diagnosis of AFRS have systemic (or even 5. Charcot–Leyden crystals, and
local) hypersensitivity to fungi. Bent and 6. Serum eosinophilia
Kuhn [90] proposed five clinical criteria for
the diagnosis of AFS: (1) nasal polyposis; Bent and Kuhn [97] proposed diagnostic for
(2) allergic mucin; (3) characteristic com- AFRS (Table 3.15).
puted tomographic (CT) scan findings show- Currently, these are the most widely accepted
ing patchy hyperdense areas corresponding and used criteria for the diagnosis of AFS. More
to fungal mucin; (4) positive fungal KOH recent studies indicate that fungal protease induced
smear; and (5) type I hypersensitivity diag- production of Th-2 cytokines attracts eosinophils,
nosed by history, skin test, or serology. and the subsequent products of eosinophilic inflam-
These criteria are now referred to as major mation result in the formation of eosinophilic
criteria. mucin. Non-contrast CT scan of paranasal sinus
shows a heterogeneity of signals seen in involved
Schubert and Goetz [96] histopathological cri- sinus (Fig. 3.25), characterized as “starry-sky” or
teria for the diagnosis of AFS: “serpiginous” pattern. The presence of intermittent
hyperdense (corresponding to the deposition of
1. Allergic mucin is present on gross and/or his- heavy metals within eosinophilic mucin) and
topathological evaluation. hypodense signals on CT scan is referred to as
94 K. Davraj et al.
“double-density” sign. Treatment of this disease is surgical clearance of the disease with the reduction
not without controversies. The mainstay of treat- of the risk of recurrence. Utilization of antifungal
ment is the surgical removal of disease with all therapy has been mentioned by some authors in the
mucin to provide good ventilation and facilitate the literature, however, the evidence for or against the
delivery of topical therapy. Steroids can be used in same is sparse [98].
pre and/or postoperative setting to reduce the
inflammatory load and facilitate the more efficient
3.9 art I: Invasive Fungal
P
Sinusitis
Table 3.15 Diagnostic criteria for AFRS
Endoscopic Invasive fungal sinusitis is a potentially lethal
Stage findings Diagnostic criteria entity which if untreated can cause lot of morbid-
Stage 0 No edema off Confirmed type 1
ity and mortality for the patient. It is generally
mucosa and hypersensitivity by
allergic mucin history, skin prick tests, seen in immunocompromised patients and can
or by serology involve intra-orbital or intracranial compartments.
Stage 1 Edema of • Nasal polyposis The incidence and prevalence rate is increasing
mucosa with and • Characteristic CT progressively with more and more uses of antibi-
without allergic finding
mucin otics, chemotherapy drugs, immune-suppressive
Stage 2 Polypoidal • Positive fungal strain or drugs, steroids, intensive care intervention, pro-
edema with or culture long life expectancy in immune deficiency
without allergic • Asthma patients. The risk of invasive fungal infection is
mucin
more in transplanted patients. Invasive fungal
Stage 3 Polyps in the • Fungal elements with
sinus with fungal eosinophilic mucin sinusitis is defined by the presence of fungal
debris or allergic without tissue invasion hyphae within the mucosa, submucosa, bone, or
mucin • One-sided blood vessels of the paranasal sinuses. Invasive
predominance sinonasal fungal infection is a silently progressive
• Bone erosion on
radiology disease that, may invade the adjacent intracranial
• Charcot–Leyden and intra-orbital compartments incurring serious
crystals morbidity. Early recognition and prompt treat-
• Eosinophilia in blood ment are needed in these patients. Aggressive
a b
Fig. 3.25 (a) Axial and (b) coronal non-contrast CT scan corresponding to allergic fungal mucin can be seen. Bony
of paranasal sinus of a patient with extensive allergic fun- thinning and remodeling leading to severe thinning and
gal sinusitis. Expansion of the involved sinuses occupied dehiscence of the roof of posterior ethmoids and the lat-
by the soft tissue density with patchy hyperdense areas eral wall of the sphenoid sinus can be appreciated
treatment in form of antifungal agents and exten- 3.9.1 Clinical Presentations

sive surgical debridement has improved the out-
come in these patients. These patients need to be Invasive fungal infection is characterized by a mass
continuously monitored in follow-up to prevent within one or more paranasal sinuses with evidence
any recurrences. It is broadly divided into two of invasion of contiguous structures such as the
subtypes, acute invasive (fulminant) and chronic base of the skull, orbit, and brain [93]. The patients
invasive. Chronic invasive can be granulomatous have symptoms of chronic rhinosinusitis such as
or non-granulomatous types. sinus pain, nasal discharge, headache, low-grade
fever, and intermittent epistaxis. Maxillary sinus
1. Acute Invasive Fungal Rhinosinusitis seems to be major site for the start of tissue inva-
It is associated with unacceptably high rates sion. Invasion of the fungus into the maxillary floor
of morbidity and mortality. The exact factors leads to palatal erosions. The involvement of orbital
underlying the pathophysiology are unclear, tissue, orbital apex, and cavernous sinuses are pos-
but the environmental load of the fungus, the sible when the extension of infection extends
specific strains, and the immune status of the beyond the ethmoid and sphenoid sinuses. The
host are believed to promote invasive dis- orbital apex syndrome is more commonly seen
ease. A favorable micro-aerophilic local with chronic type and it can present in the form of
environment is considered the trigger that proptosis (Fig. 3.26), orbital neuropathy, and
initiates the proliferation and invasion of a diminished vision [101, 102]. Invasion of adjacent
fungal species that is usually a harmless structures such as the cavernous sinus and anterior
commensal of the upper respiratory tract. cranial fossa may lead to epidural abscess, paren-
Central to the pathophysiology of this dis- chymal cerebritis or abscess, meningitis, cavernous
ease is its angio-invasiveness. Invasive fun- sinus thrombosis, osteomyelitis, mycotic aneurism,
gal rhinosinusitis is characterized by invasion stroke, and hematogenous dissemination [103].
of the organism into the vascular wall, with Granulomatous fungal sinusitis commonly pres-
subsequent hemorrhage or ischemia [99]. ents as proptosis or an enlarging, painless, and
The main challenges encountered in the irregular mass in the cheek, orbit, nose, or parana-
management of this disease include the pres- sal sinuses mimicking an orbital tumor.
ence of the blood-brain barrier that hinders
antifungal penetration intra-cerebrally, the
morbidity of surgery, and the gravity of the 3.9.2 Diagnosis
disease’s complications on the central ner-
vous system. Vascular events are poorly tol- Acute onset of symptoms with the rapid progres-
erated in the central nervous system and one sion of the disease along with the uncontrolled
of the main causes of reported mortalities in comorbid condition especially diabetes and the
the published literature on cerebrally inva- presence of crusting with unhealthy nasal mucosa
sive fungal sinusitis. on nasal endoscopic examination are the features
2. Chronic Invasive Fungal Rhinosinusitis that raised the possibility of invasive fungal
Chronic invasive fungal rhinosinusitis often sinusitis. The nasal endoscopic examination
occurs in healthy individuals, sometime reveals black-to brown crust with unhealthy, con-
patients may have history of CRS, controlled gested mucosa. Biopsy is the gold standard way
medical comorbidities such as diabetes. to confirm the invasion of the fungus into the tis-
Aspergillus fumigatus is the most common sue. The presence of the fungal strains in the
agent isolated [100, 101]. Chronic granuloma- unhealthy nasal mucosa in fungal smear exami-
tous invasive fungal rhinosinusitis is also nation is very much helpful in establishing the
known as primary paranasal granuloma and clinical diagnosis. Mucor species are mostly seen
indolent fungal sinusitis. in acute invasive fungal sinusitis whereas
96 K. Davraj et al.
Aspergillus species are mostly seen chronic inva- sibility of tissue necrosis. Hypodense lesion with
sive fungal sinusitis. osteitis and periostitis and presence of seques-
trum are the other clinical features for acute inva-
sion. In the chronic form, sinus opacification
3.9.3 Imaging appears hyperdense due to the metallic ions
concentrated by the fungus with localized ero-
CT suggests the diagnosis by showing mucosal sion of the sinus wall (Fig. 3.27). It is also invalu-
thickening or the presence of adjoining soft tissue able to assess for bony erosion into adjacent
thickening without erosion of the bony sinus wall orbital and cranial cavities [104, 105]. Sometimes,
in acute invasive form. The absence of enhance- tissues outside sinuses are more involved than
ment of nasal mucosa/turbinates raised the pos- within the sinus (Fig. 3.27b). The dense calcifica-
tion is generally seen in the chronic form of inva-
sive fungal sinusitis. CEMRI is more useful than
CT for indicating the involvement of peri-sinus
soft tissues such as orbit, brain parenchyma. A
decrease in signal intensity on T1-weighted
images and a marked decrease in signal intensity
on T2-weighted images is characteristic of fungal
disease, especially that is caused by aspergillus
(Fig. 3.27c) [104, 105].
3.9.4 Pathology
Histopathology shows the presence of fungal

hyphae in tissue with surrounding inflammatory
infiltrate with the predominance of neutrophils
and associated with foci of necrosis. Invasive
fungal rhinosinusitis is defined by the presence of
fungal hyphae within the mucosa, submucosa,
Fig. 3.26 Left orbital apex syndrome with facial nerve palsy bone, or blood vessels of the paranasal sinuses.
(Courtesy—Dr. Hitesh Verma, Associate Professor, AIIMS, Chronic invasive fungal rhinosinusitis is charac-
New Delhi, India) terized by the dense accumulation of hyphae
a b c
Fig. 3.27 (a) Axial contrast-enhanced CT scan shows tissue and right cavernous sinus infiltration, (c)
right ethmoid and sphenoid sinusitis with the destruction (Courtesy—Dr. Hitesh Verma, Associate Professor,
of the lateral wall of the right sphenoid sinus (arrow). AIIMS, New Delhi, India), T1-weighted MR images
There is invasion of the right cavernous sinus with occlu- show characteristic high signal intensity within the left
sion of the right internal carotid artery. (b) Right orbital maxillary, left posterior ethmoid, and sphenoid sinuses
infiltrating mucosa, blood vessels, and adjacent adult dose of voriconazole is 6 mg/kg twice a day
tissues as muscles and bones, which often exhibit on day one followed by 4 mg/kg twice a day for
necrosis and a nonspecific inflammatory infil- 7 days with the option to decrease to 200 mg
trate. Granulomatous invasive fungal rhinosinus- orally, twice a day thereafter. Therapy for those
itis is characterized by non-caseating granuloma with the overt bone disease should be for at least
with scanty fungal hyphae) within Langerhans- 3–6 months and possibly for 12 months or longer.
type giant cells, together with surrounding vascu- Other regime is 3–6 week course of conventional
litis and perivascular fibrosis. amphotericin B (1 mg/kg/day) or liposomal
amphotericin B (3–5 mg/kg/day) usually secures
a remission and should be followed by itracon-
3.9.5 Treatment azole or voriconazole for 6 months. Posaconazole
(tablets or liquid) is an alternative to control the
The standard management involves a combina- disease and to prevent recurrences.
tion of surgical debridement of necrotic tissues
and long-term antifungal treatment, guided by
culture results if possible, to prevent relapse. The 3.9.6 Outcome and Follow-Up
surgical approach is determined by the CT find-
ings. Patients with angioinvasion might benefit Patients with granulomatous fungal sinusitis are
from a more aggressive therapeutic approach, believed to have a better prognosis than those
such as higher dose of intravenous therapy, early with invasive fungal rhinosinusitis, although
surgical debridement, more intense assessment granulomatous invasive fungal rhinosinusitis
of response, and alternative therapy if the tends to have a high relapse rate. Overall, mor-
response is inadequate and consideration of sup- bidity and mortality appear to be lower than the
plementary gamma interferon therapy [106]. acute invasive disease. Regular follow-up is indi-
Amphotericin B is the initial antifungal choice cated and should continue for about 5 years. A
for mucormycosis. Amphotericin B and CT scan 1 month after surgery (Fig. 3.28) and a
Posaconazole are the drugs used to treat mucor- prolonged course of antifungal chemotherapy,
mycosis. For invasive aspergillosis—The usual with imaging repeated every 3 or 4 months and
Fig. 3.28 Radiology after completion of treatment (Courtesy—Dr. Hitesh Verma, Associate Professor, AIIMS, New
Delhi, India)
98 K. Davraj et al.
endoscopy every 2–3 months to evaluate recur- 13. Favre JJ, Chaffanjon P, Passagia JG, Chirossel

JP. Blood supply of the olfactory nerve. Meningeal
rence should be done [107]. The post-surgical relationships and surgical relevance. Surg Radiol
cavity can be managed after certain period of Anat. 1995;17:133–8.
follow-up. 14. Vaidyanathan S, Barnes M, Williamson P, et al.

Treatment of chronic rhinosinusitis with nasal pol-
yposis with oral steroids followed by topical steroids.
Ann Intern Med. 2011;154:293–302.
References 15. Van den Velde S, Quirynen M, van Hee P, van

Steenberghe D. Halitosis associated volatiles in breath
1. Gouveri E, Katotomichelakis M, Gouveris H, of healthy subjects. J Chromatogr B Anal Technol
Danielides V, Maltezos E, Papanas N. Olfactory dys- Biomed Life Sci. 2007;853:54–61.
function in type 2 diabetes mellitus: an additional 16. Panigrahi S, Sankaran S, Mallik S, Gaddam B,

manifestation of microvascular disease? Angiology. Hanson AA. Olfactory receptor-based polypeptide
2014;65(10):869–76. sensor for acetic acid VOC detection. Mater Sci Eng
2. Sahin-Yilmaz A, Naclerio RM. Anatomy and physi- C Mater Biol Appl. 2012;32:1307–13.
ology of the upper airway. Proc Am Thorac Soc. 17. Fokkens WJ, Lund VJ, Mullol J et al. European posi-
2011;8(1):31–9. tion paper on rhinosinusitis and nasal polyps 2012.
3. Antunes MB, Gudis DA, Cohen NA. Epithelium, cilia, Rhinol Suppl 2012;(23):3 p preceding table of con-
and mucus: their importance in chronic rhinosinusitis. tents, 1–298.
Immunol Allergy Clin N Am. 2009;29(4):631–43. 18. Erskine SE, Verkerk MM, Notley C, et al. Chronic rhi-
4. Lund VJ. Nasal physiology: neurochemical receptors, nosinusitis: patient experiences of primary and sec-
nasal cycle, and ciliary action. Allergy Asthma Proc. ondary care – a qualitative study. Clin Otolaryngol.
1996;17(4):179–84. 2015;41:8–14.
5. Morris LG, Burschtin O, Lebowitz RA, Jacobs JB, 19. Ferguson BJ. Eosinophilic mucin rhinosinusitis: a

Lee KC. Nasal obstruction and sleep-disordered distinct clinicopathological entity. Laryngoscope.
breathing: a study using acoustic rhinometry. Am J 2000;110:799–813.
Rhinol. 2005;19(1):33–9. 20. Bhattacharyya N. Contemporary assessment of the
6. Haavisto LE, Sipilä JI. Acoustic rhinometry, rhino- disease burden of sinusitis. Am J Rhinol Allergy.
manometry and visual analogue scale before and after 2009;23(4):392–5.
septal surgery: a prospective 10-year follow-up. Clin 21. Tatar EC, Tatar I, Ocal B, et al. Prevalence of bioflms
Otolaryngol. 2013;38(1):23–9. and their response to medical treatment in chronic rhi-
7. Singh A, Patel N, Kenyon G, Donaldson G. Is nosinusitis without polyps. Otolaryngol Head Neck
there objective evidence that septal surgery Surg. 2012;146(4):669–75.
improves nasal airflow? J Laryngol Otol. 22. Seiberling KA, Conley DB, Tripathi A, et al.

2006;120(11):916–20. Superantigens and chronic rhinosinusitis: detec-
8. Eduardo Nigro C, Faria Aguar Nigro J, Mion O, tion of staphylococcal exotoxins in nasal polyps.
Ferreira Mello J, Louis Voegels R, Roithmann R. A Laryngoscope. 2005;115(9):1580–5.
systematic review to assess the anatomical cor- 23. Conley DB, Tripathi A, Seiberling KA, et al.

relates of the notches in acoustic rhinometry. Clin Superantigens and chronic rhinosinusitis: skewing
Otolaryngol. 2009;34(5):431–7. of T–cell receptor V beta–distributions in polyp–
9. Morgan NJ, MacGregor FB, Birchall MA, Lund derived CD4+ and CD8+ T cells. Am J Rhinol.
VJ, Sittampalam Y. Racial differences in nasal fossa 2006;20(5):534–9.
dimensions determined by acoustic rhinometry. 24. Lanza DC, Kennedy DW. Adult rhinosinusitis defined.
Rhinology. 1995;33(4):224–8. Otolaryngol Head Neck Surg. 1997;117:S1S7.
10. Merkle J, Kohlhas L, Zadoyan G, Mösges R,
25. Van Zele T, Claeys S, Gevaert P, et al. Differentiation
Hellmich M. Rhinomanometric reference intervals of chronic sinus diseases by measurement of inflam-
for normal total nasal airflow resistance. Rhinology. matory mediators. Allergy. 2006;61(11):1280–9.
2014;52(4):292–9. 26. Bhattacharyya N. The economic burden and symptom
11. Milardi D, Cacciola A, Calamuneri A, Ghilardi
manifestations of chronic rhinosinusitis. Am J Rhinol.
MF, Caminiti F, Cascio F, Andronaco V, Anastasi 2003;17(1):27–32.
G, Mormina E, Arrigo A, Bruschetta D, Quartarone 27. Zhang N, Van Zele T, Perez-Novo C, et al. Different
A. The olfactory system revealed: Non- invasive map- types of T–effector cells orchestrate mucosal inflam-
ping by using constrained spherical deconvolution mation in chronic sinus disease. J Allergy Clin
tractography in healthy humans. Front Neuroanat. Immunol. 2008;122(5):961–8.
2017;11:32. 28. Lund VJ, Mackay IS. Staging in rhinosinusitis.

12. Hendrix P, Griessenauer CJ, Foreman P, Shoja MM, Rhinology. 1993;31(4):183–4.
Loukas M, Tubbs RS. Arterial supply of the upper 29. Zalmanovici A, Yaphe J. Intranasal steroids for

cranial nerves: a comprehensive review. Clin Anat. acute sinusitis. Cochrane Database Syst Rev.
2014;27:1159–66. 2009;4:CD005149.
30. Harvey R, Hannan SA, Badia L, Scadding G. Nasal in children and adolescents. J Paedr. 1988;113(1Pt
saline irrigations for the symptoms of chronic 1):15–23.
rhinosinusitis. Cochrane Database Syst Rev. 47. Schofield G, Farooque S. Recommended manage-

2007;3:CD006394. ment and recent advances in allergic rhinitis. Drug
31. Martinez-Devesa P, Patiar S. Oral steroids for
Rev. 2014:21–8.
nasal polyps. Cochrane Database Syst Rev. 48. Finn R. John Bostock, hay fever, and the mechanism
2011;7:CD005232. of allergy. Lancet. 1992;340(8833):1453–5. https://
32.
Bassiouni A, Naidoo Y, Wormald PJ. When doi.org/10.1016/0140-6736(92)92634-r.
FESS fails: the inflammatory load hypothesis in 49.
Björkstén B, Clayton T, Ellwood P, Stewart
refractory chronic rhinosinusitis. Laryngoscope. A, Strachan D, ISAAC Phase III Study Group.
2012;122:460–6. Worldwide time trends for symptoms of rhinitis and
33. Bent JP, Cuilty-Siller C, Kuhn FA. The frontal cell conjunctivitis: Phase III of the International Study
as a cause of frontal sinus obstruction. Am J Rhinol. of Asthma and Allergies in Childhood. Pediatr
1994;8:185–91. Allergy Immunol. 2008;19(2):110–24. https://doi.
34. Wormald PJ, Hoseman W, Callejas C, et al. The inter- org/10.1111/j.1399-3038.2007.00601.x.
national frontal sinus anatomy classification (IFAC) 50. Stempel DA, Woolf R. The cost of treating allergic
and classification of the extent of endoscopic fron- rhinitis. Curr Allergy Asthma Rep. 2002;2(3):223–30.
tal sinus surgery (EFSS). Int Forum Allergy Rhinol. https://doi.org/10.1007/s11882-002-0023-0.
2016;6(7):677–96. 51.
McCaig LF, Nawar EW. National Hospital
35. Draf W. Endonasal micro-endoscopic frontal sinus Ambulatory Medical Care Survey: 2004 emergency
surgery: the fulda concept. Oper Tech Otolaryngol department summary. Adv Data. 2006;372:1–29.
Head Neck Surg. 1991;2(4):234–40. 52. Asher MI, Montefort S, Björkstén B, et al. Worldwide
36. Saini AT, Govindaraj S. Evaluation and decision mak- time trends in the prevalence of symptoms of asthma,
ing in frontal sinus surgery. Otolaryngol Clin N Am. allergic rhinoconjunctivitis, and eczema in childhood:
2016;49(4):911–25. ISAAC Phases One and Three repeat multicountry
37.
Mamman-Prasad E, Murillo JL, Titelbaum cross-sectional surveys [published correction appears
JA. Infectious disease rounds: Pott’s puffy in Lancet. 2007 Sep 29;370(9593):1128]. Lancet.
tumour with intracranial complications. N J Med. 2006;368(9537):733–43. https://doi.org/10.1016/
1992;89(7):537–9. S0140-6736(06)69283-0.
38. Fokkens WJ, Lund VJ, Mullol J, et al. EPOS 2012: 53. Scadding GK, Durham SR, Mirakian R, et al. BSACI
European position paper on rhinosinusitis and nasal guidelines for the management of allergic and non-
polyps 2012. A summary for Otorhinolaryngologists. allergic rhinitis. Clin Exp Allergy. 2008;38(1):19–42.
Rhinology. 2012;50(1):1–12. https://doi.org/10.1111/j.1365-2222.2007.02888.x.
39. Epstein VA, Kern RC. Invasive fungal sinusitis and 54. Smith HE, Hogger C, Lallemant C, Crook D, Frew
complications of rhinosinusitis. Otolaryngol Clin N AJ. Is structured allergy history sufficient when
Am. 2008;41(3):497–524. assessing patients with asthma and rhinitis in general
40. Siedek V, Kremer A, Betz CS, Tschilsner U, Berghaus practice? J Allergy Clin Immunol. 2009;123(3):646–
A, Leunig A. Management of orbital complications 50. https://doi.org/10.1016/j.jaci.2008.11.005.
due to rhinosinusitis. Eur Arch Otorhinolaryngol. 55. Nasser M, Fedorowicz Z, Aljufairi H, McKerrow

2010;267(12):1881–6. W. Antihistamines used in addition to topi-
41. el-Silimy O. The place of endonasal endoscopy
cal nasal steroids for intermittent and persis-
in the treatment of orbital cellulitis. Rhinology. tent allergic rhinitis in children. Cochrane
1995;33(2):93–6. Database Syst Rev. 2010;7:CD006989. https://doi.
42. Chandler JR, Langenbrunner DJ, Stevens ER. The org/10.1002/14651858.CD006989.pub2.
pathogenesis of orbital Complications in acute sinus- 56. Klimek L, Bachert C, Pfaar O, et al. ARIA guideline
itis. Laryngoscope. 1970;80(9):1414–28. 2019: treatment of allergic rhinitis in the German
43. Maniglia GJ, Arnold JE, Ganz E. Intracranial
health system. Allergol Select. 2019;3(1):22–50.
abscesses secondary to nasal, sinus and orbital infec- https://doi.org/10.5414/ALX02120E.
tions in adults and children. Arch Otolaryngol Head 57. Rondón C, Canto G, Blanca M. Local allergic rhinitis:
Neck Surg. 1989;115:1424–9. a new entity, characterization and further studies. Curr
44. Clayman GL, Adams GC, Paregh DR, Koopmann
Opin Allergy Clin Immunol. 2010;10(1):1–7. https://
CF Jr. Intracranial complications of PNS, Sinusitis: doi.org/10.1097/ACI.0b013e328334f5fb.
a combined institute review. Laryngoscope. 58. van Cauwenberge P, Bachert C, Passalacqua G, et al.
1991;101(3):234–9. Consensus statement on the treatment of allergic rhi-
45.
Lerner DN, Choi SS, Zalzal GH, Johnson nitis. European Academy of Allergology and Clinical
DL. Intracranial complication of sinusitis in child- Immunology. Allergy. 2000;55(2):116–34. https://doi.
hood. Ann Otol Rhino Laryngol. 1995;104(4 Pt org/10.1034/j.1398-9995.2000.00526.x.
1):288–93. 59. Small M, Piercy J, Demoly P, Marsden H. Burden
46. Johnson DL, Markle BM, Wiedermann BL, Hanahan of illness and quality of life in patients being
L. Treatment of intracranial abscesses a/w sinusitis treated for seasonal allergic rhinitis: a cohort sur-
100 K. Davraj et al.
vey. Clin Transl Allergy. 2013;3(1):33. https://doi. 72. Akdis CA, Akdis M. Mechanisms of allergen-

org/10.1186/2045-7022-3-33. specific immunotherapy. J Allergy Clin Immunol.
60. Rodrigo GJ, Neffen H. Efficacy of fluticasone furoate 2011;127(1):18–29. https://doi.org/10.1016/j.
nasal spray vs. placebo for the treatment of ocular jaci.2010.11.030.
and nasal symptoms of allergic rhinitis: a systematic 73. Demoly P, Passalacqua G, Pfaar O, Sastre J, Wahn
review. Clin Exp Allergy. 2011;41(2):160–70. https:// U. Management of the polyallergic patient with
doi.org/10.1111/j.1365-2222.2010.03654.x. allergy immunotherapy: a practice-based approach.
61. Bielory L. Ocular symptom reduction in patients with Allergy Asthma Clin Immunol. 2016;12:2. https://doi.
seasonal allergic rhinitis treated with the intrana- org/10.1186/s13223-015-0109-6.
sal corticosteroid mometasone furoate. Ann Allergy 74.
Akdis CA, Barlan IB, Bahceciler N, Akdis
Asthma Immunol. 2008;100(3):272–9. https://doi. M. Immunological mechanisms of sublingual immu-
org/10.1016/S1081-1206(10)60453-X. notherapy. Allergy. 2006;61(Suppl 81):11–4. https://
62. Corren J. Intranasal corticosteroids for allergic rhi- doi.org/10.1111/j.1398-9995.2006.01159.x.
nitis: how do different agents compare? J Allergy 75. Untersmayr E, Jensen-Jarolim E. The role of protein
Clin Immunol. 1999;104(4 Pt 1):S144–9. https://doi. digestibility and antacids on food allergy outcomes. J
org/10.1016/s0091-6749(99)70310-6. Allergy Clin Immunol. 2008;121(6):1301–10. https://
63. Bryson HM, Faulds D. Intranasal fluticasone pro-
doi.org/10.1016/j.jaci.2008.04.025.
pionate. A review of its pharmacodynamic and phar- 76. Pattanaik D, Lieberman P. Vasomotor rhinitis. Curr
macokinetic properties, and therapeutic potential in Allergy Asthma Rep. 2010;10:84–91.
allergic rhinitis. Drugs. 1992;43(5):760–75. https:// 77. Brandt D, Bernstein JA. Questionnaire evalua-

doi.org/10.2165/00003495-199243050-00009. tion and risk factor identification for nonallergic
64. Daley-Yates PT, Baker RC. Systemic bioavailabil-
vasomotor rhinitis. Ann Allergy Asthma Immunol.
ity of fluticasone propionate administered as nasal 2006;96(4):526–32.
drops and aqueous nasal spray formulations. Br 78. Settipane RA, Charnock DR. Epidemiology of rhinitis:
J Clin Pharmacol. 2001;51(1):103–5. https://doi. allergic and nonallergic. In: Baraniuk JN, Shusterman
org/10.1046/j.1365-2125.2001.01325.x. D, editors. Nonallergic Rhinitis. New York: Informa;
65. Daley-Yates PT, Kunka RL, Yin Y, Andrews SM,
2007. p. 23–34.
Callejas S, Ng C. Bioavailability of fluticasone propi- 79. Blom HM, Van Rijswijk JB, Garrelds IM, Mulder
onate and mometasone furoate aqueous nasal sprays. PG, Timmermans T, Gerth van Wijk R. Intranasal
Eur J Clin Pharmacol. 2004;60(4):265–8. https://doi. capsaicin is efficacious in nonallergic, noninfectious
org/10.1007/s00228-004-0763-y. rhinitis. A placebo-controlled study. Clin Exp Allergy.
66. Bousquet J, Van Cauwenberge P, Bachert C, et al. 1997;27:1351–8.
Requirements for medications commonly used 80. Sarin S, Undem B, Sanico A, Togias A. The role of the
in the treatment of allergic rhinitis. European nervous system in rhinitis. J Allergy Clin Immunol.
Academy of Allergy and Clinical Immunology 2006;118:999–1014.
(EAACI), Allergic Rhinitis and its Impact on Asthma 81. Sin B, Togias A. Pathophysiology of allergic and non-
(ARIA). Allergy. 2003;58(3):192–7. https://doi. allergic rhinitis. Proc Am Thorac Soc. 2011;8:106–14.
org/10.1034/j.1398-9995.2003.00054.x. 82. Lindberg S, Malm L. Comparison of allergic rhinitis
67. Graft D, Aaronson D, Chervinsky P, et al. A pla- and vasomotor rhinitis patients on the basis of a com-
cebo- and active-controlled randomized trial of pro- puter questionnaire. Allergy. 1993;48:602–7.
phylactic treatment of seasonal allergic rhinitis with 83. Scarupa MD, Kaliner MA. Nonallergic rhinitis, with a
mometasone furoate aqueous nasal spray. J Allergy focus on vasomotor rhinitis. WAO. 2009;2:20–5.
Clin Immunol. 1996;98(4):724–31. https://doi. 84. Aksoy F, Yildirim YS, Veyseller B, et al. Midterm
org/10.1016/s0091-6749(96)70119-7. outcomes of out fracture of the inferior turbinate.
68. Garavello W, Romagnoli M, Sordo L, Gaini RM,
Otolaryngol Head Neck Surg. 2010;143(4):579–84.
Di Berardino C, Angrisano A. Hypersaline nasal 85. Elwany S, Gaimaee R, Fattah HA. Radiofrequency
irrigation in children with symptomatic sea- bipolar submucosal diathermy of the inferior turbi-
sonal allergic rhinitis: a randomized study. Pediatr nates. Am J Rhinol. 1999;13(2):145–9.
Allergy Immunol. 2003;14(2):140–3. https://doi. 86. Woodhead CJ, Wickham MH, Smelt GJ, et al. Some
org/10.1034/j.1399-3038.2003.00021.x. observations on submucous diathermy. J Laryngol
69. Tomooka LT, Murphy C, Davidson TM. Clinical
Otol. 1989;103(11):1047–9.
study and literature review of nasal irrigation. 87. Cavaliere M, Mottola G, Iemma M. Comparison of
Laryngoscope. 2000;110(7):1189–93. https://doi. the effectiveness and safety of radiofrequency tur-
org/10.1097/00005537-200007000-00023. binoplasty and traditional surgical technique in treat-
70. Bochner BS, Hamid Q. Advances in mechanisms ment of inferior turbinate hypertrophy. Otolaryngol
of allergy. J Allergy Clin Immunol. 2003;111(3 Head Neck Surg. 2005;133(6):972–8.
Suppl):S819–23. https://doi.org/10.1067/mai.2003.149. 88. Jourdy D. Inferior turbinate reduction. Oper Tech
71. Bousquet J, et al. WHO position paper – allergen Otolaryngol. 2014;25:160–70.
immunotherapy: therapeutic vaccines for allergic dis- 89. Ashleigh Halderman MD, Raj Sindwani
eases. Allergy. 1998;53(Suppl. 44):4–42. MD. Surgical management of vasomotor rhini-
tis: a systematic review. Am J Rhinol Allergy. 100. Sharif MS, Ali S, Nisar H. Frequency of granulo-
2015;29:128–34. matous invasive fungal sinusitis in patients with
90. Sharma S. Understanding allergic fungal rhino- clinical suspicion of chronic fungal rhinosinusitis.
sinusitis. Glob J Otolaryngol. 2018;13(3):GJO. Cureus. 2019;11(5):e4757. https://doi.org/10.7759/
MS.ID.555865. cureus.4757.
91. Thompson GR III, Patterson TF. Fungal dis- 101. Alrajhi AA, Enani M, Mahasin Z, Al-Omran
ease of the nose and paranasal sinuses. J Allergy K. Chronic invasive aspergillosis of the parana-
Clin Immunol. 2012;129(2):321–6. https://doi. sal sinuses in immunocompetent hosts from Saudi
org/10.1016/j.jaci.2011.11.039. Arabia. Am J Trop Med Hyg. 2001;65(1):83–6.
92. Montone KT. Pathology of fungal rhinosinusitis: a https://doi.org/10.4269/ajtmh.2001.65.83.
review. Head Neck Pathol. 2016;10(1):40–6. https:// 102. Soler ZM, Schlosser RJ. The role of fungi in
doi.org/10.1007/s12105-016-0690-0. diseases of the nose and sinuses. Am J Rhinol
93. Raz E, Win W, Hagiwara M, Lui YW, Cohen B, Allergy. 2012;26(5):351–8. https://doi.org/10.2500/
Fatterpekar GM. Fungal sinusitis. Neuroimaging ajra.2012.26.3807.
Clin N Am. 2015;25(4):569–76. https://doi. 103. Hirabayashi KE, Idowu OO, Kalin-Hajdu E, et al.
org/10.1016/j.nic.2015.07.004. Invasive fungal sinusitis: risk factors for visual acuity
94. Cojocari L, Sandul A. Literature review. Noninvasive outcomes and mortality. Ophthalmic Plast Reconstr
fungal rhinosinusitis. Romanian J Rhinol. Surg. 2019;35(6):535–42. https://doi.org/10.1097/
2017;7(26):75–81. IOP.0000000000001357.
95. Berlucchi M, Pedruzzi B. Allergic fungal sinusitis 104. Reddy CE, Gupta AK, Singh P, Mann SB. Imaging
in children. J Aller Ther. 2012;S5:004. https://doi. of granulomatous and chronic invasive fungal
org/10.4172/2155-6121.S5-004. sinusitis: comparison with allergic fungal sinusitis.
96. Schubert MS, Goetz DW. Evaluation and treatment of Otolaryngol Head Neck Surg. 2010;143(2):294–
allergic fungal sinusitis. I. Demographics and diag- 300. https://doi.org/10.1016/j.otohns.2010.02.027.
nosis. J Allergy Clin Immunol. 1998;102(3):387–94. 105. Siddiqui AA, Bashir SH, Ali Shah A, et al. Diagnostic
https://doi.org/10.1016/s0091-6749(98)70125-3. MR imaging features of craniocerebral Aspergillosis
97. Bent JP III, Kuhn FA. Diagnosis of aller- of sino-nasal origin in immunocompetent patients.
gic fungal sinusitis. Otolaryngol Head Acta Neurochir. 2006;148(2):155–66. https://doi.
Neck Surg. 1994;111(5):580–8. https://doi. org/10.1007/s00701-005-0659-3.
org/10.1177/019459989411100508. 106. Smith NL, Denning DW. Clinical implications
98. Head K, Sharp S, Chong LY, Hopkins C, Philpott of interferon-γ genetic and epigenetic variants.
C. Topical and systemic antifungal therapy Immunology. 2014;143(4):499–511. https://doi.
for chronic rhinosinusitis. Cochrane Database org/10.1111/imm.12362.
Syst Rev. 2018;9(9):CD012453. https://doi. 107. Krishnan KU, Agatha D, Selvi R. Fungal rhinosi-
org/10.1002/14651858.CD012453.pub2. nusitis: a clinicomycological perspective. Indian
99. Panda NK, Sharma SC, Chakrabarti A, Mann J Med Microbiol. 2015;33(1):120–4. https://doi.
SB. Paranasal sinus mycoses in north India. org/10.4103/0255-0857.148407.
Mycoses. 1998;41(7–8):281–6. https://doi.
org/10.1111/j.1439-0507.1998.tb00339.x.
Granulomatous Disease
and Faciomaxillary Trauma 4
Gaurav Gupta, Pooja D. Nayak, Manju Silu,
Shashank Nath Singh, and Harpreet Kocher
Contents
4.1 art A: Granulomatous Disease of the Nose and Paranasal Sinuses
P 104
4.1.2 Other Granulomatous Pathology 111
4.2 Part B: Atrophic Rhinitis 111
4.2.1 athology
P 112
4.2.2 Management Aim 113
4.2.3 Surgical Management 113
4.3 Part C: Maxillofacial Trauma 114
4.3.2 Imaging 115
4.3.3 Timing of Surgical Intervention 116
4.3.4 Airway Management During Surgery 116
4.3.5 Management of Nasal Bone Fractures 117
4.3.6 Zygomatic Fractures 118
4.3.7 Fractures of Midface 118
4.3.8 Orbital Fractures 119
4.3.9 Postoperative Care 119
References 119
Granulomatous diseases can affects any body. It is

broadly classified into specific and non specific
G. Gupta (*) · P. D. Nayak · M. Silu type. bacterial & fungal granulomatous diseases
ENT, SP Medical College, are the specific type of diseases. Granulomatosis
Bikaner, Rajasthan, India with polyangiitis (Wegeners’ granulomatosis),
e-mail: drgauravgupta24@gmail.com
sarcoidosis, Churg-Strauss syndrome, NK/T
S. N. Singh cell lymphoma are the types of non specific dis-
ENT, SMS Medical College,
Jaipur, Rajasthan, India eases. Granuloma is the characterstic feature
formed by the aggregation of macrophages.
H. Kocher
ENT, Yatharth Superspeciality Hospital, Macrophages surrounds by the layer of leuko-
Greater Noida, UP, India cytes. Each granulomatous disease generates
104 G. Gupta et al.
s pecific h istopathological feature. majority of dis- chronic inflammatory reaction, characterized by

eases are managed by specific medical manag- the focal accumulation of concentric layers of cells
ment. Atrophic rhinitis is characterized by consisting of activated macrophages called epithe-
progressive atrophy of nasal mucosa and bones lioid cells and multinucleated giant cells sur-
within the turbinates. The symptoms are foul smell rounded by lymphocytes and fibroblasts. It is a
with recurrent nasal crusting, headache, epistaxis, type IV hypersensitivity reaction. It is a protective
and nasal obstruction. The endoscopic examina- defense reaction by the host, where the immune
tion reveals roomy nasal cavity with brownish- system attempts to wall off substance that is for-
green crust and atrophy of turbinates. The natural eign but is unable to eliminate. Two factors con-
ostium of maxillary and sphenoid sinuses is visible tributes to the formation of granuloma.
on routine diagnostic endoscopy. The exact etiol-
ogy is unknown for primary type but is usually 1. The inducer agent, which is a pathogen or for-
initiates at puberty with female preponderance, eign body, the intrinsic toxicity of which can
indicative of endocrine inequality. Malnutrition, damage the tissues.
autoimmunity, and hereditary factor are the other 2. The vigorous immune-inflammatory T-cell-
important etiological factors. Prior nasal surgery, mediated response is evoked by the pathogen/
trauma, and chronic sinusitis are the common etio- foreign body recruiting macrophages and
logical factors for secondary type. A broad range phagocytosis secreting tissue damaging sub-
of bacterial flora has been cultured in atrophic rhi- stances, during the activated stage.
nitis. The primary aim of conservative treatment is
regular cleaning of the nasal cavity. Nasal douches, Several granulomatous diseases have a predi-
25% glucose in glycerine, human placental extract, lection to involve the airways. These diseases are
etc. are tried to improve symptomatology. Surgical often characterized by a local inflammatory
approaches are focused on narrowing of the nasal response in the airways, particularly in the upper
cavity by medialization of turbinates, by increas- nasal passages.
ing the nasal septum thickness, and by narrowing Etiology:
of the vestibule.
The major function of the facial skeleton is 1. Infective
providing support to sphincter muscles. Facial 2. Inflammatory
injuries account 10% of accidental trauma. The 3. Neoplastic
lines of management include the establishment of
secured airway, controlled breathing, mainte- 1. Infectious Granulomatous Disease:
nance of circulation, disability assessment, and (A) Bacterial
exposure of all injuries. The majority of facio- (B) Fungal
maxillary traumas are managed by semi-rigid (C) Protozoal
internal fixation. The outcomes are generally
assessed by fine dental occlusion, re- (A) Bacterial Granulomatous Disease:
establishment of facial esthetics. 1. Tuberculosis—It is a form of extrapul-
monary tuberculosis. Nasal tuberculosis
is usually secondary either to pulmonary
4.1 Part A: Granulomatous tuberculosis or tuberculosis of facial skin
Disease of the Nose (Fig. 4.1).
and Paranasal Sinuses Primary disease of the nose is rare.
Nasal secretions, nasal vibrissae, and the
4.1.1 Introduction inherent resistance offered by nasal
mucosa and ciliary clearance are the pos-
Granulomatous disorders comprise a large number sible explanation for the lower occur-
of diseases sharing the histological denominator of rence of nasal tuberculosis. Tuberculosis
granuloma formation. Granuloma is defined as a in the head and neck region is uncommon
4 Granulomatous Disease and Faciomaxillary Trauma 105
Fig. 4.2 The endoscopic photograph is showing cheesy

Fig. 4.1 The clinical photograph is showing nasal tuber- material (red arrow) in sphenoid sinus with erosion of
culosis. Nasal tip and overlying skin is involved by tumor posterior wall with dural breach (white arrow) (Courtesy—
Dr. Hitesh Verma, Associate Professor, AIIMS, New
Delhi, India)
and constitutes 2–6% of all types of
TB. In the last decades, extrapulmonary bacillus Mycobacterium leprae. The nose
tuberculosis is rising due to HIV co- is one of the chief organs that is affected
infection. Mycobacterium tuberculosis is by this disease. It is frequently deformed
the causative bacteria and it is spread by and disfigured and it contributes to the
droplet formation. Nasal TB remains characteristic facies of leprotic patients.
asymptomatic until it has progressed to Patients can be classified into three
the advance stage. The most common groups, each with slightly different signs
presenting symptom is nasal obstruction, and symptoms:
discharge, epistaxis, crusting, and post- • Paucibacillary (PB), or tuberculoid
nasal discharge. On examination, nasal disease: Characterized by one or a
granuloma and ulceration can be found few hypo- pigmented or hyper-pig-
in cartilaginous septum, cleft of the nasal mented skin macules that exhibit loss
ala, or facial abscesses may be present. of sensation due to infection of the
Sphenoid sinus, petrous apex involve- peripheral nerves supplying the
ment can present with retropharyngeal region. In these patients, nasal presen-
abscess by extension of abscess along the tation is with skin lesions extending
periosteum [1] (Fig. 4.2). Incisional or up to the nasal vestibule. The nasal
punch biopsy from the affected site is the mucosa is not involved.
preferred method of diagnostic sampling • Multibacillary (MB), or leproma-
for ENT lesions, and tissue should be tous disease is characterized by gen-
sent for: histopathology, staining for eralized or diffuse involvement of the
acid-fast bacilli (fluorochrome or ZN skin, a thickening of the peripheral
staining), culture. The treatment policy nerves has the potential to involve
for nasal tuberculosis is administered as other organs, the eyes, nose, testes,
per national guidelines. Nasal tuberculo- and bone. The nodular form of this
sis is consider as bony tuberculosis & it condition is the most advanced form
is managed by minimum 9 month of the disease. Patient can present
therapy. nasal discharge and, crusting. On
2.
Leprosy: It is a slowly progressive, examination, nodular thickening of
chronic infectious disease caused by the nasal mucosa in the anterior end of
106 G. Gupta et al.
the inferior turbinate is seen. Other

features are Collapse of the anterior
bridge of the nose with the destruc-
tion of anterior nasal spine, destruc-
tion of bony and cartilaginous
portions of nasal septum.
• Borderline, or dimorphous,
Hansen’s disease is the most com-
mon form. Frequently, the initial
form consisting of a few lesions,
either evolves into the other forms or
resolves spontaneously.
Scrapings of the nasal mucosa and skin
biopsy shows the presence of acid-fast
lepra bacilli which are present in the
foamy appearing histiocytes called lepra
cells. The treatment of leprosy is in the Fig. 4.3 The clinical photograph is showing complete
form of Multi Drug Therapy (MDT), stenosis of the left nasal cavity (Courtesy—Dr. Pirabhu S,
which is the combination of two or three Mch candidate, AIIMS, New Delhi, India)
of the following drugs: Rifampicin,
Dapsone, Clofazimine [2]. (c) Sclerotic/Cicatricial: Nasal deformi-
3.
Rhinoscleroma: It is found worldwide ties, anosmia, oral anesthesia, dys-
including Central America, Chili, Central phonia, dysphagia, and stridor could
Africa, India, Indonesia, and Middle East happen (Fig. 4.3).
countries. The disease usually presents in The diagnosis of Rhinoscleroma is
the second and third decades of life with clinched with histological confirmation.
slight female predominance. The The diagnostic histological changes are
Klebsiella rhinoscleromatis is the caus- seen only in the granulomatous phase.
ative organism. It is generally found in Dense infiltration by lymphocytes,
rural areas with poor socioeconomic con- plasma cells, Russell bodies, and the
ditions. The exact pathogenesis of the pathognomonic large Mikulicz cells are
disease is unclear. Transmission of this the histopathological features seen.
disease is via airborne routes. Humans Mikulicz cells are foamy macrophages
are the only identified host. It is a slowly with numerous cytoplasmic vacuoles
progressive disease with insidious onset containing viable and nonviable
and indolent course. Nasal cavity is pri- Klebsiella bacilli. They are sparse or
marily affected in 95–100% of cases. absent in the initial catarrhal and final
Nasopharynx, nasal sinuses, pharynx, sclerotic stages and abundant in the pro-
larynx, trachea, and bronchi may also be liferative phase. Extensive fibrosis and
involved. The disease progresses through few inflammatory cells are the histologi-
three sequential and overlapping phases. cal findings in the fibrotic phase. Intra-
(a) Catarrhal/Rhinitis: Patients present cytoplasmic bacilli are best demonstrated
with non-specific rhinitis. by special staining using periodic
(b) Granulomatous/Florid: Foul smell- acid-Schiff (PAS), Giemsa, Gram, silver,
ing purulent discharge, epistaxis, or Warthin-Starry stains, and type III
nasal obstruction, and crusting. On Klebsiella antigen can be detected
examination, bluish red, rubbery by immunohistochemistry. Antibiotics
granulomatous lesions are seen. that demonstrated efficacy includes
s treptomycin, doxycycline, tetracyclines, resolve spontaneously within 3 months

rifampicin, second and third-generation of appearance. Tertiary Syphilis is char-
cephalosporins, sulfonamides, clofazi- acterized by the formation of Gumma.
mine, ciprofloxacin, and ofloxacin. K. Gummas are granulomatous, nodular
rhinoscleromatis is an intracellular bacte- lesions with variable central necrosis and
rium; it responds well to prolonged it develops as early as 2 years after initial
courses of rifampicin and fluoroquino- infection. These lesions most commonly
lones, as these antibiotics can achieve affect the skin and bones. Nasal features
high concentrations in macrophages. are mucosal ulcerations, necrosis of nasal
Fluoroquinolones are recommended for septum, ozoena or atrophic rhinitis, ste-
their excellent activity against Gram- nosis, and atresia of vestibules,
negative bacilli, intracellular efficacy, Perforations of palate, and external defor-
and low toxicity profile. The current rec- mities in the form of saddle nose. Lesions
ommendation consists of a combination rarely heal spontaneously but resolve
of ciprofloxacin and doxycycline for at rapidly with appropriate antibiotic ther-
least 6 months. Combination therapy is apy. Congenital syphilis is divided into
preferred due to the high relapse rates of stages: early manifestations appearing in
the disease. Surgical debridement can the first 2 years of life, late manifesta-
also be considered if there is significant tions appears after 2 years, and residual
airway obstruction or cosmetic defor- stigmata. Dark ground microscopy from
mity. Other rarer complications to keep lesions of primary and secondary syphilis
in mind include stenosis leading to respi- and serology are the mainstay of diagno-
ratory obstruction (Fig. 4.3), hemor- sis. Penicillin is the drug of choice and
rhage, intracranial invasion, and treatment duration is based on the type of
malignancy transformation [3]. lesion [4, 5].
4. Syphilis: Syphilis is an infectious vene- (B) Fungal Granulomatous Disease:
real disease caused by the spirochete 1.
Rhinosporidiosis—It is caused by
Treponema pallid. Syphilis is acquired Rhinosporidium seeberi. Greater than
by direct contact, usually sexual, with 90% cases are reported from India, Sri
active primary or secondary lesions. Lanka, and Pakistan. It is most prevalent
Infection also occurs when organisms in southern India. The disease is mostly
cross the placenta to infect the fetus in a seen in individuals from ages 15–40.
pregnant woman. T. pallidum’s only Males tend to be affected more than
known natural host is human. Syphilis is females by a ratio of 4:1, most likely
a multistage disease with diverse and because of greater levels of outdoor
wide-ranging manifestations. Clinical activity among males. There is no known
manifestations separate the disease into vector for rhinosporidiosis. Nasal infec-
stages. Primary syphilis rarely involves tion generally occurs after swimming or
the nasal cavity. A single chancre at the bathing in stagnant freshwater ponds,
site of inoculation develops an average of lakes, or rivers that contain the organism.
3 weeks after exposure. It is indurate and Eye infection is believed to occur from
progresses to non-purulent ulceration dust or air. Mature sporangia measure
with regional lymphadenopathy. approximately 100–300 microns. They
Secondary syphilis occurs within are filled with large numbers of daughter
3 months of initial infection and is some- cells that are called endospores.
times quite subtle or disseminated muco- Symptoms are variable and depend on
cutaneous rash and adamant coryza. the location of the polyps. The nose and
Manifestations of secondary syphilis the nasopharynx are the most common
108 G. Gupta et al.
immune systems develop either trivial

clinical histoplasmosis or are totally
asymptomatic. The immunocompro-
MT
mised are more prone to develop dissem-
inated disease. Histoplasma antigen
detection in the urine and/or serum most
sensitive method for diagnosing dissemi-
Septum
nated histoplasmosis and acute pulmo-
nary histoplasmosis. Culture is the gold
standard test but it takes up to 6 weeks to
become positive. Patients with progres-
sive disseminated histoplasmosis and
those with AIDS should be treated with
IT amphotericin B.
(C) Protozoal Granulomatous Disease:
1. Nasal leishmaniasis—In over 90% of
Fig. 4.4 Rhinosporidiosis of the right nasal cavity.
mucosal lesions—whether primary or
MT(middle turbinate), IT (inferior turbinate) (Courtesy—
Dr. Hitesh Verma, Associate Professor, AIIMS, New secondary—the nose is the only site with
Delhi, India) the disease [7]. Mucosal involvement is
usually secondary to cutaneous lesions.
The nasal mucosa is one of the preferred
sites of infection, occurring in about 70% sites, especially the cartilaginous septum,
of cases. Patients may present with uni- vestibule, lower turbinates, and the floor
lateral nasal obstruction and bleeding. of the nose. Nasal obstruction, rhinorrhea,
Other symptoms may include local pruri- epistaxis are the common symptoms [7].
tus, coryza, sneezing, rhinorrhea, and On examination, we can find edematous
nasal discharge. Other structures in the anterior septal mucosa, septal nodules,
upper aero-digestive tract can also be septal perforation. Leishmaniotic facies
affected, leading to obstruction, cough, (“tapir nose”) when thickening and hyper-
hemoptysis, or painful swallowing.On emia of the nasal skin, upper lip, palate
examination red, swollen sessile, or pharynx, resulting in severe deformity.
pedunculated polyps in the nasal mucosa Leishmaniasis is diagnosed by detecting
or the ocular conjunctivae are noted it (or DNA) in tissue specimens.
(Fig. 4.4). The presence of sporangia Miltefosine is the drug of choice and
with endospores is diagnostic feature. doses for persons whose weight is from
The only effective treatment surgical 30 to 44 kg, 50-mg BD. For persons who
excision of the polyps. Excision with weight 45 kg or above, 50-mg/TDS for 28
electro-coagulation of the base of the consecutive days. Sodium stibogluconate,
lesion appears to be the treatment of ketoconazole, itraconazole, and flucon-
choice in minimizing the risk of recur- azole are other drugs used in the
rence [6]. literature.
2. Histoplasmosis: It is a fungal infection 2. Inflammatory Granulomatous Disease:
caused by Histoplasma capsulatum. (A) Granulomatosis with polyangiitis
Liver, spleen, lymph nodes, bone mar- (Wegener granulomatosis)—It is a
row, skin, and mucosa may be involved in systemic disorder that is character-
1% of the cases [1]. It is typically ized by necrotizing vasculitis of small
acquired via inhalation of airborne micro- arteries and veins. The mean age at
conidia. Most of the people with normal diagnosis is 55 years and Men and
women are similarly affected. Patients nasal biopsy can provide a definitive
may present with constitutional com- diagnosis of WG. The c-ANCA test is
plaints like fever, night sweats, highly sensitive for GPA, but a negative
fatigue, loss of appetite, and weight. result does not exclude the diagnosis.
It is Multisystem autoimmune dis- The main agents used to induce remis-
ease. Clinical features of WG can be sion are glucocorticoids, cyclophospha-
divided into three categories. mide, and/or methotrexate [7, 8].
• Type 1 GPA—It is characteristic (B) Sarcoidosis—It frequently involves
by prolonged upper respiratory the lymphatic system, lungs, liver,
tract infection. spleen, and bones. It occurs most
• Type 2 GPA—Pulmonary involve- commonly between the ages of 20
ment is often present and is asso- and 40 years with women are slightly
ciated with a cough, hemoptysis, more often affected than men. The
and cavitary lesions on chest etiology of sarcoidosis is unknown.
radiography. It is characterized by a seemingly
• Type 3 GPA is a widely dissemi- exaggerated immune response
nated form of the systemic dis- against an unknown antigen.
ease and commonly consists of Sarcoidosis is manifested by the
upper and lower airway involve- presence of multiple noncaseating
ment, cutaneous lesions, and pro- granulomas in affected organ tissues.
gressive renal involvement. The sarcoid granuloma consists of a
History, examination, radiologic, and central area of tightly packed epithe-
biochemical data findings help in diagno- lioid cells surrounded by lympho-
sis. The nasal cavity examination usually cytes and fibroblasts. The lung is the
shows septal perforation with or without primary organ affected by sarcoid-
granulomatous tissue (Fig. 4.5). Patients osis. Approximately 40% of patients
also have abnormal erythrocyte sedimen- have extrapulmonary involvement.
tation rate, hemoglobin, serum creati- The involvement of the nose and
nine, and serum c-ANCA levels. These paranasal sinuses by sarcoidosis is
serologic findings in conjunction with relatively infrequent with the inci-
dence ranging between 1% and 6%.
Symptoms of nasal involvement are
nasal obstruction, epistaxis, dys-
pnea, nasal pain, epiphora, and anos-
mia. Nasal sarcoidosis commonly
affects the mucosa of the septum and
inferior turbinate. On examination,
the nasal mucosa is dry and friable
with crusts. Submucosal nodules
with a characteristic yellow color
may be noted. In more advanced dis-
ease, irregular polypoid, friable
mucosa is seen and bleeds readily.
More severe infiltration may lead to
septal perforation or oronasal fistu-
Fig. 4.5 Nasal endoscopy is showing large septal perfo-
ration with crusting and atrophy of surrounding tissue
lae. Diagnosis is based on a combi-
(Courtesy—Dr. Hitesh Verma, Associate Professor, nation of histologic, radiographic,
AIIMS, New Delhi, India) immunologic, and biochemical data.
110 G. Gupta et al.
Pulmonary findings of either hilar plasm antibody (ANCA). CSS is

lymphadenopathy or pulmonary characterized by necrotizing vasculi-
fibrosis are common. Biochemical tis of small and medium-sized ves-
examination shows elevated serum sels, Necrotizing extravascular
or urinary calcium. Serum angioten- granulomas, eosinophilia of the ves-
sin-converting enzyme (ACE) eleva- sels and perivascular tissue. CSS
tions occur in 83% of patients with consists of three phases:
active sarcoidosis, which has become 1. A prodromal phase with allergic
very useful for the diagnosis and for rhinitis and asthma
monitoring of relapse. The diagnosis 2. an eosinophilic infiltrative phase
of sarcoidosis is confirmed by the with chronic eosinophilic pneu-
presence of noncaseating granulo- monia (Loeffler syndrome) or
mas, composed of multiple epitheli- gastroenteritis, and
oid cells and Langerhans giant cells 3. A systemic, life-threatening vas-
in the nasal mucosa. Negative stains culitis with granulomatous
for fungus and acid-fast bacilli help inflammation.
to support the diagnosis. Stage I sar- The patients presented with nasal crusing &
coidosis undergo spontaneous remis- polyposis, distringuished from GPA is by
sion within 2 years without specific extensive polyposis on both side & asthma.
treatment. Sarcoidosis with elevated The c-ANCA test result is also negative in
ACE values or extrapulmonary CSS, although perinuclear antineutrophil
involvement usually requires treat- cytoplasmic antibodies (p-ANCAs) is
ment; this statement applies to most found in 70% of patients. Glucocorticoids is
cases of nasal sarcoidosis. The the treatment for CSS whereas cyclophos-
mainstay of treatment for sarcoid-
phamide may be helpful in life-threatening
osis is systemic corticosteroids. cases or in patients with poor prognostic
Methotrexate has been used to treat factors. Rituximab (B-cell-depleting mono-
nasal sarcoidosis successfully. Nasal clonal antibody) has been used with favor-
symptoms may be treated with nasal able responses in patients with CSS
saline irrigations and topical nasal refractory to conventional treatments. The
steroids. Secondary infections anti-IgE monoclonal antibody omalizumab
treated with culture-directed antimi- has demonstrated a corticosteroid-sparing
crobial therapy. Surgery is advisable effect in refractory or relapsing
in medically controlled symptomatic EGPA. Mepolizumab an interleukin-5
nasal obstruction or chronic sinus- antagonist monoclonal antibody (IgG1
itis, in selected patients [8, 9]. kappa) is being studied for its efficacy in
(C) Churg–Strauss syndrome— CSS [8, 10].
Eosinophilic granulomatosis with (D) T-cell lymphoma—It is extra-nodal
polyangiitis (EGPA) traditionally NK/T-cell lymphoma, nasal type
termed, Churg–Strauss syndrome is (ENKL) is a rare form of non-
a rare systemic necrotizing vasculitis Hodgkin’s lymphoma. Disease
that affects small-to-medium-sized causing destruction of the midline
vessels. It occurs equally among structures of the palate and nasal
men and women with mean age of fossa, so it is also known as midline
50 years. Autoimmunity is evident lethal granuloma. Histopathology
with the presence of hypergamma- shows the presence of polymorphic
globulinemia, increased levels of lymphoid infiltrate of mature,
immunoglobulin E (IgE), rheuma- immature, and atypical lympho-
toid factor, and Antineutrophil cyto- cytes, plasma cells, histiocytes,
eosinophils with necrosis of cells. sis. Therapy for localized disease is

Immunohistochemical studies dem- radiotherapy. Chemo-radiotherapy
onstrate positivity for T-cell mark- is the treatment for advanced lesion
ers like CD2, CD7, CD45RO, and [11, 12]. The chemotherapy regi-
CD43 and natural killer cell marker mens are mentioned in Chap. 10.
CD57.35. The causative role of
EBV in the pathogenesis of T-cell
lymphoma has been strongly sug- 4.1.2 Other Granulomatous
gested. Initial symptoms are nasal Pathology
obstruction, pus, and serosangui-
nous nasal discharge. As the disease Inflammatory Pseudotumor (IPT)—It is benign
progresses, unilateral mucosal idiopathic non-neoplastic inflammatory disease
ulceration with extension into the and it can involve any organ. It presents with his-
palate, maxillary sinus, and upper tory of the progressive, locally destructive mass
lip is seen (Fig. 4.6). Oronasal fis- lesion. Radiologically, it is infiltrative in sur-
tula and nasal septal perforations rounding structures so it can mimic as skull base
are frequently present. The charac- osteomyelitis and invasive fungus sinusitis. It is
teristic clinical feature with necro- isointense on T1 and hypointense on T2 MRI
tizing atypical cell exudates on images. It most commonly involves orbit whereas
histopathology suggests the diagno- nose and paranasal sinus involvement are rela-
tively rare. Immunoglobulin G4 level can be
raised in IPT. The final diagnosis of IPT is based
on characteristic histopathology finding where
tissue shows the presence of dense lymphoplas-
mocytic infiltration with obliterative phlebitis,
storiform fibrosis. Lymphoplasmocytic infiltra-
tion is seen in IgG4 related granulomatous lesions
with serum IgG level above 135 mg/dl. The most
accepted treatment modality is systemic steroid,
radiotherapy alone, or in combination. Surgery
and immune-suppression are also mentioned as
modality in few reports [13].
4.2 Part B: Atrophic Rhinitis
Atrophic rhinitis is a chronic inflammatory condi-

tion characterized by progressive atrophy of the
nasal mucosa and underlying bone of the turbi-
nates leading to the formation of thick crusts and a
constant foul smell (Ozaena) in the nose. The natu-
ral ostium of the sinuses is visible in routine nasal
endoscopy without effort. It can be of two types—
Primary and Secondary. Histopathological exam-
ination reveals the presence of squamous
epithelium instead of ciliated columnar epithe-
Fig. 4.6 The clinical photograph is showing reddish skin
lium. The choice of investigation is prescribed on
over the right half of nose with widening of ala of the right
side (Courtesy—Dr. Hitesh Verma, Associate Professor, the basis of history for secondary atrophic rhini-
AIIMS, New Delhi, India) tis. The selection of management is based on
112 G. Gupta et al.
symptomatology and response. The first line of to their arrested development. Young and Taylor
management is to increase mucosal clearance by [16] have proposed that atrophic rhinitis is of two
nasal douches. The last management option is the types, depending upon the vascular involvement
closure of the nasal cavity for certain period. into two types. Type I is major subtype (50% to
Primary Atrophic rhinitis is multi-factorial in 80%) and is characterized by endarteritis obliter-
origin. Hereditary, as the disease is known to ans, periarteritis, and periarterial fibrosis of ter-
involve more than one member in the same family. minal arterioles as a result of chronic infection
In some cases, it usually involves females more with round cell and plasma cell infiltration. Type
than males and starts at puberty. The disease is self- II is minor subtype (20% to 50%) and shows cap-
limiting, tends to cease after menopause thus hor- illary vasodilation with active bone resorption.
monal influence cannot be ruled out. It is more Infection affects the surfactant system leading to
common in hot and humid climate specially in the surfactant deficit [17] through several mecha-
low socioeconomic group. Nutrition has also been nisms including, the absence of noteworthy SP-A
shown to play a vital role as deficiency of vitamin gene up-regulation and diminution of SP-A pro-
A, D, or iron or some other dietary factors have tein reserves, also inflammatory cytokines pro-
been associated with the disease and are likely duced in response to sepsis inhibiting the
causes. Autoimmune process in which viral infec- synthesis of surfactant leading to decrease the
tion or some other unspecified agents trigger anti- efficiency of mucociliary clearance also, surfac-
genicity of nasal mucosa. The antibody released tant deficiency impairs opsonization and phago-
causes destruction of the nasal mucosa is also pos- cytosis of bacteria thus developing into a vicious
tulated. The most widely accepted fact is the infec- cycle of colonization of nasal mucous by bacteria
tive process where in various organisms have been and causing destruction overtime.
cultured from cases which are Klebsiella ozaenae,
(Perez bacillus), diphtheroids, P. vulgaris, E. coli, 4.2.1.1 Clinical Features
Staphylococci, and Streptococci. They are all con- The disease is commonly seen in females and
sidered to be secondary invaders responsible for starts around puberty. Merciful anosmia is a term
foul smell rather than the primary causative organ- characterized by the foul smell from the nose but
ism. Specific infections like syphilis, lupus, lep- the patient herself is unaware of the smell due to
rosy, and rhinoscleroma are the etiology for marked anosmia which accompanies these
secondary atrophic rhinitis which may cause degenerative changes thus making the patient a
destruction of the nasal structures leading to atro- social outcast. Patient may also complain of nasal
phic changes. Atrophic rhinitis can also result from obstruction in spite of unduly wide nasal cham-
long-standing purulent sinusitis, radiotherapy to bers. This is due to large crusts filling the nose
the nose, or excessive surgical removal of turbi- with atrophy of nerve ending. Epistaxis may
nates [14]. Unilateral Atrophic Rhinitis—changes occur when the crusts are removed. Complain of
in the wider side of the nasal cavity is sometimes decreased hearing and fullness of ear due to
seen in cases of marked septal deviation. obstruction to eustachian tube. On examination,
anterior rhinoscopy shows the nasal cavity to be
full of greenish or grayish black dry crusts cover-
4.2.1 Pathology ing the turbinates and septum, which bleeds if
removed (Fig. 4.5). On removal of crusts, nasal
The characteristic feature is squamous metapla- cavities appear roomy with atrophy of turbinates
sia of the normal ciliated columnar epithelium which may be reduced to mere ridges and the
along with its endarteritis obliterans is seen in the posterior wall of nasopharynx can be easily seen.
mucosa, periosteum, and bone leading to atrophy Nasal mucosa appears pale and dermatitis of the
of seromucinous glands, venous blood sinusoids, nasal vestibule may be present. Septal perfora-
and nerve elements [15]. The bone of turbinates tions can be seen leading to saddle nose defor-
undergoes resorption causing the widening of mity. Atrophic changes may also be seen in the
nasal chambers. Paranasal sinuses are small due pharyngeal mucosa which appears as dry and
glazed with crusts leading to atrophic pharyngi- crusts and the associated infection, putrefying
tis. Sometimes the atrophic changes may extend smell, and to further check crust formation. alka-
to the laryngeal mucosa causing cough and line nasal douching solution is made by dissolv-
hoarseness of voice typical of Atrophic Laryngitis. ing a teaspoonful of powder containing soda
middle ear effusion, tympanic membrane retrac- bicarbonate one part, sodium biborate one part,
tions due to obstruction to eustachian tube causes sodium chloride two parts in 280 ml of water.
hearing-impairment in the minority of cases [18]. Saline acts as solvent and it washes thick mucus,
Paranasal sinuses are usually small and underde- crust, and debris. Nasal douches also increase
veloped with thick walls. The presence of 2 or mucosal humidification and ciliary function. The
more features beyond 6 months are in favor of solution is run through one nostril and comes out
atrophic rhinitis: recurrent epistaxis, episodic from the other. It loosens the crusts and removes
anosmia, nasal purulence, crusting, surgical thick tenacious discharge. Initially, irrigations are
intervention in two or more sinuses, and presence done two to three times a day but later once every
of chronic inflammatory disease [19]. 2–3 days is sufficient. After crusts are removed,
the nose is painted with 25% glucose in glycer-
4.2.1.2 Investigations ine. This inhibits the growth of proteolytic organ-
Mainly aim to establish the diagnosis by exclud- isms which are responsible for foul smell. In
ing secondary causes of atrophic rhinitis and other place of this antibiotic spray can also be used like
granulomatous conditions. Low hemoglobin and Kemicetine antiozena solution contains chloro-
peripheral blood smear show microcytic hypo- mycetin, oestradiol, and vitamin D2 but antibiot-
chromic picture pointing towards iron deficiency ics are not having much role in the treatment of
anemia. As bacterial infection is seen, there is atrophic rhinitis. Budesonide based nasal wash
raised total leukocyte count (TLC) and differen- (2 ml in 1000 ml saline irrigation solution) is also
tial leukocyte count (DLC) show lymphocytosis. recommended after saline nasal douches to
Commonly, low Serum protein and plasma vita- improve symptomatology.
min levels are seen due to malnutrition. Other Other treatment strategies that have shown
tests done to rule out secondary causes are the benefit are oestradiol spray which has been found
erythrocyte sedimentation rate (ESR) which is to increase vascularity of nasal mucosa and
raised in tuberculosis and granulomatous infec- regeneration of seromucinous glands for Young
tion. Blood sugar is to rule out diabetes mellitus. and Taylor Type1 not Type 2. Placental extract,
VDRL test is to diagnose secondary to syphilis. when injected submucosally in the nose may pro-
Chest X-ray and Mantoux test/enzyme-linked vide some relief. A potassium iodide oral prepa-
immunosorbent assay (ELISA) for tuberculosis. ration promotes and liquefies nasal secretion
Skin biopsy is to get the diagnosis of leprosy. [20]. Mitomycin C, platelet-rich plasma, and
Nasal biopsy is for granulomatous diseases such ozone were tried as an adjuvant treatment with
as lupus, leprosy, scleroma, and gumma. CT scan nasal douches but both medications were not
of paranasal sinuses shows mucoperiosteal thick- showed any significant benefit. Nasal endoscopic
ening of paranasal sinuses, loss of definition of surveillance is recommended twice a year to
osteomeatal complex due to resorption of eth- clear crusting and to remove adhesion till symp-
moidal bulla and uncinate process, hypoplastic toms persist.
maxillary sinuses, enlargement of the nasal cavity
with the erosion of the lateral nasal wall, and atro-
phy of inferior and middle turbinates. 4.2.3 Surgical Management
The surgeries can be broadly classified into four

4.2.2 Management Aim categories with different aims.
Complete cure is not yet possible. Goal of treat- 1. Surgeries for narrowing the nasal cavities—
ment is to maintain nasal hygiene by removal of Nasal chambers are very wide in atrophic rhi-
114 G. Gupta et al.
nitis and air currents dry up secretions leading 3. Surgeries to increase lubrication of dry nasal
to crusting. Narrowing the size of the nasal mucosa: There are two main techniques used
airway helps to relieve the symptoms. Among one is Raghav Sharan’s operation [22], in which
the techniques followed for narrowing the implantation of maxillary sinus mucosa is done
nasal cavities initially Wilson injected in the nostril. And the other is Wittmack’s tech-
Submucosal a mixture of 50% Teflon in glyc- nique, where implantation of the Stenson’s duct
erin paste. Then insertion of the implant under is done (parotid duct) into the maxillary antrum.
the mucoperiosteum of the floor and lateral 4. Surgeries to improve the vascularity of the
wall of the nose and the mucoperichondrium nasal cavities: Sympathetic tone causes vaso-
of the septum was done and the types of constriction and emptying of the venous
implants used can be classified into two sinusoids via the arteriovenous anastomosis.
(a) Living tissue implants A reduction in sympathetic tone causes venous
(i) Autogenous—dermofat, bone, sinusoids dilatation along with the increase in
cartilage blood supply by decreasing the vasoconstric-
(ii) Homogenous—placenta tion which is being utilized in these proce-
(iii) Heterogenous—bioimplant dures that are satellite ganglion block, cervical
(b)
Synthetic implants—acrylic, silicone, sympathectomy, pterygopalatine fossa block,
Teflon, proplast and juxta-nasal sympathectomy.
2. Surgeries to promote regeneration of normal Number of surgical options is mentioned in
mucosa: Young’s operation [21]—In it both literature but no control trial is performed till
the nostrils are closed completely just within date for the efficacy of different procedures
the nasal vestibule by raising flaps. They are [20].
opened after 6 months or later. In these cases,
mucosa may revert back to normal and crust-
ing reduced. To avoid the discomfort of bilat- 4.3 Part C: Maxillofacial Trauma
eral nasal obstruction, modified Young’s
operation was devised which aims to partially 4.3.1 Introduction
close the nostrils instead of complete closure.
It is also claimed to give the same benefit as Maxillofacial trauma presents in emergency as
Young’s (Fig. 4.7). part of polytrauma or standalone facial trauma.
The common causes include motor vehicle acci-
dents, fall from height, or assault. Maxillofacial
trauma is very commonly associated with neuro-
logical and eye trauma, along with possibility of
solid viscera injury. This necessitates team
approach to this entity. Like any trauma, princi-
ples of Advanced Trauma Life Support (ATLS)
should be followed and attention to Airway,
Breathing, Circulation, Disability, and Exposure
(ABCDE) be done appropriately.
Non-comminuted maxillary fractures seldom
bleed profusely. At the same time, in severe frac-
tures nasal packing alone to control bleeding may
be insufficient as splayed walls of the nasal cav-
ity and/or palatal process of maxilla will not
allow the packing to generate enough pressure to
Fig. 4.7 The clinical photograph is showing modified
control bleeding. In such cases, airway securing
Young’s operation. The catheter is placed to prepare small
size nostril (Courtesy—Dr. Hitesh Verma, Associate followed by both oral and nasal packing can be
Professor, AIIMS, New Delhi, India) considered (Fig. 4.8a, b).
a b
Fig. 4.8 (a) Patient with nasoethmoidal and bilateral minuted nasoethmoidal complex and bilateral maxillary
maxillary fracture who needed securing of airway and fractures leading to splaying of lateral nasal wall. Bleeding
oral and nasal packing to control bleeding. (b) 3D CT in such a case may not be controlled by nasal packing
reconstruction of the same patient shows severely com- alone
4.3.1.1 Assessment of a Maxillofacial

Trauma Patient
The mechanism of injury is crucial to under-
standing the extent and pattern of trauma. The
direction, amount of force, and object with which
trauma is sustained gives an insight into the pat-
tern of injury, hence a careful history about the
circumstances how the trauma was sustained
needs to be enquired. Careful attention to the
scalp and facial wounds for laceration, contami-
nation, and foreign material/debris impaction is
needed. Facial skeleton should be assessed in a
structured protocol to evaluate frontal bones,
supra, and infraorbital margins, nasal bones,
zygomatic arch and mandible. Observe for any
step deformity or discontinuity. Intraoral assess- Fig. 4.9 Hematoma in floor of mouth of and edentulous
patient who had fracture mandible
ment for occlusion, hematoma in the floor of
mouth, missing/fractured/avulsed teeth is imper-
ative (Fig. 4.9). Orbital assessment for telecan- vascular ailments along with any coagulopathies,
thus, mobility, acuity, pupillary size, and reaction should be ruled out which may have a bearing on
should be done. Anterior rhinoscopy is done for wound healing and postoperative complications.
septal fracture/hematoma. Sensation over the
face along the distribution of infraorbital and
mental nerves is important in preoperative period 4.3.2 Imaging
in a conscious patient. This may prevent potential
postoperative medicolegal issues. Coexistent Multidetector CT scan with three-dimensional
medical conditions like renal, hepatic, or cardio- shaded surface display is standard for evaluation
116 G. Gupta et al.
Fig. 4.11 Image shows fracture of right ramus of man-

dible. Also seen are midline maxillary fracture, right side
Le Fort 2 maxillary fracture, and fracture of the frontal
bone
Fig. 4.10 3D shaded surface display with fractures
involving left fronto-zygomatic buttress, left angle of
mandible, right parasymphysis, midline maxillary, and nasotracheal intubation is adequate. For Le Fort 2
left frontal process of the maxillary bone and Le Fort 3 fractures, a submental intubation or
tracheotomy is considered.
(Fig. 4.10). X-ray of the skull in anteroposterior,
lateral, and submentovertical view along with 4.3.4.1 Mandibular Fractures
X-ray mandible lateral oblique view may be done Based on the location, they are divided into con-
if CT scan is not available. dylar/subcondylar, parasymphyseal (between
mandibular canines)/symphyseal (between cen-
tral mandibular incisors), ramus (Fig. 4.11)
4.3.3 Timing of Surgical (posterior border of masseter to height of sig-
Intervention moid notch), angle (third molar to posterior bor-
der of masseter), body (distal part of mandibular
In cases of midfacial, nasal, zygomaticomaxil- canine to distal mandibular second molar), and
lary complex, and frontal fractures, early opera- alveolus [23].
tive intervention may not be feasible due to Condylar fractures may be intracapsular or
concomitant significant facial swelling and/or extracapsular. Since these are often missed, a
intracranial trauma. Hence, the surgical interven- keen observation is needed during clinical exami-
tion is planned after the reduction in swelling. In nation. A small wound on the chin, malocclusion
patients with solid organ or hollow visceral with otherwise preserved mandibular arch, dif-
trauma too, a definitive management of these fuse parotid swelling, and parotid area crepitus
injuries takes priority. Only after any other vital are subtle pointers (Fig. 4.12a, b).
organ injury has been assessed and addressed, Intermaxillary fixation is done by closed
facial trauma care should be planned. (tooth-borne/bone-borne) or open techniques.
1. Tooth-borne closed techniques—Erich arch

4.3.4 A
irway Management During bars, interdental wires (Ivy loops/eyelet wires,
Surgery etc.) or lingual splints.
2. Bone-borne techniques—skeletal suspen-
For isolated mandibular, zygomaticomaxillary sion wires, IMF screws, external fixators,
complex, and Le Fort 1 fractures of midface, an hybrid systems.
a b
Fig. 4.12 (a) Left parotid swelling and ear bleeding in a injury. (b) Same patient showing malocclusion due to
patient with the left condylar fracture. The patient was condylar fracture
otherwise well preserved with no other apparent facial
Category 1 Fracture In this, fracture segments

Open techniques are preferable and are based
are generally maintained position by their infe-
on AO/ASIF guidelines. These methods include-
rior attachment with upper lateral cartilage. It
two plate fixation, reconstruction plate, lag
occurs in less severe form of trauma and grade 1
screws. Fracture line can be accessed by tran-
fractures come under category 1 fracture.
soral/transbuccal approach (body/symphysis/
Chevallet was the first documenting person so it
parasymphysis), transcervical-submandibular
was also known as Chevallet fracture.
approach (angle), transcervical-retromandibular
approach (ramus/subcondylar), or endoscopic
Category 2 Fracture Nasal bones, frontal pro-
approach (subcondylar). Some fractures of
cess of the maxilla, and septal bones are involved
ascending ramus and angle can be plated by tran-
in this fracture. It is seen in the more severe form
soral approach using a transbuccal device for
of trauma. Grade 2 and above fractures come
fixation.
under category 2 fractures. It is also known as
Jarjavay fracture (C shaped fracture).
4.3.5 M
anagement of Nasal Bone
Category 3 Fracture It involves all nasal bone
Fractures
with orbit, ethmoid bone, and any other facial
bone. Clinically, patient may have pig-like
Nasal fracture is classified into five subtypes on
appearance. It is also classified into two, depend-
clinical basis
ing upon skull base involvement. In type 2, ante-
rior cranial base, posterior wall of frontal sinus,
• Grade 0—No displacement.
and optic nerve is involved.
• Grade 1—The deviation of nose is less than
50% of width of bridge of nose.
• Grade 2—The deviation of nose is more than For evaluation of nasal bone fractures, clinical
50% to almost equal of width of bridge of assessment is most informative. Additionally,
nose. X-rays (Water’s view, lateral view) and in select
• Grade 3—The deviation of nose is more than cases (nasoethmoidal fractures, minimally
width of bridge of nose. depressed fractures at rhinion/ nasion) CT may
• Grade 4—It almost reaching to the cheek. be requisitioned.
For simple fractures, closed reduction with
Nasal fractures are also divided on the basis of Asch or Walsham forceps with digital manipula-
patterns of damage. tion is carried out (Fig. 4.13a, b). Septal straight-
118 G. Gupta et al.
a b
Fig. 4.13 Preoperative (6a) and postoperative (6b) image of a patient with nasal bone fracture who underwent closed
reduction
ening is done if required. If significant septal and displaced fracture of zygomatic arch are
cartilage and septal fracture are present, emer- reduced and fixed by coronal approach. Non-
gency septoplasty can be considered. Telescoping comminuted depressed fractures of arch that are
of fragments with significant comminution may cosmetically and functionally significant can
merit external fixation using lead plates or ortho- undergo closed reduction by temporal (Gilles) or
pedic plates [24]. vestibular (Keen) approach using periosteal or
Rowe zygoma elevator.
4.3.6 Zygomatic Fractures

4.3.7 Fractures of Midface
Fractures of zygomaticomaxillary complex (ZMC)
(also called trimalar, tripod, tetrapod, quadrapod) These are usually classified as Le Fort 1 (floating
may lead to infraorbital anesthesia, trismus, diplo- palate), Le Fort 2 (floating maxilla), and Le Fort 3
pia, enophthalmos, palpable bony suture line (craniofacial dysjunction). However, in the current
abnormalities, and flattened malar prominence. scenario of high-velocity injuries, fracture lines
Clinical evaluation includes the assessment of may not follow lines of least resistance, which was
malar depression, mouth opening, ocular examina- the basis of this classification, and mixed fractures
tion for mobility and diplopia, and sensation over are more common presentation [23].
area of V2 division. Open reduction and fixation by Impacted maxillae need to be disimpacted
miniplates of ZMC fractures are carried out by using Rowe disimpaction forceps. Definitive
using a combination of approaches: vestibular for management is preferably by intermaxillary fixa-
zygomaticomaxillary buttress, subciliary/subtarsal/ tion and open reduction and internal fixation
transconjunctival for infraorbital rim, and brow/ using miniplates. Fractures can be accessed by
eyebrow for lateral orbital rim [23]. Comminuted vestibular incision (Le Fort 1), a combination of
vestibular and infraorbital/transconjunctival/sub- 4.3.9 Postoperative Care

ciliary incisions (Le Fort 2), or coronal incision
(Le Fort 3). Systemic steroids and elective postoperative ven-
tilatory support can be considered in patients
with significant facial swelling with controlled
4.3.8 Orbital Fractures extubation in ICU/postoperative recovery.
Rigorous attention to oral hygiene and mouth
A high index of suspicion is required to diag- opening exercises is essential to prevent infection
nose orbital fractures, hence there is a need for and trismus.
evaluating visual acuity, visual field, and cheek
area sensation in all patients of facial trauma. In
children, there is also a possibility of trapdoor References
fractures of the orbital floor due to elasticity of
bones [23], hence even in the paucity of radio- 1. Verma H, Panda S, Sikka K, Irugu DVK, Thakar
A. Primary spheno-petro-clival tuberculosis. Indian
logical findings, it is important to have a com- J Otolaryngol Head Neck Surg. 2019;71(Suppl
plete visual examination. ‘Blow-in’ fractures, 3):1796–9.
whereby the roof of the orbit may cave in due to 2. Fischer M. Leprosy – an overview of clinical features,
frontal area injury, are also likely to be associ- diagnosis, and treatment. J Dtsch Dermatol Ges.
2017;15(8):801–27.
ated with intracranial trauma. “Blowout” frac- 3. Mukara BK, Munyarugamba P, Dazert S, Löhler
tures, generally a result of blunt trauma to orbit J. Rhinoscleroma: a case series report and review
may be either of the medial wall (fracture into of the literature. Eur Arch Otorhinolaryngol.
ethmoidal cells), or floor of orbit (fracture into 2014;271(7):1851–6.
4. Tsang SH, Sharma T. Syphilis. Adv Exp Med Biol.
maxillary antrum) and can result in enophthal- 2018;1085:219–21.
mos or diplopia due to tethering of inferior or 5. Fernández-López C, Morales-Angulo
medial rectus muscle. These are radiologically C. Otorhinolaryngology manifestations secondary to
evaluated by CT done in all three planes oral sex. Acta Otorrinolaringol Esp. 2017;68(3):169–80.
6. Almeida FA, Feitoza Lde M, Pinho JD, et al.
(Fig. 4.14). Force duction test helps in con- Rhinosporidiosis: the largest case series in Brazil. Rev
forming the entrapped muscle. Soc Bras Med Trop. 2016;49(4):473–6.
The orbital floor defect can be approached by 7. Vega Braga FL, Machado de Carvalho G, Caixeta
subciliary approach, entrapped contents freed, Guimarães A, et al. Otolaryngological manifestations
of Wegener’s disease. Acta Otorrinolaringol Esp.
and defect repaired using titanium mesh, split 2013;64(1):45–9.
calvarial grafts, or rib cartilage graft. There are 8. Kohanski MA, Reh DD. Granulomatous diseases and
reports of successful endoscopic repair of orbital chronic sinusitis, Chapter 11. Am J Rhinol Allergy.
floor fractures [25]. 2013;27(Suppl 1):S39–41.
9. Send T, Tuleta I, Koppen T, et al. Sarcoidosis of
the paranasal sinuses. Eur Arch Otorhinolaryngol.
2019;276(7):1969–74.
10. Seccia V, Baldini C, Latorre M, et al. Focus on the
involvement of the nose and paranasal sinuses in
eosinophilic granulomatosis with polyangiitis (Churg-
Strauss Syndrome): nasal cytology reveals infiltration
of eosinophils as a very common feature. Int Arch
Allergy Immunol. 2018;175(1–2):61–9.
11.
Allen PB, Lechowicz MJ. Management of
NK/T-cell lymphoma, nasal type. J Oncol Pract.
2019;15(10):513–20.
12. Tse E, Au-Yeung R, Kwong YL. Recent advances in
the diagnosis and treatment of natural killer/T-cell lym-
phomas. Expert Rev Hematol. 2019;12(11):927–35.
13. Ryu G, Cho H, Lee KE, et al. Clinical signifi-

cance of IgG4 in sinonasal and skull base inflam-
Fig. 4.14 Blowout fracture of left inferior orbital wall
120 G. Gupta et al.
matory pseudotumor. Eur Arch Otorhinolaryngol. 19. Ly TH, deShazo RD, Olivier J, Stringer SP, Daley W,
2019;276:2465–73. Stodard CM. Diagnostic criteria for atrophic rhinosi-
14. RA S, Kaliner MA. Nonallergic rhinitis, Chapter 14. nusitis. Am J Med. 2009;122(8):747–53.
Am J Rhinol Allergy. 2013;27(Suppl 1):S48–51. 20. Mishra A, Kawatra R, Gola M. Interventions for

15. Chen HS. Desquamation and squamotransforma-
atrophic rhinitis. Cochrane Database Syst Rev.
tion of rhinomucosa as a prodromal sign of atrophic 2012;2:CD008280.
rhinitis. J Otorhinolaryngol Related Specialties. 21. Young A. Closure of nostrils in Atrophic Rhinitis. J
1984;46(6):327–8. Laryngol. 1967;81:514–5.
16. Taylor M, Young A. Histopathological and histo-
22. Sharan R. Transplantation of the maxillary sinus

chemical studies in atrophic rhinitis. J Laryngol Otol. mucosa in atrophic rhinitis. Indian J Otolaryngol.
1961;75:574–89. 1978;30:14–6.
17. El-Anwar MW, et al. Surfactant protein A expres- 23. Fonseca RJ. Oral and maxillofacial trauma. 3rd ed. St.
sion in chronic rhinosinusitis and atrophic rhinitis. Int Louis, MO: Elsevier; 2018.
Arch Otorhinolaryngol. 2015;19(2):130–4. 24. Kochar HS. An innovative approach to external fixa-
18. Bist SS, Bisht M, Purohit JP. Primary atrophic rhini- tion of severe nasal bone fractures with orthopedic
tis: a clinical profile, microbiological and radiological plates. Ear Nose Throat J. 2011;90:102–4.
study. ISRN Otolaryngol. 2012;2012:404075. 25. Chen CT, Chen YR. Endoscopically assisted repair
of orbital floor fractures. Plast Reconstr Surg.
2001;108:2011–8.
Diagnostic Method
and Instrumentation in Rhinology 5
Gagandeep Singh, Immaculata Xess, Ankur Goyal,
Ashu Seith Bhalla, Shamim Ahmed Shamim,
Hitender Gautam, Zareen Lynrah,
Pradip Kumar Tiwari, Ripu Daman Arora,
Nikhil Singh, and Nitin M. Nagarkar
Contents
5.1 Part A: Diagnosis of Fungal Infections of Nose and Paranasal Sinuses 122
5.1.2 Diagnosis of Invasive FRS 123
5.1.3 Specimens 123
5.1.4 Sample Transport 124
5.1.5 Sample Processing 124
5.1.6 Culture and Antifungal Susceptibility Testing (AFST) 124
5.1.7 Serologic Tests 124
5.2 Part B: Intervention Radiology for Rhinology 126
5.2.1 re-Requisites
P 127
5.2.2 Image-Guided Sampling 127
5.2.3 DSA Assessment of Vascularity and Collateralization 128
5.2.4 DSA Embolization in Trauma Setting 129
5.2.5 DSA Embolization in Epistaxis 129
5.2.6 DSA Embolization in Tumors 130
5.2.7 DSA Embolization in AVMs 133
5.2.8 Sclerotherapy for Sinonasal Low-Flow Malformations 133
5.3 art C: Nuclear Medicine Perspective
P 134
5.4 art D: Bacteriology and Virology
P 142
5.4.2 Staining Procedures 143
Z. Lynrah · P. K. Tiwari
G. Singh · I. Xess · H. Gautam ENT, NIGRIMS, Shillong, Meghalaya, India
Microbiology, AIIMS, New Delhi, India
R. D. Arora (*) ·N. Singh · N. M. Nagarkar
A. Goyal · A. S. Bhalla ENT, AIIMS, Raipur, Chhattisgarh, India
Radiology, AIIMS, New Delhi, India e-mail: neelripu@gmail.com
S. A. Shamim
Nuclear Medicine, AIIMS, New Delhi, India
122 G. Singh et al.
5.4.3 C ulture Media Are Required to Isolate the Bacteria from the Clinical
Specimens 144
5.4.4 Nucleic Acid Amplification Techniques (NAAT) 144
5.4.5 Antibiotic Sensitivity, Resistance, and Prevention 145
5.4.6 Viruses in ENT 145
5.4.7 Laboratory Diagnosis of Viral Diseases 145
5.5 Part E: Advanced Instruments in Rhinology 146
References 153
Fungal rhino-sinusitis is one of the major sub- involved in the majority of rhinosinusitis. Acute
types of chronic rhino-sinusitis. It is classified infection generally starts with viruses and super-
into invasive and none-invasive types. Surgical added bacterial infection usually prolongs the
clearance is the primary treatment method for disease duration and can complicate the out-
non-invasive type. Non-invasive fungal sinusitis comes. The acute type is more complicated than
may convert into invasive type to some extent. the chronic type. The evaluation is required gen-
The invasive is managed by debridement & long erally in poor responder to the standard line of
term antifungal therapy. The prognosis of inva- the management, complicated cases, and in
sive type is poor than non-invasive type. chronic rhinosinusitis cases. The correct identifi-
Prophylactic, incomplete & unnecessary prolong cation of the causative organism is possible by
treatment raised the possibility of drug resis- knowing the correct way of sample collection,
tance. Proper identification of the causative transportation technique, etc. Endoscopes, micro-
organism, drug sensitivity against it & treatment debrider, radiofrequency ablation, coblator, etc.
duration reduces the risk of relapse of disease & revolutionized the outcomes of surgery by
drug resistance which intern improves the quality improving the surgical field exposure, by provid-
of life. The correct diagnosis of causative fungal ing finer details and by controlling the surgical
organism is possible if the samples extract in cor- bleeding. Navigation system allows expansion of
rect way, timely transport to the laboratories, etc. endoscopic surgical approaches. Recent advances
New serological tests allow early identification of in the instruments allow dealing of central skull
tissue invasion. Radiological interventions are base lesions by transnasal route. The quality of
commonly done for tissue diagnosis especially in life is improved significantly in comparison to
hidden areas which requires extensive exposure traditional open trans-cranial approaches.
for biopsy such as high infratemporal fossa, cra-
nial tumour eroding middle & posterior skull
base. Interventions are also indicated to control 5.1 art A: Diagnosis of Fungal
P
traumatic bleeding & to reduce the vascularity of Infections of Nose
vascular lesions. The procedures are performed and Paranasal Sinuses
under image guidance in head and neck region
include those performed for obtaining diagnostic 5.1.1 Introduction
information or for therapeutic intent. Nuclear
Medicine uses radiopharmaceuticals for diagnos- Fungi are ubiquitous in the environment and we
tic and therapeutic purposes. It plays an impor- are exposed to them on a regular basis. In few
tant role in identifying the unknown etiological individuals, fungi can cause allergic manifesta-
factor, the staging of mass lesions of nose and tions or even invasive disease in the nose and
paranasal sinuses pathology, to assess the treat- PNS, depending on underlying conditions and
ment response. Bacteria’s and viruses are are collectively termed as fungal rhinosinusitis
5 Diagnostic Method and Instrumentation in Rhinology 123
Table 5.1 Common agents associated with fungal except mucormycosis and cryptococcosis. The
rhinosinusitis
galactomannan test is specific for invasive asper-
Allergic fungal rhinosinusitis Invasive fungal Sinusitis gillosis. Newer techniques like the lateral flow
(AFRS) (IFS)
devices for detecting Aspergillus antigens and
• Aspergillus flavus • Rhizopus oryzae
• Aspergillus fumigatus • Rhizopus microsporus polymerase chain reaction for detecting fungal
• Aspergillus niger • Lichtheimia DNA in tissue specimens are under evaluation.
• Other Aspergillus species corymbifera As the nose and paranasal sinuses are in close
• Fusarium spp. • Apophysomyces proximity to the eye and brain, invasive type
• Alternaria spp. elegans
• Cladosporium spp. • Aspergillus flavus infections should be managed aggressively.
• Curvularia spp. • Aspergillus fumigatus Classification of FRS: Based on histopathol-
• Bipolaris spp. ogy, clinical features, and laboratory investiga-
tions (Fig. 5.1) [1–4].
(FRS) (Table 5.1). FRS affects all age groups and
socioeconomic status. FRS is neglected and often
misdiagnosed in developing countries. Correct 5.1.2 Diagnosis of Invasive FRS
sample collection to establish an appropriate
diagnosis is of paramount importance. Nasal A high degree of suspicion should be kept for estab-
swabs are considered inferior and biopsy speci- lishing a diagnosis of invasive FRS, especially in
mens are the most conclusive. Once the biopsy is the immunocompromised patient with facial pain.
collected it should be transported immediately to The nares and oral cavity should be carefully exam-
the laboratory, immersed in normal saline in a ined for necrotic areas. Early nasal endoscopic eval-
sterile leak-proof container. Samples should uation by an otolaryngologist is essential for
always be well labeled and accompanied with sampling the site. Computed tomography (CT)
complete clinical details. The samples should be shows sinus involvement and may reveal bony ero-
processed as early as possible to avoid over- sions or extension of the infection. Magnetic reso-
growth of commensal flora. Samples can be nance imaging (MRI) should be performed to assess
stored at 4 °C if the processing is being delayed, intracranial and cavernous sinus involvement.
however, if mucormycosis is being suspected the Maxillary and ethmoid sinuses are the most com-
samples should not be stored at 4 °C and main- mon sites for invasive FRS. The diagnosis is depen-
tained at room temperature. Biopsy samples are dent on histopathologic/direct demonstration of
processed depending on the presumptive diagno- fungal elements. Isolation of the infecting fungus is
sis made by the clinician. All biopsies should be necessary to guide therapy [1, 5].
homogenized to release the fungal elements in all
non-mucormycosis cases. However, if the diag-
nosis of mucormycosis is made, the biopsy speci- 5.1.3 Specimens
men should not be homogenized as it will damage
the delicate fungal elements of the Mucorales and Tissue biopsy is the ideal sample. It should be
inhibit the recovery in culture. These should obtained from the necrotic part of the affected site
instead be cut into small pieces and simply placed under direct visualization. Nasal scrapings have
on the culture media. In routine, Mucorales are low yield, however, may be obtained in patients
recovered on the culture within 3–4 days of cul- with bleeding diathesis. Nasal swabs should be
ture and Aspergillus sp. grow within 5–7 days. avoided as fungal elements get trapped in fibers.
Obtaining a biopsy specimen may not always be Moist swabs should be obtained, if at all used, as
feasible. In such situations, non-culture tech- drying of the sample will cause fungi to lose their
niques aid in establishing the diagnosis. The viability. Serum samples can be sent for galacto-
beta-D-glucan is a pan-fungal marker, it is posi- mannan antigen detection and Beta-1,3- Glucan
tive in all cases of invasive fungal infections detection and other serological markers [6, 7].
124 G. Singh et al.
Fig. 5.1 Classification
of fungal rhinosinusitis Acute invasive
FRS
Granulomatous
Invasive FRS FRS
Fungal Chronic FRS

rhinosinusitis
(FRS)
Fungal ball
(Mycetoma)
Non-Invasive
FRS
Allergic FRS
5.1.4 Sample Transport pauci-septate, typically 8–15 μm in width with

right angle branching are suggestive of mucor-
All tissue samples for fungal culture should be sent mycosis (Fig. 5.3a). Hyphae which are septate,
to the laboratory in a sterile container immersed in 4–8 μm in width with acute angle branching are
sterile saline. Samples should be transported imme- suggestive of aspergillosis (Fig. 5.3b).
diately or within two hours of collection. Serum
can be stored at 4 °C, if there is a delay in transport.
However, if mucormycosis is being suspected the 5.1.6 Culture and Antifungal
samples should not be stored at 4 °C and main- Susceptibility Testing (AFST)
tained at room temperature. Lower temperature
causes the Mucorales to lose their viability. Once a culture is obtained on SDA, it can be
identified based on colony characters and micro-
scopic features on lacto-phenol cotton blue
5.1.5 Sample Processing (LCB) mount. Aspergillus spp. are usually vel-
vety to granular downy colonies where as those
The samples should be processed as early as pos- of mucormycetes are usually cottony, filling up
sible, once received in the laboratory. The tissue the entire tube/culture plate. AFST can be per-
samples should be examined carefully for any formed in cases which do not respond to standard
necrotic or hemorrhagic areas. A small portion treatment. AFST is performed by the micro-broth
should be obtained from these areas for further dilution test for determining the minimum inhibi-
processing as the fungal load is relatively higher. tory concentrations (MICs) of antifungal drugs.
Depending on the presumptive diagnosis,
whether aspergillosis or mucormycosis, the sam-
ple should be processed according to Fig. 5.2. 5.1.7 Serologic Tests
The processed samples can be examined by
direct microscopy using KOH-Calcofluor White 5.1.7.1 Beta-1,3,-Glucan (BDG)
stain for fungal elements and cultured on SDA Indicated for the presumptive diagnosis of inva-
with and without antibiotics. Swabs can be plated sive fungal disease through detection of elevated
directly on Sabouraud dextrose agar (SDA) levels of BDG in serum [6]. BDG is a qualitative
plates. The Hyphae which are broad, aseptate, or test & values are reported as follows:
Fig. 5.2 Shows the

method of processing
tissue samples based on Tissue sample
presumptive diagnosis
Suspected Suspected
invasive invasive
aspergillosis mucormycosis
Cut the sample

Homogenize
into small
the tissue
pieces (2–3mm)
KOH-Calcofluor KOH-Calcofluor
Culture Culture
white stain white stain
a b
Fig. 5.3 Calcofluor white-KOH mount under 40× foldings indicating mucormycosis (b) Dichotomous
magnification (a) Broad aseptate hyphae are observed branching at acute angle (arrow) suggestive of asper-
with right angle branching (arrow) and ribbon-like gillosis/hyalohyphomycosis
• <60 pg/mL: NEGATIVE more than 30% of Candida isolates in neonatal

• ≥80 pg/mL: POSITIVE (in an at-risk patient) intensive care units.
• 60–79 pg/mL: EQUIVOCAL; additional sam- False positives may be found under the fol-
pling is necessary lowing circumstances:
A negative BDG may be seen in patients (a) Bacteremic patients.

infected with (b)
Antibiotics; only amoxicillin/clavulanate
and piperacillin/tazobactam (of note, anti-
• Cryptococcus neoformans fungal therapy does not significantly affect
• Mucorales (Mucor, Rhizopus, etc.) the performance of the assay).
(c) Hemodialysis with cellulose membranes.
Lower levels of BDG are found in the cell wall (d) Patients treated with iv products manufac-
of Candida parapsilosis, which may comprise tured using cellulose filters.
126 G. Singh et al.

(e)
Surgical gauzes/sponges—transient false • False-positive Galactomannan results have
positives in surgical patients. been shown in patients receiving Plasmalyte
for intravenous hydration or if Plasmalyte is
False negatives may be seen in the following used for BAL collection.
circumstances:
1. Immune complex formation. 5.1.7.3 Aspergillus-Specific Lateral

Flow Device (LFD)
Utility of BDG: Point of care test based on monoclonal antibody
(mAb JF5) to detect an extracellular mannopro-
• A pre-emptive approach is recommended, tein antigen that is secreted exclusively during
whereby surveillance is carried out in at-risk active growth of Aspergillus species. Patient’s
patients. BAL fluid samples do not need pre-treatment.
• Twice weekly testing has been recommended Test results can be available within 10–15 min of
as a screening strategy; both in invasive asper- sample receipt. LFD test results are read by the
gillosis as well as invasive candidiasis, this naked eye, and they have previously been shown
increases the sensitivity, specificity as well as to be reproducible between different studies and
positive predictive value (PPV) of the assay. different laboratories [8].
5.1.7.2 Galactomannan Antigen

Detection 5.1.7.4 Polymerase Chain Reaction
The galactomannan (GM) assay is a fairly specific
(PCR)
Can be performed in samples that have a high
and sensitive test for invasive aspergillosis. Also
degree of suspicion of fungal etiology however,
found in Histoplasma capsulatum and Fusarium
direct microscopy as well as culture do not yield
spp. The aspergillus galactomannan is an immune-
any results. A pan-fungal or genus-specific PCR
enzymatic sandwich microplate assay. The assay
can be performed. Extra caution should be taken
uses EBA-2 monoclonal antibodies which detect
while collecting samples for PCR as even little
Aspergillus galactomannan. This test has been
contamination with any mucosal surface may
approved for diagnostic use by the U.S. Food and
result in a false-positive PCR due to commensal
Drug Administration for BAL and serum speci-
fungi [9, 10].
mens only. When used in conjunction with other
diagnostic procedures it can be used to aid in the
diagnosis of invasive aspergillosis. Galactomannan
assay with serum but not BAL fluid may have 5.2 art B: Intervention
P
prognostic value. Twice a week monitoring of neu- Radiology for Rhinology
tropenic patients is often recommended. Patients
with an index of ≥0.5 in serum and ≥1.0 in BAL Radiology has expanded horizons not only in the
are considered to be positive for galactomannan diagnosis of rhinological diseases but also in the
antigen. Specimens testing positive should be management of such patients. Radiological inter-
retested to confirm the positive result [7]. ventions are commonly done for tissue diagnosis
as well as for bleeding control. Interventional
Cautions: Radiology (IR) Procedures performed under
• The concomitant use of mold-active, antifun- image guidance in the head and neck region
gal therapy may result in reduced sensitivity. include those performed for obtaining diagnostic
• There are reports of positive galactomannan information or for therapeutic intent (Table 5.2).
test results in patients receiving piperacillin/ Only the interventions pertaining to sinonasal
tazobactam. lesions are discussed in this chapter. The internal
• Patients with intestinal mucositis caused by carotid artery interventions are not included in
chemotherapy and irradiation, which allows this chapter. Also, the infrahyoid neck is only
extra absorption of dietary galactomannan. briefly covered.
Table 5.2 Types of IR procedures in head and neck 5.2.1 Pre-Requisites

Diagnostic interventions Therapeutic interventions
Image-guided FNAC Drainage procedures The general pre-requisites include
and Biopsy • Retropharyngeal
• Infratemporal fossa collections
1. Platelet count SHOULD BE ABOVE 50,000/
Assessment of Embolization for
cross-circulation and • Epistaxis (including mm3.
vascularity on DSA trauma) 2. Prothrombin time within 5 s of control or

• Pseudoaneurysms International Normalized Ratio (INR) ≤1.4.
• Preoperative
3. Short admission, especially for vascular

embolization (JNA,
Glomus tumor) procedures.
• Arteriovenous 4. Renal function tests, whenever intravenous

malformations contrast is to be injected.
• Tumor erosion of arteries
5. Intravenous access, prior to starting the

Venous sampling Jugular vein catheterization
procedure.
Sclerotherapy for venous
and lymphatic 6. Informed consent.
malformations 7. Aspirin and clopidogrel to be stopped 5 days
Carotid artery stenting for prior and low molecular weight heparins
blowout 1 day prior to the procedure.
Miscellaneous:
• Pterygopalatine ganglion
block
• Radiofrequency ablation 5.2.2 Image-Guided Sampling
of masses
• Alcohol ablation of
Ultrasound (USG) guidance is routinely used for
thyroid nodules
sampling of non-palpable lesions of the head and
DSA digital subtraction angiography, JNA Juvenile naso-
pharyngeal angiofibroma neck. Even for palpable lesions, ultrasound guid-
ance may permit targeting the solid viable por-
tions of the lesion (Fig. 5.4). Advantages of
ultrasound include real-time imaging, excellent
Radiological interventions can be divided into tissue contrast without radiation/intravenous con-
endovascular and non-vascular procedures. trast and thus it is commonly used for sampling
of neck nodes and masses, thyroid nodules, and
• Non-vascular procedures are aimed at obtain- salivary gland lesions [11].
ing tissue diagnosis, especially when the sino- CT guidance is used for deep-seated lesions
nasal masses are deep-seated or involves the (for example in infratemporal fossa), bony lesions
infratemporal fossa (ITF). (example mandible) and for regions obscured by
• Vascular interventions are primarily done overlying bones or air from the aerodigestive
to manage oronasal bleed from arterial tract. Shortest path should be employed and
causes (including trauma) and preoperative wherever feasible, sampling should be done
embolizations to reduce intraoperative along the largest dimension of the lesion.
blood loss. Subzygomatic (sigmoid notch/transcondylar)
approach is commonly employed for targeting
Majority of the radiological interventions can infratemporal lesions (Fig. 5.4).
be done with local anesthesia and conscious Other approaches for suprahyoid lesions
sedation. General anesthesia is required for small include retromandibular, paramaxillary, submas-
children and when large doses of glue emboliza- toid, transoral, and posterior [11]. While most
tion needs to be done (since the latter cause’s sinonasal lesions are sampled through the nasal
pain). route, large aggressive lesions with lateral exten-
128 G. Singh et al.
a b
Fig. 5.4 (a) Ultrasound image showing sampling from necrotic nodal mass. (b) Axial CT image shows transcondylar
approach for targeting infratemporal masses. Arrowheads denote needle
sion into ITF or beyond can be approached are usually sufficient if the needle throw is 2 cm.
through CT guidance. Similarly lesions with Upto 5 cores may be required if length of biopsy
extension into premaxillary or buccal space can needle hub is 1 cm.
be sampled under USG guidance. Addition of
USG allows sampling of most solid, non-necrotic
components where the yield is likely to be higher. 5.2.3 DSA Assessment
Coaxial technique is preferred for deep-seated of Vascularity
lesions so that access is retained for repeated and Collateralization
passes and there is no repetitive trauma to the
intervening tissues. Also, it saves time and mul- Digital subtraction angiography (DSA) is done
tiple samples can be taken via the outer needle. for assessment of vascularity of masses of supra-
This employs 16G outer needle and 18G inner hyoid neck and skull base as well as cross-
biopsy needle. Fine needle aspiration cytology is circulation prior to surgery. For cross-circulation
best done with on-site pathologist and/or micro- assessment, the common carotid artery ipsilateral
biologist to assess the adequacy of the sample to the side of the neoplasm is manually com-
[Rapid On Site Evaluation (ROSE) by the pathol- pressed, while contrast is injected into the contra-
ogist to check for the cellular adequacy so as to lateral internal carotid artery and DSA acquisition
reduce recalling of the patients for a second sit- is done in the frontal projection (Matas maneu-
ting]. FNAC is done with a 21–23 gauge hypo- ver) [12]. Opacification of ipsilateral brain paren-
dermic/spinal needle and two-three excursions chyma through patent anterior communicating
are usually sufficient. When clinico-radiological artery indicates preserved cross-circulation
diagnosis is infection, then aspiration of the liq- (Fig. 5.5).
uefied/necrotic content is useful both for identi- Allcock maneuver involves dominant vertebral
fying the pathogen as well as therapeutic artery injection [12] with manual carotid com-
purposes. However, if the neoplasm is suspected, pression to look for posterior communicating
then FNAC/biopsy from the solid component artery patency and is done if cross-circulation is
should be done. Biopsy cores are taken in case not preserved. Carotid balloon occlusion test is
the cytology smears are inadequate or the lesion done by inflating an occlusion balloon in the ipsi-
is predominantly solid. 18G cores have much bet- lateral internal carotid artery (cervical portion) for
ter yield than 20G cores. Two-three biopsy cores 20 min and evaluating ischemic tolerance. Latter
a b c
Fig. 5.5 DSA runs showing examples of crossing artery. (b) DSA run through left ICA shows preserved
circulation. (a) DSA run through right internal carotid cross-circulation. (c) DSA run through right ICA shows
artery ICA (with compression of left carotid) shows pre- absent cross-circulation
served cross-circulation through the anterior communicat-
can be done in the most basic form by clinical though the patient is bleeding. Most common
neurological assessment (motor, touch sensation, cause of this finding is arterial spasm secondary
language, memory, judgment tests) or more accu- to trauma as well as hypovolemia. In such case,
rately by doing electroencephalography (EEG). empirical embolization of bilateral internal max-
Various imaging-based perfusion assessment illary arteries and ipsilateral facial artery is done
studies (Single photon emission CT SPECT using using gelfoam. Table 5.3 outlines the commonly
Tc99m HMPAO) can also be done. The test is used embolizing agents and sclerosants.
positive in case any neurological deficit or EEG/
SPECT abnormality is detected. Though consid-
ered safe, there is mild risk of arterial dissection, 5.2.5 DSA Embolization in Epistaxis
thrombosis, and distal infarction (3.5%) [12].
Matas and Allcock’s maneuver are safer alterna- The first step in non-traumatic epistaxis is to
tives to balloon occlusion test and can accurately identify the cause. This is done by nasal examina-
predict the results of latter [12]. tion, endoscopy, and CT angiography. If no defi-
nite cause is apparent or there is abnormal cluster
of vessels or arteriovenous malformation, then
5.2.4 D
SA Embolization in Trauma endovascular embolization is usually done. This
Setting is particularly applicable to posterior epistaxis.
Depending on the finding on diagnostic runs,
Arterial embolization procedures are commonly appropriate embolization agent is used. If no sig-
performed in the emergency setting for traumatic nificant finding is seen and bleeding cannot be
oronasal bleed not responding to packing. localized to one side, then empirical emboliza-
Selective arterial runs of bilateral internal maxil- tion of bilateral internal maxillary arteries is done
lary and facial arteries are mandatory to identify using gelfoam/PVA particles. If bleeding can be
the source of the bleed. DSA may show pseudoa- localized to one side, then the superior labial
neurysm due to traumatic injury of the artery or branch (nasal septal branches) of ipsilateral facial
abnormal parenchymal blush due to bleeding artery is also embolized [13]. Internal maxillary
from small arterioles (Fig. 5.6). Former is usually artery is embolized distal to the origin of the mid-
treated by selective coil embolization while the dle meningeal artery so that sphenopalatine and
latter is managed by occluding the culprit artery descending palatine arteries are embolized [13].
using gelfoam. Sometimes the diagnostic runs Most common cause of failed embolization is
may not show any abnormality on DSA, even bleeding from anterior and posterior ethmoidal
130 G. Singh et al.
Fig. 5.6 Traumatic maxillary bleed. (a) Shows contrast extravasation from internal maxillary artery in the DSA run.
(b) After gelfoam embolization, the extravasation has stopped
Table 5.3 Commonly used embolizing and sclerother- operative blood loss and morbidity. This is usu-
apy agents ally done within 72 h of surgery but should not be
Sclerotherapy done more than 5–7 days earlier. This is to pre-
Embolizing agents agents vent revascularization by recruitment of collater-
Mechanical: Coil, Microcoil, 3% STDS
Vascular Plug, Gelfoam pledgets
als. Endovascular embolization is usually done.
Particulate: PVA particles, Polidocanol Percutaneous/endoscopic direct intralesional
Embospheres, Gelfoam slurry embolization may also be done, especially if arte-
Liquid: Glue Bleomycin rial feeders are small and difficult to catheterize
Ablative: Alcohol or if there is significant supply from the internal
Chemo-embolic agents: carotid artery. Common lesions where preopera-
Chemotherapy drug with lipiodol
tive embolization is done include juvenile naso-
STDS sodium tetradecyl sulfate pharyngeal angiofibroma and glomus tumors
(Figs. 5.7 and 5.8).
arteries (branches of ophthalmic artery); this It may also be done for other hypervascular
requires surgical ligation. Reported success rates neoplasms like hemangiopericytoma, nerve
of embolization in epistaxis are 71–95% [13]. In sheath tumors, plasmacytomas, and metastases.
diseases like hereditary hemorrhagic telangiecta- Commonly used embolizing agent is polyvinyl
sia where multiple sessions may be needed, the alcohol (PVA) particles 300–500 μ in size.
main arteries must be kept patent and proximal Gelfoam can also be used. Glue is used if there is
embolization with coils should not be done. excessive arteriovenous shunting or for direct
embolization. Direct intratumoral glue injection
can be done through percutaneous or nasal route,
5.2.6 DSA Embolization in Tumors depending on the tumor location and extent.
All the feeding arteries (usually from external
Usual indication of embolization in tumor setting carotid artery branches) need to be embolized so
is in the preoperative period to reduce the intra- that the entire tumor blush disappears. The goal is
Fig. 5.7 DSA runs showing parenchymal blush of JNA. vidian branch and (c) Demonstrates percutaneous target-
(a) Shows predominant supply from internal maxillary ing of JNA component in the infratemporal fossa
artery. (b) Depicts supply from internal carotid artery via
Fig. 5.8 Glomus tumor. (a) Sagittal T2w MRI image ICA and ECA with intense blush. (c) There is predomi-
shows hyperintense mass with flow voids within. (b) DSA nant supply from the posterior auricular artery
image RT common carotid artery runs shows splaying of
to deposit the embolizing agent at arteriolar/cap- surgically because of distorted anatomy, large
illary level to reduce vascularity. Feeders from tumor size, post-radiation changes, fistula, and
the internal carotid and vertebral arteries are usu- infection [14]. CT angiography is usually done
ally not embolized because of the risk of stroke. first to assess the tumor and its relationship with
Few series have also tried selective chemo- adjacent vessels. CT also helps to identify any
embolization where chemotherapy drugs are pseudoaneurysm or active contrast extravasation.
injected selectively into the feeding arteries of In such a case the corresponding artery is usually
the tumor. This may increase the local effect of blocked with coils at the site of injury. If no site
the drug on the tumor and reduce systemic toxic- of arterial injury is identified, then tumor emboli-
ity. This has been mostly tried in laryngeal can- zation is done to reduce bleeding.
cers but results have been heterogenous. Carotid blowout syndrome is a complication
Sometimes tumors may erode adjacent arteries of extensive or recurrent squamous cell carci-
and lead to bleeding. This is difficult to control noma of the head and neck in which there is rup-
132 G. Singh et al.
Fig. 5.9 (a) Frontal and (b) lateral DSA runs in a patient with locally invasive laryngeal cancer with carotid blowout
show contrast extravasation from the distal common carotid artery
Fig. 5.10 Face AVM. (a) and (b) DSA runs in lateral projection arterial phase and late venous phase respectively show
abnormal cluster of vessels getting supply from the internal maxillary artery and showing early venous shunting
ture or bleeding from the carotid artery or its such a case and thus endovascular treatment is
branches (Fig. 5.9). This may be due to tumor preferred. There are two options in carotid blow-
eroding the vessel wall or post-radiation changes out. One is permanent occlusion of the carotid
or postoperative exposure. Surgical ligation of artery by coils or detachable balloons. However,
the carotid artery is technically challenging in if the balloon occlusion test is positive, then cov-
ered stent (stent graft) may be used to prevent 5.2.8 Sclerotherapy for Sinonasal
cerebral ischemia. However, the latter does not Low-Flow Malformations
have good long-term outcome.
Low-flow vascular malformations include venous
and lymphatic malformations are commonly
5.2.7 DSA Embolization in AVMs treated by sclerotherapy. Cystic masses in the
region of glabella need to be carefully evaluated
Arteriovenous malformations (AVMs) in the to rule out meningocele. MRI is usually recom-
face/nose/ITF may present with pulsatile swell- mended prior to any management to map out the
ing and/or bleeding (epistaxis) (Fig. 5.10). Lip entire extent of the lesion, muscle involvement,
is often involved in such cases. Glue mixed proximity to the course of nerves, orbit, and air-
with lipiodol is the commonly used embolizing ways. Direct puncture of the lesion followed by
agent. In case of large venous varices, espe- contrast phlebography is done initially to decide
cially when causing osteolysis of mandible, the type of sclerosant, estimate its volume and
coils are used to pack the venous side of the look for draining veins (Fig. 5.11). The intent of
AVM. Absolute alcohol may also be used; how- sclerotherapy is the alleviation of symptoms
ever, has the propensity to cause side effects (pain, bleeding, swelling, mass effect) and rarely
due to tissue necrosis. Onyx (ethylene vinyl curative. Sodium tetradecyl sulfate (STDS) is the
alcohol copolymer) can also be used especially commonly used sclerosant especially in case of
in cases where there is direct arteriovenous fis- macrocystic lesions and 3% concentration is used.
tula. For bleeding control; many times, percuta- Polidocanol is less effective, less painful, and
neous direct embolization is also done after incites less edema; used when the risk of side
endovascular control. The potential sites of effects is more especially in case of small cystic
dangerous anastomoses between internal and spaces. Bleomycin is the agent of choice for
external carotid circulations need to be kept in microcystic lesions and incites the least inflam-
mind in case of midline face lesions to avoid mation, thus can be used if the lesion is close to
inadvertent blindness and stroke. These include airways. However, the cumulative dose of bleo-
nasal bridge, glabella and orbits and the anasto- mycin should not exceed the safety limits to avoid
mosis is between ophthalmic and ethmoid pulmonary toxicity. Orbital extension is frequent
arteries with internal maxillary and facial artery in sinonasal lesions, thus there is potential risk of
branches. Also, such lesions usually have some orbital inflammation post sclerotherapy. Hence
drainage into the cavernous sinus as well. risk versus benefit to be assessed based on patient
Fig. 5.11 Low-flow malformations of face. (a) Axial vein. (c) Axial T2w MRI image shows hyperintense lym-
T2w MRI image shows hyperintense microcystic venous phatic malformation involving right parotid. (d)
malformation in the left upper lip. (b) Corresponding Corresponding phlebogram image shows macrocystic
phlebogram shows spongy pattern without any draining pattern
134 G. Singh et al.
symptoms and vision. Usual technique is foam ter patient comfort [16]. With advances in the
sclerotherapy for both STDS and polidocanol to hardware of interventional radiology and increas-
increase the surface area of contact with the endo- ingly available expertise, the use of IR is going to
thelial wall and to slow down the clearance. The expand in ENT surgery. Both specialties need to
usual gap between sclerotherapy sessions is work together for decision making to enhance
6–8 weeks. Sclerotherapy or alcohol ablation may patient care.
also be done for benign cystic lesions like colloid
thyroid nodules, plunging ranula, salivary gland
cysts [14]. 5.3 art C: Nuclear Medicine
P
Perspective
5.2.9 Complications 5.3.1 Introduction
Common complications of non-vascular proce- Nuclear Medicine is a medical speciality that

dures include pain and vasovagal reaction. There uses radiopharmaceuticals for diagnostic and
is minor risk of bleeding and infection. Injury to therapeutic purposes. Recognition of nuclear
adjacent structures like major vessels and nerves medicine as a branch dates back to 1946 when
is uncommon if a safe path has already been Sam Seidlin became the first to report the success
identified on imaging. Also, the use of thinner of radioactive iodine (131I) in treating a patient
needles further reduces the risk. Prior radical with advanced thyroid cancer. Since then, there
neck surgery and radiation therapy increase the have been many discoveries and development of
risk of vascular complications (1). Injury to numerous diagnostic and therapeutic agents. The
nerves remains a theoretical risk in sampling pro- most commonly used radiotracers in diagnostic
cedures. Complications of sclerotherapy include nuclear medicine are 99mTc (Technetium) labeled
pain and swelling for 5–7 days, trismus (in case for planar and SPECT (Single Photon Emission
of lesions in the masseteric muscles), and skin Computed Tomography) imaging, and 18F
discoloration in case of superficial lesions or (Fluoride) and 68Ga (Gallium) labeled for PET
extravasation of sclerosant. In case of malforma- imaging. Nuclear Medicine plays an important
tions around/near the nerves (example parotid role in nasal, nasopharyngeal, and paranasal
lesions), there is a risk of sensory/motor loss due sinus pathologies, by offering different types of
to post-procedural edema. These neuropathic fea- investigations. Its use is indicated in infective
tures are usually transient. Vascular interventions pathologies and some benign and malignant
may lead to puncture site hematomas, skin / pathologies.
mucosal discoloration/ulcers (due to ischemia),
and rarely non-target embolization (leading to 5.3.1.1 Skull Base Osteomyelitis
stroke or blindness) due to particle reflux and
dangerous arterial anastomosis between internal Three Phase Bone Scintigraphy
and external carotid circulations [15]. Facial Three phase bone scintigraphy is commonly used
nerve paralysis may occur in case of emboliza- for skeletal infection imaging including skull base
tion of the superficial temporal artery or if there osteomyelitis (SBO). Three planar phases of the
is lot of post-embolization edema (alcohol/glue bone scan are: flow, pool, and delayed. Flow
use). Some patients may develop post- images demonstrate blood flow to the region of
embolization syndrome (fever, malaise, pain). interest. Pool phase shows the soft tissue
There is the potential risk of raised intracranial distribution of radiotracer around the region.
tension post cavernous sinus thrombosis, if Delayed images depict the bone uptake of radio-
venous drainage is not properly mapped. tracer in the area. Sometimes additional SPECT/
IR provides a minimally invasive treatment CT images are also taken. Conventional imaging
option with considerably less morbidity and bet- for SBO is CT (Computerized tomography) is
commonly performed investigation since it is rel- assess the functional activity of the disease. This
atively easy and fast method and detects deminer- feature can be used for response assessment,
alization and bone destruction. However, CT especially in immune-compromised patients in
cannot detect the early functional changes that whom clinical features and laboratory parameters
characterize bone infections and suffers a definite may not be reliable, which helps in making the
delay in detecting bony structure alterations [17]. decision of change or discontinuation of antibiot-
Magnetic Resonance Imaging (MRI) is suggested ics. However, the disadvantage of planar bone
to visualize intracranial spread, thrombosis, and scintigraphy is that the ongoing osteoblastic activ-
soft tissue involvement. Both these conventional ity of the healing process may appear as false
imaging techniques give anatomical details and positive on scan. In such cases, WBC labeled
do not allow assessment of disease activity and its imaging will differentiate between infection and
response to treatment. In SBO, bone scintigraphy bone remodeling. The negative predictive value of
is indicated for the diagnosis and the extent of dis- bone scintigraphy in SBO is much higher and can
ease, to evaluate disease activity status, and for rule out active infection.
assessment of response to treatment. In active
SBO, there will be increase in flow, pool activity, 18
F FDG PET/CT
and uptake in delayed images. With SPECT/CT 18
F FDG PET/CT can be used for SBO, since it is
imaging the anatomical extent of the disease can easily available and has higher resolution than
be corroborated with functional activity. planar and SPECT imaging (Fig. 5.13). As it is
Occasionally flow and pool activity may not be not a bone-specific agent, it can differentiate
significantly increased, particularly in cases of between bone infection and osteoblastic changes
chronic osteomyelitis. In these cases, diagnosis is in bone healing. However, it is non-specific and
made on the basis of delayed and SPECT images can be positive in other non-infectious etiologies,
(Fig. 5.12). The advantage of bone scan over con- like malignancy, and has higher radiation expo-
ventional anatomical imaging is its ability to sure to the patient than 99mTc bone scintigraphy.
Fig. 5.12 A 40 years old diabetic patient presented with region. (b) CT and fused SPECT-CT images reveal the
pain and discharge in the left ear for past 3 months and focal concentration of radiotracer in left mastoid air cells
was referred to rule out skull base osteomyelitis. (a) which show loss of pneumatization on CT
Delayed planar images show uptake in the left mastoid
136 G. Singh et al.
Fig. 5.13 53 years old male, with known left skull base CT shows focal area of radiotracer uptake in the left sty-
osteomyelitis, post-left radical mastoidectomy, referred loid process and mastoid air cells, suggestive of residual
for FDG PET/CT to rule out residual disease. FDG PET/ disease
Fig. 5.14 Sixty years old female, with clinical suspicion of skull base osteomyelitis and inconclusive bone scan, under-
went 18F-WBC PET/CT, which revealed the involvement of left temporomandibular joint and sphenoid
WBC Labeled Imaging fungal infections as well. The disadvantage of

White blood cells (WBC) labeling is a specific WBC labeled imaging is that the process is cum-
tool for infection imaging, particularly in differ- bersome with low yields and requires dedicated
entiating bone infection from bone remodeling lab facility.
(Fig. 5.14). In this technique, autologous WBCs
are labeled with radionuclide ex vivo. The com- Tumor Imaging
monly used SPECT based tracers are 99mTc (A) Carcinoma Nasopharynx
HMPAO (hexamethylpropylene amine oxime) Conventional imaging of choice for the stag-
and 111In oxine and PET-based tracer is 18F labeled ing of Nasopharyngeal carcinoma (NPC) is
WBC. SPECT based tracers have less resolution MRI. 18F-FDG PET/CT is the preferred
as compared to PET-based tracers. Since leuko- investigation for metastatic evaluation of
cytes are directly labeled, this modality can detect NPC (Fig. 5.15). MRI has high specificity,
ongoing infections anywhere, and can find use in sensitivity, and accuracy for T staging of the
Fig. 5.15 62 year old male with biopsy proven nasopha- vical lymph nodes. (c) Axial fused PET/CT images show-
ryngeal carcinoma underwent 18F-FDG PET/CT for staging parenchymal lung nodule with uptake in right lung
ing. (a) MIP image reveals uptake in primary, cervical lower lobe, superior segment. (d) Axial fused PET/CT
lymph node, lung, liver, and skeletal lesions. (b) Coronal images showing multiple liver metastases. (e) Axial fused
section of head and neck showing intense FDG uptake in PET/CT images in bone window showing increased
ill-defined lesion occupying the roof of nasopharynx with uptake with lytic lesion in left ilium suggestive of bone
intracranial extension. Also seen, multiple FDG avid cer- metastases
tumor. 18F-FDG PET/CT has a limited role PET/CT can detect residual disease in the
in T staging of tumor and tends to miss background of postoperative and RT changes
lesions in the skull base and cavernous and therefore has a role to play in response
sinuses due to physiologically high uptake assessment in these groups of patients.
of FDG in the brain and in early-stage tumor (B) Sinonasal Tumors
invasion and because of the lower resolution Sinonasal neoplasms are rare in occurrence
of PET compared with MRI [18]. Since MRI and comprise only 3% of all head and neck
and CT depend on size criteria, it may be cancers. Sinonasal tumors can be of epithe-
difficult to differentiate between small lial (carcinomas) or mesenchymal (sarco-
benign and malignant nodes. 18F-FDG PET/ mas) origin. Epithelial tumors are the most
CT has high accuracy in assessing N stage of common and originate from the epithelial
tumor. 18F-FDG PET/CT has a sensitivity of lining, accessory salivary glands, neuroen-
97–100% and specificity of 73–97% in docrine tissue, and olfactory epithelium.
assessing cervical lymph nodes in patients Mesenchymal tumors derive from the sup-
with NPC, and MRI has a sensitivity of porting tissue. Since their presentation is
84–92% and specificity of 73–97% [19]. similar to rhinosinusitis, by the time of diag-
However, PET/CT is not comparable to MRI nosis they are usually much advanced.
in the detection of retropharyngeal nodes Common benign tumors in this region are
close to the primary, use of contrast enhanced papilloma and schwannoma. These benign
CT with PET may improve this detection. tumors are routinely imaged with CT and
According to NCCN guidelines (v1.2015) MRI. However, in the presence of malignant
18
F-FDG PET/CT is recommended for imag- transformation 18F-FDG PET/CT has shown
ing of distant metastases (chest, liver, bone) to have increased uptake. Therefore, PET/
for WHO class 2–3/N2–3 disease. 18F-FDG CT may have a role to play in cases with sus-
138 G. Singh et al.
picion of co-existent malignant (ii) Mesenchymal Tumors:

components. Mesenchymal tumor is a rare neoplasm
(i) Juvenile Nasopharyngeal Angiofibroma arising from any mesenchymal tissue
(JNA): such as bone or soft tissue. This tumor is
These are benign yet locally aggressive common in extremities, rarely occurs in
in disease pathology. Conventionally CT sinonasal region. Some of them secrete
and MRI are used to confirm diagnosis fibroblast growth factor 23 (FGF23)
and disease extent. However residual dis- which is responsible for phosphaturia
ease and recurrence rate for JNA is high, and tumor-induced osteomalacia (TIO)
ranging from 15% to 50%, which are not [20]. They can present with muscle
well detected on conventional imaging. weakness, bone pain, and fractures.
18
F-FDG PET/CT may be able to detect These tumors are small and hence diffi-
active residual/recurrent disease but due cult to diagnose. Initial whole body
to physiological high FDG uptake in screening is done with 18F-FDG PET/CT
brain, intracranial extension and lesion followed by 68Ga-DOTANOC PET/CT
close to skull base may not be well appre- (SSTR scintigraphy), any suspicious
ciated. With this consideration, lesion is further evaluated with MRI and
68
Ga-PSMA PET/CT and 68
Ga- histopathology.
DOTANOC PET/CT have been done for (iii) Lymphoma:
few patients in our department, which are The nasal cavities and paranasal sinuses
showing promising results (Fig. 5.16). are rarely affected by primary Non-
Fig. 5.16 12 year old boy with juvenile nasopharyngeal gland and avid mass. Whereas MIP image of PSMA (b)
angiofibroma, underwent 68Ga DOTANOC (a) and 68Ga shows physiological uptake in lacrimal and salivary
PSMA (b) PET/CT for baseline evaluation. Images reveal glands along with the avid mass (On going thesis- Dr.
ill-defined lobulated mass occupying entire nasal cavity Prabhu, Dept of ENT, AIIMS, New Delhi, under guidance
and left maxillary sinus, with erosion of sphenoid and of Prof. Alok Thakar (ENT) & Prof Rakesh Kumar
extension into left infratemporal fossa. MIP image of (Nuclear Medicine)
DOTANOC (a) shows physiological uptake in pituitary
Fig. 5.17 39 year old male, with NK Tcell lymphoma of ity and involving the nasal septum and nasopharynx, with
nasal cavity, underwent 18F-FDG PET/CT for staging. diffuse FDG uptake. (c) FDG avid extension of mass into
MIP image (a) reveals FDG avid mass involving the nasal infra-orbital region of right eye and right ethmoid seen.
cavity and diffuse uptake in axial and appendicular skele- No other lesion noted in rest of the body
ton. (b) Irregular soft tissue thickening of right nasal cav-
Hodgkin lymphoma (NHL). Most com- metastatic evaluation and disease activity
mon NHL in the head and neck region is response assessment (Fig. 5.17).
of the Waldeyer ring, in which palatine (iv) Mucosal Melanoma:
tonsil is most common followed by naso- Mucosal malignant melanoma is a very
pharynx. Primary nasopharyngeal lym- rare tumor counting for approximately
phoma constitutes 8% of all head and 0.8–1.3% of all melanomas. Sinonasal
neck lymphomas. 18F-FDG PET/CT is malignant melanoma (SNMM) accounts
useful for the detection of the Primary roughly for 4% of all head and neck mel-
Nasopharyngeal lymphoma (PNL), its anomas and sinonasal malignancies [22].
extent of disease, and response evalua- In routine practice of head & neck radio-
tion. Studies have revealed that 18F-FDG logical assessment, CT and MRI are used
PET/CT is not reliable to differentiate for initial diagnosis. These modalities
between PNL and NPC [21]. The nasal have their limitation in metastatic evalua-
cavities and paranasal sinuses are rarely tion and detection of residual/recurrent
affected by primary NHL, these can be disease. 18F-FDG-PET/CT imaging has
differentiated from squamous carcino- higher sensitivity and specificity over
mas of these areas on conventional imag- conventional imaging in the staging of
ing due to their sub-mucosal origin. malignant melanoma [23]. Therefore,
18
F-FDG PET/CT also has a role in the 18
F-FDG-PET/CT can be a one-stop-
140 G. Singh et al.
Fig. 5.18 50 years old female, with known malignant mel- axial skeleton. (b) Axial CT and Pet/CT fused images show-
anoma, underwent 18F-FDG-PET/CT post-surgery and ing mucosal thickening in lateral wall of left nasal cavity
radiotherapy to look for disease status. (a) MIP image show- with FDG uptake, suggestive of residual disease. (c) FDG
ing increased uptake in the region of nasal cavity, lungs, and avid parenchymal metastatic nodule in right lung lower lobe
shop imaging for detection of primary as evaluation of the osseous involvement of

well as metastatic diseases (Fig. 5.18). the cribriform plate, fovea ethmoidalis,
Studies have shown the use of 18F-FDG- and lamina papyracea. MRI assesses the
PET/CT in staging, restaging post- soft tissue extent and dural involvement
surgery, and response assessment of of the disease. Like other neuroectoder-
SNMM [24]. However, non-specific mal tumors, ENB shows MIBG (Meta-
mucosal FDG uptake in local infective or iodo benzyl guanidine), a nor-epinephrine
inflammatory conditions may lead to analog, concentration. 123I labeled MIBG
misinterpretation of PET. for diagnostic planar and SPECT and 131I
(v) Olfactory Neuroblastoma: labeled MIBG for therapeutic indications
Olfactory neuroblastoma also known as are already in use for extra-nasal neuro-
Esthesioneuroblastoma (ENB) is a rare blastoma. MIBG scintigraphy has been
neuroectodermal tumor of the nasal cav- found to be useful in differentiating
ity, comprising 2% of all sino-nasal neo- olfactory neuroblastomas from other
plasms [25]. Imaging plays an important nasal tumors [26]. 18F-FDG-PET/CT is
role in the diagnosis and staging of olfac- used for staging, restaging, and follow up
tory neuroblastoma. CT is essential for of ENB [27]. Some studies have shown
Fig. 5.19 33 years old male, with suspected nasal neuro- nasal cavity with intense tracer uptake. (b) Sagittal CT
endocrine carcinoma, post three cycles of docetaxel, and PET/CT fused images showing mass occupying the
underwent 68Ga DOTANOC PET/CT. (a) Axial CT and right nasal cavity. Biopsy revealed olfactory
PET/CT fused images showing sift tissue mass in right neuroblastoma
the superior diagnostic role of Choline- DOTANOC in tumor and response to 90Y
based PET (18F or 11C labeled) over FDG DOTATATE (Fig. 5.19) [30].
PET, however, more data is required to (vi) Occult Primary:
establish this [28]. High expression of Carcinomas of unknown primary (CUP)
Somatostatin Receptors (SSTR), particu- account for 5–10% of head and neck can-
larly SSTR-1 and 2, has been docu- cers [31]. Oropharynx is one of the most
mented in tumor cells of neuroblastoma common sites of origin of head and neck
[29]. Extending from this knowledge occult primaries, accounting for nearly
Savelli et al. have reported SSTR scintig- 90% of CUPs, the nasopharynx and
raphy and peptide receptor radionuclide hypopharynx are relatively less common
therapy (PRRT) in a case of ENB, they ‘hot spots’ for occult primary tumors
have reported good uptake of 68Ga [32]. When conventional imaging, i.e.,
142 G. Singh et al.
CT and MRI, fail to localize occult pri- tium), 90Y (yttrium), or 225Ac (actinium)
mary, PET/CT becomes the next investi- labeled DOTATE. Olfactory neuroblastoma
gation of choice. FDG PET/CT scan has like other neuroblastomas is amenable to
an overall staging accuracy of 69–78%, a 131
I-MIBG therapy. JNA has been shown to
positive predictive value of 56–83%, a express both SSTRs and PSMA, therefore,
negative predictive value of 75–86%, a theoretically can receive PRRT or PSMA
sensitivity of 63–100%, and a specificity labeled 177Lu or 225Ac therapy.
of 90–94% in CUP [33]. Apart from the
localization of primary, PET also assists
in identifying more feasible sites for 5.4 art D: Bacteriology
P
biopsy. However, FDG PET/CT also has and Virology
its drawbacks, the presence of infective/
inflammatory pathology in nasal cavity 5.4.1 Introduction
and paranasal sinuses may give rise to
false positives. Antonie Philips van Leeuwenhoek was the first
(C) Sentinel Lymph Node Scintigraphy scientist who observed bacteria. Bacteria are sin-
Sentinel lymph node biopsy is based on the gle cell organism seen by light microscopy which
identification of the predictable pattern of unlike viruses is able to multiply by binary fission
lymphatic drainage to a primary tumor, and as well as survive outside other cells. After birth,
its role as an effective filter for tumor cells the nasopharynx of a new born does not remain a
[34]. Histopathological confirmation of the sterile site for more than 48 h. With rapid acquisi-
involvement of sentinel lymph node helps in tion of colonizing bacteria initially from the
limiting unnecessary neck dissections. There maternal genital tract and later followed by organ-
are various techniques for the identification ism which are either ingested or received from
of the sentinel lymph nodes, commonly used carrier skin. The normal indigenous flora consists
are the dye method and radiotracer method. of gram-positive and gram-negative, aerobic and
In the radiotracer method, the radiolabeled anaerobic bacteria including the oral streptococci,
colloid suspension is injected at the primary Bacteroides species, Corynebacterium species,
site, and planar and SPECT/CT images are and Neisseria species.
acquired at 15, 30, and 60 min from injec-
tion. SPECT/CT provides anatomical confir- 5.4.1.1 Bacteriology of Nose and PNS
mation of lymph node level of the sentinel Common cold (Rhinitis) is defined as an inflam-
lymph node. During surgery, the exact loca- mation of the nasal mucous membrane or lining.
tion of the nodes may be confirmed using a Bacterial agents are responsible for 10–15% of
hand-held gamma detector probe. These cases of rhinitis which include Chlamydia pneu-
identified lymph nodes are then biopsied to moniae, Mycoplasma pneumoniae, and Group A
look for the spread of malignancy, and assist streptococci [36]. Maxillary sinus is the most com-
in decisions regarding neck dissection. Few monly involved sinus. The subsequent order of
sentinel lymph node scintigraphy studies frequency of sinus involvement is the ethmoid,
have been done for sino-nasal malignancies, frontal, and sphenoid sinuses) [37]. Streptococcus
showing an increment in the identification of pneumoniae and Haemophilus influenzae are the
involved nodes of up to 14% [35]. most common etiological agents among
( D) Therapeutic Potential community-acquired cases (50–60%). Moraxella
Tumors expressing somatostatin receptors catarrhalis is responsible for around 20% of cases
(SSTR) like NET of the nose and paranasal in children. Methicillin-resistant Staphylococcus
sinuses, may be considered for peptide aureus (MRSA) concern is emerging. Among
receptor radionuclide therapy (PRRT) tar- anaerobes, Prevotella spp. Fusobacterium spp.,
geting these receptors, such as 177Lu (lute- are found [38]. Among chronic sinusitis, common
pathogens are S. pneumoniae, H. influenzae, and 2 . Sinusitis is the clinical diagnosis. Maxillary
M. catarrhalis. Other pathogens that are less fre- sinusitis is the most common type of sinus-
quently seen are anaerobic streptococci, Prevotella itis, and specimen is collected by aspiration
spp., and Fusobacterium spp. M. catarrhalis is and subjected to culture and susceptibility
one of the possible agent in chronic sinusitis in testing [36, 40]. Therapy can be modified
children [36]. according to the etiological agent and treat-
Nosocomial sinusitis is a relatively common ment response. As nasal cavity is colonized
occurring complication, mainly in critical care. heavily with respiratory flora, contamination
Risk factors are nasal intubation, nasal-enteric of sample collected from paranasal sinuses is
tube. Bacterial species that are prevalent in envi- quite common. To help in differentiating true
ronment of hospital are the common etiological infection from contamination, quantitative
agents for nosocomial cases including, methods can be helpful. Colony count of at
Staphylococcus. aureus, Pseudomonas spp., least 104 colony-forming units per milliliter
Klebsiella pneumonia, etc. Such infections are (CFUs/mL) of aspirated material is sugges-
commonly polymicrobial and multidrug resistive of infection.
tant. During the last three decades, extra- 3. General instructions for specimen transport:
pulmonary tuberculosis (EPTB) has gained The specimen should reach the laboratory as
special attention because of the human immuno- soon as possible. Ideally specimen must
deficiency virus (HIV) pandemic. Mycobacterium reach the laboratory within <2 h. If specimen
tuberculosis most frequently reaches the lung and is taken in odd hours, it can be store at 4 °C
rarely involves paranasal sinuses and nasophar- (This only applies to Virus etiology as men-
ynx. It reaches the nose and facial bones through tioned with Coronavirus). For suspected
blood stream or lymphatics. Antral lavage exami- Bacterial etiology, we can keep the specimen
nation for AFB and culture for Mycobacterium at room temperature maximum for 24 h. It
tuberculosis can facilitate early diagnosis, there should not be refrigerated, Sinus drainage is
by avoiding surgical intervention. unacceptable for smear or culture because of
contamination with naturally occuring flora.
Steps and Site of Specimen Collection [39]
1. Rhinitis: The sample is collected from ante- Nasal smear is also useful to evaluate eosino-
rior nares. If pus is found on anterior rhinos- phils. It may help in diagnosing the suspected
copy, dry swab is applied over it to collect cases of allergic rhinitis. Even in uncomplicated
sample. If no pus is found, the swab is moist- cold, polymorpho-nuclear leukocytes predomi-
ened first and then the anterior nares are nance in nasal secretions can be seen and does
swabbed. Swab specimen should be taken not always a marker for bacterial superinfection.
from at least 1 cm inside the nares. The trans- Routine microbiological investigations like
port medium for the swab is mainly for staph- bacterial cultures or antigen detection are
ylococcal carriers. To culture the lesion, the required when specific bacterial etiological agent
sample is to be collected from the advancing like group A streptococcus, nasal diphtheria, or
margin of the lesion. For nasopharyngeal Bordetella pertussis is suspected.
swab, flexible swab stick is inserted per nasal,
it is passed through the nasal cavity till it
impinges on the nasopharynx, and then rotate 5.4.2 Staining Procedures
for 5–10 s. Swab can be moistened with
Stuart’s or Amie’s medium. (This moistening • Gram Stain: It divides the bacteria into Gram-
is only for bacterial etiology suspected). Thin positive and Gram-negative bacteria.
wire or flexible swab is dipped into transport • Ziehl–Neelsen Technique: It divides the bac-
medium. Transport to laboratory teria into acid fast and non-acid fast.
immediately. Mycobacterium tuberculosis being acid fast,
144 G. Singh et al.
is presumptively diagnosed with this 3. Loeffler’s serum slope and Potassium tellurite
technique. agar (PTA): It is used for isolation of
• Albert Stain: It is performed for Corynebacterium Corynebacterium diphtheriae.
diphtheriae, will appear as green bacilli with 4. Blood agar and Pike’s medium (Blood agar
purple-blue metachromatic granules and in typi- containing crystal violet and sodium azide):
cal arrangement. For Streptococcus spp.
5. Robertson’s cooked meat medium (RCM),

PRAS (pre-reduced anaerobic sterilized)
5.4.3 C
ulture Media Are Required transport medium, Stuart’s transport medium
to Isolate the Bacteria for anaerobes.
from the Clinical Specimens
Growth from the medium can be identified by
1. Primary Plating Medias are blood agar,
conventional biochemical tests, automated iden-
MacConkey agar, chocolate (Heated blood tification system, or MALDI-ToF {Matrix-
agar) agar. It is for isolation of aerobic bacte- assisted laser desorption/ionization (MALDI),
ria (Figs. 5.20, 5.21, and 5.22). and the mass analyzer is time-of-flight (TOF)
2. Lowenstein-Jensen (LJ) medium: It is used analyzer}.
for isolation of Mycobacterium tuberculosis.
5.4.3.1 Storage of Media
Bacterial cultures are generally stored on agar
plates or in stab cultures in the refrigerator at
4 °C. Long-term storage methods should be con-
sidered for maximum bacterial viability like:
1. Freezing samples
2. Freeze-drying (Lyophilization)
5.4.4 N
ucleic Acid Amplification
Techniques (NAAT)
It is increase the yield of sample. The various

Fig. 5.20 MacConkey Agar NAATs used are Polymerase chain reaction
Fig. 5.21 Blood Agar Fig. 5.22 Chocolate Agar

(PCR), Real-time polymerase chain reaction, degenerative alterations of the ciliary ultrastruc-
Ligase chain reaction (LCR), Transcription- ture (shortening and focal or even general loss of
mediated amplification (TMA), Nucleic acid the cilia), the cytoplasm (contraction of the cyto-
sequence-based amplification (NASBA), and plasm, or even shortening of the upper portion of
Strand displacement amplification (SDA) [41]. the cell body), the nucleus (chromatin margin-
The PCR technique involves three basic steps ation with a ground-glass appearance and intra-
to amplify the number. nuclear inclusions). The range of viruses that
commonly infects the respiratory tract is notori-
1 . DNA extraction from the organism ously wide (rhinovirus, coronavirus, respiratory
2. Amplification of extracted DNA syncytial virus [RSV], adenovirus, parainfluenza
3. Gel electrophoresis of the amplified product virus, coxsackievirus, cytomegalovirus).
However, no specific cytomorphologic alteration
has been found till date that could represent a
5.4.5 Antibiotic Sensitivity, turning point in epidemiology, despite viral infec-
Resistance, and Prevention tions accounting for the bulk of human infectious
diseases, or in prognosis and therapy. Some have
Testing for antibiotic sensitivity is often done by strongly linked with the carcinogenesis of several
the Kirby-Bauer method or automated antibiotic tumor types, particularly Burkitt’s lymphoma
susceptibility system. Small disc containing anti- and nasopharyngeal carcinoma (NPC) with
biotics are placed onto a plate upon which bacte- Epstein-Barr virus (EBV).
ria are growing. If the bacteria are sensitive to the
antibiotic, a clear ring, or zone of inhibition, is
seen around the disc indicating poor growth. 5.4.7 L
aboratory Diagnosis of Viral
Antibiotic resistance occurs when bacteria Diseases
change in some way that reduces or eliminates
the effectiveness of drugs, chemicals, or other Laboratory Diagnosis of Common Cold [37]:
agents designed to cure or prevent infections. The The culture, antigen detection, PCR, or serologic
bacteria survive and continue to multiply causing methods are the commonly employed diagnostic
more harm. Bacteria can do this through several methods for viral pathogens that cause the com-
mechanisms. To preserve the potency of existing mon cold. As such, routine diagnostic methods
antibiotics, overall antibiotic use must be neither required nor of any help in cases with
decreased. Physicians, pharmacists, and the gen- common cold. It is only helpful when therapy
eral public must avoid the careless use of these with an antiviral agent is required for specific
valuable drugs. Antibiotics must be prescribed etiological agent. As such, viruses have been
only for bacterial infections and in the proper infrequently isolated from patients with acute
dose for the correct amount of time. sinusitis. Timing of sinus aspiration may be
responsible for this. Sinus aspiration is usually
done in persistent sinusitis when case has been
5.4.6 Viruses in ENT symptomatic for at least 7–10 days [42].
Normally, by this time, viral infection may be
Viruses are the smallest unicellular organisms, diminishing. Respiratory viruses have been
are obligate intracellular. Viruses are the most recovered from approximately 10% of sinus aspi-
primitive microorganisms infecting man. Viral rates. Approximately 30–40% of sinus aspirates
infections are responsible for rhinitis in 20–25% in cases with acute sinusitis are not positive for
of cases. In rhino-pathologies of viral origin, the any bacteria. It is presumed that many of these
microscopic picture is characterized by fairly infections are, in fact, viral. Nasopharyngeal and
aspecific cellular changes gathered under the oropharyngeal swab is also collected to evaluate
term “ciliocytophthoria,” which comprises virus. Swab should be Dacron or polyester
146 G. Singh et al.
flocked swab. For transport of samples for viral improved, handling of diseased and normal
detection, Viral transport medium (VTM) con- healthy mucosa is improved, access to difficult
taining antifungal and antibiotic supplements to area is also improved so the disease clearance
be used. Avoid repeated freezing and thawing of is better than with cold instruments which in
specimen. Transport the sample to laboratory at term reduce the chances of recurrence and
4 °C. If specimen is required to be stored, store at residual disease. Sinonasal region is sur-
4 °C less than equal to 5 days while at -70 °C for rounded by vital structures such as brain and
>5 days. orbit. Inadvertent injury to these vital struc-
tures can create devastating complications.
5.4.7.1 Detection Methods for Viruses Powered instrument also reduces the rate of
Direct Demonstration of Virus is done by elec- complications and fear to handle disease close
tron microscopy, immune-electron microscopy, to these vital structures, which in turn reduces
Fluorescent microscopy, Light microscopy. the morbidity, mortality, and financial burden
ELISA, direct immunofluorescence (IF), on community. Endoscopes, debrider, coblator,
Immunochromatography (ICT) test, flow through navigation system, ultrasonic aspirator, radio-
assays are the methods for detection of viral anti- frequency ablation, etc. are advances in the last
gens. Hemagglutination Inhibition assay (HAI), two decades.
neutralization test, and complement fixation test
(CFT) are the conventional techniques for detec-
1. Endoscopes—It is prepared by using fiber
tion of the specific antibodies. Enzyme-linked optics and powerful lens systems to provide
immunosorbent assay (ELISA) is a technique lighting and visualization of the relatively
used to detect antibodies to infectious agents in a inaccessible areas through conventional instru-
sample. Antibodies are made in response to infec- ments. The portion of the endoscope inserted
tion and so an antibody ELISA can indicate into the body can be rigid or flexible. Hopkins
whether or not an animal has been in contact with rod lens system was developed to provide
a certain virus. Molecular methods include endoscopes of different length, diameter, and
RT-PCR is for RNA and DNA detection. The iso- angle to provide visualization in certain areas.
lation of virus is done by animal inoculation The rigid endoscopes commonly used are 2.7,
method, embryonated egg inoculation method, 3, and 4 mm in diameter. 2.7 mm is for pediat-
and by tissue cultures such as organ culture, ric and 4 mm is for adult nasal procedures.
explant culture, cell line culture [43]. Visualization is better with the increase in
diameter of endoscopes as more light can
transmit to the surgical field. The working
5.5 art E: Advanced
P length of nasal endoscopes is 18 cm. Nasal
Instruments in Rhinology endoscopes are available in various degrees
such as 0, 15, 30, 45, 70, and 90° (Fig. 5.23)
The normal anatomy of the nose and paranasal [44]. 0° and 30° endoscopes are the most com-
sinuses is highly variable and complicated. monly used endoscopes. With the increase in
Certain parts were very difficult to access with degrees, we can see more hidden part of nose
existing cold instruments so clearance of dis- and paranasal sinuses. Seventy degree endo-
ease from these areas was difficult. With the scope is useful for visualization of frontal
advent of the concept of functional endoscopic sinus and maxillary sinus floor. All the endo-
sinus surgery, preservation of uninvolved scopes are now autoclavable. 0° nasal endo-
mucosa is very important so outcome of sur- scope comes with green color coding. Fifteen
gery is better. It improves the quality of life to and thirteen degrees endoscopes comes with
great extent. With the advancement in instru- white and red color coding. Color coding for
mentation in the field of rhinology, the knowl- 45°, 70°, 90° endoscopes are blue, yellow, and
edge of normal anatomy and its variation is black respectively.
Fig. 5.23 Nasal
endoscopes
Video endoscopes are mechanically simi- greater than that of standard halogen sources,
lar to fiber-endoscopes. They have charged with white rather than yellow-tinted light
couple device (CCD) ‘chip’ and supporting quality. In comparison to halogen light,
electronics mounted at the tip, to and fro wir- xenon is more robust and efficient, with
ing replacing the optical bundle and further greater life, less heat creation. The drawback
electronics and switches occupying the site of of xenon bulbs is the cost to install and
the ocular lens on the upper part of the control replace, it takes a few seconds to attain full
head [45]. A CCD chip is an array of 33,000– glow and give off more glare.
100,000 individual photo pixel receiving pho- Digital cameras use chips that process
tons reflected back from the mucosal surface color information. Modern 3-chip cameras
and producing electrons in proportion to the have spate chips to process each of the three
light received. The advantages are improved primary colors, red, blue, and green. This
image quality, improved monitor view, remov- markedly enhances video quality [46].
ing the necessity to grasp the instrument close 2. Microdebrider—Microdebrider is a powered
to the surgeon eye has hygienic advantages instrument. It is an extremely helpful surgical
and it also improved instrument design and tool in modern endoscopic sinus surgery [47].
handling techniques. The only limiting factor Handpiece, interchangeable blades, and
is no direct viewing. Endoscopic observation machines are the components of microde-
can further increase by the light source and brider. The handpiece is connected with suc-
digital camera. tion and irrigation source which is cylindrical
Light Source further augment visualiza- or piston drip in design (Fig. 5.24). The blades
tion by increasing light output. With the have cylindrical back part for easy connection
advent of the xenon light source (peak wave- with handpiece. It contains two hollow shafts.
lengths in the 800–1000 nm range), visual- The outer shaft allows suction and irrigation
ization has markedly improved. Xenon through and around the blades whereas the
sources have been observed to be 3 times inner shaft rotates or oscillates with in outer
148 G. Singh et al.
Fig. 5.24 Microdebrider hand piece, blades, and machine (Courtesy—Dr. Hitesh Verma, Associate Professor, AIIMS,
New Delhi, India)
shaft. For surgical ease, blades are available in sheared bits of debrided tissue are sucked by
wide range in term of size and angles. Straight the suction effect. Microdebrider also
edge blades allow clear tissue cut without improves surgical field by its suction and irri-
injury to surrounding mucosa whereas ser- gation mechanism. The Advantages are the
rated edge blades allow rapid tissue removal. preservation of surrounding healthy mucosa,
Frontal sinus and the deeper part of maxillary it allows precise tissue removal and decreases
sinus can be accessed by more angled blades. surgical time [49]. It is commonly used for
Recent modification in design increases the the removal of polyp and tumor tissue of
application of microdebrider such as inferior nose and paranasal sinuses. Current technol-
turbinate reduction, correction of septal spur ogy advances have added cauterization of
[48]. The mode and speed can be control by bleeders by delivering bipolar cautery effect
footplate of microdebrider. via the end of the blade. These blades them-
Microdebrider acts by indrawn of soft tis- selves are surrounded by layers of insulation
sue by the suction portal. This tissue is causing a sandwiching of the inner and outer
sheared off by the revolving blade between electrodes [50].
the inner and outer cannulas. Irrigation is 3. Coblator—Coblator term is originated from
classically incorporated into the device, “Controlled ablation”. It is a kind of bipolar
applied by another set of tubing, and pumped radiofrequency ablation that works at rela-
into the blade to assist the movement of tively low temperatures (typically 60–70 C)
debrided tissue. The irrigation helps to pre- by unsettling molecular bonds and allowing
vent blockage of the device by the debrided tissues to melt [51, 52]. Soft tissue melting
tissue. The slower the revolving speed of the makes use of bipolar radiofrequency energy.
blade, the big is the tissue nibble. At higher This energy is made to flow through a conduc-
speed rates, the instrument becomes less tive medium like normal saline. When current
effective for debridement of tissue but it is from radiofrequency probe passes through
more effective for drilling of bone. Oscillation saline medium it breaks saline into sodium
mode is used for tissue debridement and it is and chloride ions. These highly energized ions
around 5000 rotations per minute. Other form a plasma field strong enough to break
mode is rotation, it is used for drilling and it organic molecular bonds within soft tissue
is around 15,000 rotations per minute. The causing its dissolution. The excellent conduc-
tivity of saline is used in this technology. This (e) Fifth stage (stage of thermal dissipation
conductivity is responsible for high energy of energy): This stage is essentially due
plasma generation. Low temperature limits to the combination of plasma ions, active
the thermal damage to surrounding tissues atoms, and molecules. Plasma contains
with a depth of penetration 2–4 mm. The H and OH ions. These ions makes
stages of plasma generation are (Fig. 5.25). plasma destructive. Hydroxy radicals
(a) First stage is characterized by the transi- causes protein degradation. When cobla-
tion from bubble to film boiling. This tion is being used to perform surgery the
decreases heat emission and causes interface between the plasma and dis-
increase in surface temperature. sected tissue acts as a gate for charged
(b) Second stage is vapor film pulsation.
particles.
Tissue ablation occurs during this stage. Radiofrequency generator, foot pedal, irriga-
(c) Third stage—Reduction of amplitude of tion system, and wand are the components of
current across the electrodes. coblator (Fig. 5.26). Radiofrequency (RF)
(d) Fourth stage: Dissipation of electron
generator generates RF signals. It is managed
energy at the metal electrode surface. by the microprocessor. This generator is com-
petent in adjusting the settings as per the type
Fig. 5.25 Active

Diagrammatic Electrodes
representation of
mechanism in coblation
Passive
wand. (Coblation wand Electrode
has two electrodes, i.e.,
Base electrode and
active electrode. These
electrodes are separated
by ceramic. Saline flows SALINE HIGH FREQUENCY
between these two SOLUTION CURRENT DISTRIBUTION
FLOW IN QALINE SOLUTION FLOW
electrodes. Current
generated flows between
TISSUE
these two electrodes via
the saline medium.
Saline gets broken down
ZONE OF PLASMA GENERATION
into ions thereby AND ELECTIC CHARGE
forming active plasma
which ablates tissue
Fig. 5.26 Radio frequency generator, irrigation system and wand (Courtesy—Dr. Hitesh Verma, Associate Professor,
150 G. Singh et al.
of wand inserted. It automatically senses the (b) The head mount universal tracker is

type of the wand and adjusts settings accord- attached to the patient.
ingly. For coblation, the plasma setting is 7 (c) Registration: It relates the patient in OT
and for cauterization, non-plasma setting is 3. to pre-op acquired image data sets and is
Foot pedal control has two color-coded ped- used to establish the relation between
als. The yellow one is for coblation and the two coordinate systems. It is done by
blue one is for RF cautery. This device also using anatomical landmarks that are vis-
emits different sounds when these pedals are ible on patient and image data, e.g.,
pressed indicating to the surgeon which mode Tragus, outer canthus, inner canthus,
is getting activated. There are different types nasion. The position of the tip of probe is
of wands available to perform coblation pro- identified by tracking device and coordi-
cedure optimally [53–55]. nates are fed back to navigation soft-
The efficiency of ablation can be improved ware. With the use of fiducial markers
by its intermittent application, copious irriga- the registration process is complete
tion, and by using cold saline. Cold saline can (Fig. 5.27) [56, 57].
be prepared by placing the saline pack in a (d) Tracking—It is the mechanism of fol-
refrigerator overnight. lowing the position of patient/instru-
It is primarily useful in adenotonsillec- ments within the operative field. It
tomy, removal of vascular lesion of sinonasal provides dynamic positional informa-
region. The advantages are less bleeding, lim- tion. Tracking system must be precise,
ited surrounding tissue damage. consistently accurate, fast enough to pro-
4 . Surgical Navigation System vide >25 readings/s, insensitive to
It is also known as image-guided surgery changes in air temperature, unaffected
(IGS) and has emerged as a critical tool during by metal objects. Tracking systems are
the era of endoscopic surgery. Structures in based on either magnetic field or based
the skull base are either embedded or closely on infra-red light sensors [58].
adherent to the bone, making this region ideal The Mechanism is that every point in the
for IGS. Steps of image guidance machine for patient’s sinuses/surface landmarks has x, y, z
rhinology and skull base surgery are coordinate (Real coordinates). The patient’s
(a) Preoperative 0.5–1 mm cuts in all plans CT scan image will also have a corresponding
of radiology of nose and paranasal x, y, z coordinates (Virtual coordinates). IGS
sinuses are acquired in CD and it needs works by matching and correlating the real
to be uploaded in IGS machine. and virtual coordinates. It produces 3D local-
ization information for navigation during sur-
Fig. 5.27 Registration and tracking for navigation system (Courtesy—Dr. Hitesh Verma, Associate Professor, AIIMS,
New Delhi, India)
ambient temperature so that boiling of liquid

occurs due to pressure reduction. Cavitation is
formed on the minus side of a pressure cycle,
when the tip of probe is retracting with suffi-
cient frequency and amplitude, resulting in
the formation of shock waves. Cells expands
and burst by increasing pressure. It is more
confined to the tissues with high water propor-
tion such as fat, mass lesion. Blood vessels,
nerves, and other healthy tissue mostly unaf-
fected by the process. Gas and fluid are aspi-
rated by negative pressure device. It works by
generating the ultrasonic waves up to the
range of 23 KHx [61]. The steps for the CUSA
application are (Fig. 5.29).
(a) Irrigation fluid came out from handpiece
with a speed of 3–40 ml/min. Aspiration
Fig. 5.28 Navigation system (Courtesy—Dr. Hitesh
Verma, Associate Professor, AIIMS, New Delhi, India) of gas and liquid occurs at the tip with a
maximum pressure of 500 mmHg.
(b) When the vibrating tip comes in contact
gery. The components of navigation system with tissue, it breaks cells.
are head-mounted universal tracker, Overhead (c) Twenty-four kilo hertz generating hand-
optical tracking camera, Optical LEDs placed piece is useful to break tough, fibrous, and
on the universal tracker, navigation pointer calcified tumors while the small 35 kHz
and other navigation devices, Monitor and handpiece is useful during procedures
Software: simultaneous view of axial, coronal, requiring precision, tactile feedback, and
and sagittal sections (Fig. 5.28) and the frontal delicate control.
sinus outflow pathway with an orange line. (d) A wide variety of tips enables customiza-
This surgical plan may be imported into the tion of the handpiece for each procedure,
navigation system. depending on the consistency, location,
Clinical applications of IGS are in and depth of the targeted tissue.
(a) FESS, esp. revision sinus surgeries Suction and Irrigation mechanism of CUSA
because no recognizable anatomical land- draws tissue toward the vibrating tip and cre-
marks [59]. ates a tip/tissue pairing effect. It keeps the
(b) Extensive mass lesion of nose and PNS operating site clear [62, 63]. It can be useful in
with distorted anatomy. all kind of surgeries in the field of rhinology
(c) Extended endoscopic surgery for skull and skull base such as inferior turbinoplasty,
base such as pituitary surgery, nasal tumor septoplasty, DCR, FESS, etc. The advantages
with intracranial extension [60]. are safety, reduction in operating time, quality
(d) Excision or drainage of petrous apex and improvement, and facilitation of selective
internal auditory meatus tumors by trans- surgeries.
phenoid approach. 6 . Radiofrequency Ablation—It acts by ablation
5 . Ultrasonic Aspirator—It is called by Cavitron with minimally invasive and usually appropri-
ultrasonic surgical aspirator (CUSA). The ate for inoperable patients with other comor-
machine is worked by the mechanism of cre- bidities. It requires a less hospital stay or can
ation of cavitation. It is a process of creation be performed on an outpatient basis. It pre-
of the vapor form of liquid when the machine serves more normal healthy tissue [64–66].
is subjected to diminish pressure at sustained RF ablation has been used for the treatment of
152 G. Singh et al.
Fig. 5.29 Ultrasonic aspirator (Courtesy—Dr. Hitesh Verma, Associate Professor, AIIMS, New Delhi, India)
Fig. 5.30 RF ablation circuit and machine (Courtesy for figure b and c Dr. Hitesh Verma, Associate Professor, AIIMS,
New Delhi, India)
various neoplasms, including metastasis from The nature of the thermal hurt depends on
a variety of primary tumors [67, 68]. The act the tissue temperature and the duration of heat-
by deposition of power into tumors induces ing. Successful ablation can only be achieved
thermal injury resulting in a tumoricidal
by optimizing heat production and minimizing
effect. RF ablation involves the flow of electri- heat loss. Successful RF ablation can be
cal alternating current through tissues whereby reduced when tissues are heated to greater than
ionic shakeup and resistive heating of the tis- 100 °C and/or when charring of tissues occurs.
sues occurs. In order to set up this current, the An important element of effective ablation is
RF ablation system requires a closed-loop cir- the extent of the ablation zone. In order to
cuit comprised of an electrical generator, a assure eradication of microscopic tumoral
needle electrode, a patient (a resistor), and extensions, the ablation zone needs to include
large dispersive electrodes (or “grounding areas beyond the tumor margin. This is called
pads”) (Fig. 5.30). the ablation margin, and safe ablation margins
varies depending on the organ being ablated one axial holes) allows the fluid to reach hid-
and should preferably be approximately 1 cm. den recesses. It is useful to lavage of sinuses
Principles of RF ablation is based on and to remove fungal muck in non-invasive
(a) Joule heating—rapid alternating current fungal sinusitis.
(~460–480 kHz) passing through a resis-
tive medium is converted into thermal
energy
(b) RF ablation: electrode → tissue →
References
ground pads
(c) AC current → ionic agitation → friction 1. Chakrabarti A, Denning DW, Ferguson BJ, Ponikau J,
causes tissue heating Buzina W, Kita H, Marple B, Panda N, Vlaminck S,
Kauffmann-Lacroix C, Das A, Singh P, Taj-Aldeen SJ,
RF acts by tissue heating (protein denatur- Kantarcioglu AS, Handa KK, Gupta A, Thungabathra
ation), tissue boiling (water vaporization and M, Shivaprakash MR, Bal A, Fothergill A, Radotra
tissue disruption) which leads to breakdown BD. Fungal rhinosinusitis: a categorization and defi-
of cell membranes, vascular thrombosis, red nitional schema addressing current controversies.
Laryngoscope. 2009;119(9):1809–18.
cell fragmentation, and cell death. It is primar- 2. Callejas CA, Douglas RG. Fungal rhinosinusitis:
ily used for inferior turbinate reduction. what every allergist should know. Clin Exp Allergy.
Superficial ulceration of mucosa, crusting, 2013;43(8):835–49.
and adhesion are the complications of RF in 3. Grosjean P, Weber R. Fungus balls of the parana-
sal sinuses: a review. Eur Arch Otorhinolaryngol.
rhinology. 2007;264(5):461–70.
7. Hydrodebrider—The mucosal biofilm forma- 4. Chakrabarti A, Rudramurthy SM, Panda N, Das A,
tion is the major cause of failure in FESS Singh A. Epidemiology of chronic fungal rhinosinus-
[69]. It protects bacteria from immune-sys- itis in rural India. Mycoses. 2015;58(5):294–302.
5. Patterson TF, Thompson GR, Denning DW, et al.
tem and antibiotic penetration [70, 71]. It Practice guidelines for the diagnosis and manage-
leads to the generation of strong antimicro- ment of aspergillosis: 2016 update by the infec-
bial resistance to usual medical and surgical tious diseases society of America. Clin Infect Dis.
treatments. Hydrodebrider allows controlled 2016;63(4):e1–e60.
6. Cho HJ, Hong SD, Kim HY, Chung SK, Dhong
delivery of a shear force to the mucosal sur- HJ. Clinical implications of serum galactomannan
face of the sinonasal cavity and has claimed measurement in patients with acute invasive fungal
as a useful adjunct in the disruption of the rhinosinusitis. Rhinology. 2016;54(4):336–41.
biofilm structure. It is thought to be worked 7. Theel ES, Doern CD. β-D-glucan testing is impor-
tant for diagnosis of invasive fungal infections. J Clin
by providing a controlled shear energy that Microbiol. 2013;51(11):3478–83.
helps mechanically in dislocation of mucosal 8. Heldt S, Hoenigl M. Lateral flow assays for the diag-
biofilm [72]. It consists of an endoscopic suc- nosis of invasive aspergillosis: current status. Curr
tion irrigator with 270° articulation designed Fungal Infect Rep. 2017;11(2):45–51.
9. Valero C, de la Cruz-Villar L, Zaragoza Ó, Buitrago
to apply irrigation under pressure during MJ. New panfungal real-time PCR assay for diagno-
sinus surgery. The handpiece delivers a rotat- sis of invasive fungal infections. J Clin Microbiol.
ing spray of pressurized saline at 5 ml/s, 2016;54(12):2910–8.
enabling access to all of the sinuses but for 10. Arvanitis M, Anagnostou T, Fuchs BB, Caliendo AM,
Mylonakis E. Molecular and nonmolecular diagnostic
frontal sinus, the handpiece includes a stream- methods for invasive fungal infections. Clin Microbiol
lined 2.2 mm diameter tip and fixed 80° artic- Rev. 2014;27(3):490–526.
ulation for accessing the frontal sinus. It 11. Gupta S, Henningsen JA, Wallace MJ, Madoff DC,
works by providing simultaneous suctioning Morello FA, Ahrar K, et al. Percutaneous biopsy of
head and neck lesions with CT guidance: various
and irrigation. It is important to allow recircu- approaches and relevant anatomic and technical con-
lation and avoid pooling of solution. The siderations. Radiogr Rev Publ Radiol Soc N Am Inc.
multidirectional irrigation (five radial and 2007;27(2):371–90.
154 G. Singh et al.
12. Kikuchi K, Yoshiura T, Hiwatashi A, Togao O,

related to olfactory neuroblastoma revealed by
Yamashita K, Honda H. Balloon test occlusion of single-photon emission CT. Am J Neuroradiol.
internal carotid artery: Angiographic findings predic- 2000;21(4):717–20.
tive of results. World J Radiol. 2014;6(8):619–24. 27. Dublin AB, Bobinski M. Imaging characteristics of
13. Krajina A, Chrobok V. Radiological diagnosis and olfactory neuroblastoma (Esthesioneuroblastoma). J
management of epistaxis. Cardiovasc Intervent Neurol Surg B Skull Base. 2015;77(1):1–5.
Radiol. 2014;37(1):26–36. 28. Wu H-b, Wang Q-s, Zhong J-m, Zhou W-l, Li H-s,
14. Gandhi D, Gemmete JJ, Ansari SA, Gujar SK,
Qiao-yu W. Preliminary study on the evaluation of
Mukherji SK. Interventional neuroradiology of olfactory neuroblastoma using PET/CT. Clin Nucl
the head and neck. AJNR Am J Neuroradiol. Med. 2011;36:894–8.
2008;29(10):1806–15. 29. Watanabe N, Nakanishi Y, Kinukawa N, et al.

15. Broomfield S, Bruce I, Birzgalis A, Herwadkar A. The Expressions of somatostatin receptor subtypes
expanding role of interventional radiology in head (SSTR-1, 2, 3, 4 and 5) in neuroblastic tumors; spe-
and neck surgery. J R Soc Med. 2009;102(6):228–34. cial reference to clinicopathological correlations
16.
Kulkarni SS, Shetty NS, Dharia TP, Polnaya with international neuroblastoma pathology classi-
AM. Pictorial essay: Vascular interventions in extra fication and outcomes. Acta Histochem Cytochem.
cranial head and neck. Indian J Radiol Imaging. 2014;47(5):219–29.
2012;22(4):350–7. 30. Savelli G, Bartolomei M, Bignardi M. Somatostatin
17. Fayad LM, Carrino JA, Fishman EK. Musculoskeletal receptors imaging and therapy in a patient affected
infection: role of CT in the emergency department. by esthesioneuroblastoma with meningeal metas-
Radiographics. 2007;27:1723–1736 (Stacy GS, Kapur tases. A classic example of theranostic approach.
A (2011) Mimics of bone and soft tissue neoplasms. J Neurooncol. 2016;127:617–9. https://doi.
Radiol Clin N Am 49:1261–1286. org/10.1007/s11060-016-2067-3.
18. Mohandas A, Marcus C, Kang H, Truong M-T,
31. Pavlidis N, Briasoulis E, Hainsworth J, Greco

Subramaniam RM. FDG PET/CT in the management FA. Diagnostic and therapeutic management of
of nasopharyngeal carcinoma. Am J Roentgenol. cancer of an unknown primary. Eur J Cancer.
2014;203(2):146–57. 2003;39(14):1990–2005.
19. Kao CH, Hsieh JF, Tsai SC, et al. Comparison of 32. Cianchetti M, Mancuso AA, Amdur RJ, Werning JW,
18-fluoro-2-deoxyglucose positron emission tomogra- Kirwan J, Morris CG, Mendenhall W. Diagnostic
phy and computed tomography in detection of cervical evaluation of squamous cell carcinoma metastatic to
lymph node metastases of nasopharyngeal carcinoma. cervical lymph nodes from an unknown head and neck
Ann Otol Rhinol Laryngol. 2000;109:1130–4. primary site. Laryngoscope. 2009;119(12):2348–54.
20. Chong WH, Molinolo AA, Chen CC, Collins
33. Calabrese L, Jereczek-Fossa BA, Jassem J, et al.

MT. Tumor-induced osteomalacia. Endocr Relat Diagnosis and management of neck metastases from
Cancer. 2011;18(3):R53–77. https://doi.org/10.1530/ an unknown primary. Acta Otorhinolaryngol Ital.
ERC-11-0006. 2005;25(1):2–12.
21. Cho K-S, Kang D-W, Kim H-J, Lee J-K, Roh
34. Ross GL, Soutar DS. Sentinel node biopsy in head
H-J. Differential diagnosis of primary nasopha- and neck cancer: preliminary results of a multicenter
ryngeal lymphoma and nasopharyngeal carcinoma trial. Ann Surg Oncol. 2004;11:690–6.
focusing on CT, MRI, and PET/CT. Otolaryngol 35. Ene P, Popescu RC, Voiculescu S, et al. Sentinel lymph
Head Neck Surg. 2012;146(4):574–8. https://doi. node — work hypothesis in sinonasal carcinoma
org/10.1177/019459981143471 treatment. Maedica (Buchar). 2011;6(4):308–12.
22. Thompson L, Wieneke J, Miettinen M. Sinonasal tract 36. Scott B. In: Tille PM, editor. Bailey & Scott’s diag-
and nasopharyngeal melanomas: a clinicopathologic nostic microbiology. 13th ed: Elsevier Mosby; 2014.
study of 115 cases with a proposed staging system. 37. Bennett JE, Dolin R, Blaser MJ, editors. Mandell:
Am J Surg Pathol. 2003;27:594–611. Mandell, Douglas and Bennett’s principles and prac-
23. Swetter S, Carroll L, Johnson D, Segall G. Positron tice of infectious diseases. 8th ed: Elsevier; 2015.
emission tomography is superior to computed tomog- 38. Kasper DL, Fauci AS, Hauser SL, Longo DL, Jameson
raphy for metastatic detection in melanoma patients. JL, Loscalzo J (eds) Harrison: Harrison’s principles of
Ann Surg Oncol. 2002;9:646–53. internal medicine, 19th ed. McGraw Hill; 2015.
24. Goerres GW, Stoeckli SJ, von Schulthess GK, Steinert 39. Garcia LS, Isenberg HD, editors. Isenberg: clini-

HC. FDG PET for mucosal malignant melanoma of cal microbiology procedural handbook. 2nd edition
the head and neck. Laryngoscope. 2002;112(2):381–5. update. ASM Press; 2007.
25. Howell MC, Branstetter BF, Snyderman CH. Patterns 40. Lee VS, Davis GE. Culture-directed topical antibi-
of regional spread for esthesioneuroblastoma. AJNR otic treatment for chronic rhinosinusitis. Am J Rhinol
Am J Neuroradiol. 2011;32:929–33. https://doi. Allergy. 2016;30(6):414–7. https://doi.org/10.2500/
org/10.3174/ajnr.A2401. ajra.2016.30.4380.
26. Sasajima T, Kinouchi H, Tomura N, Watara J, Mizoi 41. Rom D, Bassiouni A, Eykman E, et al. The association
K. High uptake of 123I-metaiodobenzylguanidine between disease severity and microbiome in chronic
rhinosinusitis. Laryngoscope. 2019;129(6):1265–73. 58. Azuma R, Bishop G. Improving static and dynamic
https://doi.org/10.1002/lary.27726. registration in an optical see-through hmd. In:
42.
Aring AM, Chan MM. Current concepts in Proceedings of the 21st annual conference on com-
adult acute rhinosinusitis. Am Fam Physician. puter graphics and interactive techniques. New York:
2016;94(2):97–105. ACM Press; 1994. p. 197–204.
43. Liu P, Lu L, Xu M, et al. A novel multiplex PCR for 59. Metson R. Image-guided sinus surgery: lessons

virus detection by melting curve analysis. J Virol learned from the first 1000 cases. Otolaryngol Head
Methods. 2018;262:56–60. https://doi.org/10.1016/j. Neck Surg. 2003;128:8–13.
jviromet.2018.09.010. 60. Neumann AM Jr, Pasquale-Niebles K, Bhuta T, Sillers
44. Chandra RK, Conley DB, Kern RC. Evolution of the MJ. Image-guided transnasal endoscopic surgery of
endoscope and endoscopic sinus surgery. Otolaryngol the paranasal sinuses and anterior skull base. Am J
Clin N Am. 2009;42(5):747–52. Rhinol. 1999;13:449–54.
45.
Marsh BR. Historic development of broncho- 61. Chan KK, Watmough DJ, Hope DT, Moir K. A new
esophagology. Otolaryngol Head Neck Surg. motor-driven surgical probe and its in vitro compari-
1996;114(6):689–716. son with the Cavitron Ultrasonic Surgical Aspirator.
46. Wootton C. Digital image formats, Chapter 6. In: A Ultrasound Med Biol. 1986;12:279–83.
practical guide to video and audio compression: from 62. Deppe G, Malviya VK, Malone JM Jr. Use of

sprockets and rasters to macro blocks. Burlington, Cavitron Ultrasonic Surgical Aspirator (CUSA) for
MA: Focal Press; 2005. p. 115–46. palliative resection of recurrent gynecologic malig-
47. Sindwani R, Manz R. Technological innovations in nancies involving the vagina. Eur J Gynaecol Oncol.
tissue removal during rhinologic surgery. Am J Rhino 1989;10:1–2.
Allergy. 2012;26(1):65–9. 63. Chopp RT, Shah BB, Addonizio JC. Use of ultra-
48. Beswick DM, Rodriguez KD, Olds CE, et al.
sonic surgical aspirator in renal surgery. Urology.
Quantification of maxillary sinus accessibility via 1983;22:157–9.
a middle meatal antrostomy. Am J Rhinol Allergy. 64. Gillams AR. The use of radiofrequency in cancer. Br
2015;29(5):394–6. J Cancer. 2005;92:1825–9.
49. Selivanova O, Kuehnemund M, Mann WJ, Amedee 65. Gillams A. Tumor ablation: current role in the kidney,
RG. Comparison of conventional instruments and lung and bone. Cancer Imaging. 2009;9:68–70.
mechanical debriders for surgery of patients with 66. Bilchik AJ, Rose DM, Allegra DP, Bostick PJ, Hsueh
chronic sinusitis. Am J Rhinol. 2003;17(4):197–202. E, Morton DL. Radiofrequency ablation: a minimally
50. Kumar N, Sindwani R. Bipolar microdebrider may invasive technique with multiple applications. Cancer
reduce intraoperative blood loss and operative time J Sci Am. 1999;5:356–61.
during nasal polyp surgery. Ear Nose Throat J. 67. Lencioni R, Crocetti L, Cioni R, et al. Response
2012;91(8):336–44. to radiofrequency ablation of pulmonary tumours:
51. Grobler A, Carney AS. Radiofrequency cobla-
a prospective, intention-to-treat, multicentre clini-
tion tonsillectomy. Br J Hosp Med (Lond). cal trial (the RAPTURE study). Lancet Oncol.
2006;67(6):309–12. 2008;9:621–8.
52.
Coblation product brochure. https://www.smith- 68.
Dupuy DE, Mayo-Smith WW, Abbott GF,
nephew.com/global/assets/pdf/products/surgical/ DiPetrillo T. Clinical applications of radiofre-
sportsmedicine/08427f%20multi-electrode %20tech- quency tumor ablation in the thorax. Radiographics.
nology%20brochure.pdf. Accessed July 30, 2016. 2002;22:259–69.
53. Sergeev VN, Belov SV. Coblation technology: a new 69. Potera C. Forging a link between biofilms and disease.
method for high frequency electrosurgery. Biomed Science. 1999;283:1837–9.
Eng. 2003;37(1):22–5. 70. Cavaliere R, Ball JL, Turnbull L, Whitchurch

54. Belov SV. Use of high-frequency cold plasma abla- CB. The biofilm matrix destabilizers, EDTA and
tion technology for electrosurgery with minimized DNaseI, enhance the susceptibility of nontype-
invasiveness. Biomed Eng. 2004;38(2):80–5. able Hemophilus influenzae biofilms to treatment
55. Qi B, Ren C, Wang D, Li SZ, Wang K, Zhang
with ampicillin and ciprofloxacin. Microbiology.
Y. Uniform glow like plasma source assisted by pre- 2014;3:557–67.
ionization of spark in ambient air at atmospheric pres- 71. Berlanga M, Gomez-Perez L, Guerrero R. Biofilm for-
sure. Appl Phys Lett. 2006;89:131503. mation and antibiotic susceptibility in dispersed cells
56. Albritton FD, Kingdom TI, DelGaudio JM. Malleable versus planktonic cells from clinical, industry and
registration mask: application of a novel registration environmental origins. Antonie Van Leeuwenhoek.
method in image guided sinus surgery. Am J Rhinol. 2017;110:1691–704.
2001;15:219–24. 72. Valentine R, Jervis-Bardy J, Psaltis A, Tan LW,

57. Raabe A, Krishnan R, Wolff R, Hermann E,
Wormald PJ. Efficacy of using a hydrodebrider
Zimmermann M, Seifert V. Laser surface scanning and of citric acid/zwitterionic surfactant on a
for patient registration in intracranial image-guided Staphylococcus aureus bacterial biofilm in the
surgery. Neurosurgery. 2002;50:797–801. discussion sheep model of rhinosinusitis. Am J Rhinol Allergy.
802–3 2011;25:323–6.
Tumours of Nose and
Paranasal Sinuses 6
Gyan Nayak, Hitesh Verma, Rakesh Kumar,
Rupa Mehta, Nikhil Singh, Kuldeep Thakur,
Kapil Sikka, Anchal Kakkar, and Deepali Jain
Contents
6.1 Part A: Benign Lesions of Nose and Paranasal Sinuses 158
6.1.2 Clinical Presentation 158
6.1.3 Benign Tumours of Epithelial Origin Sinonasal Papilloma 158
6.1.5 Schneiderian Papilloma (Oncocytic Type) 160
6.1.6 Schneiderian Papilloma (Exophytic Type) 160
6.1.7 Salivary Gland Adenoma 160
6.1.8 Benign Tumours of Bony and Cartilaginous Origin 161
6.1.9 Fibroosseus Lesion 162
6.1.10 Benign Vascular Tumours 164
6.1.11 Other Rare Lesions 164
6.2 Part B: Angiofibroma, Its Medical and Surgical Management 164
6.2.1 Extensions 166
6.3 Part C: Cancer of Nose and Paranasal Sinuses 173
6.3.1 etiology
A 173
6.3.2 Patterns of Tumour Spread 173
6.3.4 Histopathology 176
6.3.5 Stage with Description 176
6.4 Part D: Nasopharyngeal Carcinoma 178
6.4.1 ummary
S 178
6.4.2 Anatomy of Nasopharynx 178
6.4.3 Benign Tumours 180
6.4.4 Nasopharyngeal Carcinoma 180
R. Mehta · N. Singh
G. Nayak ENT, AIIMS, Raipur, Chhattisgarh, India
ENT, PGIMER, Chandigarh, India
A. Kakkar · D. Jain
H. Verma (*) · R. Kumar · K. Thakur · K. Sikka Pathology, AIIMS, New Delhi, India
ENT, AIIMS, New Delhi, India
158 G. Nayak et al.
6.5 Part E: Pathology of Lesions of the Nose and Paranasal Sinuses 187

6.5.1 inonasal Neoplasms
S 187
6.5.2 Carcinomas 187
6.5.3 Sinonasal Papillomas 192
6.5.4 Mesenchymal Neoplasms 193
6.5.5 Other Malignant Neoplasms 196
6.5.6 Fibroosseous Lesions 197
6.5.7 Nasal Polyps 197
References 198
6.1 art A: Benign Lesions

P ral, germ cell tumours, and other tumour-like
of Nose and Paranasal conditions like reparative granuloma [1].
Sinuses
6.1.1 Introduction 6.1.3 Benign Tumours of Epithelial

Origin Sinonasal Papilloma
The benign tumours of the nose and paranasal
sinus represents a vast and varied group of 6.1.3.1 Inverted Papilloma
lesions. These tumours are often diagnosed late (Shneiderian Papilloma,
due to their rarity of the condition and similar Inverting Type)
presentation to chronic rhinosinusitis. These WHO has classified sinonasal papilloma into
lesions are usually indolent and diagnosis can be three histopathological subgroups: exophytic
delayed. It is prudent to consider the diagnosis of papilloma, inverted papilloma (IP), and onco-
benign tumours of the nose and paranasal sinuses cytic papilloma [1]. Inverted papilloma is the
in the setting of unilateral nasal symptoms with most common tumour among these subgroups.
bleeding. With the advent of endoscopes, instru- IP is also known as Ringertz tumour or
mentation, and navigation system, it is possible Schneiderian papilloma, and arises from the lat-
to detect in the early stage and initiate safe treat- eral nasal wall and is a locally aggressive tumour
ment thus, reducing morbidity. with the tendency to recur after its excision.
These tumours were first described by Ward in
1884 and later characterised by Ringertz in 1935.
6.1.2 Clinical Presentation Inverted papillomas constitute 0.5–4% of sinona-
sal tumours and the chances of turning into
The clinical presentation in the majority of the malignancy reaches up to 5% [2]. Males are more
condition mimics the symptoms of chronic rhino- commonly affected with M:F ratio of 3.4:1 and
sinusitis like nasal obstruction, nasal discharge, commonly presents in the 6th–7th decade of life.
postnasal drip, hyposmia, or anosmia. Nasal The various risk factors associated with inverted
bleeding can be seen in vascular tumours and papilloma are nickel, organic solvents, welding
inverted papilloma. Facial deformity, telecanthus fumes, etc. [3, 4] A close association between the
can be seen in fibrosseous lesions of maxillofa- human papillomavirus (HPV) and inverted papil-
cial bones. Although visual symptoms are rare loma has also been suggested but the evidence is
but visual blurring and diplopia can be presenting inadequate to validate its role in its etiopathogen-
complaints due to the pressure effect on the esis [5].
orbital contents. WHO classified Sinonasal Histologically, the classical hallmark appear-
tumours according to their tissues of origin viz. ance is digitiform proliferation of squamous epi-
epithelial, mesenchymal, hematolymphoid, neu- thelium into the underlying stroma with an intact
6 Tumours of Nose and Paranasal Sinuses 159
basement membrane. There is well-differentiated

columnar or ciliated respiratory epithelium with
variable degrees of squamous differentiation [6].
HPV and Inverted Papilloma The role of HPV

and inverted papilloma has been studied to find
out its correlation in its etiopathogenesis.
Kashima et al. suggested on the basis of poly-
merase chain reaction detection of HPV DNA in
specimens to be etiologically related to sinonasal
papillomas, inverted papillomas, and squamous
cell carcinomas [5]. McLachlin et al., in a study
of 22 patients, found HPV DNA to be present in
inverted papilloma as well as its association with
squamous cell carcinoma (SCC), which sug-
gested its role in the etiopathogenesis and malig-
nant transformation [7]. Retrospective studies
have concluded that HPV infection might repre-
sent the initiation in the oncogenesis of inverted
papilloma [8, 9].
In contradiction to the above studies, many

Fig. 6.1 The inverted papilloma arising from the left
studies have shown conflicting evidence. Kraft osteomeatal complex
et al. detected HPV-11 in only 1 out of 29 inverted
papillomas. There was no evidence of HPV Table 6.1 Krouse’s classification of inverted papilloma
where inverted papilloma is associated with SCC Stage Tumour extension
[10]. A study of 66 patients did show HPV isola- 1 Disease limited to the nasal cavity
tion; however, subsequent analysis revealed that 2 Disease extends to ethmoid sinus and medial
the presence of HPV DNA was neither a statisti- and superior wall of maxillary sinus
cally significant predictor of the recurrence of 3 Tumour involves lateral and inferior aspects
inverted papilloma nor was it a statistically sig- of the maxillary sinus or extension into the
frontal or sphenoid sinus
nificant risk factor for associated SCCs [11].
4 Extranasal extension or malignancy
These conflicting findings suggest that HPV may
represent mere incidental colonisation rather than
a causative agent. extension (Table 6.1) [12]. Contrast-enhanced
computed tomography shows remodelling and
focal erosion and may show focal hyperostosis at
6.1.4 Clinical Presentation the attachment site (site of origin). A convoluted,
“cerebriform,” pattern is characteristic of inverted
The common symptoms include nasal obstruc- papilloma on T2/STIR and post-gadolinium
tion and epistaxis. Larger tumour size may pres- T1-weighted MR images (Fig. 6.2) [13].
ent with facial swelling and visual symptoms. Medial maxillectomy has been the standard of
The diagnostic nasal endoscopy reveals vascular, care for inverted papillomas for many decades.
friable multilobulated mass filling the nasal cav- Lateral rhinotomy or sublabial approach is still
ity, arising from the lateral nasal wall near the being used to access the tumour in resource-
osteomeatal complex (Fig. 6.1). Tumour mass limited settings. Currently, endoscopic Denker is
can extend into the maxillary and ethmoid sinus. the preferred approach for medial maxillectomy
Krause has classified the tumour depending on its [14–16]. Endoscopic Denker approach involves
160 G. Nayak et al.
Fig. 6.2 NCCT PNS orbit (coronal cut) is showing air–fluid level is visible within the sinus. MRI Nose and
homogenous mass filling both side frontal, ethmoid PNS (axial cut) are showing characteristic “cerebriform”
sinuses with focal hyperostosis (black arrow) in the region pattern (black arrow) in nasal cavity and ethmoid sinuses.
of the right frontal outflow tract. The right maxillary sinus (Courtesy—Dr. Hitesh Verma, Associate Professor,
is also filled up by secretions as the ostium is not wide and AIIMS, New Delhi, India)
drilling of the thick bone of the lateral wall of the is equal distribution among the sexes and HPV
pyriform aperture from the anteromedial part of has not been isolated from these variants.
the maxillary sinus. This significantly improves
the surgical accessibility to the posterolateral
wall and infratemporal fossa. The commonly 6.1.6 Schneiderian Papilloma
reported complications are bleeding, infraorbital (Exophytic Type)
hypoesthesia, epiphora, orbital fat exposure, alar
collapse, etc. These are the papillomas arising from the
Radiation therapy as adjuvant therapy is used Schneiderian membrane with rich papillary
for local recurrences at some centres, but this fronds and fibrovascular cores covered by layers
remains controversial [17]. However, regular fol- of epithelium [1]. Other synonyms are transi-
low- up and subsequent surgical management tional cell papilloma, fungiform papilloma, sep-
remains the treatment option for the vast majority tal papilloma. These tumours are more commonly
of recurrent cases. seen in men (2–10 times) between 20–50 years of
age. In contrast to inverted papilloma, these vari-
ants are localised more on the lower anterior
6.1.5 Schneiderian Papilloma nasal septum with no significant lateralisation.
(Oncocytic Type) They are infrequent on the lateral nasal wall.
Malignant change in exophytic papilloma is rare.
These types of papilloma are a variant of
Schneiderian papilloma where the columnar cell
lining have oncocytic features. The high content 6.1.7 Salivary Gland Adenoma
of cytochrome C oxidase and mitochondria estab-
lishes this oncocytic appearance. Other synonyms Only 25% of glandular tumours are benign in the
are cylindrical cell papilloma, columnar cell pap- nose and paranasal sinus tract. The common
illoma [1]. In contrast to inverted papilloma, there veining tumours are pleomorphic adenoma, myo-
epithelioma, and oncocytoma. Pleomorphic ade- obstruction to frontal recess, nasolacrimal duct
noma presents with non-specific signs and and can also lead to mucocele formation.
symptoms like nasal obstruction, discharge, and Osteomas have slight male preponderance and
occasional bleeding. These are more common are usually diagnosed between the second and
between 20 and 50 years of age. Most of the fifth decades.
cases arise from the submucosa of the bony and These tumours are histologically divided into
cartilaginous part of the nasal septum. Treatment three categories as shown in Table 6.2 [19].
is surgical with wide local excision. Osteomas can also be associated with Gardner
syndrome, a form of familial adenomatous pol-
yposis with epidermoid cysts, lipomas, and des-
6.1.8 Benign Tumours of Bony moid tumours [20]. High-resolution computed
and Cartilaginous Origin tomography of paranasal sinus and orbit assesses
the site of attachment and gauges the extent of the
6.1.8.1 Osteoma lesion. Differential diagnosis of nasal osteoma
Osteomas are benign, slow-growing osteoblastic includes other fibroosseous lesions like fibrous
lesions and the most common type of benign dysplasia and ossifying fibroma.
sinonasal tumours [18]. They are incidental find-
ings on computed tomography of patients with Table 6.2 Histological types of osteoma
sinus symptoms. These tumours are mostly Types of
asymptomatic and occasionally present with osteoma Histology
symptoms of headache, nasal discharge, epiph- Ivory Lobulated, made of compact dense bone
ora, forehead swelling, ocular pain, etc. The most osteoma containing a minimal amount of fibrous
tissue
common location of osteoma is in the frontal
Mature Spongy, mature bone with conspicuous
sinus followed by ethmoid, maxillary, and more osteoma fibrous tissue
rarely the sphenoid sinus (Fig. 6.3). However, Mixed Findings of both ivory and mature
rarely, the turbinates can be involved causing osteoma osteoma
Fig. 6.3 Water’s view is showing radio-opaque mass in of the right anterior ethmoid region. (Courtesy—Dr.
the region of the right ethmoid and frontal sinus floor. Hitesh Verma, Associate Professor, AIIMS, New Delhi,
NCCT PNS orbit (Coronal cut) is showing ivory osteoma India)
162 G. Nayak et al.
Treatment of osteoma depends upon the signs fibroosseous lesions is shown in Table 6.3 and
and symptoms. These tumours are slow-growing Table 6.4, respectively [1, 22].
in nature and there is a general consensus in
favour of a wait-and-watch policy provided there 6.1.9.1 Fibrous Dysplasia
are no symptoms and the lesion does not encroach Fibrous dysplasia (FD) is a benign dysplastic
critical structures like optic nerve, orbit, frontal skeletal lesion where the normal bone is replaced
mucocele, facial deformity. Local resection by by disorganised and immature bony and fibrous
endoscopic or external approach is the treatment tissue. FD may affect a single bone (monostotic)
of choice. or more than one bones (polyostotic). Monostotic
FD is more common in the craniofacial skeleton
6.1.8.2 Chondroma with the maxilla affected more commonly than
Chondromas are extremely rare and any cartilagi- the mandible. Polyostotic FD may be associated
nous tumour more than 2 cm in this site should be
considered potentially malignant unless proven Table 6.3 WHO classification of fibroosseous lesions
otherwise.
Fibroosseous conditions Subtypes
Ossifying fibroma
Fibrous dysplasia
6.1.9 Fibroosseus Lesion Osseous dysplasia (a) Periodical osseous
dysplasia, focal osseous
Fibroosseous lesions comprise a diverse group of dysplasia, florid osseous
dysplasia, familial
conditions of cranio facial skeleton which gigantiform cementoma
includes developmental lesions, reactive or dys- Central giant cell
plastic lesions, and neoplasms. These lesions are granuloma
characterised by the replacement of normal bone Cherubism
by variable fibroblastic connective tissue matrix Aneurysmal bone cyst
[21]. The WHO and Eversole classification of Solitary bone cyst
Table 6.4 Eversole classification of fibroosseous lesions

Fibrosooesus pathology Disease Subtypes
1. Bone dysplasia a. Fibrous dysplasia i. Monostotic
Ii. Polyostotic
Iii. Polyostotic with endocrinopathy (McCune–
Albright syndrome)
b. Osteitis deformans/Paget’s disease
c. Pagetoid heritable bone dysplasia
of childhood
d. Segmental odontomaxillary
dysplasia
2. Cemento-osseous a. Focal cemento-osseous dysplasia
dysplasia
b. Florid cemento-osseous dysplasia
3. Nflammatory/reactive a. Focal sclerosing osteomyelitis
process
b. Diffuse sclerosing osteomyelitis
c. Proliferative periostitis
4. Metabolic disease Hyperparathyroidism
5. Neoplastic conditions a. Ossifying fibroma
b. Juvenile ossifying fibroma i. Trabecular
ii. Psammomatoid
c. Gigantiform cemetoma
with endocrine abnormality and skin pigmenta- toms will require surgical decompression of the
tion and this variant is known as McCune– optic nerve [25, 26].
Albright syndrome [23].
FD occurs in the first two decades of life with 6.1.9.2 Ossifying Fibroma
equal preponderance in males and females. The Ossifying fibroma are true benign tumours
most common symptoms are painless swelling among all the fibroosseous lesions. Ossifying
and asymmetry of the facial skeleton. Involvement fibroma of craniofacial skeleton divided into fol-
of nose, paranasal sinuses, and foramina of the lowing types:
skull base, orbit can cause symptoms such as
nasal obstruction, headache, proptosis, visual • Ossifying fibroma of Odontogenic origin
abnormality, hyposmia/anosmia. Diagnosis of (Cemento-ossifying fibroma)
this condition requires clinical, radiological, and • Juvenile Ossifying fibroma (JOF)
histological assessment. Key radiological fea-
(a) Trabecular Juvenile Ossifying fibroma
tures on CT scan show radiolucent/radiopaque (TrJOF)
depending upon the degree of calcification lead- (b)
Psammomatoid Juvenile Ossifying
ing to a typical “ground glass” appearance fibroma (PsJOF)
(Fig. 6.4). This mottling appearance blends with • Gigantiform cementoma
the surrounding normal bones with ill-defined
margins [24]. Ossifying fibromas are generally unifocal
Histological feature depends upon the grade lesions except the gigantiform cementoma which
of ossification and calcification within the imma- are typically multifocal in presentation [22, 23].
ture matrix and the trabeculae assumes classic Radiologically OF are well-defined unilocular
“Chinese figure script” pattern [22, 23]. These mass and due to the expansile nature, the cortex is
lesions tend to become quiescent after puberty. thinned out (Fig. 6.5). The radiolucency on com-
Only cosmetic deformity can be corrected by sur- puted tomography scan can vary and depends
gical contouring of the affected site. However, upon the degree of calcification. Treatment is usu-
continuous growth in later life with visual symp- ally surgical excision by enucleation or curettage.
The recurrence rate is low in most of the cases.
Fig. 6.4 NCCT Head is showing fibrous dysplasia Fig. 6.5 Unilocular expansile mass lesion in right ante-
involving all skull base bones. (Courtesy—Dr. Hitesh rior ethmoid region. It is pushing lamina papyracea and
Verma, Associate Professor, AIIMS, New Delhi, India) eyeball laterally
164 G. Nayak et al.
6.1.10 Benign Vascular Tumours common site of origin. Symptomatology is the

same with other benign lesions and surgical exci-
6.1.10.1 Lobular Capillary sion is the treatment of choice.
Haemangioma (Pyogenic
Granuloma) 2- Dermoid
Sinonasal haemangioma accounts for up to 25%
of non-epithelial neoplasms in this region. Dermoid cyst is the commonest midline con-
Lobular capillary haemangioma are benign vas- genital mass lesion of the nasal dorsum. It is
cular lesions and are also known as haemangio- formed due to incomplete obliteration of neuroec-
matous granuloma, granuloma gravidarum, toderm of frontonasal region. It can present in the
granulation tissue-type haemangioma, etc. The form of cyst, sinus, and fistula with or without
term “pyogenic granuloma” is a misnomer as nei- intracranial extension (Fig. 6.6). Both CT and
ther there is any infective aetiology nor any gran- MRI are required to assess tract extent and for
uloma formation [27]. treatment plan (Fig. 6.7). The presence of bifid
A lobular capillary haemangioma is a circum- crista raised the possibility of intracranial exten-
scribed lesion comprising lobules of capillaries sion of the tract. MRI of the skull base region is
lined by endothelial cells and supported by prom- required in such suspected cases to map the tract
inent pericytes. The lobules are separated by extent. External rhinoplasty, vertical midline, lat-
fibro-myxoid stroma with few mitotic figures but eral rhinotomy, horizontal trans-nasal, and endo-
never atypical [28]. Most commonly affects scopic approaches are used to excise the nasal part
women in their second to third decade of life. of the tract. The choice of approach depends on the
This can be explained by the high incidence of external opening of the tract. Neurosurgical team
pregnancy during this time period. These tumours is required to excise the intracranial part [32].
may occur during the first trimester of pregnancy,
but the incidence increases until the seventh
month of pregnancy. They occur in approxi- 6.2 art B: Angiofibroma,
P
mately 2% of all pregnant females with the most Its Medical and Surgical
common presentation being a rapidly growing Management
nasal mass with recurrent epistaxis. The most fre-
quently affected site is the septum followed by Angiofibroma is first described by Hippocrates in
the turbinate and the sinuses [29]. the fifth century. Other names are, e.g., juvenile
Management of these lesions depends upon the nasopharyngeal angiofibroma, nasopharyngeal
timing and severity of presentation. Most of them fibroma, juvenile angiofibroma. It accounts for
resolve spontaneously after the end of pregnancy. 0.05% of all head and neck tumours. It is more
Surgical intervention is considered in patients with prevalent in familial adenomatous polyposis
multiple episodes of epistaxis or whose lesions fail (FAP) group patients. It is a benign, locally
to resolve after pregnancy. Endoscopic surgical aggressive unencapsulated vascular tumour. It
resection and cauterisation is the standard of care has both vascular and fibrous elements. Various
with a high success rate [30, 31]. authors proposed different theories for its origin.
The most recent and accepted theory is that it is a
vascular malformation and maybe it arises from
6.1.11 Other Rare Lesions persistent tissue of the first branchial artery. The
nasopharynx is the most common site of involve-
1- Neurogenic tumours ment. It takes origin from sphenopalatine fore-
man and extends medially in the nasal cavity,
Neurofibroma and schwannoma are the neuro- laterally into pterygopalatine fossa, and superi-
genic benign tumour of the nose and paranasal orly into the cranial cavity. The symptomatology
sinuses. Neurogenic tumours are a relatively rare can vary from unilateral nasal obstruction to life-
entity of this region. Maxillary sinus is the most threatening epistaxis. It appears grossly as
Fig. 6.6 Clinical photographs are showing cystic, fistulous external presentation. (Courtesy—Dr. Hitesh Verma,
Associate Professor, AIIMS, New Delhi, India)
Fig. 6.7 NCCT PNS is showing bifid crista galli and corresponding MRI is not showing intracranial extension of tract.
(Courtesy—Dr. Hitesh Verma, Associate Professor, AIIMS, New Delhi, India)
166 G. Nayak et al.
pinkish-grey colour lobular mass.

Microscopically, blood vessels are immature
with poorly developed surrounding muscular lay-
ers. Mutation and expression of β catenin, p-53, Nasal
C-KIT, C-MYC, VEGF receptor, and BMI-1 are ITF cavity
found in the tissue of angiofibroma. The most PMF
SPF
accepted treatment modality is surgical which
can be endoscopic or external. The choice of
approach is based on tumour extent and surgeon PP
experience. Radiotherapy and hormonal therapy
nasopharynx
are the other treatment modalities.
6.2.1 Extensions
Sphenopalatine foreman (SPF) is present in the Fig. 6.8 CECT PNS orbit is showing characteristic
lateral nasal wall. The nasal cavity communicates extensions of JNA
with the pterygopalatine fossa via a sphenopala-
tine foreman. The foreman is covered by palatine
bone inferiorly and sphenoid bone superiorly. 3. From ITF it may erode the greater wing of the
Sphenopalatine artery and nerve to the lateral sphenoid and middle cranial fossa (lateral to
nasal wall and nasopalatine nerve enter into the cavernous sinus).
nasal cavity via the foreman. Angiofibroma gets 4. It can enter the cranial cavity via the posterior
origin from the superior aspect of foreman and it wall of PPF. Foramen rotundum, vidian canal
tends to spread submucosally in close by less- are the natural communication site with the
resistant anatomical sites. It follows the standard cranium.
pathway of spread because of its fixed site of ori- 5.
Rarely Infratemporal fossa® temporal
gin and characteristic tumour behaviour. It can fossa®intracranial by the erosion of squa-
extend medially into the nasal cavity, paranasal mous part of the temporal bone.
sinuses, nasopharynx, and oropharynx. It can
invade within the cancellous bone of the basisphe- Demographic Features [35] It is seen in the
noid region. The lateral extension involves the first two decades of life. It is found exclusively in
pterygopalatine fossa (PPF), where It can push the males and it may be explained by the presence of
posterior wall of the maxilla anteriorly which is high androgen, oestrogen receptors. Nasal
known as the Holmen–Miller sign. It further obstruction (70–90%) and recurrent epistaxis
extends laterally and it involves the infratemporal (40–60%) are the most common ways of presen-
fossa (ITF), temporal fossa, and cheek (Fig. 6.8). It tation. Facial pain, persistent rhinosinusitis, and
can extend behind the pterygoid plates (PP) [33]. headache are the other symptoms. Conductive
Superiorly, it enters into the intracranial cavity hearing loss and ear fullness occur after the
mostly via inferior orbital fissure, orbit, superior blockage of eustachian tube opening in the naso-
orbital fissure (Fig. 6.9) [34]. The intracranial pharynx. Proptosis and facial asymmetry appears
extension is found in 10–20% of cases but dural in the advanced stage. Clinical examination
infiltration is very rare. Other pathways are: shows the presence of mucoid discharge in the
nasal cavity, anterior displacement of the soft
1. Nasal cavity®ethmoid roof®erosion of fovea palate, and widening of space behind the last
ethmoidalis or cribriform plate®intracranial. upper molar. Nasal endoscopy reveals a single
2. Nasal cavity®erosion of skull base at planum large pinkish-red lobular mass filling choana and
and sphenoid sinus roof® or lateral wall and posterior part of the nasal cavity. It pushes the
intracranial. posterior part of the middle turbinate anteriorly.
Investigations extension of tumour which indeed helps in decid-

Contrast CT of the nose and paranasal sinuses is ing the treatment policy [36, 37]. Erosion of ante-
the first basic investigation (Fig. 6.8). Angiofibroma rior most of vidian canal favours the theory that it
is highly intense after contrast administration arises from medial most of PPF [38]. CT angiogra-
because of rich vascularity. Angiofibroma spreads phy is helpful by providing feeder detail preopera-
in a characteristic way, so CT also helps in con- tively (Fig. 6.10). Digital subtraction angiography
firming the diagnosis. Radiology helps in locating (DSA) is an invasive method and it also helps in
the site of origin and it also helps in mapping the the mapping of feeding vessels. DSA-based
Fig. 6.9 Contrast enhancing mass

is involving of both cavernous
sinuses, sphenoid sinus,
retropterygoid space and right ITF
Fig. 6.10 The clinical photograph is showing the widen- ated by extension of JNA in the temporal fossa and cheek
ing of space behind the last right molar with a bulged and region
displaced soft palate. Two different swellings are appreci-
168 G. Nayak et al.
Fig. 6.11 CT angiography is showing feeder and tumour blush. Loss of tumour vascularity post embolisation is visible
in DSA pictures
embolisation of feeder from the branches of exter-

nal carotid artery reduces bleeding intraopera-
tively (Fig. 6.11). It is most effective within
24–48 hrs before surgery and it can reduce 60–70%
of blood loss. Initial studies create doubt on the
effectiveness of embolisation on tumour excision
by secondary inflammation but advancement in
technology and embolisation materials improves
the surgical outcome. Selective and super-selec-
tive embolisation reduces accidental slippage of
material into the internal carotid system.
On MRI [37], angiofibroma is hypointense on
T1 and intermediate to hyperintense on T2.
Tumour shows hyperintensity after contrast
administration which appears as bags of worms
(Fig. 6.12). MRI is reserve for a condition like
doubtful diagnosis, invasion into cranial fossa,
relationship with cavernous sinus and dura, to
detect a residual tumour in the postoperative
Fig. 6.12 Bag of worm appearance in MRI T2 image
period, to assess the response of medical manage-
ment. The temporary control of the carotid system
in the neck or balloon occlusion of the internal and ascending pharyngeal artery are the other
carotid artery may be required to deal with tumour common arteries. As the tumour grows, it can
receiving major blood supply from ICA. get vascularity from other vessels of the ipsilat-
Recent studies show the presence of prostate- eral side or contralateral side (36%). Internal
specific membranous antigen in angiofibroma tis- carotid artery feeder generates when mass
sue. PMSA PET scan is indicated for the detection extends into the orbital, cranium and with gross
of residual tumour in the postoperative period where skull base involvement but vidian artery can
MRI raised residual possibility (Fig. 6.13) [39]. supply tumour in early stage because of its
proximity with the site of origin. Tumour
Feeding vessels The branches of the internal receives feeder from the ophthalmic artery and
maxillary artery are the most common feeder. sometimes direct branch from the internal
Sphenopalatine is the most common feeding carotid artery. The vertebral and basilar artery
branch of the maxillary artery. Palatine arteries can also provide feeders [40].
6.2.1.1 Staging System • Stage IIb—JNA occupies PPF completely

Sessions proposed the first staging system. with or without erosion of orbital bones.
Chandler, Fisch, Radkowski, Pittsburgh, Andrew, • Stage IIc—extension into ITF with or without
Onerci staging systems are the other staging sys- cheek or posterior to the pterygoid plate
tem proposed at different points of time [35]. (Fig. 6.14c).
Radkowski staging system is the most popular • Stage IIIa—skull base bone erosion with min-
staging system. imal intracranial extension.
• Stage IIIb—gross intracranial extension ±
• Stage 1a—JNA is limited to the nasal cavity cavernous sinus (Fig. 6.9).
and/or nasopharynx (Fig. 6.14a).
• Stage 1b—extension into one or more parana- Syndermann’s staging system [41] is based
sal sinuses. on residual tumour blush post embolisation
• Stage IIa—minimal extension into PPF (Fig. 6.11). Residual tumour blush is because of
(Fig. 6.14b). blood supply from the internal carotid artery.
• Stage 1—Tumour is confined medial to mid-

point of PPF, nasal cavity, and no vascularity
after embolisation.
• Stage 2—Tumour extention into paranasal
sinuses and lateral part of PPF without any
residual vascularity.
• Stage 3—Extracranial tumour beyond stage 2
(ITF, orbit, skull base erosion) without resid-
ual vascularity.
• Stage 4—Stage 3 tumour with residual
vascularity.
• Stage 5—Intracranial extension. M (medial)
and L (lateral) are used for medial and lateral
to the cavernous sinus.
Diagnosis The typical demographic profile of a

Fig. 6.13 PMSA PET scan showing dye uptake in sphe- patient with a characteristic radiological spread
noid sinus and close by intracranial part. (Ongoing the-
pattern is sufficient enough to make a diagnosis.
sis—Dr. Prabhu, Dept of ENT, AIIMS, New Delhi, under
the guidance of Prof. Alok Thakar (ENT) and Prof Rakesh The biopsy is not indicated because it can lead to
Kumar (Nuclear Medicine)) excessive bleeding.
a b c
Fig. 6.14 Different stages of JNA. (a) stage Ia, (b) stage IIa, (c) stage IIc
170 G. Nayak et al.
6.2.1.2 Histopathology septectomy increases space within the nasal cav-

It is circumscribed, non-capsulated mucosa cov- ity. Literature supports the use of endoscopic exci-
ered lobular mass lesion. Colour depends on the sion till stage IIIa of the Radkowski staging system
vascular component of the tumour (pinkish-white [44]. Tumour removal in toto or piecemeal showed
to red). Microscopically, it is formed by fibro- a similar recurrence pattern if the extension of
cellular stoma with spindle cells and haphazardly tumour is well assessed intraoperatively.
arranged dense collagen matrix with the irregular Open anterior (lateral rhinotomy, Weber
vascular pattern. The vessels are dilated and lacks Ferguson or maxillary swing) and lateral approach
true muscle layer [42]. (subtemoral approach with or without craniotomy)
is indicated for large volume tumour with gross
Differential Diagnosis Angiomatous polyp, skullbase involvement and when tumour is lateral to
infected antrochoanal polyp, benign (hemangi- ICA, significant residual vascularity after emboliza-
oma, paraganglioma) or malignant tumour tion (equal to more than 50%) (Figs. 6.16 and 6.17).
(hemangiopericytoma) are differential tumours
for angiofibroma. The demographic features,
clinical features, and pattern of spread helps in
differentiating these tumours from JNA [35, 43].
6.2.1.3 Treatment
Surgical treatment is the gold standard treatment. SS
The choice of approach can vary between centres
based on the surgeon's experience and hospital
setup. The majority of centres are shifted from JNA
open surgical methods (lateral rhinotomy, Weber–
Fergusson, transpalatal, sublabial, midfacial
degloving, Le Fort 1 approach) to endoscopic IT
method because of improving anatomical knowl-
edge, advancement in technology, and expertise
[44]. Endoscopic Denker’s, septal window, ante-
rior maxillotomy, and small posterior sublabial
Fig. 6.15 Endoscopic picture is showing a bloodless
incision allow easy dealing of ITF extension of field with coblator while separating JNA from the
JNA by endoscopic approach (Fig. 6.15). Posterior surrounding
a b c
Fig. 6.16 Maxillary swing approach. (a) Weber–Fergusson’s incision is made, (b) plating for postoperative approxi-
mation, (c) raising of palatal flap
a b
c Zygomatic arch mandible
Temporal
fossa
angiofibroma
Temporalis muscle
Fig. 6.17 Preauricular subtemporal approach for right side. (a) JNA 3b, (b) flap elevation, (c) exposure of tumour
Excision of residual tumour lies in close prox- inexperienced surgeon, and early age of onset are
imity with ICA, dura, optic nerve and cavernous the major factors for tumour residual.
sinus is challenging as tumour handling can lead
to significant morbidity [45]. Hypotensive anaes- Medical Management Immunohistochemistry
thesia, reverse Trendelenburg position, proper shows the presence of oestrogen α, oestrogen β,
decongestion, preoperative embolisation, and androgen, and vascular endothelial growth factor
coblation of peritumoral tissues are the measures (VEGF) receptors in tumour tissue. It is an oes-
to reduce the amount of intraoperative bleeding trogen suppressive tumour and testosterone
significantly (Fig. 6.15). Large-volume tumour, responsive tumour. Diethylstilbestrol was ini-
an extension of tumour into vidian canal and tially used for shrinkage but it has a long list of
infiltration into the cancellous bone of skull base, adverse effects. Flutamide therapy is a non-
172 G. Nayak et al.
Fig. 6.18 Radiology is

showing a reduction of
the stage from
pretreatment II C to II A
of the Radkowski stage
Fig. 6.19 Clinical photograph is showing bilateral proptosis, with fullness in the right cheek. CECT is showing hyper-
intense mass with 360-degree involvement of the bilateral carotid artery
steroidal, anti-androgenic drug without feminis- trol rate ranging from 70 to 90%. The side effects
ing side effects and limited reversible adverse are cataract, panhypopituitarism, growth retarda-
effects. The dose is 10 mg/kg/day for 6 weeks. tion, temporal lobe necrosis, and secondary
The response rate ranged from 7 to 44% and it malignancy. Recent techniques such as IMRT
was found more in post-puberty patients can reduce the risk of complication rate, but lim-
(Fig. 6.18). It is also effective in reducing episode ited literature is available [48, 49].
number and amount of blood loss in the preoper-
ative period [46, 47]. Surveillance The advised radiological investi-
Radiotherapy is indicated for unresectable gation is MRI and it can be performed after pack
tumours (Fig. 6.19), in patients with persistent removal or at 3 months postoperative period after
residual lesion even after multiple surgeries and [46]. The surrounding inflammation interferes in
when residual lies close to the vital structure the diagnosis of residual lesion. PMSA PET scan
where surgery is very much challenging. The is indicated when MRI is doubtful. When no
dose ranges from 30 to 55 Gy with tumour con- lesion is found in 5 years’ follow-up period, then
Fig. 6.20 Preoperative
CECT and postoperative
surveillance (3-months
interval) MRI scan for
residual detection
the patient can be labelled as disease-free nickel refining processes, alkaline battery man-
(Fig. 6.20). ufacture industry, leather tanning, soldering,
welding has been reported to cause cancer of
paranasal sinuses.
6.3 art C: Cancer of Nose
P Squamous cell carcinoma has been associated
and Paranasal Sinuses with softwood dust, nickel, mustard gas, asbestos
industry workers. African mahogany appears to
Cancers of the nose and PNS are very rare, and be the most carcinogenic of all agents.
account for 0.2–0.8% of all neoplasms. Overall, Adenocarcinoma, especially the interstitial vari-
they form <3% of all head and neck cancers. The ant, is mostly associated with hardwood dust in
symptoms of nose and PNS tumours are similar the furniture industry, clothes and leather indus-
to those of common disorders such as chronic try. Biologically active compounds in wood dust
rhinosinusitis and thus cause a delay in diagnosis. impair mucociliary clearance and predispose to
The commonest age of presentation is in the fifth carcinogenesis [51].
and sixth decade of life with a male predilection Human Papilloma Virus (HPV) infection has
(Male:Female:: 2:1) [50]. The most commonly an increased risk of malignant transformation of
involved sinus is the maxillary (70%) > ethmoid inverted papilloma. However, no significant asso-
(20%) > frontal and sphenoid sinuses. A wide ciation between cigarette smoking and alcohol in
variety of histologies may be encountered sinonasal cancers has been noted.
although Squamous Cell Carcinoma (SCC) is the
most common malignant tumour. The TNM stag-
ing system is slightly complex and different for 6.3.2 Patterns of Tumour Spread
different regions of the nose and paranasal
sinuses. A correct documentation of staging is The most common route of spread is by local
required for treatment planning, prognostication, invasion. Orbit and cranium are seperate from
and information transfer. nose and paranasal sinuses by thin bone. The
paranasal sinuses other than the maxillary sinus
are in close proximity to orbit and cranial cavity
6.3.1 Aetiology which makes them more vulnerable even at low
volume of tumour. Natural foreman allows early
Several carcinogenic compounds have been spread of tumour.
identified with inhalation of these carcinogens
being responsible for ~40% of reported sinona- Local Invasion Periosteum, perichondrium, and
sal malignancies. Exposure to industrial fumes, dura appear to act as a momentary fence and
174 G. Nayak et al.
oppose tumour growth to some degree [52, 53].

The bone of the anterior maxilla, medial wall and
floor of orbital, roof of the frontal sinus and olfac-
tory cleft are very thin and readily destroyed by
tumour. The clinical presentation is based on the
area of involvement. Maxillary sinus tumours
generally present with medial spread or anterior/
inferior wall breach. Inferior orbital fissure and
thin orbital floor allows early orbital involvement
but periorbita is the relatively tough lining that
limits orbital tissue involvement to certain extent.
Posterior breach involves infratemporal fossa,
pteryomaxillary space and pterygoid plates
which is relatively rare [54]. Öhngren described a
line running from the medial canthus of the orbit
to the angle of the mandible. Superiorly based
tumours are more aggressive and poorly differen-
tiated, whereas inferiorly based tumours are more
amenable to treatment with a better prognosis.
Fig. 6.21 Tumour of left maxillary sinus involving ITF,
Orbit is involved by the lateral and inferior spread pterygoid plates, pterygoid muscles, and nasal cavity
of ethmoid and frontal sinus tumours. Anterior
cranial fossa is involved by the superior spread of
tumours. Cavernous sinus is involved by lateral common. The usual manifestations are unilateral
spread, nasopharynx by inferior spread, nasal nasal obstruction, persistent sinusitis, recurrent
cavity and ethmoid sinuses by anterior spread of epistaxis, foul-smelling nasal discharge, facial
sphenoid sinus tumours. pain, etc. Epiphora is due to blockage of the
nasolacrimal duct (Fig. 6.22).
• Regional spread: Nodal disease is a marker of Oral symptoms are seen in 25–30% of patients.
locally advanced disease and lymphatic spread These symptoms manifest in the form of loose
to regional nodes is seen in around 25–35% of teeth, pain in maxillary teeth, and palatal fullness
patients. Submandibular and jugulodigastric (Fig. 6.23). Muscles of mastication, nerves are
nodes are the most commonly involved lymph involved by tumour extension into infratemporal
nodes by anteriorly placed tumours, when fossa or by pterygoid muscle infiltration and
tumour breaches anterior bony wall, whereas, patients are present with symptoms of trismus.
posteriorly placed tumours involve retropha- Numbness of the cheek is the sign of inferior
ryngeal lymph nodes. Anterior spread has a orbital nerve infiltration. Distortion of nose and
better prognosis than posterior spread. face is a late feature (Fig. 6.22). Pattern of eye-
• Distant metastases: It is unusual at the time of ball displacement is helpful in pinpointing the
presentation and develops in less than 20% of involved sinus. Auditory manifestations are in the
patients with adenocarcinomas, whereas, for form of hearing loss, secondary to serous otitis
SCC, it is around 10% [55]. The most com- media due to nasopharyngeal extension. Cranial
mon sites for metastases are bone, brain, liver, nerve II, III, IV, V1, V2, and VI nerves are seen
lung, and skin (Fig. 6.21). after orbital apex and cavernous sinus involve-
ment. Cranial nerve involvement is a manifesta-
tion of advanced disease; it indicates poor
6.3.3 Clinical Features prognosis.
The clinical presentation is depending on the site Diagnosis Clinical staging requires detailed
of involvement. Nasal symptoms are the most local examination with neck evaluation for cervi-
cal lymphadenopathy, cranial nerve function, and obtain tissue for biopsy (Fig. 6.24). Contrast CT
ophthalmological evaluation. Nasal endoscopy is scan of nose and paranasal sinuses 3–5 mm axial,
done with a diagnostic purpose to see the charac- coronal, and sagittal images are required to docu-
teristic of mass and with a therapeutic purpose to ment staging of the tumour. Coronal images are
obtained for involvement of the orbital floor and
skull base and axial images are obtained for
extension through the posterior wall of the maxil-
lary sinus into the pterygopalatine fossa and
infratemporal fossa (Fig. 6.25). It also helps to
evaluate the tumour involvement of the retro-
orbital and orbital apex region. Sometimes,
reconstructed images are required to pinpoint
bony erosion. However, the limitations of CT
scan are in the evaluation of periorbita, dural
involvement to see whether the tumour has
invaded or is just abutting these structures. It is
Fig. 6.22 Nasal mass (Right) with fullness of right nasal

cavity ulceration of skin in medial canthus and lateral/
inferior displacement of right eyeball (clinical stage is
T4). (Courtesy—Dr. Hitesh Verma, Associate Professor, Fig. 6.24 Nasal endoscopy is revealing a mass in the left
AIIMS, New Delhi, India) nasal cavity (clinical stage T2)
Fig. 6.23 Palatal bulge

and ulceration with
loosening of teeth by
inferior spread of
maxillary sinus tumour
176 G. Nayak et al.
Fig. 6.25 CECT Nose and PNS showing the extent of a sinonasal tumour (T4a stage). MRI is showing right periorbital
infiltration with retained section in right maxillary sinus (T4a stage)
difficult to differentiate tumour from soft tissues with the potential of inducing paraneoplastic syn-
and secretions owing to their similar densities. drome by releasing peptides. Sinonasal undiffer-
MRI is prescribed in such cases as it provides us entiated carcinoma, melanoma, and
better soft tissue details and it differentiates hemangiopericytomas are other common differ-
tumour from secretion [54, 56]. Angiography and ential diagnoses for sinonasal tumours [57, 58].
embolisation have limited indications in highly
vascular malignant lesions, such as hemangio- Staging it is devised for carcinomas of the max-
pericytoma. Histopathology is compulsory for illary sinus, ethmoid sinus, and the nasal cavity
tissue diagnosis. Unusual presentation and abnor- and is not applicable to mesodermal tumours,
mal recurrence are the indications for PET scan. olfactory neuroblastoma (OAN) for which other
grading systems have been devised. TNM
Classification (AJCC 2018) is proposed for nose
6.3.4 Histopathology and paranasal sinuses lesions [59].
Squamous cell carcinoma (SCC) is the leading

histopathological diagnosis. Adenocarcinoma 6.3.5 Stage with Description
and adenoid cystic carcinoma accounts for
around 10% of nose and PNS tumours. The 6.3.5.1 T Staging
tumours have a male preponderance and are seen Maxillary Sinus
mostly in sixth to seventh decades of life. Sino-
nasal tumour mostly arise from the lateral nasal • T1 Tumour confined to the maxillary antrum
wall whereas tumours arise from paranasal mucosa without bone erosion.
sinuses. SCC is well-differentiated in a majority • T2 Tumour produces bone erosion or destruc-
of cases (85%). Esthesioneuroblastoma origi- tion, except the posterior wall of the antrum,
nates from basal cells of the olfactory epithelium. and it also includes tumour extension into the
It accounts for less than 5% of sinonasal malig- hard palate and/or middle meatus.
nancies and it has bimodal age distribution (peak • T3 Tumour infiltrates in whichever of the sub-
at 20 and 50 of age). It has female preponderance sequent: maxillary sinus posterior wall, sub-
cutaneous tissues over maxillary sinus, N Staging

ethmoid sinus, medial wall and floor of orbit, • NX Local lymph nodes cannot be assessed.
pterygomaxillary space. • N0 No local lymph node metastasis.
• T4a Tumour infiltrates in whichever of the • N1 Metastasis in a solitary ipsilateral lymph
subsequent: anterior orbit stuffing, pterygoid node, 3 cm or less in maximum measurement
plates, cheek skin, cribriform plate, infratem- exclusive of extranodal extension.
poral fossa, sphenoid or frontal sinuses • N2
(Fig. 6.25). • N2a—Metastasis in a solitary ipsilateral
• T4b Tumour infiltrates in whichever of the lymph node, more than 3 cm but not more
subsequent: apex of orbit, dura, brain, cranial than 6 cm in maximum measurement exclu-
nerves except maxillary division of trigeminal sive of extranodal extension.
nerve, nasopharynx, or clivus. • N2b—Metastasis in several ipsilateral lymph
nodes, none more than 6 cm in maximum
Ethmoid Sinus measurement exclusive of extranodal
extension.
• T1 Tumour confined to the ethmoid sinuses • N2c—Metastasis in bilateral or contralateral
with or without bony erosion. lymph nodes, none more than 6 cm in greatest
• T2 Tumour extends into the nasal cavity. dimension, without extranodal extension.
• T3 Tumour extends into anterior orbit and/or • N3a Metastasis in a lymph node more than
maxillary sinus. 6 cm in greatest dimension without extranodal
• T4a Tumour infiltrates in whichever of the extension.
subsequent: anterior orbital stuffing, skin over • N3b Metastases in a solitary or several lymph
nose or cheek, negligible anterior intracranial nodes with clinical extranodal extension.
extension, pterygoid plates, sphenoid or fron-
tal sinuses. The staging template is mentioned in Table 6.5.
• T4b Tumour infiltrates in whichever of the The staging system for olfactory neuroblas-
subsequent: orbit apex of orbit, dura, brain, toma is first proposed by Kadish and then it was
cranial nerves except maxillary division of tri- modified by Morita [60]:
geminal nerve, nasopharynx, or clivus. Stage 1: Tumour confined to nasal cavity
Stage 2: Tumour confined to the nasal cavity
Nasal Cavity and paranasal sinuses
• T1 Tumour involves only one subunit of the Stage 3: Extension of tumour away from nose
subsequent: septum, floor, lateral wall, and and paranasal sinuses (intra-orbit or intracranial)
vestibule of the nasal cavity. Stage 4: Any previous stage with cervical
• T2 Tumour involves two subunits or ethmoid. lymph node or distal metastasis
• T3 Tumour infiltrates into the orbit anteriorly
and/or maxillary sinus. Table 6.5 Staging template
• T4a Tumour invades any of the following: Stage
anterior orbital stuffing, skin over nose or O Tis N0 M0
cheek, negligible anterior intracranial exten- I T1 N0 M0
sion, pterygoid plates, sphenoid or frontal II T2 N0 M0
III T1/2 N1 M0
sinuses.
T3 N0/1 M0
• T4b Tumour infiltrates in whichever of the
IVa T1/2/3 N2 M0
subsequent: apex of orbit, dura, brain, middle T4a N0/1/2 M0
cranial fossa, cranial nerves except maxillary IVb T4b Any N M0
division of trigeminal nerve, nasopharynx or Any T N3 M0
clivus. IVc Any T Any N M1
178 G. Nayak et al.
Dulgurov proposed a new staging system for in about 10% of cases. Nasopharyngosocopic
esthesioneuroblastoma [61]: examination reveals growth and provides a suit-
able area for biopsy under direct visualisation.
• T1 is confined to the nose and PNS without The use of immunohistochemical markers will
superior ethmoid cells and sphenoid sinus help to differentiate NPC from other malignan-
involvement. cies in the nasopharynx.
• T2 is T1 + sphenoid sinus with or without ero- Computed tomography has been the corner-
sion of cribriform plate. stone of radiological staging for many years;
• T3 is any stage with intraorbital and intracra- however, magnetic resonance imaging has been
nial extension without dural infiltration. used increasingly because of its superior defini-
• T4 is brain parenchyma involvement. tion in detecting soft tissue changes and intracra-
nial involvement. Bone scan and positron
The presence of regional and distal metastasis emission tomography are other reliable investiga-
is marked as N1 and M1. Dural involvement is tions to look for distant metastasis.
noticed in 25% and lymph node metastasis in 5% In recent years, treatment of NPC had under-
of cases. Hyems et al. proposed a histopathologi- gone several paradigm shifts resulting in improved
cal grading system on the basis of tumour cell prognosis. Advances in the planning and delivery
architecture, degree of differentiation, nuclear of radiation treatment and the addition of chemo-
pleomorphism, mitotic index, tumour necrosis, therapy have been demonstrated to improve dis-
and nature of the matrix. They graded histology ease control rates in locally advanced NPC. In
into four subtypes where type 1 is least aggres- general, patients with stage 1 are treated by radia-
sive and type 4 is most aggressive [62]. tion therapy alone, whereas, stage II, III, and IV
Surgical and other management for sinonasal are treated by concurrent radiotherapy and che-
malignancies is mentioned in Chaps. 7 and 10. motherapy. Surgery should be considered as a
first-line treatment of residual or recurrence dis-
ease at the primary site (rT1 and limited rT2).
6.4 art D: Nasopharyngeal
P Technical advances have enabled surgeons to per-
Carcinoma form endoscopic or robotic surgeries as salvage,
reducing the morbidity from traditional open
6.4.1 Summary resections. Patients with NPC cases are followed
up and assessed with office-based rigid and/or
Nasopharyngeal carcinoma (NPC) is the most fibro-optic nasal endoscopy. Positron emission
common neoplasm arising in the nasopharynx tomography–computed tomography, CT, or MRI
which shows remarkable geographical difference scan should be carried out at 3 months from com-
in incidence across the world. NPC is uncommon pletion of treatment to assess response.
in the United State but is endemic in many areas
in the world, particularly southeastern China and
Hong Kong where the incidence is as high as 6.4.2 Anatomy of Nasopharynx
20–30 cases per 100,000 population. The main
factors believed to be associated with the devel- It is also known as postnasal space, located in the
opment of NPC are EBV, genetic, and environ- centre of the head behind the nasal cavity and
mental; however, we are still unable to assimilate above the oropharynx. It is a region where thor-
these information to translate knowledge into ough clinical examination as well as adequate
prevention, early detection, and improved sur- exposure for surgical resection is difficult.
vival outcome. The most common clinical pre- Anatomically, the roof is formed by the body of
sentation is palpable cervical lymphadenopathy sphenoid bone, sphenoid further slants downwards
(50%) followed by blood-stained nasal discharge in front of arch of atlas and body of axis to form
(41%), deafness (30%), and cranial nerve palsy the posterior wall. The floor is formed by the upper
surface of the soft palate. The lateral wall is formed separated from the apex of the lateral recess by
by the eustachian tube opening in the upper part only a thin layer of fibroconnective tissue.
and superior constrictor muscle in the lower part. Blood supply of the nasopharynx is from
Fossa of Rosenmuller, also called lateral pharyn- branches of the internal maxillary artery, ascend-
geal recess, is an important structure lying in the ing pharyngeal artery and venous drainage is to
lateral wall, which is bounded anteriorly by torus the pterygoid plexus. Sensory supply is from
tubarius and levator palatine muscle, posteriorly branches of the maxillary nerve and lymphatic
by the posterior wall of the nasopharynx and retro- supply drains into the retropharyngeal and cervi-
pharyngeal space, laterally by parapharyngeal cal lymph nodes.
space, and inferiorly by the upper edge of superior
constrictor muscle (Fig. 6.26a, b). Its superior Tumours of Nasopharynx A broad range of
boundary is the skull base with important open- neoplasms arise in the nasopharynx from epithe-
ings including foramen spinosum, foramen ovale, lial to mesenchymal, lymphoid, and neuroecto-
and carotid canal. The internal carotid artery is dermal cells (Table 6.6) [63].
Fossa of Rosenmuller
Torus tubaris
Nasopharynx Eustachian tube

on axial
section
Fig. 6.26. Axial view of nasopharynx and the endoscopic view of nasopharynx from left choana
Table 6.6 (Pathology fourth edition WHO classification)

Carcinomas Nasopharyngeal Non- 8072/3 Soft tissue Nasopharyngeal 9160/0
carcinoma keratinising tumours angiofibroma
SCC
Keratinising 8071/3 Haemato- Diffuse B cell 9680/3
SCC lymphoid lymphoma
Basaloid 8083/3 tumours Extra-osseous 9734/3
SCC plasmacytoma
Nasopharyngeal 8260/3 Extramedullary 9930/3
papillary myeloid sarcoma
adenocarcinoma
Salivary Adenoid cystic 8200/3 Notochordal Chordoma 9370/3
gland carcinoma tumours
tumours Salivary gland anlage
tumours
Benign and Hairy polyp
borderline Ectopic pituitary 8272/0
lesions adenoma 9350/1
Craniopharyngioma
180 G. Nayak et al.
6.4.3 Benign Tumours in the majority of any population, IgG VCA

and EA will be raised; however, in NPC, the
It Includes salivary gland tumours, hyperplastic IgA VCA and EA raises [67]. EBV antigens
lymphoid tissue, adenoid hypertrophy, nasopha- are also present on NPC cells and express lytic
ryngeal cyst, papilloma, juvenile angiofibroma, antigens (latent membrane proteins 1, 2, 3)
and choanal polyps. and nuclear antigens (Epstein–Barr nuclear
antigens 1–6). In NPC, EBNA-1 is always
Malignant Tumours Include lymphomas, sali- expressed and LMP-1 is consistently
vary gland tumours, and NPC. expressed in significant levels. EBNA-1 is
responsible for maintaining viral episome in
the tumour cells, whereas LMP-1 has been
6.4.4 Nasopharyngeal Carcinoma shown to induce cellular growth by inducing
epithelial hyperplasia and altered keratin gene
Nasopharyngeal carcinoma (NPC) has unique expression [68, 69]. In addition, expression of
epidemiology, pathogenesis, and evolving treat- LMP-1 and EBNA-1 is not seen in normal
ment modalities which have undergone several nasopharyngeal epithelium cells.
paradigm shifts over the last 30 years. Recent • Genetic factor: The association of human leu-
advances in the treatment planning and delivery kocyte antigen (HLA) alleles with NPC is
of radiation therapy and the better understanding well established; HLA A2, Bw46, B17,
of the delivery of chemotherapeutic agents over Bw58, DR3, and DR9 have been consistently
the decades have contributed to the improvement found more prevalent in NPC in contrast to
in prognosis. Globally NPC is a rare cancer with the general population [70]. These haplotypes
80,000 new cases reported per year and accounts are associated with an increased risk for
for 0.7% of all cancers [64]. Compared with NPC. Deletions in chromosomes 3, 9, and 11
other cancer types, NPC is uncommon with a have been described in NPC. Family clusters
very unique pattern of geographical distribution. with NPC are not uncommon as NPC in a
In non-endemic areas like North America and first-degree family member could be as high
Europe, the incidence rate is low (<1 case per as eight times [71].
100,000 population) whereas in high-risk areas • Environment factors: It has been seen that
such as Hong Kong and Southern China, the diets high in preservatives containing nitrosa-
annual age-standardised incidence rate among mines such as salted fish, eggs, and vegetables
male is as high as 20–30 cases per 100,000 popu- are associated with NPC. Other environmental
lation and 8–15 cases per 100,000 population factors associated with NPC include chemical
[65, 66]. A most common site is the fossa of fumes and wood dusts [72].
Rosenmüller followed by the superior posterior
wall of the nasopharynx. Clinical Features The most common presenta-
tion in NPC is palpable cervical lymphadenopa-
Aetiology The main factors believed to be asso- thy (50%) mainly high level V and level II. Others
ciated with NPC include Epstein–Barr Virus may present with nasal symptoms (30%), oto-
(EBV), genetic and environmental factors. logical symptoms (20%), cranial nerve palsy
20% (III, IV, V, VIth nerves), or distant metastasis
• Epstein–Barr Virus: Epstein–Barr Virus is a 3% (spine is the commonest site of distant metas-
herpesvirus with a central DNA core and an tasis). Unilateral secretory otitis media present-
enveloped capsid. Infection with EBV occurs ing as deafness (30%) in adults is a warning sign
in early childhood and tends to be asymptom- and is believed to be secondary to eustachian tube
atic. In acute and convalescent phase of infec- dysfunction.
tion, the immunoglobulins (IgG and IgM) to
antigens (nuclear core early antigen [EA] or Around 1% of NPC cases may have dermato-
the viral capsid antigen [VCA]) rises. Hence, myositis as a paraneoplastic syndrome which can
develop concurrently with NPC, late after diag- Multislice computed tomographic scan of
nosis, or months before the NPC is clinically head, neck, and chest is an essential investiga-
apparent [73]. tion particularly useful in delineating clival and
skull base erosion. Magnetic resonance imaging
Assessment Patients should be assessed with provides superior definition in detecting soft tis-
rigid and fibro-optic nasal endoscopy which sue changes and intracranial involvement
reveals exophytic mass that may occupy the (Fig. 6.28a, b).
whole postnasal space (Fig. 6.27). Ulcerated
growth may be present and in about 10% of NPC Diagnosis The gold standard in the diagnosis
patients, the lesion is submucosal. of NPC is the histopathological confirmation.
The immunohistochemical markers such as
cytokeratin, epithelial cell markers, and
Epstein–Barr encoded ribonucleic acid (EBER)
will help in differentiating NPC from other
malignancies.
Cytology Fine-needle aspiration with immuno-

histochemical staining for EBER from enlarged
neck lymph node can often differentiate between
metastasis from undifferentiated carcinoma and
squamous cell carcinoma.
Other Staging Investigations Other staging

investigations include chest radiograph, CT scan
of lungs and liver, liver ultrasound, and bone
scan. Among these, bone scan has the highest
pick-up rate, which is consistent with the skele-
ton being the most common distant site of metas-
Fig. 6.27 Endoscopic view of nasopharyngeal tumour: A tasis. Positron emission tomography (PET-CT) is
tumour can be seen obliterating the right nasal choana another imaging tool; however, literature is scant
b
a
Fig. 6.28 (a) Contrast-enhanced computed tomography (axial section) of left nasopharyngeal carcinoma. (b) T2w
axial section, left nasopharyngeal carcinoma
182 G. Nayak et al.
on the efficacy and cost-effectiveness of using enables more flexible adjustment of the beam
PET-CT as a sole staging tool to assess the pri- direction.
mary and regional metastasis. A recent meta- • Radiotherapy (RT) is the mainstay for the rad-
analysis has confirmed the reliable performance ical treatment of NPC (stage I).
of PET-CT in the evaluation of distant metastasis, • Concurrent chemoradiotherapy followed by
with a pooled sensitivity of 83% and specificity adjuvant cisplatin and fluorouracil or neo-
of 97% [74]. adjuvant chemotherapy followed by concur-
rent chemoradiotherapy offers significant
EBV DNA copies may be measured by poly- improvement in overall survival in stage III
merase chain reaction techniques which correlate and IV diseases [75, 76].
with the stage of disease and are useful as an indi-
cator of treatment response. Immunoserology NCCN Guideline [77]
(VCA-IgA, EA-IgA, EBVNA1-IgA) and EBV
DNA can be used as screening methods. • T1, N0, M0: Definitive radiotherapy to naso-
Pathology: WHO histological classification: pharynx and elective RT to neck.
Three types: • T1, N1–3; T2–4, N0–3: Clinical trials (pre-
ferred) or Concurrent chemo/RT followed by
• Type I—Keratinising squamous cell carcinoma adjuvant chemotherapy or induction chemo-
• Type IIa—Differentiated non-keratinising therapy followed by chemo/RT or concurrent
carcinoma chemo/RT not followed by chemotherapy.
• Type IIb—undifferentiated non-keratinising • Any T, any N, M1: Clinical trials (preferred)
carcinoma or Platinum-based combination chemotherapy
• Type III—Basaloid squamous cell carcinoma followed by RT or concurrent systemic ther-
apy/RT as clinically indicated or observation
In endemic areas, the non-keratinising sub- or concurrent chemo/RT or RT or surgery in
type constitutes most cases (>95%) and is invari- select patients with oligometastatic disease.
ably associated with EBV infection. On • Cetuximab or nimotuzumab, monoclonal anti-
histopathology, abundant lymphoid cells are seen bodies in combination with induction chemo-
intermixed with malignant epithelial cells. therapy has shown better overall survival and
3-years’ disease-free survival in patients with
Staging of Nasopharyngeal Cancers The locally advanced NPC treated with intensity-
eighth edition of AJCC Classification and staging modulated radiotherapy [78].
[59] is given in Table 6.7.
Treatment of Local Recurrence
• Differential diagnoses include lymphoma, Brachytherapy, high-dose external reirradiation,
extramedullary plasmacytoma, melanoma, or surgery has comparable results in terms of
rhabdomyosarcoma, and adenoid cystic treatment outcome in patients with early local
carcinoma. recurrence, but their toxicity profile is quite dif-
ferent. Nasopharyngectomy is mainly reserved
Treatment: Non-keratinising NPC is a radio- for lesions that do not involve skull base or inter-
sensitive tumour and radiotherapy is the mainstay nal carotid artery (rT1 and limited rT2) whereas
of treatment, whereas surgery is reserved for sal- external beam reirradiation is an alternative to
vage of radiation failure. surgery for rT2 disease and is often the only
option for more advanced disease (advanced rT2,
• Intensity-modulated radiation therapy tech- rT3–4). Brachytherapy is only suitable for small
niques are the standard of care, and integrating recurrences confined to the central nasopharynx.
CT or MRI images into the 3D planning sys- Few radioresistant tumours like adenoid cystic
tem provides accurate spatial information on carcinoma should be treated with upfront surgery
the normal organ and tumour target which followed by radiotherapy.
Table 6.7 Staging: eighth edition of AJCC Classification and staging

T category T criteria
Tx Primary tumour cannot be assessed.
T0 No tumour recognised, but EBV-positive cervical lymph node(s).
T1 Tumour limited to nasopharynx, or involvement of oropharynx and/or nasal cavity
without parapharyngeal space infiltration.
T2 Tumour with involvement to parapharyngeal space and/or neighbouring soft tissue
involvement (medial pterygoid, lateral pterygoid, prevertebral muscles).
T3 Tumour with infiltration of bony structures at the skull base, cervical vertebra,
pterygoid structures, and/or paranasal sinuses.
T4 Tumours with intracranial extension, involvement of cranial nerves, hypopharynx,
orbit, parotid gland, and/or extensive soft tissue infiltration beyond the lateral
surface of the lateral pterygoid muscle.
N category N criteria
Nx Regional lymph nodes cannot be assessed.
N0 No regional lymph node metastasis.
N1 Unilateral metastasis in cervical lymph node(s) and/unilateral or bilateral metastasis
in retropharyngeal lymph node(s), 6 cm or smaller in greatest dimensions, above the
caudal border of cricoid cartilage.
N2 Bilateral metastasis in cervical lymph node(s) 6 cm or smaller in greatest dimension,
above the caudal border of the cricoid cartilage.
N3 Unilateral or bilateral metastasis in cervical lymph node(s), larger than 6 cm in
greatest dimension, and/or extension below the caudal border of cricoid cartilage.
M category M criteria
M0 No distant metastasis
M1 Distant metastasis
When T is … And N is… And M is… Then the stage group is…
Tis N0 M0 Stage 0
T1 N0 M0 Stage I
T1,N0 N1 M0 Stage II
T2 N0 M0 Stage II
T2 N1 M0 Stage II
T1,T0 N2 M0 Stage III
T2 N2 M0 Stage III
T3 N0 M0 Stage III
T3 N1 M0 Stage III
T3 N2 M0 Stage III
T4 N0 M0 Stage IVA
T4 N1 M0 Stage IVA
T4 N2 M0 Stage IVA
Any T N3 M0 Stage IVA
Any T Any N M1 Stage IVB
Surgery in form of nasopharyngectomy should 1. Trans-palatine approaches

be considered as a first-line treatment of residual
or recurrence disease at the primary site (rT1 and Indications:
limited rT2). • Benign and malignant tumours of the poste-
rior nasopharyngeal wall (2 cm or less in size)
Surgical Approaches to Nasopharynx • Access to tumour extending to clivus and
Anterior approaches: craniocervical junction
184 G. Nayak et al.
Contraindications: 6. Facial translocation:

• Nasopharyngeal tumours size >2 cm Indications:
• Significant intracranial extension • Extensive tumours (T4) of anterior and
• Tumours extending to parapharyngeal middle skull base extending into orbit,
space, infratemporal fossa, cavernous paranasal sinus, and posterior cranial fossa
sinus, and peritubal space with intracranial involvement
2. Transmandibular–transcervical approach: • Contraindications:
Indications: • Bilateral involvement of ICA
• Nasopharyngeal tumours extending into • Bilateral involvement of optic chiasma
the anterior infratemporal fossa • Lesion extending into posterior cranial
Contraindications: fossa
• Dural invasion >2 cm2 and intracranial
involvement Robotic Nasopharyngectomy Transoral robotic
• Invasion of parasellar and posterior infra- nasopharyngectomy has many advantages which
temporal region include good visualisation of the lateral aspect
3. Lateral approaches: infratemporal fossa
of nasopharynx and avoidance of cutting palatal
type C: muscles including tensor veil palatine which
Indications: can cause velopharyngeal insufficiency. This
• Tumour that extends into the temporal new technique is a feasible operation for salvage
bone with the involvement of the of recurrent nasopharyngeal carcinoma mainly
epipharynx rT1 and limited rT2 NPC. Early results have
• Contraindications: shown a high control rate, low morbidity, and
• Advanced disease extending to sella, comparable operating time to open surgeries. It
contralateral middle fossa, anterior skull is indicated in [79]:
base
4. Anterolateral approach: Maxillary swing
1. Smaller tumours in posterior wall/roof of

technique (Fig. 6.16) nasopharynx.
Indications: 2.
Fossa of Rosenmuller without lateral
• Nasopharyngeal tumours with limited exten- extension.
sion into the anterior infratemporal region 3. Tumour should be more than 1 cm from ICA
Contraindications: and the course of ICA should not be medial to
• Lesions involving petrous ICA and petrous the medial pterygoid plate.
apex
• Lesions extending into parasellar and/or Contraindications:
posterior infratemporal region
5. Combined approaches: Subtemporal–preau-
1 . Tumour located less than 1 cm from ICA
ricular infratemporal fossa approaches 2. Tumour extending lateral to lateral pterygoid
(Fig. 6.17) plate
Indications: 3. Tumour with invasion of pterygopalatine

• Large tumours (T4) involving infratempo- fossa or maxillary sinus
ral space extending into the nasopharynx,
cavernous sinus, and middle cranial fossa A major disadvantage is the lack of tactile
Contraindications: sensation which makes the surgeon unaware
• Bilateral ICA involvement that the tip of the instrument has reached the
• Bilateral involvement of optic chiasma bony clivus or the inability to palpate ICA
• Lesion extending into posterior cranial which is in the lateral aspect of the area of
fossa dissection.
Endoscopic Nasopharyngectomy A minimally recurrent NPC, image-guided 125I is an effective

invasive, safe, and efficacious option for selected treatment modality with better survival and mini-
primary and locally radiorecurrent tumours with mal damage [83].
comparable survival to open approaches. This
technique approaches the nasopharynx through Immunotherapy Expression of EBV antigens
the natural orifices with added high magnifica- is important as these antigens are being targeted
tion and avoids the inherent morbidities associ- in immunotherapy such as viral-specific adoptive
ated with open procedures. However, long-term cell therapy. These strategies may emerge as the
evaluation with longer follow-up data is required. main modality of treatment and can offer a dura-
Three types of nasopharyngeal endoscopic resec- ble remission in advanced nasopharyngeal carci-
tion (NER) are: noma [84].
1. Type I NER: Involves resection of posterior Photodynamic Therapy (PDT) FDA-approved

wall of nasopharynx therapy involves a combination of light-activated
2. Type II NER: Involves resection of tumours photosensitiser, visible light, and molecular oxy-
extending superiorly to the sphenoid sinus gen to selectively destroy tissue. Antitumour
3. Type 3 NER: Is trans-pterygoid approach to effect is derived by three mechanisms: the
posterolateral nasopharynx with removal of destruction of tumour-associated vasculature,
eustachian tube and pterygoid plates direct cytotoxic effect, and induction of inflam-
matory reaction against tumour cells. Photofrin,
Initial results are promising with local control first-generation FDA-approved photosensitiser,
comparable to conventional open surgical tech- is administered via intravenous injections with
niques, with most series having a 2-years’ local 24–48 hours incubation with light of wavelength
control of over 80% [80, 81]. 630 nm. Its longer clearance time is a drawback
of photofrin-mediated PDT. A number of second-
TreatmentofRegional Recurrence Reirradiation generation photosensitisers (5-Aminolevulinic
for nodal failure is associated with poor results and acid, hexyl-ALA, and Meta-tetra (hydroxyphe-
high complications. Neck dissection remains the nyl) chlorine) were discovered and have potential
treatment of choice for residual or metastatic neck advantages over first-generation drugs including
disease whenever possible. Prognosis often better tumour selectivity, faster clearance, and
remains poor in neck residue patients. Surgical higher chemical purity. Light sources commonly
salvage of nodal recurrence has a 5-years’ local used for PDT include laser diode, laser, filtered
control of 66% and 5-years’ overall survival of broadband light, and light-emitting diodes. It can
37% [82]. be used in residual and recurrent cases and initial
studies have shown improvement in recurrent
Distant Recurrence The traditional first-line tumours of less than 10 mm in depth [85].
chemotherapeutic regimen for metastatic NPC is
a combination of cisplatin and 5-fluorouracil andFollow-Up With the introduction of a concur-
the median overall survival is around 12 months. rent chemoradiation regimen, recurrence has
dropped to less than 10%. Most failures occur
Brachytherapy This modality can be used within 2 years of treatment. Patients with NPC
either as a primary treatment modality or in the cases are followed up and assessed with office-
management of recurrent cancers. For patients based rigid and/or fibro-optic nasal endoscopy.
with T1–2 NPC, it can be used either as two- Positron emission tomography–computed
dimensional high-dose-rate brachytherapy or tomography, CT, or MRI scan should be carried
three-dimensional image high-dose-rate brachy- out at 3 months from completion of treatment to
therapy with acceptable complications. For assess response.
186 G. Nayak et al.
Outcome In general, patients with non-viral- expression of thyroid transcription factor-1 (TTF-
associated nasopharyngeal carcinoma (i.e. HPV- 1) and therefore can be confused with metastatic
negative, EBV-negative tumours) had worse papillary thyroid carcinoma histologically but
outcomes than patients with viral-associated these lesions are thyroglobulin-negative.
tumours. The average 5 years survival rates with
treatment are [86]: These tumours commonly arise from surface
epithelium in the posterior and superior aspect of
• Stage I: 100% the nasopharynx. Histologically, tumour cells
• Stage II: 90% have a papillary architecture with mild nuclear
• Stage III: 67% atypia and invasive growth pattern. On immuno-
• Stage IV A: 67% histochemistry, these tumours are TTF-1 V,
• Stage IV B: 69% CK-7, CK-19, and CEA positive. Complete sur-
• Stage IV C:18% gical excision is the treatment. Adjuvant radia-
tion therapy is advised in case of incomplete
Adenoid Cystic Carcinoma Adenoid cystic excision [89].
carcinoma (ACC) arising from minor salivary
glands in this region is relatively rare and has a Chordoma Chordoma is a low-grade malig-
progressive clinical course. These lesions are nant tumour arising from notochord remnants
characterised by local infiltration and neural showing epithelial–mesenchymal differentia-
invasion and can extend from the nasopharynx tion. They mostly arise from clivus in the head
into the orbital cavity, along the cranial nerve and neck region in 25–35% of cases. These
canal and anterior skull base. Most often, they lesions are slow-growing and invade local struc-
tend to be locally aggressive and have high ten- tures, and malignant transformation occurs in
dency of recurrence. Magnetic resonance imag- third to fourth decade of life. Metastasis is rare
ing is the investigation of interest as it detects and if occurs, metastasise to lungs, bones, skin,
perineurial invasion and has a superior definition and lymph nodes. They can have varied presen-
in detecting soft tissue changes. It is widely used tations, depending on their location. Cranial
for monitoring the response of treatment. tumours may present with chronic intractable
Complete surgical resection is an important goal headache, cranial neuropathy, inferior extension
in the treatment; however, close resection mar- results in nasal or nasopharyngeal mass, nasal
gins in an anatomically complex area, adjuvant obstruction, nasal bleeding, and cerebrospinal
therapy becomes an integral part of treatment rhinorrhoea. Histologically shows lobular
[87]. Endoscopic surgery is becoming a promis- growth pattern separated by connective tissue
ing approach for early-stage disease. septae (typical multivacuolated physaliferous
cells). Immunohistochemistry shows positivity
ACC grows slowly, recurs frequently, and for cytokeratin, vimentin, and S-100 [90].
metastasises to distant organs, particularly lungs, Staging is done by radiological investigations
and therefore, its long-term prognosis is poor. (CECT/CEMRI) and is a prerequisite for appro-
The solid component of tumour on histology, priate management. Treatment options include
advanced tumour stage, and the perineurial inva- surgery (gross total resection) +/− radiotherapy
sion appears to be associated with an unfavour- or radiotherapy. Endonasal endoscopic skull
able prognosis. base approach has allowed a high rate of gross as
well as microscopic clearance of disease [91].
Nasopharyngeal Papillary Adenocar Due to the locally invasive nature of the lesion,
cinoma Primary nasopharyngeal papillary ade- complete excision may not be possible leading
nocarcinoma is an extremely rare tumour which to a high recurrence rate. Five and 10 years over-
is reported to occupy 0.48% of all types of NPC all survival rates are 50% and 20%. Tumour
[88]. These tumours have features resembling necrosis and volume of tumour more than 70 ml
papillary carcinoma thyroid with nuclear positive are independent poor prognostic factors.
6.5 art E: Pathology of Lesions

P where in the body but are important in the sinona-
of the Nose and Paranasal sal tract due to differential diagnostic
Sinuses considerations. They include benign and malig-
nant tumours of epithelial, mesenchymal, neuro-
Lesions of the nose and paranasal sinuses include ectodermal, and hematolymphoid origin, as
inflammatory lesions as well as benign and shown in Table 6.8 [92, 93].
malignant neoplasms. With increasing ease of
availability of high-throughput molecular diag-
nostic platforms, newer genetically defined enti- 6.5.2 Carcinomas
ties are being identified, leading to escalating
complexity of classification systems. This chap- Carcinomas are tumours of epithelial origin.
ter covers the salient diagnostic features and Sinonasal carcinomas represent fewer than 5% of
genetic alterations in the frequently encountered all head and neck tumours. They may arise from
lesions of this region. the respiratory epithelium of the sinonasal region,
or from the subepithelial mucoserous glands.
They are diagnosed primarily based on morphol-
6.5.1 Sinonasal Neoplasms ogy and immunohistochemistry. However,
improvements in molecular techniques in recent
The nasal cavity and paranasal sinuses play host years have led to a more specific categorisation of
to a wide spectrum of benign and malignant neo- sinonasal carcinomas, with many poorly differ-
plasms. These neoplasms may be exclusive to entiated tumours being redefined into more spe-
this region, may occur here more frequently than cific categories based on molecular genetic
at other head and neck sites, or may occur else- features.
Table 6.8 Classification of sinonasal tumours

Epithelial Mesenchymal Others
Malignant Benign Malignant Borderline Benign
Squamous cell Sinonasal Biphenotypic Glomangiopericytoma Leiomyoma Neuroectodermal
carcinoma and papillomas sinonasal sarcoma Olfactory
variants neuroblastoma
Ewing sarcoma
Mucosal melanoma
SMARCB1- Respiratory Undifferentiated Solitary fibrous tumour Hemangioma Lymphomas
deficient epithelial pleomorphic Extranodal NK/T cell
sinonasal lesions sarcoma lymphoma
carcinoma Respiratory Plasmacytoma
epithelial Plasmablastic
adenomatoid lymphoma
hamartoma
Seromucinous
hamartoma
NUT carcinoma Salivary gland Malignant Fibromatosis Schwannoma Sinonasal
tumours peripheral nerve teratocarcinosarcoma
Pleomorphic sheath tumour
adenoma
Neuroendocrine Fibrosarcoma Epithelioid Neurofibroma Ectopic pituitary
carcinomas hemangioendothelioma adenoma
Adenocarcinoma Rhabdomyosarcoma Meningioma
Sinonasal Synovial sarcoma
undifferentiated
carcinoma
(SNUC)
Leiomyosarcoma
Angiosarcoma
188 G. Nayak et al.
6.5.2.1 Squamous Cell Carcinoma (SCC) 6.5.2.2 SMARCB1-Deficient Sinonasal

SCC is a carcinoma with squamous differentia- Carcinoma
tion, arising from the sinonasal surface epithe- SMARCB1-deficient sinonasal carcinomas are
lium. SCCs occur de novo, or, less frequently, by recently identified aggressive neoplasms charac-
malignant transformation of sinonasal papillo- terised by biallelic inactivating alterations (dele-
mas. They are classified as keratinising and non- tions, intragenic mutations) in the SMARCB1
keratinising types. The keratinising type of SCC tumour suppressor gene on 22q11.2, which can
is associated with smoking and resembles kera- be demonstrated by loss of immunoexpression of
tinising SCC at other head and neck sites. It dis- INI1, the protein product of this gene. Prior to
plays nests and cords of atypical squamous cells their identification, they were mostly diagnosed
with evidence of maturation, i.e. keratinisation, in as non-keratinising SCC or sinonasal undifferen-
a desmoplastic stroma. Keratinising SCCs are tiated carcinoma (SNUC). These tumours show a
graded as well into moderately or poorly differen- variable admixture of basaloid (Fig. 6.30a), plas-
tiated tumours based on the extent of keratinisa- macytoid (Fig. 6.30b), and rhabdoid cells with
tion (Fig. 6.29a). Non-keratinising SCC has been abundant eccentric eosinophilic inclusion-like
found to be associated with transcriptionally cytoplasm (Fig. 6.30c). In addition, they may
active high-risk HPV. It is morphologically char- also show oncocytic cells in a glandular pattern,
acterised by ribbon-like and nested architecture, mimicking adenocarcinomas. Inverted papilloma-
and pushing borders (Fig. 6.29b). Tumour cells like growth, pagetoid spread along respiratory
appear basaloid, with scant cytoplasm and ovoid epithelium, and clefting artefact around tumour
nuclei (Fig. 6.29c). These tumours are not graded islands are other features that may be present.
as keratinising SCC are HPV-related tumours Necrosis, frequent mitoses, and intracytoplasmic
demonstrate diffuse p16 staining, and are HPV clear vacuoles are present in the tumour cells. On
positive by in DNA and mRNA situ hybridisation immunohistochemistry, they show loss of INI1
techniques. Rare morphological subtypes of SCC immunostaining (Fig. 6.30d), are diffusely
occasionally encountered in the sinonasal tract cytokeratin-positive, and show variable staining
include spindle cell (sarcomatoid) SCC, lympho- with p63, p40, CK5/6, and neuroendocrine mark-
epithelial carcinoma, papillary SCC, basaloid ers [95, 96].
SCC, and verrucous carcinoma. SCCs are immu-
nopositive for cytokeratins including CK5/6, epi- 6.5.2.3 NUT Carcinoma
thelial membrane antigen (EMA), and squamous NUT carcinoma is a novel, poorly differentiated,
markers p63 and p40. Staining with these markers aggressive carcinoma characterised by NUTM1
is extremely helpful in establishing the diagnosis gene rearrangements with various fusion part-
of spindle cell SCC [94]. ners, most frequently BRD4. NUT carcinomas
a b c
Fig. 6.29 Keratinising squamous cell carcinoma show- cinoma showing large rounded nests with smooth borders
ing irregular nests of cells with abundant pink cytoplasm (b) containing tumour cells with scant cytoplasm (c)
and keratin pearls (a); non-keratinising squamous cell car-
a b
c d
e f
Fig. 6.30 SMARCB1-deficient sinonasal carcinoma with staining (d); NUT carcinoma showing undifferentiated
“blue” basaloid cells showing empty vacuoles (a), “pink” basaloid cells (e) with foci of abrupt squamous differen-
plasmacytoid (b) and rhabdoid (c) cells, and loss of INI1 tiation (f)
have been described at midline locations in the lining epithelium of the sinonasal region. They
head and neck including the sinonasal region and present as exophytic masses that extensively
parotid gland, and in the mediastinum and lung. invade surrounding tissue. They show a variety of
These tumours are composed of sheets and nests histological patterns, including papillary
of undifferentiated basaloid cells (Fig. 6.30e), (Fig. 6.31a), tubular, solid, and mucinous. Mixed
with foci of abrupt squamous differentiation patterns are frequent. Mucinous, goblet, and
including clear cells and squamous eddies signet-
ring cells containing intracytoplasmic
(Fig. 6.30f). The tumour cells may display spin- mucin are present; intraluminal and extracellular
dling and peripheral palisading. Interspersed mucin may also be seen. The tumour cells are
inflammatory cells may be present. The tumour cuboidal to columnar with pseudostratified nuclei
cells show diffuse immunopositivity with cyto- (Fig. 6.31b) showing variable crowding and loss
keratin, p63, p40, and NUT protein [97]. of polarity which increase with increasing grade
from low through intermediate to high. The
6.5.2.4 Adenocarcinoma tumour cells are immunopositive for CK20,
Sinonasal adenocarcinomas are glandular neo- CDX2 (Fig. 6.31c), villin, and MUC2, similar to
plasms that arise from glandular cells in the colonic adenocarcinomas; variable staining for
respiratory mucosa. Non-salivary-type sinonasal CK7, EMA, and CEA is also seen. Focal positiv-
adenocarcinomas are classified as intestinal and ity for neuroendocrine markers is frequent.
non-intestinal types. Mutations have been identified in KRAS, HRAS,
Intestinal-type adenocarcinomas (ITACs) are TP53 genes, like in colonic adenocarcinomas.
sinonasal glandular neoplasms that resemble gas- Solid, mucinous, and signet ring patterns have
trointestinal adenocarcinomas, hence the name. been found to be associated with poor prognosis
They develop through intestinal metaplasia of the in these tumours [98].
190 G. Nayak et al.
a b c
d e f
Fig. 6.31 Intestinal-type adenocarcinoma with papillary intestinal- type adenocarcinoma with tubuloglandular
structures (a) lined by tall columnar cells with stratifica- pattern (d), cuboidal cells (e) and CK7 positivity (f)
tion of nuclei (b) immunopositive for CDX2 (c); non-
Non-intestinal-type adenocarcinomas high-grade carcinomas with evidence of neuro-

(NITACs) are sinonasal adenocarcinomas that do endocrine differentiation. NECs are graded as
not show the features of salivary gland neoplasms well, moderately or poorly differentiated NEC
and do not have an intestinal phenotype. They based on mitotic count and presence of necrosis.
show papillary, tubuloglandular (Fig. 6.31d), Poorly differentiated NEC includes small cell
solid architecture with a single layer of cuboidal NEC and large cell NEC, of which the former
to columnar cells lacking cilia (Fig. 6.31e), with outnumbers the latter. Small cell NEC (Fig. 6.32a)
mild to moderate (in low grade) or severe (in high is composed of small- to medium-sized cells with
grade) nuclear pleomorphism. Low-grade scant cytoplasm and hyperchromatic nuclei
tumours have well-formed back-to-back glands; (Fig. 6.32b). Similar to pulmonary small cell
high-grade tumours have predominantly solid NEC, nuclear molding, crushing, and necrosis
pattern with sheet-like growth of tumour cells. are prominent; frequent mitoses are present.
Scant intracytoplasmic or intraluminal mucin Large cell NEC shows cells with abundant cyto-
may be present. Tumour cells are immunoposi- plasm, and vesicular nuclei with coarse chroma-
tive for CK7 (Fig. 6.31f) and are negative for tin and prominent nucleoli, arranged in nests and
CK20, CDX2, and villin. INI1 expression is trabeculae. Frequent mitoses and comedo
retained, unlike in SMARCB1-deficient sinona- necrosis are identified. Both small cell and large
sal carcinomas with glandular architectural pat- cell NEC show positivity for at least one neuro-
terns [99]. endocrine marker, i.e. chromogranin, synapto-
physin (Fig. 6.32c), CD56. Cytokeratin shows a
6.5.2.5 Neuroendocrine Carcinomas characteristic paranuclear dot-like staining pat-
(NECs) tern. TTF-1 is frequently positive in small cell
Neuroendocrine carcinomas (NECs) in the sino- NEC, and should not be mistaken as evidence of
nasal tract are relatively rare, with the majority pulmonary origin. Well-differentiated (carcinoid)
being poorly differentiated NECs, which are and moderately differentiated (atypical carci-
a b c
d e f
Fig. 6.32 Small cell neuroendocrine carcinoma showing ated carcinoma with nests and trabecular arrangement (d)
lobular architecture (a), sheets of cells with scant cyto- of monomorphic malignant cells with brisk mitoses (e)
plasm, stippled chromatin, and nuclear molding (b) that and cytokeratin positivity (f)
are positive for synaptophysin (c); sinonasal undifferenti-
noid) NEC are extremely rare in the sinonasal entiation, which are arranged in sheets, lobules,
tract. Pituitary adenoma, ectopic or extending or trabeculae (Fig. 6.32d). Cells have scant to
from the sella, should be excluded prior to mak- moderate amount of cytoplasm, ill-defined cyto-
ing this diagnosis [100]. plasmic borders, large round vesicular to hyper-
chromatic nuclei, prominent nucleoli, and brisk
6.5.2.6 Sinonasal Undifferentiated mitotic activity (Fig. 6.32e). However, they are
Carcinoma (SNUC) relatively isomorphic appearing. There usually is
SNUC is a high-grade undifferentiated epithelial abundant necrosis and apoptosis. Surface dyspla-
malignancy lacking specific differentiation, i.e. sia is not present. Tumour cells are immunoreac-
without glandular or squamous features by histo- tive with pan-cytokeratin (Fig. 6.32f), CK7,
logical or immunohistochemical examination. It CK19, and epithelial membrane antigen, while
is a highly aggressive carcinoma with uncertain CK5/6 and CK14 are negative. Focal positivity
histogenesis and morphological overlap with with neuroendocrine markers and p63 may be
other malignant tumours (Table 6.9). It is postu- present. However, p40, a more specific marker of
lated that the cell of origin of this neoplasm may squamous differentiation is negative or maybe
be related to both the Schneiderian membrane seen in occasional cells only. Neuroendocrine
and olfactory epithelium. SNUC is now consid- markers like chromogranin and synaptophysin
ered a diagnosis of exclusion and has become may show focal positivity. Tumour cells are neg-
less common with the description of specific ative for NUT, INI1 expression is retained, and
genetically defined tumour entities, such as p16 may be positive, regardless of HPV status. A
SMARCB1-deficient carcinoma, SMARCA4- subset of SNUCs have recently been found to
deficient carcinoma, and NUT carcinoma. show mutation in IDH1 and 2 genes, which can
SNUC is composed of atypical, overtly malig- be identified by IDH immunohistochemistry and
nant cells lacking squamous or glandular differ- sequencing [101].
192 G. Nayak et al.
Table 6.9 Differential diagnosis of undifferentiated tumours of the sinonasal tract

Neoplasm Morphological features Immunohistochemistry
Non-keratinising SCC Basaloid cells with nuclear PanCK +; p63/ p40 +; INI1 retained
pleomorphism; focal keratinisation,
intercellular bridges
Basaloid SCC Basaloid cells with peripheral PanCK +; p63/ p40 +; INI1 retained
palisading
Olfactory neuroblastoma Lobular or diffuse architecture, NSE, CG, synaptophysin, calretinin +;
fibrillary background, ganglionic S100 + in sustentacular cells; PanCK
differentiation may be positive, EMA negative
NUT carcinoma Primitive basaloid cells PanCK, p63, p40 +; NUT1 +; INI1
Abrupt keratinisation +/− retained
SMARCB1-deficient Variable admixture of basaloid, PanCK +; p63, p40, CD34,
sinonasal carcinoma plasmacytoid, rhabdoid cells; no true neuroendocrine markers +/−; INI1 loss
keratinisation; relatively uniform nuclei
Small cell neuroendocrine High N:C ratio with nuclear molding; Neuroendocrine markers +; PanCK
carcinoma abundant mitoses, necrosis, apoptosis dot-like +; INI1 retained
Large cell neuroendocrine Organoid nesting pattern, trabeculae; Neuroendocrine markers +; PanCK
carcinoma large cells, coarse salt-and-pepper dot-like +; INI1 retained
chromatin, prominent nucleoli +/−
HPV-related Biphasic: Basal & ductal cells; S100, p40, p63 + in basal cells;
multiphenotypic sinonasal cribriform architecture frequent; surface CK7, CD117 + in ductal cells; p16, HR
carcinoma dysplasia present HPV ISH +; INI1 retained
Adenoid cystic carcinoma, Basaloid cells in solid sheets; focal CD117, p40, MYB +
grade III cribriform pattern; small cells with
angulated nuclei; surface dysplasia
absent
Sinonasal undifferentiated Large round nuclei of uniform size; p63, p40, NE markers focal +/−; PanCK
carcinoma mitoses, apoptosis ++ +; INI1 retained
Ewing sarcoma Small to medium cells with scant CD99, FLI1, NKX2.2 +; PanCK negative
vacuolated cytoplasm, fine chromatin;
necrosis
Adamantinoma-like Ewing Basaloid cells with peripheral PanCK, p40, CD99, FLI1, NKX2.2 +;
sarcoma palisading; basement membrane-like INI1 retained
material seen
Rhabdomyosarcoma Primitive round to spindle cells; Myogenin, desmin, MyoD1 +
rhabdomyoblasts; multinucleated cells
Lymphoma (Extranodal Dispersed cells; angiocentricity, Leukocyte common antigen, lineage-
NK/T cell lymphoma, nasal angiodestruction; abundant necrosis specific markers (CD3, CD56) +; EBV
type) EBER +
Mucosal melanoma Pleomorphic, with epithelioid, S100,SOX10,HMB-45,Melan-A+;PanCK-
plasmacytoid, and spindled cells;
peritheliomatous pattern; melanin may
be present
6.5.3 Sinonasal Papillomas types viz. inverted (Fig. 6.33a–c), exophytic, and

oncocytic, whose features are summarised in
Sinonasal papillomas are benign epithelial neo- Table 6.10.
plasms arising from sinonasal mucosa. They are Malignant transformation of sinonasal papil-
also known as Schneiderian papillomas, as they lomas follows a papilloma–dysplasia–carcinoma
originate from the Schneiderian epithelium lining sequence. Dysplasia may be keratinising or non-
the nasal cavity. While they are benign tumours, keratinising, with the latter being more subtle and
they may be locally destructive, may recur, and difficult to identify. Histological features indica-
on occasion may even undergo malignant tive of malignant transformation in a papilloma
transformation. Sinonasal papillomas are of three include the presence of extensive exophytic pap-
a b c
Fig. 6.33 Sinonasal inverted papilloma with endophytic submucosal proliferation of rounded nests (a) of immature
squamous cells lacking atypia (b); transmigrating neutrophils are prominent (c)
Table 6.10 Salient features of different types of sinona- expression, and p53 expression in >25% of
sal papillomas tumour cells [92, 94].
Inverted type Exophytic type Oncocytic type
Most common Rare Least common
type 6.5.4 Mesenchymal Neoplasms
Lateral nasal Nasal septum Lateral nasal
wall, paranasal wall, paranasal
sinuses sinuses Biphenotypic sinonasal sarcoma is a recently
Endophytic Exophytic Exophytic and/ described entity. It is a low-grade malignancy
growth pattern polypoid or endophytic with a distinctive genetic signature and propen-
growth growth sity for local recurrence but not metastasis, which
Nests, Papillary Nested and is exclusive to the sinonasal region. It is charac-
ribbon-like structures with papillary
growth pattern; delicate architecture terised by t(2;4) resulting in fusion of the PAX3
edematous fibrovascular gene with MAML3, NCOA1/2, FOXO1, or
stroma cores WWTR1 genes. These tumours are seen most
Multilayered Multilayered Multilayered commonly in females in the fourth to sixth
non-keratinising squamous or cuboidal to
decades of life. They are histologically character-
immature respiratory columnar
squamous cells, epithelial cells, epithelial cells ised by infiltrating monomorphic spindle-shaped
with variable with with abundant cells arranged in fascicles, herringbone, and sto-
respiratory mucocytes; rare eosinophilic riform pattern in a collagenous background. At
epithelial cells transmigrating cytoplasm;
places, tumour cells may show evidence of
and mucocytes; neutrophils; intraepithelial
transmigrating koilocytic mucous cysts, Schwannian or rhabdomyoblastic differentiation.
neutrophils are change may be neutrophilic Entrapped epithelial invaginations with or with-
prominent seen microabscesses out squamous metaplasia is a typical feature of
Mutually Association KRAS this tumour. Tumour cells have minimal nuclear
exclusive EGFR with low-risk mutations
mutations and HPV types 6 pleomorphism; mitoses are infrequent. These
low-risk HPV and 11 tumours display dual neural and myogenic dif-
association ferentiation histologically and immunohisto-
Low to Very low risk of Low to chemically, hence the nomenclature
intermediate malignant intermediate risk
“biphenotypic.” Differential diagnosis of biphe-
risk of transformation of malignant
malignant transformation notypic sinonasal sarcoma includes all spindle
transformation cell tumours that may occur in this region, as
shown in Table 6.11 [102–104].
illomatous growth in an inverted papilloma, 6.5.4.1 Rhabdomyosarcoma (RMS)

decreased transmigrating neutrophils, atypical Rhabdomyosarcoma is a malignant soft tissue
mitoses, necrosis, bone invasion, increased Ki-67 tumour with skeletal muscle differentiation.
194 G. Nayak et al.
Table 6.11 Differential diagnosis of common spindle cell neoplasms of the sinonasal tract
Tumour Histopathological features IHC Genetics
Biphenotypic sinonasal Spindle cells in short fascicles S100, SMA, muscle- PAX3
sarcoma Elongated nuclei specific actin, calponin, rearrangements
Epithelial invaginations Staghorn desmin/myogenin (patchy),
vasculature PAX3, β-catenin (focal)
Glomangiopericytoma Plump oval/spindle cells in short β-Catenin, SMA, cyclinD1 CTNNB1
fascicles, syncytium mutations
Round to oval nuclei Staghorn
vasculature
Perivascular hyalinisation
Solitary fibrous tumour Bland spindle cells in patternless STAT6, CD34, bcl2, CD99 NAB2-STAT6
pattern fusion
Alternating hypo- and
hypercellular areas
Ropey collagen
Malignant: Increased cellularity,
atypia, mitoses
Monophasic synovial Plump oval to spindle cells in CD99, bcl2, TLE1, SSX-SS18 fusion
sarcoma fascicular/herringbone pattern, cytokeratins, EMA
scant cytoplasm; branching
vasculature
Malignant peripheral Spindle cells with tapered nuclei, SOX10, S100 (focal), Neurofibromatosis
nerve sheath tumour myxoid background H3K27me3 loss type 1
Nuclear atypia, necrosis, mitoses
Spindle cell Herringbone, fascicular Desmin (more diffuse than MYOD1 mutations
rhabdomyosarcoma architecture BSNS), myoD1; PAX3
Greater atypia, mitoses negative
Leiomyosarcoma Spindled cells in long fascicles SMA, SMMHC, desmin,
Bright eosinophilic cytoplasm caldesmon
Cigar-shaped nuclei
Fibromatosis Spindled cells in broad fascicles Nuclear β-catenin CTNNB1 mutation
Collagenised/myxoid matrix
Infiltrating margins
Fibrosarcoma Cellular spindle cell tumour in Vimentin
fascicular/ herringbone pattern
Inflammatory Spindle cells admixed with ALK1, SMA ALK translocations
myofibroblastic tumour inflammatory cells
Schwannoma Cellular Antoni A and hypocellular S100, SOX10, GFAP, NSE
Antoni B areas
Benign spindle cells with fibrillary
cytoplasm
Wavy, buckled nuclei
Verocay bodies
Cystic, hemorrhagic areas
Meningioma Whorled architecture, cells in EMA, vimentin,
syncytium, intranuclear inclusions, progesterone receptor
calcification
Phosphaturic Stellate to spindled cells with Vimentin, FGF-23, FGFR1 gene
mesenchymal tumour vesicular nuclei; smudgy matrix; somatostatin receptors fusions
grungy calcification; staghorn (SSTR)
vessels; osteoclastic giant cells
RMS is the most common sinonasal sarcoma in Embryonal RMS is seen in young patients,
children and young adults. There are three histo- i.e. the first decade of life. It is composed of
logical subtypes of RMS, viz. embryonal, alveo- small round, polygonal and spindle cells with
lar, and spindle cell/sclerosing RMS. scant cytoplasm and hyperchromatic nuclei in a
myxoid to collagenous stroma. There is vari- tumour cells are designated as sclerosing
able evidence of rhabdomyoblastic differentia- RMS. Desmin and myogenin show variable
tion in the form of cells with bright pink staining but myoD1 is strongly positive in this
cytoplasm and eccentric nuclei. Strap cells and, RMS subtype. MYOD1 mutations are seen in
rarely, cytoplasmic cross-striations may also be spindle cell/sclerosing RMS.
seen. The botryoid variant of embryonal RMS All RMS may aberrantly express CK, EMA,
presents as a polypoidal mass with linear con- synaptophysin, chromogranin, INSM1, and
densation of tumour cells beneath the surface CD99; hence, immunohistochemistry should be
epithelium, forming a hypercellular “cambium” interpreted with caution [105].
layer. Embryonal RMS shows diffuse strong
desmin positivity and variable reactivity with 6.5.4.2 Schwannoma
myogenin and myoD1. FGFR4/RAS/AKT path- Schwannomas are benign nerve sheath tumours
way mutations have been identified in embryo- that originate from Schwann cells. They are
nal RMS. unencapsulated tumours, with cellular Antoni A
Alveolar RMS is seen in adolescents and and hypocellular Antoni B areas. Antoni A areas
young adults. It displays small to medium are composed of elongated spindled cells with
round blue cells arranged in an alveolar pattern wavy, buckled nuclei having tapered ends.
with intervening fibrovascular septa. Nuclear palisading and Verocay bodies are pres-
Multinucleated tumour cells are frequent, and ent. Antoni B areas consist of a hypocellular,
are a clue to the diagnosis; rhabdomyoblasts myxoid stroma with reticular appearance and
may also be seen. The solid variant of alveolar infiltration by inflammatory cells, particularly by
RMS does not show the alveolar pattern with histiocytes. Perivascular hyalinisation and degen-
fibrovascular septa but has sheet-like growth of erative changes such as haemorrhage, cystic
tumour cells. Alveolar RMS are diffusely posi- areas, and nuclear atypia are commonly seen.
tive for myogenin and stain positively at least Schwannomas show diffuse strong S100
focally with desmin. Alveolar RMS harbour positivity.
PAX3FOX01 (in 70–90% of cases) or PAX7
FOX01 (in 10% of cases) gene fusions. These 6.5.4.3 Nasopharyngeal Angiofibroma
are of prognostic significance, with the former These are benign, locally aggressive fibrovascular
having worse outcomes than the latter. Fusion- neoplasms seen almost exclusively in adolescent
negative alveolar RMS have a prognosis similar males. They arise from a nidus in the posterolat-
to embryonal RMS. eral wall of the nasal cavity. The growth of these
Spindle cell/sclerosing RMS are the rarest tumours is believed to be testosterone hormone-
RMS subtypes and occur at all ages. In adults, dependent. They are characterised by submucosal
they frequently occur at head and neck locations. haphazard proliferation of thin- and thick-walled
They are comprised of intersecting fascicles of blood vessels which are surrounded by spindled
spindle-shaped cells with eosinophilic cyto- to stellate shaped fibroblasts in a collagenous
plasm. Those with prominent stromal hyalinisa- stroma (Fig 6.34a, b). There is minimal nuclear
tion and nested or cord-like arrangement of atypia, and mitoses are rare. Necrosis may be seen
Fig. 6.34 Nasopha a b
ryngeal angiofibroma
showing a spindle cell
tumour with many blood
vessels (a) from which
the spindle cells
emanate (b)
196 G. Nayak et al.
following embolisation, accompanied by intra- 6.5.5.2 Sinonasal

vascular foreign material. On immunohistochem- Teratocarcinosarcoma
istry, the tumour cells are immunopositive for Sinonasal teratocarcinosarcoma (SNTCS) is an
androgen receptor and beta-catenin. The display extremely uncommon malignant neoplasm with
genetic alterations are including loss of the Y aggressive behaviour. It is characterised by the
chromosome and m utations in exon 3 of the presence of a combination of ectodermal, mesen-
CTNNB1 (beta-catenin) gene in the majority of chymal, and neuroectodermal components in
cases. Patients with familial adenomatous polypo- varying proportion. The ectodermal component
sis having a germline APC gene mutation are consists of squamous or glandular epithelium;
more likely to develop angiofibromas [106]. “fetal”-appearing squamous epithelium with
clear polygonal cells is typical of SNTCS. The
mesenchymal component consists of malignant
6.5.5 Other Malignant Neoplasms spindle cells; differentiation along various lin-
eages can be seen, including osteoid, cartilage,
6.5.5.1 Olfactory Neuroblastoma smooth muscle, and skeletal muscle differentia-
Olfactory neuroblastoma, previously also known tion. The neuroectodermal component consists of
as esthesioneuroblastoma, originates from the spe- small round blue cells resembling ONB. The
cialised sensory olfactory neuroepithelium present divergent differentiation seen in SNTCS is attrib-
near the cribriform plate of ethmoid. On histology, uted to its origin from a multipotential adult
ONB shows a wide morphological spectrum, somatic stem cell. The presence of individual
based on the grade of the tumour. Hyams grade is components in small biopsies frequently leads to
the most accepted grading system. Low-grade misdiagnosis and delay in management, which
tumours (grade 1 and 2) consist of monomorphic further worsens the outcome of this highly malig-
small round blue cells with stippled/“salt and pep- nant tumour [109].
per” chromatin arranged in lobules separated by
fibrovascular septae that are richly vascularised 6.5.5.3 Extranodal NK/T Cell
[62]. A variable amount of neurofibrillary matrix Lymphoma, Nasal Type
is interspersed between the tumour cells. Extranodal NK/T cell lymphoma, nasal type
Sustentacular cells are present at the periphery of (ENKTL) is the most frequently encountered
the lobules. High-grade tumours show tumour lymphoma in the sinonasal tract. It has a strong
cells arranged in sheets. Atypia and mitoses are association with Epstein–Barr virus (EBV).
increased, and necrosis may be present. Rosettes Biopsies show diffuse infiltrates of abnormal
may be seen in ONB: Homer Wright pseudoro- lymphoid cells of variable size with irregular,
settes are identified in Hyams grades 1 and 2, and folded nuclei. Angiocentricity, angioinvasion,
Flexner–Wintersteiner true rosettes in Hyams angiodestruction, and necrosis are prominent and
grades 3 and 4. Calcification may be present. serve as clues to the diagnosis when present.
ONBs stain positively with synaptophysin, chro- Variable cellularity, presence of necrosis, and
mogranin, INSM1, and neuron-specific enolase. admixed inflammatory cells can cause overlap
Calretinin positivity has also been documented with inflammatory processes, and obscure the
and may be helpful in diagnosis. While cytokeratin diagnosis. The most common immunophenotype
may be positive focally, EMA is usually negative. of the tumour cells is positivity for cytoplasmic
p63 and p40 are also usually negative. S100 stains CD3, CD56, CD57, TIA-1, perforin, and gran-
the sustentacular cells. Dense core neurosecretory zyme B. EBV detection by in situ hybridisation
granules are present on ultrastructural examination for EBV-encoded RNA (EBER) can be used for
of the tumour cells [107, 108]. confirmation [107].
6.5.6 Fibroosseous Lesions more frequently affected than the gnathic bones.
JPOFs consist of compact stellate to spindle-
6.5.6.1 Ossifying Fibroma shaped cells with scant stroma, accompanied by
Ossifying fibromas are benign fibroosseous numerous rounded, bluish deposits of woven
lesions of the jaw and craniofacial bones. They bone known as psammomatoid bodies or ossi-
are classified into three specific variants viz. cles, as they resemble psammoma bodies. Similar
Cemento-ossifying fibroma, Juvenile trabecular to JTOF, osteoblastic rimming is absent. Larger
ossifying fibroma (JTOF), and Juvenile psam- bone deposits may fuse to form irregular angu-
momatoid ossifying fibroma (JPOF). lated trabeculae. Cystic degeneration and sec-
Cemento-ossifying fibromas (COFs) are ondary cyst formation may be seen [110].
tumours of odontogenic origin, which occur in
the third and fourth decades of life, with a female 6.5.6.2 Fibrous Dysplasia
preponderance. The mandible is more frequently Fibrous dysplasia (FD) is a benign condition in
involved than the maxilla. Microscopically, COF which normal bone is replaced by disorganised
demonstrates a variably cellular, fibroblastic pro- immature bone and fibrous tissue. Clinical types
liferation in a fibrotic stroma, accompanied by include monostotic FD, polyostotic FD, and
deposition of mainly woven and scant lamellar McCune–Albright syndrome characterised by
bone, osteoid and cementum-like material polyostotic fibrous dysplasia, café-au-lait spots,
arranged in irregular islands, trabeculae, and and multiple endocrinopathies. The maxilla is
spheroids. The fibroblastic cells are bland, stel- involved more frequently than the mandible. FD
late to spindle-shaped, with normo- to hyperchro- is slightly more common in females and occurs in
matic nuclei that lack atypia and mitoses. The young adults. Histologically, FD shows replace-
bone shows osteoblastic rimming. Osteoclastic ment of the medullary cavity of normal bone by a
giant cells and secondary cyst formation are rare. cellular fibroblastic stroma containing narrow
COFs are associated with mutations in CDC73 curvilinear (C shaped) and irregularly shaped
(HRPT2) gene. Multiple lesions occur in patients (Chinese letter pattern) trabeculae of woven bone
with hyperparathyroidism-jaw tumour syndrome that lack osteoblastic rimming. FD is character-
attributed to this mutation. GNAS mutations, ised by activating missense mutations in the
characteristic of fibrous dysplasia, are absent. GNAS gene, which is seen in all three forms
Juvenile trabecular ossifying fibroma (JTOF) [111].
occurs in the first and second decades of life with
equal sex distribution and involves the maxilla
more frequently than the mandible. JTOF is com- 6.5.7 Nasal Polyps
posed of a hypercellular stellate to spindle cell
proliferation with minimal atypia and occasional 6.5.7.1 Inflammatory Nasal Polyp
mitoses. Stroma shows sparse collagen. These are polypoid Inflammatory swellings of
Elongated curved and branched trabecular depos- the sinonasal mucosa with multifactorial aetiol-
its of osteoid which mineralise at the centre and ogy. They are lined by respiratory mucosa on
lack osteoblastic rimming are present. These may three sides, which may undergo squamous meta-
ossify and form lamellar bone. Clusters of osteo- plasia. The basement membrane of the epithe-
clastic giant cells may be seen and secondary cyst lium is thickened and hyalinised. The underlying
formation is not uncommon and can aid in dis- lamina propria is expanded, edematous, and con-
tinction from COF. tains seromucous glands. Fibroblasts and small
Juvenile psammomatoid ossifying fibroma blood vessels may be seen in the stroma. A mixed
(JPOF) occurs over a wide age range with mean chronic inflammatory cell infiltrate is usually
age in second to fourth decades of life and equal present. Secondary changes may be identified,
sex distribution. The paranasal sinuses and peri- including ulceration, formation of granulation
orbital bones, i.e. ethmoid and frontal bones are tissue, fibrosis, infarction, nuclear atypia in stro-
198 G. Nayak et al.
mal fibroblasts, cartilaginous or osseous metapla- 7. McLachlin CM, Kandel RA, Colgan TJ, Swanson
DB, Witterick IJ, Ngan BY. Prevalence of human
sia, and mucous gland hyperplasia. papillomavirus in sinonasal papillomas: a study
using polymerase chain reaction and in situ hybrid-
6.5.7.2 Antrochoanal Polyp ization. Mod Pathol. 1992;5:406–9.
AC polyp is a distinct clinical type of inflamma- 8. McKay SP, Grégoire L, Lonardo F, Reidy P,
Mathog RH, Lancaster WD. Human papillomavi-
tory polyp arising from the maxillary sinus and rus (HPV) transcripts in malignant inverted papil-
extending into the nasal cavity through the maxil- loma are from integrated HPV DNA. Laryngoscope.
lary ostium. It is histologically similar to inflam- 2005;115:1428–31.
matory polyps, but seromucous glands are 9. Cheung FM, Lau TW, Cheung LK, Li AS, Chow SK,
Lo AW. Schneiderian papillomas and carcinomas: a
diminished or absent, and they lack eosinophils. retrospective study with special reference to p53 and
Atypical stromal cells are more frequent, as is p16 tumor suppressor gene expression and associa-
infarction, accompanied by neovascularisation. tion with HPV. Ear Nose Throat J. 2010;89:E5–E12.
10. Kraft M, Simmen D, Casas R, Pfaltz M. Significance
of human papillomavirus in sinonasal papillomas. J
6.5.7.3 Allergic Nasal Polyp Laryngol Otol. 2001;115:709–14.
These are an inflammatory response of sinonasal 11. Jenko K, Kocjan B, Zidar N. In inverted papillo-
mucosa to inhaled fungal allergens, mediated by mas HPV more likely represents incidental colo-
eosinophils. They present as polypoid mucosal nization than an etiological factor. Virchows Arch.
2011;459:529–38.
fragments with inflammation. Abundant sepa- 12. Krause JH. Development of a staging system for
rately lying mucinous material containing inverted papilloma. Laryngoscope. 2000;110:965–8.
degranulated eosinophils and Charcot Leyden 13. Ojiri H, Ujita M, Tada S, et al. Potentially distinc-
crystals, i.e. allergic mucin is found, which may tive features of sinonasal inverted papilloma on MR
imaging. AJR Am J Roentgenol. 2000;175(2):465–8.
contain fungal hyphae that are difficult to iden- 14. Lawson W, Patel ZM. The evolution of management
tify. Fungal elements are not seen within tissue for inverted papilloma: an analysis of 200 cases.
fragments or blood vessels, unlike in invasive Otolaryngol Head Neck Surg. 2009;140:330–5.
fungal sinusitis. Histochemical stains like PAS-D 15. Lee TJ, Huang SF, Huang CC. Tailored endoscopic
surgery for the treatment of sinonasal inverted papil-
and Gomori methenamine silver may be used to loma. Head Neck. 2004;26:145–53.
highlight the fungal hyphae. It is not required to 16. Sham CL, Woo JK, van Hasselt CA, et al. Treatment
identify fungal elements to give the diagnosis. results of sinonasal inverted papilloma: an 18-year
study. Am J Rhinol Allergy. 2009;23:203–11.
17. Mendenhall WM, Hinerman RW, Malyapa
RS. Inverted papilloma of the nasal cavity and para-
References nasal sinuses. Am J Clin Oncol. 2007;30:560–3.
18. Eller R, Sillers M. Common fibro-osseous lesions
1. Barnes L, Eveson JW, Reichart P, Sidransky D, eds. of the paranasal sinuses. Otolaryngol Clin N Am.
Pathology and Genetics of Head and Neck tumors. 2006;39:585–600.
2. Wood JW, Casiano RR. Inverted papillomas and 19. Fu YS, Perzin KH. Non-epithelial tumors of the
benign nonneoplastic lesions of the nasal cavity. Am nasal cavity, paranasal sinuses, and nasopharynx. A
J Rhinol Allergy. 2012 Mar-Apr;26(2):157–63. clinicopathologic study. Cancer. 1974;33:1289–305.
3. Sham CL, Lee DL, van Hasselt CA, et al. A case- 20. Alexander AA, Patel AA, Odland R. Paranasal sinus
control study of the risk factors associated with osteomas and Gardner’s syndrome. Ann Otol Rhinol
sinonasal inverted papilloma. Am J Rhinol Allergy. Laryngol. 2007;116:658–62.
2010;24:e37–40. 21. Speight PM, Carlos R. Maxillofacial fibro-osseous
4. Dietmer T, Wiener C. Is there an occupational etiol- lesions. Curr Diagn Pathol. 2006;12:1–10.
ogy of inverted papilloma of the nose and sinuses. 22. Eversole R, Su L, Elmofty S. Benign fibro-ossous
Acta Otolaryngol (Stockh). 1996;116:762–5. lesions of the craniofacial complex a review. Head
5. Kashima HK, Kessis T, Hruban RH, Wu TC, Neck Pathol. 2008;2:177–202.
Zinreich SJ, Shah KV. Human papillomavirus in 23. Waldron CA. Fibroosseous lesions of the jaws. J
sinonasal papillomas and squamous cell carcinoma. Oral Maxillofac Surg. 1993;51:828–35.
Laryngoscope. 1992;102:973–6. 24. Kransdorf MJ, Moser RP Jr, Gilkey FW. Fibrous
6. Ringert N. Pathology of malignant tumors arising dysplasia. Radiographics. 1990;10:519–37.
in the nasal and paranasal cavities and maxilla. Acta 25. Stompro BE, Wolf P, Haghihi P. Fibrous dysplasia of
Otolaryngol (Stockh). 1938;27(suppl):31–42. bone. Am Fam Phys. 1989;39:179–84.
26. Moore AT, Buncic JR, Munro IR. Fibrous dysplasia 41. Snyderman CH, Pant H, Carrau RL, Gardner P. A
of the orbit in childhood. Clinical features and man- new endoscopic staging system for angiofibromas.
agement. Ophthalmology. 1985;92:12–20. Archives of Otolaryngology—Head and Neck
27. Angelopoulos AP. Pyogenic granuloma of the oral Surgery. 2010;136(6):588–94.
cavity: statistical analysis of its clinical features. J 42. Schuon R, Brieger J, Heinrich UR, Roth Y, Szyfter
Oral Surg. 1971;29:840–7. W, Mann WJ. Immunohistochemical analysis
28. Cawson RA, Binnie WH, Speight PM, Barrett AW, of growth mechanisms in juvenile nasopharyn-
Wright JM. Lucas pathology of tumors of oral tis- geal angiofibroma. Eur Arch Otorhinolaryngol.
sues. 5th ed. Missouri: Mosby; 1998. p. 252–4. 2007;264(4):389–94.
29. Zarrinneshan A, Zapanta P, Wall S. Nasal pyo- 43. Thompson LDR, Fanburg-Smith JC. Update on select
genic granuloma. Otolaryngol Head Neck Surg. benign Mesenchymal and Meningothelial Sinonasal
2007;136:130–1. tract lesions. Head Neck Pathol. 2016;10(1):95–108.
30. Patil K, Mahima VG, Lahari K. Extragingival pyogenic https://doi.org/10.1007/s12105-016-0697-6.
granuloma. Indian J Dent Res. 2006;17:199–202. 44. Boghani Z, Husain Q, Kanumuri VV, et al. Juvenile
31. Marx RE, Stern D. Oral and maxillofacial pathology: nasopharyngeal angiofibroma: a systematic review
a rationale for diagnosis and treatment. Chicago: and comparison of endoscopic, endoscopic-assisted,
Quintessence Publishing Co; 2003. p. 21–3. and open resection in 1047 cases. Laryngoscope.
32. Herrington H, Adil E, Moritz E, et al. Update on cur- 2013;123(4):859–69. https://doi.org/10.1002/
rent evaluation and management of pediatric nasal lary.23843.
dermoid. Laryngoscope. 2016;126(9):2151–60. 45. Nicolai P, Villaret AB, Farina D, et al. Endoscopic
https://doi.org/10.1002/lary.25860. surgery for juvenile angiofibroma: a critical review
33. Szymańska A, Szymański M, Czekajska-Chehab of indications after 46 cases. American Journal of
E, Szczerbo-Trojanowska M. Two types of lateral Rhinology and Allergy. 2010;24(2):e67–72.
extension in juvenile nasopharyngeal angiofibroma: 46. Gates GA, Rice DH, Koopmann CF Jr, Schuller
diagnostic and therapeutic management. Eur Arch DE. Flutamide-induced regression of angiofibroma.
Otorhinolaryngol. 2015;272(1):159–66. https://doi. Laryngoscope. 1992 Jun;102(6):641–4.
org/10.1007/s00405-014-2965-y. 47. Thakar A, Gupta G, Bhalla AS, Jain V, Sharma SC,
34. Gołąbek W, Szymańska A, Szymański M, Czekajska- Sharma R, Bahadur S, Deka RC. Adjuvant therapy
Chehab E, Jargiełło T. Juvenile nasopharyngeal with flutamide for presurgical volume reduction in
angiofibroma with intracranial extension–diagnosis juvenile nasopharyngeal angiofibroma. Head Neck.
and treatment. Otolaryngol Pol. 2019;74(2):1–7. 2011 Dec;33(12):1747–53.
https://doi.org/10.5604/01.3001.0013.5275. 48. Mallick S, Benson R, Bhasker S, Mohanti
35. Nicolai P, Schreiber A, Villaret AB. Juvenile BK. Conformal radiotherapy for locally advanced
Angiofibroma: evolution of management. juvenile nasopharyngeal angio-fibroma. J
Int J Pediatr. 2012;412545:11. https://doi. Cancer Res Ther. 2015;11(1):73–7. https://doi.
org/10.1155/2012/412545. org/10.4103/0973-1482.150349.
36. Schick B, Kahle G. Radiological findings in angiofi- 49. Mallick S, Benson R, Bhasker S, Mohanti BK. Long-
broma. Acta Radiol. 2000;41(6):585–93. term treatment outcomes of juvenile nasopharyn-
37. Szymańska A, Szymański M, Czekajska-Chehab geal angiofibroma treated with radiotherapy. Acta
E, Szczerbo-Trojanowska M. Invasive growth pat- Otorhinolaryngol Ital. 2015;35(2):75.
terns of juvenile nasopharyngeal angiofibroma: 50. Goldenberg D, Golz A, Fradis M, et al. Malignant
radiological imaging and clinical implications. tumors of the nose and paranasal sinuses: az retro-
Acta Radiol. 2014;55(6):725–31. https://doi. spective review of 291 cases. Ear Nose Throat J.
org/10.1177/0284185113506189. 2001;80:272–7.
38. Lloyd G, Howard D, Lund VJ, Savy L. Imaging 51. Shah UK, Hybels RL, Dugan J. Endoscopic manage-
for juvenile angiofibroma. J Laryngol Otol. ment of low-grade papillary adenocarcinoma of the
2000;114(9):727–30. ethmoid sinus: case report and review of the litera-
39. Thakar A, Sakthivel P, Prashanth A, Bhalla AS, ture. Am J Otolaryngol. 1999;20:190–4.
Sharma SC, Kumar R. Comparison of 68Ga-PSMA 52. Suárez C, Ferlito A, Lund VJ, et al. Management
PET/CT and contrast-enhanced MRI on residual dis- of the orbit in malignant sinonasal tumors. Head
ease assessment of juvenile nasal Angiofibroma. Clin Neck. 2008;30(2):242–50. https://doi.org/10.1002/
Nucl Med. 2020 Feb 11; https://doi.org/10.1097/ hed.20736.
RLU.0000000000002951. 53. Lyon BM, Donald PJ. Radical surgery for nasal cav-
40. Overdevest JB, Amans MR, Zaki P, Pletcher SD, ity and paranasal sinuses. Otolaryngologic Clincs of
El-Sayed IH. Patterns of vascularization and surgical North America. 1991;24:1499–521.
morbidity in juvenile nasopharyngeal angiofibroma: 54. Madani G, Beale TJ, Lund VJ. Imaging of sino-
a case series, systematic review, and meta-analysis. nasal tumors. Semin Ultrasound CT MR.
Head Neck. 2018;40(2):428–43. https://doi. 2009;30(1):25–38. https://doi.org/10.1053/j.
org/10.1002/hed.24987. sult.2008.10.013.
200 G. Nayak et al.
55. Kraus D, Sternman BM, Levine HL, et al. Factors and solvents and risk of nasopharyngeal carcinoma.
inuencing survival in ethmoid sinus cancer. Arch Cancer Epidemiol Biomark Prev. 2001;10:1145–3.
Otolaryngol Head Neck Surg. 1992;118:367–72. 73. Peng JC, Sheen TS, Hsu MM. Nasopharyngeal
56. Lloyd G, Lund VJ, Howard D, Savy L. Optimum carcinoma with dermatomyositis: analysis of
imaging for sinonasal malignancy. J Laryngol 12 cases. Arch Otolaryngol Head Neck Surg.
Otol. 2000;114(7):557–62. https://doi. 1995;121(11):1298–1.
org/10.1258/0022215001906174. 74. Chang MC, Chen JH, Liang JA, et al. Accuracy
57. Bishop JA. Recently described neoplasms of the of whole-body FDG-PET and FDG-PET/CT in
sinonasal tract. Semin Diagn Pathol. 2016;33(2):62– M staging of nasopharyngeal carcinoma: a sys-
70. https://doi.org/10.1053/j.semdp.2015.12.001. tematic review and meta-analysis. Eur J Radiol.
58. Andreasen S, Kiss K, Mikkelsen LH, et al. An update 2013;82:366–3.
on head and neck cancer: new entities and their his- 75. Simo R, Robinson M, Lei M, Sibtain A, Hickey
topathology, molecular background, treatment, and S. Nasopharyngeal carcinoma: United Kingdom
outcome. APMIS. 2019;127(5):240–64. https://doi. National Multidisciplinary Guidelines. J Laryngol
org/10.1111/apm.12901. Otol. 2016;130:97–3.
59. Lydiatt WM, Patel SG, O’Sullivan B. Head and 76. Al-Sarraf M, LeBlanc M, Giri PG, et al.
neck cancers- major changes in the American joint Chemoradiotherapy versus radiotherapy in patients
committee on cancer eighth edition cancer staging with advanced nasopharyngeal cancer: phase III
manual. CA Cancer J Clin. 2017;67:122–7. randomized intergroup study 0099. J Clin Oncol.
60. Morita A, Ebersold MJ, Olsen KD, et al. 1998;16(4):1310–7.
Esthesioneuroblastoma: prognosis and management. 77. Version 3.2019, 06/09/19 © National Comprehensive
Neurosurgery. 1993;32:706–15. Cancer Network, Inc. 2019.
61. Dulguerov P, calcaterra T. Esthesioneuroblastoma: 78. Peng H, Tang LL, Liu X, Chen L, Li WF, Mao
the UCLA experience 1970-1990. Laryngoscope. YP. Anti-epidermal growth factor receptor ther-
1992;102:843–9. apy concurrently with induction chemotherapy
62. Hyam VJ, Batsakis JG. Michaels. Tumour of the in locoregionally advanced nasopharyngeal carci-
upper respiratory tract and ear. Washington DC: air noma. Cancer Sci. 2018;109:1609–6.
force institute of. Pathology. 1988:240–8. 79. Tsang RK, To VS, Ho AC, Ho WK, Chan JY, Wei
63. Sarradin V, Siegfried A, Uro-Coste E, Delord WI. Early results of robotic assisted nasopharyngec-
JP. WHO classification of head and neck tumours tomy for recurrent nasopharyngeal carcinoma. Head
2017: Main novelties and update of diagnostic meth- Neck. 2015;37(6):788–3.
ods. Bull Cancer. 2018;105(6):596–2. 80. Castelnuovo P, Nicolai P, Turri-Zanoni M, Battaglia
64. Jemal A, Bray F, Center MM, et al. Global cancer P, Bolzoni Villaret A, Gallo S, Bignami M. Dallan
statistics. CA Cancer J Clin. 2011;61:69–90. endoscopic endonasal nasopharyngectomy in
65. Huang TR, Zhang SW, Chen WQ, et al. Trends selected cancers. Otolaryngol Head Neck Surg.
in nasopharyngeal carcinoma mortality in 2013;149(3):424–30.
China, 1973–2005. Asian Pac J Cancer Prev. 81. Ho AS, Kaplan MJ, Fee WE, et al. Targeted endo-
2012;13:2495–2. scopic salvage nasopharyngectomy for recurrent
66. Yu MC, Yuan JM. Epidemiology of nasopharyngeal nasopharyngeal carcinoma. Int Forum Allergy
carcinoma. Semin Cancer Biol. 2002;12:421–9. Rhinol. 2012;2(2):166–3.
67. Henle G, Henle W. Epstein-Barr virus–specific IgA 82. Wei W, Lam K, Ho C, et al. Efficacy of radical neck
serum antibodies as an outstanding feature of naso- dissection for the control of cervical metastasis after
pharyngeal carcinoma. Int J Cancer. 1976;17(1):1–7. radiotherapy for nasopharyngeal carcinoma. Am J
68. Miller WE, Earp HS, Raab-Traub N. The Epstein- Surg. 1990;160(4):439–2.
Barr virus latent membrane protein 1 induces 83. Yan H, Mo Z, Xiang Z, Rong D, Zhang Y, Chen
expression of the epidermal growth factor receptor. J G, et al. CT-guided 125I brachytherapy for locally
Virol. 1995;69:4390–8. recurrent nasopharyngeal carcinoma. J Cancer.
69. Paine E, Scheinman RI, Baldwin AS Jr, et al. 2017;8(11):2104–3.
Expression of LMP1 in epithelial cells leads to the 84. Jain A, Chia WK, Toh HC. Immunotherapy for
activation of a select subset of NF-kappa B/Rel fam- nasopharyngeal cancer-a review. Chin Clin Oncol.
ily proteins. J Virol. 1995;69:4572–6. 2016;5(2):22.
70. Simons MJ, Wee GB, Chan SH, et al. Probable iden- 85. Stoker SD, Indrasari SR, Herdini C, Hariwiyanto
tification of an HLA second-locus antigen associ- B, Karakullukcu B, Dhamiyati W, Widayati K,
ated with a high risk of nasopharyngeal carcinoma. Romdhoni AC, Fles R, Haryana SM, Wildeman MA,
Lancet. 1975;1:142–3. Tan IB. Photodynamic therapy as salvage therapy for
71. Ung A, Chen CJ, Levine PH, et al. Familial and spo- patients with nasopharyngeal carcinoma experienc-
radic cases of nasopharyngeal carcinoma in Taiwan. ing local failures following definitive radiotherapy.
Anticancer Res. 1999;19:661–5. Photodiagn Photodyn Ther. 2015;12(3):519–5.
72. Hildesheim A, Dosemeci M, Chan CC, et al. 86. Lee AWM, Ng WT, Chan LK, et al. The strength/
Occupational exposure to wood, formaldehyde, weakness of the AJCC/UICC staging system
(7th edition) for nasopharyngeal cancer and sug- 99. Rampinelli V, Ferrari M, Nicolai P. Intestinal-
gestions for future improvement. Oral Oncol. type adenocarcinoma of the sinonasal tract: an
2012;48(10):1007–3. update. Curr Opin Otolaryngol Head Neck Surg.
87. Liu TR, Yang AK, Guo X, et al. Adenoid cystic 2018;26:115–21.
carcinoma of the nasopharynx: 27-year experience. 100. Leivo I. Sinonasal adenocarcinoma: update on clas-
Laryngoscope. 2008;118:1981–8. sification, Immunophenotype and molecular fea-
88. Wang X, Yan H, Luo Y, Fan T. Low-grade nasopha- tures. Head Neck Pathol. 2016;10:68–74.
ryngeal papillary adenocarcinoma: a case report 101. Montone KT. The differential diagnosis of
and review of the literature. Onco Targets Ther. Sinonasal/ nasopharyngeal neuroendocrine/
2016;9:2955–9. Neuroectodermally derived tumors. Arch Pathol Lab
89. Zhang WL, Ma S, Havrilla L, Cai L, Yu CQ, Shen Med. 2015;139:1498–507.
S. Primary thyroid-like low-grade nasopharyngeal 102. Agaimy A, Franchi A, Lund VJ, Skálová A,

papillary adenocarcinoma: a case report and litera- Bishop JA, Triantafyllou A, Andreasen S, Gnepp
ture review. Medicine. 2017;96:47. DR, Hellquist H, Thompson LDR, Rinaldo A,
90. Crapanzano JP, Ali SZ, Ginsberg MS, Zakowski Ferlito A. Sinonasal undifferentiated carcinoma
MF. Chordoma: a cytologic study with his- (SNUC): from an entity to morphologic pattern
tologic and radiologic correlation. Cancer. and Back again-a historical perspective. Adv Anat
2001;93(1):40. Pathol. 2019 Dec 24; https://doi.org/10.1097/
91. Fernandez-Miranda JC, Gardner PA, Snyderman PAP.0000000000000258.
CH, Devaney KO, Mendenhall WM, Suárez C, 103. Kakkar A, Rajeshwari M, Sakthivel P, Sharma
Rinaldo A, Ferlito A. Clival chordomas: a patho- MC, Sharma SC. Biphenotypic sinonasal sar-
logical, surgical, and radiotherapeutic review. Head coma: a series of six cases with evaluation of role
Neck. 2014;36(6):892–6. of β-catenin immunohistochemistry in differential
92. Tumors of the nasal cavity, paranasal sinuses and diagnosis. Ann Diagn Pathol. 2018;33:6–10.
skull base. In: El-Naggar AK, JKC C, Grandis JR, 104. Gross J, Fritchie K. Soft tissue special issue:
Takata T, Slootweg PJ, editors. WHO classifica- Biphenotypic Sinonasal sarcoma: a review with
tion of head and neck tumors. IARC: Lyon; 2017. emphasis on differential diagnosis. Head Neck
p. 11–61. Pathol. 2020 Jan 16; https://doi.org/10.1007/
93. Nasal cavity and paranasal sinuses. In: LDR T, s12105-019-01092-4.
Wenig BM, Muller S, Nelson B, editors. Diagnostic 105. Kane SV, Kakkar A, Oza N, Sridhar E, Pai
pathology: head and neck. Philadelphia: Elsevier; PS. Phosphaturic mesenchymal tumor of the nasal
2016. p. 2–189. cavity and paranasal sinuses: a clinical curiosity pre-
94. Weindorf SC, Brown NA, McHugh JB, Udager senting a diagnostic challenge. Auris Nasus Larynx.
AM. Sinonasal Papillomas and carcinomas: a con- 2018;45:377–83.
temporary update with review of an emerging 106. Kohashi K, Kinoshita I, Oda Y. Soft tissue special
molecular classification. Arch Pathol Lab Med. issue: skeletal muscle tumors: a Clinicopathological
2019;143:1304–16. review. Head Neck Pathol. 2020 Jan 16; https://doi.
95. Kakkar A, Antony VM, Pramanik R, Sakthivel P, org/10.1007/s12105-019-01113-2.
Singh CA, Jain D. SMARCB1 (INI1)- deficient 107. Purgina B, Lai CK. Distinctive head and neck
sinonasal carcinoma: a series of 13 cases with bone and soft tissue neoplasms. Surg Pathol Clin.
assessment of histological patterns. Hum Pathol. 2017;10:223–79.
2018;83:59–67. 108. Rooper LM, Bishop JA. Sinonasal small round blue
96. Agaimy A, Hartmann A, Antonescu CR, Chiosea SI, cell tumors: an Immunohistochemical approach.
El-Mofty SK, Geddert H, et al. SMARCB1 (INI-1)- Surg Pathol Clin. 2017;10:103–23.
deficient Sinonasal carcinoma: a series of 39 cases 109. Agaimy A. Poorly differentiated sinonasal tract
expanding the morphologic and Clinicopathologic malignancies: a review focusing on recently
Spectrum of a recently described entity. Am J Surg described entities. Cesk Patol. 2016;52:146–53.
Pathol. 2017;41:458–71. 110. Sable M, Kakkar A, Garg K, Suri V. Sinonasal
97. Kakkar A, Antony VM, Irugu DVK, Adhikari N, Jain Teratocarcinosarcoma: an underdiagnosed entity
D. NUT midline carcinoma: a series of five cases, posing diagnostic challenges. Turk Neurosurg.
including one with unusual clinical course. Head 2017;27:468–71.
Neck Pathol. 2018;12:230–6. 111. Hameed M, Horvai AE, Jordan RCK. Soft tissue
98. Bishop JA, Westra WH. NUT midline carcino- special issue: gnathic fibro-osseous lesions and
mas of the sinonasal tract. Am J Surg Pathol. osteosarcoma. Head Neck Pathol. 2020 Jan 16;
2012;36:1216–21. https://doi.org/10.1007/s12105-019-01094-2.
Extended Procedures
7
Pankuri Mittal, Hitesh Verma, Amit Kesari,
R. S. Virk, Kshitiz Charya, Smriti Panda,
Alok Thakar, Rajesh Kumar Meena,
Ramesh S. Doddamani, Manish Gupta,
Rohit Verma, Vikas Gupta, Ganakalyan Behera,
Amit Shanker, Namrita Mahmi, M. Ravi Sankar,
and Arulalan Mathialagan
Contents
7.1 art A: Extended Endoscopic Approach
P 205
7.1.1 Contraindications of EEAs 213
7.1.2 Limits of EEAs 214
7.2 art B: Anatomy and Surgical Approaches to Pterygopalatine Fossa,
P
Pterygomaxillary Fissure and Infratemporal Fossa 214
7.2.1 Surgical Approach to PPF and ITF 215
7.3 Part C: Pituitary Tumours and Surgical Management 220
7.3.1 natomy
A 220
7.3.2 Physiology 221
7.3.3 Postoperative Care 225
7.3.4 Pearls of Pituitary Surgery 225
7.4 art D: Open Techniques for Nose and Paranasal Sinuses
P 225
7.4.1 Indications for Open Approaches 226
7.4.2 Relative Contraindications for Surgical Resection of Nose/Paranasal
Sinus Tumours 226
P. Mittal · H. Verma (*) · S. Panda · A. Thakar M. Gupta

N. Mahmi ENT, MMIMSR, MMU, Ambala, Haryana, India
Department of ENT, AIIMS, New Delhi, India R. Verma
e-mail: drhitesh10@gmail.com ENT, DMC, Ludhiana, Punjab, India
A. Kesari · M. R. Sankar · A. Mathialagan V. Gupta · G. Behera
Neurootology, SGPGIMS, Lucknow, UP, India ENT, AIIMS, Bhopal, MP, India
R. S. Virk A. Shanker
ENT, PGIMER, Chandigarh, India ENT, Brighton and Sussex University Hospital NHS,
K. Charya Brighton, UK
Indus Hospital, Mohali, Punjab, India
R. K. Meena · R. S. Doddamani
Neurosurgery, AIIMS, New Delhi, India
204 P. Mittal et al.
7.4.3 Preoperative Work-Up 227

7.4.4 lassification of Approaches to Nose and PNS
C 227
7.4.5 Soft Tissue Approaches 227
7.4.6 Bony Approaches 229
7.5 art E: Open Anterior Skull Base Approaches: Indications
P
and Complications 233
7.5.1 Diagnostic Work-Up 234
7.5.2 The Subcranial Approach 236
7.5.3 Reconstruction 236
7.6 art F: Lacrimal Sac Anatomy and DCR
P 238
7.6.1 Pathology—Dacryocystitis 238
7.6.2 Preoperative Tests/Investigations 238
7.7 Part G: Sinus Mucocele 243
7.7.1 etiology
A 243
7.7.2 Pathology 243
7.7.4 Imaging 244
7.7.5 Treatment 244
7.7.6 Results 244
7.8 Part H: Choanal Atresia and Management 245
7.8.1 Aetiology 246
7.8.2 Patho-physiology 246
7.8.4 Diagnosis and Evaluation 247
7.8.5 Treatment 247
7.8.6 Preliminary Airway Management 248
7.8.7 Definitive Surgical Management 248
7.8.8 Prevention of Restenosis After Surgery 250
7.8.9 Use of Laser in Surgery 250
7.8.10 Syndromes Associated with Choanal Atresia 250
7.9 Part I: Cerebrospinal Fluid Rhinorrhea 250
7.9.1 pplied Physiology
A 251
7.9.2 Applied Anatomy 251
7.9.3 Classification 251
7.9.4 Patient Evaluation 252
7.9.5 Differential Diagnosis 252
7.9.6 Investigations 252
7.9.7 Treatment 254
7.9.8 Grafting Techniques 258
7.10 Part J: Optic Nerve Anatomy and Management 259
7.11 art K: Skull Base Reconstruction in Extended
P
Endoscopic Approaches 264
7.11.2 Principles of Skull Base Reconstruction 264
7.11.3 Endonasal Mucosal Flaps 265
References 270
7 Extended Procedures 205
Good radiology, better-quality visualization, mechanism violation and external scar. The
advances in technology and in-depth anatomical proper surgical technique and regular follow-up
knowledge allows removal of central skull base reduces the risk of restenosis. Choanal atresia is
lesion by transnasal route. CECT and MRI scan the stenosis/atresia of the posterior choana. It can
in all planes at 1 mm interval is required to map present in isolation or as a part of the syndrome.
the extent of the lesion. The diagnostic cerebral It can be bony, membranous or mixed types.
angiography (DSA) is indicated in selected cases, Endoscopic direct visualization is the gold stan-
to obtain information regarding vascularity of the dard way to confirm the diagnosis. Transnasal
lesion and possible involvement of surrounding and transpalatal are the most accepted approaches.
major neurovascular bundle. Extended endo- CSF rhinorrhea is developed by the abnormal
scopic approaches are divided into median and communication of the nasal cavity with the cra-
paramedian type. Median approaches are for nial cavity. The aetiology is broadly classified
midline lesions. It is further divided on the basis into traumatic and non-traumatic types. The
of site of involvement such as frontal sinus, crib- numbers of haematological and biochemical
riform plate, planum sphenoidalis, etc. parameters are mentioned for confirmation of the
Paramedian approaches are for lateral lesions. It presence of CSF fluid within the nasal cavity but
is further divided into anterior, middle and poste- β-2-transferrin is the most specific for CSF. HRCT
rior approaches. Intraorbiral and transorbital temporal bone with MR cisternography is the
comes under the anterior subtype. Cavernous most accepted radiological investigation combi-
sinus, petrous apex and infratemporal area lesions nation to localize the site of leak. Traumatic ones
are managed by the middle approach. Condylar, are mainly managed by a conservative approach
hypoglossal canal and jugular fossa lesions are but non-traumatic ones require surgical repair.
delt by posterior approach. Pituitary gland lies Optic nerve comes in a lateral relationship with
behind and above the sphenoid sinus. Number of the posterior ethmoid and sphenoid sinus. Direct
hormones are secreted by the pituitary gland. and indirect injuries are the types of optic nerve
Pituitary adenomas are dealt by both medical and injury. No management option is available for
surgical ways. These adenomas are the most direct injury. The indirect optic neuropathy is
common lesions managed by extended endo- managed by both medical and surgical way. The
scopic approaches. Tumours involving the skin, extended surgical approaches create a large sur-
extending beyond the mid-pupillary line, tumour gical cavity and iatrogenic communication of the
infiltration into the orbital tissue and palatal bone nasal cavity with the cranial cavity. The flaps are
erosion are the indications for open approaches. used to separate these cavities and to improve the
Open extra-cranial approaches are further subdi- outcome of repairs.
vided into soft tissue and bony approaches.
Moure’s Lateral Rhinotomy Incision and Weber–
Ferguson incisions are the most commonly used 7.1 art A: Extended Endoscopic
P
soft tissue approaches. Transcranial approaches Approach
to the anterior skull base are divided into anterior
and anterolateral approaches depending upon the Extended endoscopic endonasal approaches
tumour extensions. The lacrimal system is for (EEAs) have come up as a good substitute to tra-
sucking the tears. The obstruction of nasolacri- ditional open approaches. Advance technology
mal duct requires the creation of new communi- allows superior visualization and better control
cation between the sac and nasal cavity. of instruments with precision in disease clear-
Dacryocystorhinostomy is of two types: endo- ance. The extent of EEAs is from cribriform plate
scopic and external. The endoscopic method pro- to clivus and C2 vertebrae. The major drawback
vides almost equal results with an open approach. of open approaches is the manipulation of the
The endoscopic approach is devoid of complica- cerebrum, blood vessels and cranial nerves. The
tions of external approach such as lacrimal pump other disadvantages of traditional approaches are
EEA
Approaches to the median skull Approaches to the paramedian

base (access to structures in the skull base (access to structures
sagittal plane) in the coronal plane)
• Transfrontal • Anterior coronal Middle coronal Posterior coronal

• Transcribriform plane plane plane
• Transtuberculum/ • Supraorbital Petrous apex • Transcondylar
Transplanum • Transorbital Petroclival • Transhypoglossal
• Transsellar Quadrangular space • Jugular foramen
• Transclival Superior cavernous
• Transodontoid sinus
Infratemporal
approach
Fig. 7.1 Extended endoscopic approaches
large incision size, prolonged exposure time, further defined based on the anatomy of the cor-
bleeding, frontal lobe symptoms, prolonged hos- ridor and target areas and their relationship with
pitalization and medical care, etc. The rate of critical structures (Fig. 7.1) [1, 2]. The choice of
complications is drastically reduced by endo- approach is based on the extent of the lesion and
scopic approaches. In the last two decades, more in a number of situations; a combination of close-
and more centres have moved towards endo- by approaches is required.
scopic approaches to the skull base and intracra-
nial lesion because of the improvement in 1. Access to the median skull base (sagittal
knowledge in endoscopic anatomy, hi-tech endo- plane): anterior to posterior direction
scopic equipment, micro-instruments, refining (A) Transfrontal Approach (Fig. 7.2)
the expertise of the surgeon and EEAs have a The indications are chronic refractory
lack of disadvantages of open approaches. frontal sinusitis not responding to other
Sphenoid sinus is the entry route for the majority management, fibro-osseous lesions of
of skull base lesions. Internal carotid artery, cav- frontal sinus, posterior table CSF rhinor-
ernous sinus, optic nerve and maxillary division rhoea, recurrent mucoceles, and other
of trigeminal nerve are the close-by vital struc- lesions of frontal sinus like dermoid. The
tures, so good preoperative radiological assess- surgery starts with complete exposure of
ment and selection of correct instruments with bilateral frontal recesses. Superior septal
copious saline irrigation to prevent thermal window is created anterior to anterior
trauma is the key for surgical success in EEAs. attachment of middle turbinate and ante-
The complexity of lesion is the deciding factor rior to cribriform plate area to visulaized
for two-hands or four-hands technique. both frontal sinuses. The final step is the
EEA can be classified into approaches to removal of the interfrontal sinus septum
median skull base and paramedian skull base, to create one large frontal sinus. It pro-
according to the orientation of the surgical field vides wide access to remove the disease
(target area) under two main categories and are and to deal with posterior table.
Frontal sinues
Cribriform plate
Fig. 7.2 CT scan of nose & PNS revealing heterogenous mass filling fronal sinuses, nasal cavity with surrounding
osteogenesis. Right figure is showing healed postoperative cavity after transfrontal approach
a b c Septal
perforation
Left
olfactory
cleft
Fig. 7.3 Recurrent adenocarcinoma of left olfactory cleft. (a) endoscopic photo, (b) contrast-enhancing mass in the left
nasal cavity and olfactory cleft, (c) healed postoperative cavity
Transcribriform Approach [3]

(B) omy and middle turbinate removal
Indications for exposure of the entire skull base
It is indicated for tumours involving the is done to define the posterior limit
central part of the frontal lobe and the of the lesion. Anterior and posterior
olfactory bulb region (e.g. olfactory ethmoid arteries are cauterized to
groove meningioma, esthesioneuroblas- de-vascularize the lesion. In selected
toma, adenocarcinoma) (Fig. 7.3). cases, preservation of olfaction is
Steps possible on the other side.
(i) Debulking of intranasal mass may (iii) An endoscopic modified Lothrop
required to expose the cribriform procedure (Draf III) is performed
plate region. to label the anterior limit.
(ii) Complete anterior and posterior eth- (iv) Bone lateral to tumour is drilled
moidectomy with wide sphenoidot- out and removed from frontal
Fig. 7.4 Esthesioneuroblastoma. (a) sagittal MRI T2 images (Kadish stage 3 lesion), (b) surgical cavity (NCCT head)
after combined transcribriform and transplanar approach
sinus posterior wall to planum gical exposure (Fig. 7.4). Suprasellar

sphenoidalis. Lateral limit of drill lesions are managed by this approach by
is orbital medial wall. cauterization of superior inter-cavernous
(v) Nasal septum is removed with sinus.
1 cm healthy margin from tumour (D) Trans-sphenoidal Approaches
to sphenoid sinus posteriorly and The sphenoid sinus is the entry point for
cribriform plate superiorly. a number of trans-sphenoid approaches.
(vi) Dura mater is cauterized peri- Sphenoid bone is located in the centre of
tumourally with preservation of the cranial base in intimate contact with
deep cortical vessels. Crista galli, many important arterial, venous and neu-
olfactory nerve fibres, and falx are ral structures. The pneumatization of the
separated from tumour by inferior sphenoid bone creates a natural corridor.
displacement. The next step is the identification of
(vii) The final defect is from the median sphenoid ostium. The nasal septum is
orbital margin on both sides and separated from the sphenoid rostrum.
from the posterior table of the The anterior wall of the sphenoidal sinus
frontal sinus till planum sphenoi- is enlarged circumferentially and sphe-
dalis in anteroposterior direction. noidal septae is drilled. The posterior and
(viii) Closure of defect in layers with lateral walls of the sphenoidal sinus
vascularized flap. should be visible laterally; the sellar floor
Transplanar Approach
(C) inferiorly, the sphenoethmoid planum
The limit of the corridor is from fovea above (Fig. 7.5) [4–6].
ethmoidalis over posterior ethmoid and (i) Trans-sellar Approach
cribriform plate anteriorly. The posterior Indications
limit is the sella and the lateral limit is the It allows access to pathologies of
optic nerve. It can combine with anterior the pituitary gland such as pituitary
or posterior extended approaches for sur- adenomas, Rathke’s cleft cysts, etc.
Superior orbital Optic

fissure foramen Lesser wing
Sphenoid PS
sinus ostium
TS
Greater OP OP
wing
LOCR LOCR
Foramen
rotundum CPs CPs
SF
Orbital surface
Pterygoid canal
Infratemporal
fossa crest
Spine of CPc CPc
Sphenoidal C
sphenoid
Lateral pterygoid rostrum
Vaginal process
plate
Pterygoid notch Hamulus of

Medial pterygoid medial pterygoid
plate
Fig. 7.5 The natural anatomy of sphenoid bone and endoscopic view of sphenoid sinus after wide sphenoidotomy and
removal of posterior septum (Courtesy for line diagram—Dr. Arulalan Mathialagan- Senior Resident SGPGI, Lucknow)
It provides access to the medial cav- angle formed by the convergence of

ernous sinus for pituitary adenomas the sphenoid planum with the sellar
that extend laterally behind the cav- floor is recognizable; from the intra-
ernous ICA. The first step is the cranial view, this corresponds to the
completion of the trans-sphenoidal tuberculum sellae. As one moves
approach. Bone removal over the the endoscope in an anterior direc-
sellar face extends laterally beyond tion, the sphenoid planum is visible.
the medial aspect of the cavernous The opening of the planum starts
sinuses (CS) and superiorly and with the removal of the tuberculum
inferiorly to expose both the inter- sellae, extended bilaterally in the
cavernous sinuses. Further extended direction of the optico-carotid
approaches require the creation of a recesses. The lateral extension of
wider surgical corridor to expose the opening is limited by the protu-
and work in the different areas berances of the optic nerves
around the sella (Fig. 7.6). (Fig. 7.6).
Trans-tuberculum/Transplanum (iii)
(ii) Trans-clival Approach
Approach The surgical corridor is extending
Indications from dorsal sellae to the foreman
The indications are extracellular magnum. It provides a head-on view
pituitary adenomas with suprasellar to the brainstem and vertebrobasilar
extension, meningiomas and select vascular network. It can further be
craniopharyngiomas. The access is divided into superior, middle and
obtained through a more anterior inferior approaches by location of
trajectory compared with the one dural opening of abducent and glos-
used to reach the sellar region. This sopharyngeal nerve. The internal
route requires a wider opening of carotid artery is the lateral limit for
the anterior wall of the sphenoidal middle and inferior approaches.
sinus, which is obtained by remov- Vidian artery, intraoperative naviga-
ing the superior (supreme) turbi- tion system with carotid doppler
nates and the posterior ethmoid air helps in identification of carotid
cells. Above the sellar floor, the artery [6]. The limit of bone removal
a b c
d e f
g h
Fig. 7.6 Extended endoscopic trans-seller approach drilling of intersphenoid septum with bone over sella, (e)
(courtesy—Dr. Ramesh Doddamani, Associate Professor, line diagram of figure d, (f) entry into sella turcica and
AIIMS, New Delhi). (a) Endoscopic view of right sphe- flap creation, (g) line diagram of figure f, (h) adenomatous
noid ostium, (b) separation of posterior septum from ros- tissue is visible through entry site
trum of sphenoid sinus, (c) wide sphenoidotomy, (d)
can be tailored. Abducent nerve is at the body of C2 cervical vertebrae.

risk while working in the region of Access is achieved by removal of
paraclival carotid [7]. nasal septum till floor of nasal
Transodontoid Approach
(iv) cavity. Nasopharyngeal mucosa
The indications are decompres- with underlying muscles is
sion of the brainstem in rheuma- removed from one side eustachian
toid arthritis and disintegration of tube opening to the other side [8].
the upper cervical spine. The limit C1 vertebral ring is removed after
of the surgical corridor is anterior elevation of fascia and clival bone
limit of the foramen magnum to drilling.
2. Access to Paramedian Corridor (Coronal

Plane)
The most critical and defining structure is
ICA in this plane. The paramedian skull base
may be divided into anterior (corresponding
to the orbit and anterior cranial cavity), mid-
dle (corresponding to the middle cranial, pter-
ygopalatine and infratemporal fossae) and
posterior (includes the craniovertebral junc-
tion lateral to the occipital condyles and the
jugular foramen) segments.
(A) Anterior Coronal Plane
It is further divided into the supraorbital
and transorbital approaches [9–11].
Supraorbital approach provides access to Fig. 7.7 Right transorbital intraconal approach.
anterior cranium lesion extending later- (Courtesy Dr. M. Arulalan, Senior Resident, Neuro-
ally over orbit. Transorbital is designed to Otology, Department of Neurosurgery, SGPGIMS,
Lucknow)
reach both extraconal and intraconal
lesions. The indications for the extra- found medial to petrous apex, zone 2 is
conal approach are the sinonasal lesions corridor for infrapterous access, zone 3 is
that displace, erode or invade the medial passage for suprapetrous access, zone 4 is
wall of the orbit and for orbital/optic for lateral cavernous sinus access and
nerve decompression in Graves’ disease zone 5 is for middle fossa and infratem-
or trauma. The intraconal approach is poral fossa. Except for zone 1, all zones
indicated to address intraorbital benign start with a transpterygoid approach using
space-occupying lesions, such as schwan- the maxillary sinus as the working corri-
nomas, haemangiomas and meningio- dor [12–15]. These approaches provide
mas. The steps include complete access to skull base lesions posterior to
ethmoidectomy and exposure of lamina the maxillary sinus (e.g. middle cranial,
papyracea in full extend. The next step is pterygopalatine and infratemporal fossae,
the removal of lamina. For supraorbital lateral sphenoid recess, petrous apex, cav-
lesions, periorbita is lifted off from the ernous sinus). Common pathologies
cranium base with cauterization of eth- include schwannomas, juvenile nasopha-
moid vessels. Binostril approach can be ryngeal angiofibromas, sinonasal malig-
performed by superior septectomy. For nancy and meningoencephaloceles.
intraconal compartment access, perior- (i) Transpterygoid Approach
bita is incised to expose the medial and The pterygopalatine fossa (PPF) is
inferior rectus muscles. The gap between bound by the pterygoid process
these two muscles represents the window posteriorly, the palatine bone
for intraconal access (Fig. 7.7). As oph- anteromedially and the maxilla
thalmic arteries and the optic nerves can- anterolaterally. The ITF is an ana-
not be mobilized, they constitute the tomic space located under the floor
lateral limits of the approach. of the middle cranial fossa and pos-
(B) Middle Coronal Plane terior to the maxilla. It communi-
It is further divided into five different cates medially with the
zones, according to their relationship pterygopalatine fossa through the
with specific segments of the ICA. Zone 1 pterygomaxillary fissure, anteriorly
is the boundary to approach the lesions ITF is continuous with the inferior
orbital fissure. Pneumatization of ina located from superolateral to

the sphenoid sinus extending into infero-medial: foramen rotundum,
the greater sphenoid wing bears a vidian canal and palatovaginal
lateral sphenoid recess (i.e. ptery- canal.
goid recess), which projects under The surgery begins with uncinec-
the middle fossa. The paired ptery- tomy, anterior ethmoidectomy and
goid processes comprise medial wide middle meatus antrostomy
and lateral plates, fused at their (Fig. 7.8). The sphenopalatine and
anterior cephalic aspect, the ptery- posterior nasal arteries are then
goid base. Three important foram- identified at the sphenopalatine
a b
Ethmoid
sinus
Maxillary
sinus
posterior Angiofibroma
wall
choana
c d
Sphenoid
sinus
Lateral
recess
Infratemporal
fossa
Pterygoid
plates
Fig. 7.8 Right middle coronal plane. (a) Complete expo- placement of tissue laterally after ligation of vessels, (e)
sure of posterior and part of the lateral wall of right maxil- line diagram is showing surgical field after removal of
lary sinus, (b) complete removal of posterior wall, (c) posterior maxillary sinus wall (Courtesy Dr. M. Arulalan,
ligation of terminal branches of maxillary artery, (d) com- Senior Resident, Neurootology, Department of
plete removal of pterygopalatine fossa content and dis- Neurosurgery, SGPGIMS, Lucknow)
and secondary complications, such

as infection or meningitis. A vascu-
larized reconstruction (e.g. nasosep-
tal flap) is favoured. The
reconstruction options are men-
tioned in the last section.
(ii) Trans-cavernous Approach [13]
It allows access lateral to cavernous
carotid. Pituitary macroadenomas
extending posterior to cavernous
carotid is the only indication for the
trans-cavernous approach. It allows
lateral displacement of the carotid
artery.
(iii) Petrous Apex Approach [10, 12]
Petrous apex lesions extending
towards the sphenoid sinus can be
accessed by this approach.
Extended sphenoidotomy and drill-
Fig. 7.8 (continued) ing of bone over the petrous apex
allows access.
foreman. The posterior wall of the (iv) Suprapetrous Approach
antrum is removed, revealing the It starts with complete exposure of
contents of the PPF covered with the course of internal carotid artery.
periosteum. The sphenopalatine and Lesion extending into trigeminal
posterior nasal arteries can be nerve and Meckel’s cave are man-
divided and mobilized laterally aged by suprapetrous approach.
which exposes the vidian canal. The Infra-petrous, trans-condylar
location of the vidian canal is usu- and parapharyngeal are the poste-
ally at the insertion of the medial rior coronal approaches. The surgi-
pterygoid plate on the pterygoid cal exposure in posterior coronal
process of the sphenoid bone. The approaches is improved by
vidian nerve and artery inside the Denker’s approach, septal window
canal can be coagulated and divided, and by wide maxillectomy. Zone 5
allowing for the subsequent lateral- is discussed in the next section.
ization of the contents of the ptery-
gopalatine fossa and identification
of the pterygoid base as well as the 7.1.1 Contraindications of EEAs
foramen rotundum. The base of the
pterygoid plate is drilled, and the Contraindications to an endoscopic approach to
lateral sphenoid recess is opened. the skull base include tumour extending lateral
The infratemporal approach is dis- to the midline of orbital roof, or lateral to optic
cussed in the next section. The nerve, cases where an oncological resection
objective behind reconstruction is to mandates a total maxillectomy, orbital exentera-
restore the natural isolation of the tion or resection of facial skin, and most impor-
intracranial structures from the sino- tantly lack of progressive experience in surgical
nasal cavity, avoiding a CSF leak team [16].
7.1.2 Limits of EEAs (ITF) laterally. It is formed by a narrow gap

between the lateral pterygoid plate and the infra-
Certain limitations to EEAs are significant pos- temporal surface of maxilla. The contents of
terior fossa extension with the tumour located PMF are third part of the maxillary artery and
behind the ICA, institutional limitations (lack posterior superior alveolar nerve, artery and
of transnasal Doppler, stereotactic neuro- veins.
navigation, specialized endo-bipolars and Infratemporal fossa is a three-dimensional
extraocular EMG monitoring) and tumours that space lies below the middle cranial fossa base
circumferentially encase the carotid, so the which comprises of greater wing of the sphe-
endoscopic endonasal approach cannot achieve noid and squamous temporal bone. It is bounded
a gross total resection [16, 17]. laterally by ramus of mandible, zygomatic arch
and medially by lateral pterygoid plate which
has pterygomaxillary fissure connecting it to the
7.2 Part B: Anatomy and Surgical pterygopalatine fossa. Anteriorly, it is bounded
Approaches by posterior-lateral wall of maxilla with inferior
to Pterygopalatine Fossa, orbital fissure and posteriorly with carotid
Pterygomaxillary Fissure sheath and styloid apparatus. Inferiorly, it com-
and Infratemporal Fossa municates with the neck (Figs. 7.9 and 7.10).
Infratemporal fossa contents lie in three planes
The pterygopalatine fossa (PPF), pterygomaxil- from superficial-to-deep in the axial plane. The
lary fissure (PMF) and infratemporal fossa (ITF) first layer immediately posterior to periosteum
are continuous compartments that lie lateral to of posterior wall of maxillary sinus consists of
the sphenopalatine foramen with a greater wing branches of maxillary artery. Second layer
of sphenoid forming their roof. Pterygomaxillary formed by various branches and anastomosis of
fissure (PMF) is a communication between the V2 and V3 and third layer is consist of muscles
pterygopalatine fossa medially (which in turn of ITF. This surgical anatomy is important while
communicate with the nasal cavity via the dealing with the pathology of PPF and ITF
sphenopalatine foramen) and infratemporal fossa (Fig. 7.11) [18–21].
a b
Fig. 7.9 Infratemporal fossa—bony outlines. (a) Lateral view and (b) posterior view
a b
Fig. 7.10 Computed tomography Axial sections (a) showing tumour (asterisk) involving sphenopalatine foramen and
pterygomaxillary fissure and (b) involving infratemporal fossa
and ITF are decided mainly by the type of

The surgical approach to PPF and ITF can be
lesion, its extension and experience of the surgi-
either an endoscopic approach or an open
cal team.
approach. The endoscopic approach is mainly
1. Endoscopic Approach to SPA, PPF and
the anterior approach to ITF and suited for SPF,
ITF
PPF and medial ITF which can combined with
It is indicated for sphenopalatine artery liga-
endoscopic Denker’s approach or anterior maxil-
tion, maxillary artery ligation, vidian neurec-
lotomy for lateral ITF pathology. Open
tomy, juvenile nasopharyngeal angiofibroma
approaches can be either anterolateral like max-
(Fisch Stage I, II and III JNA). Schwannomas
illary swing and midfacial degloving or lateral
of PPF and ITF are commonly arising from
like Fisch’s ITF approach C and infratemporal
the maxillary nerve and mandibular nerve,
fossa approach D (preauricular transzygomatic
paranasal sinus tumours (non-squamous) with
approach).
extension into the SPA, PPF or ITF. Temporal
lobe meningo-encephalocele is extending into
7.2.1 S
urgical Approach to PPF the infratemporal fossa. Lesions of the middle
and ITF cranial skull base, which are lying (intradural/
extradural) lateral to cavernous sinus.
Surgery of PPF and ITF can be done by either an Contraindications of Endoscopic Approach:
endoscopic approach or by an open approach. Tumours are extending to the masseteric
The endoscopic approach is mainly an anterior space and gingivobuccal sulcus. Large juve-
approach to ITF and suited for SPF, PPF and nile nasopharyngeal angiofibroma is receiv-
Medial ITF which if combined with endoscopic ing significant feeders from the internal
Denker’s approach or maxillotomy can be used carotid artery and other tumours encasing
for lateral ITF pathology. Open approaches can ICA. Tumours extending to the cavernous
be either anterolateral like maxillary swing and sinus, in around optic nerve and orbital apex,
midfacial degloving or lateral like Fisch’s ITF middle fossa and para-sellar extension are the
approach C and D. Surgical approach to PPF relative contraindications.
Surgical Steps (Fig. 7.12):

Endoscopic large meatal antrostomy is the
first step of the endoscopic approach as this
exposes the posterior-medial wall of the max-
illary sinus, which lies anterior to SPF, PPF
and ITF. Wider access can be gained by a
medial maxillectomy. Removal of the lower
part of middle turbinate creates more space
for instrumentation. This is followed by an
anterior and posterior ethmoidectomy.
Pathologies in the SPA, PPF and medial ITF
can be accessed after removal of posterior
wall of maxilla with a Kerrison’s rongeurs or
Fig. 7.11 Contents of infratemporal fossa in three planes. drill starting from the anterior lip of SPA tak-
(1) Vascular layer (with branches of internal maxillary ing care to prevent injury to the periosteum of
artery), (2) neural layer (with branches of maxillary and posterior wall of maxillary sinus, as maxillary
mandibular nerves) and (3) muscular layer. Right side artery and its branches lie directly posterior to
(asterisk) is the tumour arising from the sphenopalatine
foramen involving the nasopharynx and entering infra- it. The sphenopalatine artery can be identified
temporal fossa causing splaying of the vascular and neural just posterior to cristae on the posterior part of
layers medial wall of maxilla and maxillary artery
a b c
d e f
Fig. 7.12 Endoscopic excision of the infratemporal fossa lesion, (d) endoscopic exposure after removal of posterior
tumour. (a) Axial CT showing hypodense lesion in left wall of maxillary sinus, (e) tumour dissection from sur-
ITF, (b) zoomed image, (c) coronal section for the same rounding tissue, (f) postoperative cavity
Complications
Bleeding can occur intraoperatively due to
injury to the maxillary artery or its branches
and rarely from feeders of ICA. Injury to the
nasolacrimal duct is evident after surgery with
complaints of epiphora. Injury to V2, spheno-
palatine ganglia can lead to dry eye and numb-
ness of the face. Orbital injury can occur
during dissection of tumours, dissection
around orbital fissure and optic nerve can lead
to visual deterioration, if the optic nerve is
injured and extraocular muscle injury can lead
to diplopia. CSF leak can occur from the mid-
dle cranial fossa after tumour removal and
Fig. 7.13 Endoscopic view of right internal maxillary repair of encephaloceles. Intracranial bleeding
artery in the infratemporal fossa. (1) Internal maxillary can also occur during tumour removal from
artery, (2) sphenopalatine artery, (3) descending palatine
the intradural compartment. Complications
artery, (4) infraorbital artery, (5) infraorbital nerve, (6)
infratemporal fossa fat, (7) lateral wall of the maxillary can happen due to removal of normal struc-
sinus, (8) medial wall of the maxillary sinus tures like piriform aperture leading to numb-
ness of the vestibular area, nasal obstruction
from crusting in nasal cavity and septal perfo-
and its branches by careful dissection of peri- ration. Postoperative epistaxis can occur lead-
osteum of posterior wall of maxilla to expose ing to blood loss or aspirations [19, 22]. So,
contents of PPF, PMF and ITF (Fig. 7.13). each and every step of the procedure has to be
The maxillary artery dissection and the meticulously performed and the possible com-
control is important as it is the major vascular plication has to be anticipated and avoided.
supply to the tumours arising or located in this 2. Open Approach to PPF and ITF
area. Preoperative embolization can reduce Indications
the vascularity in vascular tumours like JNA It is indicated for the tumours of ITF with
and hemangiopericytoma. extensions to masticator space, buccinators
Lateral exposure of ITF by endoscope is space and Zygomatic space. Malignant lesions
limited by Piriform aperture, which can be of the maxillary sinus with ITF involvement
removed by modified Denker’s approach or are managed by open anterior approach. It is
by wide anterior wall maxillotomy to gain also advised for gross extension of lesion to
access to the lateral compartment of middle cranial fossa through foramen rotun-
ITF. Single surgeon endoscopic approach can dum or ovale. Parotid gland, mandible and
be converted into a two surgeon 4 handed zygomatic bone can be involved by lateral
technique after making a septal window any- extension of ITF lesions. Inferior extension of
time during surgery for better visualization, ITF lesions into parapharyngeal space is also
dexterity, dissection, for controlling the ves- managed by an open approach. Jugular fora-
sels and for tumour removal. For pathology men lesion with ITF extension is also handled
located in the middle fossa and surrounding by open approaches [23, 24]. Approaches for
skull base, a greater wing of sphenoid and malignant lesions of the nose and PNS are
pterygoids can be drilled to access the middle mentioned in Part D (Sect. 7.4).
fossa above, the petrous carotid from cavern- Contraindications
ous sinus to lateral part of temporal bone after There is no absolute contraindication to the
either displacing the maxillary artery and its open approach to ITF as this approach can be
branches downward and clipping it [14, 15]. extended or combined with other open or
endoscopic approaches for tumour removal. of tragus coursing superiorly and then anteri-
Being a lateral vector, this approach is not orly in the frontal scalp to end superior to the
suited for lesion crossing midline to other supraorbital notch near the midline. Scalp inci-
sides like contralateral sphenoid sinus and sion is elevated by giving incision in the super-
nasopharynx. Extensive malignant tumour ficial layer of deep temporal fascia to prevent
like squamous cell carcinoma and tumour injury to the frontal branch of facial nerve.
having extensive involvement of ICA or verte- Temporal muscle is incised to gain exposure of
bral artery are deemed inoperable. zygomatic arch and lateral orbital rim in
Surgical Steps
Open approaches to PPF and ITF are many.
Most commonly performed open approaches
are transmaxillary like midface degloving and
maxillary swing approach which works in an
anterior vector (Fig. 7.14), while commonly
performed lateral approaches are preauricular
transzygomatic (Fig. 7.15) approach for ITF
lesions and a preauricular fronto-temporal
orbitozygomatic for ITF lesions having major
intracranial extension.
For a preauricular transzygomatic approach,
a curvilinear incision is made in the preauricu-
lar region staying above the lower attachment Fig. 7.14 Midfacial degloving for left ITF lesion
Fig. 7.15 Preauricular transzygomatic approach. (a) poral extension, (c) flaps elevated, (d) temporal craniot-
MRI is showing dumbbell tumour with ITF involvement omy bone, (e) postoperative CT scan and (f) healed wound
of right side, (b) preauricular incision is marked with tem-
selected cases where zygomatic arch needs Temporomandibular joint dysfunction can
removed and in more advanced case orbitozy- occur due to drilling, leading to varying
gomatic osteotomy is required. Combining this degrees of trismus. Injury to ICA can occur
with pterional craniotomy, middle cranial fossa if vertical petrous carotid is involved by
can be approached. The middle fossa skull base lesion, as this approach does not give
is drilled to expose the V2, V3 and Middle access to gain control over it. Injury to
meningeal artery which can be mobilized or facial nerve and branches can lead to facial
sacrificed combining ITF and middle fossa. nerve palsy [25].
This approach can provide access for tumour Conclusion
removal medially from sphenoid sinus to cav- PPF and ITF have a complex anatomy and
ernous sinus, superiorly from middle cranial contain many neurovascular structures and a
fossa, laterally up to skin mandible and parot- clear understating of this anatomy is impor-
ids, inferiorly till parapharyngeal space and tant for surgery in this area. Medial and
lower neck if skin incision is extended below. medium-size lesions are better suited by
Control of great vessels in the neck can be endoscopic approach while laterally based
taken for lesions involving the petrous ICA. extensive tumours are better suited by open
Complications approach. Both approaches can be combined
Mandibular nerve needs to be sacrificed in selected cases for complete resection of
sometimes leading to hypoesthesia. lesions (Fig. 7.16).
Fig. 7.16 Endoscopic and midfacial degloving approach is used to excise the lesion (pre- and postoperative
radiology)
7.3 art C: Pituitary Tumours

P diabetes insipidus, CSF leak, meningitis and
and Surgical Management visual disturbance among other complications.
The endoscopic endonasal approach is the
Pituitary adenoma is the most common tumour standard surgical approach for pituitary tumours;
of the sellar region (90–95%). The adenomas hence, it will be discussed in detail in this chap-
constitute 10–15% of all intracranial tumours ter. Transcranial approaches are mentioned in
[26]. The preoperative assessment, indication Part E (Sect. 7.5).
of surgery, selection of approach and postop-
erative care are jointly done by neurosurgeon,
otolaryngologist, neuro-radiologist, endocri- 7.3.1 Anatomy
nologist and neuro-anaesthetist for a better
patient outcome [27]. The presenting symp- The pituitary gland is projected from inferior part
toms are based on the type of adenoma. Except of the hypothalamus and it maintains the func-
prolactinoma, surgery remains the treatment of tional connections via the infundibulum (pituitary
choice. The endoscopic transnasal trans-sphe- stalk). The gland has an anterior lobe called adeno-
noidal approach is the gold standard due to the hypophysis derived from the ectoderm of Rathke's
panoramic view, preservation of normal func- pouch and a posterior lobe called neurohypophysis
tion and reduced hospital stay. The use of derived from neuroectoderm prosencephalon. The
newer technologies like plasma ablation pro- intermediate lobe is rudimentary in humans and
vides a relatively bloodless field. An expertise degenerates after birth. The gland resides in the
in endoscopic techniques and the ability to use sella turcica and is covered by diaphragmatic sella
angled endoscopes is required. Detailed ana- (dural fold). Laterally it is bound by cavernous
tomical knowledge is the prerequisite as the sinus and its contents (ICA, CN III, IV, V1,V2 VI)
margin of error is very less. During postopera- and anterior and inferiorly by the sphenoid sinus
tive monitoring in ICU, one should look out for (Fig. 7.17).
Fig. 7.17 Anatomical
location and relations of
pituitary gland (1)
pituitary gland, (2) ICA
(cavernous part), (3)
cavernous sinus, (4)
oculomotor nerve (III),
(5) trochlear nerve (IV),
(6) ophthalmic nerve
(V1), (7) abducent nerve
(VI), (8) maxillary nerve
(V2), (9) optic chiasm,
(10) sphenoid sinus, (11)
ICA (clinoidal part),
(12) posterior
communicating artery
7.3.2 Physiology common clinical features include head-

ache, visual disturbance, features of
Anterior pituitary secrets the hormones under hypopituitarism and hydrocephalus.
the influence of the hypothalamus. The main Indication of surgery in these patients is
hormones are growth hormone (GH), adreno- to relieve and to prevent the mass effect
corticotrophic hormone (ACTH), thyroid-stim- of the tumour and pituitary apoplexy
ulating hormone (TSH), prolactin (PRL), [31]. As far as treatment is concerned,
gonadotropins (Luteinising hormone, LH and surgery remains the mainstay with radio-
Follicular-stimulating hormone, FSH). Posterior therapy in recurrent and invasive cases.
pituitary secrets oxytocin and vasopressin Functional Pituitary Adenoma
2.
(Figs. 7.18 and 7.19). The types of pituitary function adenoma
The list of pituitary tumours is long and dif- are based on the hormone secreted by
ferential diagnosis of sellar lesions is listed in adenoma.
Table 7.1. (i) Prolactinoma
(A) Pituitary Adenoma This is the most common type
It is the most common type of pituitary (40%) of functional adenoma [28]
lesion. The classification of adenoma is with clinical features depending
based on the size of the tumour and immu- upon the gender. Females present as
nohistochemical expression (Table 7.2) secondary oligomenorrhoea and/or
[28]. The incidence of incidentalomas is galactorrhoea whereas males pres-
10% [29, 30]. ent with galactorrhoea, impotence,
1. Non-functional Pituitary Adenoma headache and visual disturbance.
No hormone is secreted and symptoms This tumour is unique because the
are usually due to pressure effects. The medical treatment is the mainstay in
more than 90% of the patients and
includes dopamine agonists like
bromocriptine and cabergoline.
Surgical management, although
rarely required, has specific indica-
tions like failure of medical treat-
ment, patient preference, pituitary
apoplexy, CSF leak during medical
therapy [32] and pregnancy-related
issues [33].
(ii) Acromegaly
These are the growth hormone-
secreting tumours and about 10% of
these tumours occur before adult-
hood and lead to gigantism. Clinical
features include enlarged nose,
chin, hands and feet and endocrine
abnormalities include increased
GH, insulin-like growth factor (IGF
Fig. 7.18 Blood supply—Hypothalamic—Pituitary axis I) levels in serum. The morbidity
(1) anterior pituitary, (2) posterior pituitary, (3) superior and mortality in this subset of
hypophyseal artery, (4) inferior hypophyseal artery, (5) tumours is related to cardiovascular
third ventricle, (6) neuroendocrine nuclei, (7) hypothala-
mus, (8) long portal vessels, (9) short portal vessels and
complications. As far as the treat-
(10) hormone release ment is concerned, surgery remains
CRH TSH GnRH SRIF DOPAMIN

GHRH
HYPOTHLAMUS
ADH
KIDNEY
PITUTARY
WATER
RESOPTION
OXYTOCIN
ACTH TSH LH FSH PRL GH
OTHER
ADRENAL THYROID TESTES OVARY BREAST LIVER
ORGANS
CORTISOL
LACTATION LINEAR
T3,T4
GROWTH
TESTOSTERONE
INHIBIN PROGESTERONE IGF-1
ESTRADIOL
INHIBIN
Fig. 7.19 Hypothalamic pituitary axis—regulation of hormone secretion
Table 7.1 Differential diagnosis of sellar lesions Table 7.2 Classification of pituitary adenoma
Tumours Pituitary adenoma Based on size Based on character
Craniopharyngioma Microadenoma Non-functional
Meningioma (<1 cm) Clinically no function
Glioma • Enclosed (hypopituitarism due to pressure)
Chordoma • Invasive
Lymphoma Macroadenoma Functional
Metastasis (>1 cm) • Prolactinoma (Prolactin)
Cyst Rathke’s cyst • Enclosed • Acromegaly (GH)
Dermoid cyst • Invasive • Cushing disease (ACTH)
Inflammatory Bacterial Abscess • Expanding • Gonadotropin-producing
conditions Tuberculosis adenoma (LH, FSH)
Sarcoidosis • Thyrotropin-producing
Langerhans cell adenoma (TSH)
histiocytosis • Mixed (GH with PRL)
Hypophysitis Mesoadenoma
Others Pituitary apoplexy (1 cm)
Hypothalamus hamartoma
ICA aneurysms
the mainstay with medical manage- Preoperative Work-Up

ment aiming at correcting the hor- Apart from relevant history, e.g. nasal surgery
monal abnormalities. The medical and co-morbid conditions, one should look
agents include somatostatin ana- for features of various endocrine conditions
logue, dopamine agonist and GH like Cushing, acromegaly, hyperthyroidism
receptor antagonist. Radiotherapy is and hypopituitarism. Special examination
reserved for invasive and recurrent includes ophthalmological work-up (visual
cases [34]. acuity, visual field and proptosis evaluation),
(iii) Cushing Disease neurologic examination (e.g. cranial III, IV, V
These tumours are usually ACTH- and VI), endocrine assessment (hormonal
secreting microadenoma and have assessment and electrolyte evaluation), nasal
pronounced clinical features usually endoscopic examination—to look for abnor-
secondary to endocrine disturbances. mal anatomy and adequacy for nasal septal
These include truncal obesity, hyper- flap. Imaging studies include delayed post-
tension, hirsutism, glycosuria, osteo- contrast MRI, which is the modality of
porosis and psychosis. Surgery choice. MRI helps in determining the extent
remains the mainstay of treatment of tumour, cavernous sinus involvement, ICA
with medical therapy aiming to cor- involvement (signal void in T2 MRI), identi-
rect the endocrine imbalances. In fication of normal pituitary gland (neurohy-
rare cases, radiotherapy and bilateral pophysis shows increased signal intensity in
adrenalectomy have also been used T1 non-contrast) and optic chiasm. CT para-
[35]. nasal sinus must also be done as it helps in
(iv) Gonadotropin-Secreting Adenoma surgical planning, anatomical study (sinuses,
These are LH- and FSH-secreting skull base, optic nerve, Onodi cell) and also
tumours and their symptoms are helps in differential diagnosis (calcification in
usually due to mass effects; hence, craniopharyngioma).
surgery is the main choice of Aims and Principles of Pituitary Surgery
treatment. They include elimination of mass effect, res-
(v) Thyrotropin-Secreting Tumours toration of pituitary function, prevention of
These tumours secrete TSH and recurrence, complete histopathological
patients usually present with central diagnosis, and if possible, normalization of
hyperthyroidism features (palpita- hormonal production.
tion, tremors, neck swelling, weight Operative Procedure
loss, sweating, etc.). Treatment is (i) Anaesthesia
medical with somatostatin analogue General anaesthesia with orotracheal
if compressive effects are not prom- intubation is standard. The anaesthetist
inent; otherwise, surgical removal is requested for hypotensive anaesthe-
of the tumour along with medical sia (Mean Arterial Pressure between 60
therapy must be taken into and 80 mmHg, Heart rate less than 70)
consideration. in order to get a clean surgical field and
(B) Pituitary Apoplexy minimize the blood loss.
It is the sudden pituitary haemorrhage or The patient is placed in a supine
haemorrhage in adenomas and usually pres- position with 30° head up (reverse
ents with dramatic clinical features like sud- Trendelenburg position) and ceftriax-
den visual loss, headache and vomiting. one 2 g I.V. or clindamycin 600 mg IV/
Treatment is surgical removal of the tumour vancomycin 1 g iv in cases of beta-lac-
with evacuation of haematoma in order to tam allergy, is injected before starting
relieve the pressure. the surgery.
(ii) Instruments and Equipment expose it. If a Hadad flap is planned,

A three-chip or preferably HD camera then it has to be harvested before the
with a large LED monitor of 20 inches septectomy is done.
or larger (easier on the eyes) is required • Septal phase: Using the plasma
for visualizing the structures clearly. A ablation, the mucosa around the
complete Functional Endoscopic Sinus ostia and the nasal septum is ablated
Surgery set with various sized straight away and steps are repeated on the
and angled up-cut and down-cut ron- opposite side. Septectomy is per-
geurs along with high-speed drill is formed and the sphenoidal phase of
essential. Among the optional instru- surgery is started.
ments are microdebrider, plasma abla- • Sphenoidal phase: Sphenoid ostias are
tion and doppler for identification of widened on both sides using a rongeur
para-sellar carotid artery. Neuro- and the keel of sphenoid drilled away
navigation, if available, is recom- using a high-speed cutting burr. Any
mended in cases of extensive tumour bleeding from the bone is taken care of
with distorted anatomy or revision sur- with a diamond burr (Figs. 7.20 and
gery to identify the landmarks. 7.21). With the sphenoid sinus wide
Surgical Approaches
(iii) open, the mucosa from the sinus is ele-
The surgical approaches can be either vated and removed completely. After
transseptal, trans-ethmoidal or transna- this, the intersinus septum is drilled
sal [36–38]. Endoscopic transnasal away or cut with a through-cut. The
trans-sphenoidal approach is usually bone over the sella is drilled using a dia-
considered the standard approach for mond burr; if the bone is thick, a cutting
pituitary surgery because of the follow- burr is used. The thin bone is then taken
ing advantages: good panoramic view, away with a rongeur and the dura is
preservation of normal function, exposed.
reduced hospital stays and improved • Sellar phase: Using the coagulation
patient outcome. The surgery can be mode of the plasma ablator, the dura
divided into the following steps:
• Position: The surgery is started with
the proper positioning of the patient.
We use a reverse Trendelenburg
position.
• Nasal phase: Nasal cavity is decon-
gested with commercially available
sponges or by cotton pledgets
soaked in 1:10,000 Adrenaline. The
surgical corridor used is the space
between the middle turbinate and
nasal septum. Inferior turbinate is
out fractured to create space (not
always needed), the Middle turbi-
nate is lateralized and the superior
turbinate is identified and gently lat-
eralized to reveal the natural sphe-
noid ostia. Many times the sphenoid
ostia is oedematous and not clearly Fig. 7.20 Sphenoid ostia identified and area being
visible, decongestion usually will plasma ablated
is coagulated and at this point, it 7.3.3 Postoperative Care

becomes a four-hand technique with
the neurosurgeon joining the surgery. The choice of antibiotics and analgesics is
• Neurosurgical removal of tumour: depending upon the institution’s preference. The
An incision is made over the dura and patient should spend his first 24–48 h in an ICU
using saline, hydro- dissection is with physicians experienced in monitoring
done. If the tumour is soft and suck- important signs like CSF leak, visual disturbance,
able, a major part of it just bulges out nasal bleed, etc. The ICU team should be able to
with hydro- dissection. Biopsy is manage possible conditions like diabetes insipi-
taken and using curettes and suction, dus and meningitis. Routine advise includes bed
the neurosurgeon clears the tumour. rest, head-end elevation and stool softener along
Suprasellar and lateral extensions with copious saline drops to prevent crusting.
require angled endoscopes (30° or The patient should be advised strict follow-up to
45°). After ensuring complete tumour prevent crusting.
removal and examination of the sella,
the defect is repaired.
• Reconstruction of the defect: The 7.3.4 Pearls of Pituitary Surgery
fat is wrapped in oxidized cellulose
polymer. We have found that this Superior turbinate, superior margin of choana are
makes it easier to manipulate the key landmarks for sphenoidal ostium identifica-
fat. A fascia lata graft is used by tion. Adequate removal of the anterior wall of
overlay, underlay or interlay fash- sphenoid is essential for good visualization of
ion and fibrin glue is applied over sella. Recognition of medial and lateral optico-
it. A small piece of gel foam is then carotid recesses are important. The need for vascu-
applied over the glue. No nasal larized nasoseptal flap is to be considered prior to
packs are used. Readers can access sphenoidotomy. The drilling of tuberculum and
the author’s surgical video via the planum is considered in suprasellar extension. The
following link: https://youtu. delineation of carotid in cavernous sinus extension
be/L-YEssDFGGQ is important and attention to superior and inferior
inter-cavernous sinus is important.
7.4 art D: Open Techniques

P
for Nose and Paranasal
Sinuses
The surgical approaches for the nose and parana-

sal sinuses range from endoscopic to conven-
tional open techniques. The contemporary
indications for endoscopic approaches to the
paranasal sinuses and skull base have been
expanded making conventional open techniques
less frequent [39]. Absolute indications necessi-
tating either a transfacial or a transpalatal inci-
sion include skin and subcutaneous tissue
invasion, extensive involvement of the orbital fat,
Fig. 7.21 Owls eye appearance, the ostia have been wid- extraocular muscles and eyelid skin and palatal
ened and septectomy done involvement. Traditionally, intracranial exten-
sion, cavernous sinus involvement [40] and this chapter is on neoplastic disease (benign or
extension beyond the mid-pupillary line were malignant), the indications for open approaches
considered to preclude endoscopic approaches. may be listed as the following:
With advancements in neuro-navigation and
endoscopic surgical armamentarium, properly • Lesion extending beyond mid-pupillary line
selected cases with the above-mentioned disease • Skin involvement
extension can be dealt without resorting to con- • Extensive involvement of orbital fat, extraocu-
ventional open approaches. Open approaches in lar muscles and skin of the eyelid
this chapter have been classified into bone and • Involvement of the bone of the hard palate or
soft tissue approaches. Soft tissue approaches paranasal sinuses
and incisions like the Moure’s incision with lat- • Significant intracranial extension
eral rhinotomy also serve as a precursor for bony
approaches like the medial maxillectomy. Bony
approaches can further be classified into midline, 7.4.2 Relative Contraindications
paramedian and lateral approaches based on the for Surgical Resection
trajectory to the skull base. Strictly midline of Nose/Paranasal Sinus
approaches include transpalatal, lateral rhinot- Tumours
omy, medial maxillectomy and Le Fort’s
Osteotomy approach. Paramedian approaches Surgical resection with open technique with or
additionally target the infratemporal fossa with without endoscopic guidance can be attempted
the maxillary swing being the best example. but resection may not offer oncological clearance
Lateral approach to the paranasal sinus and the of the disease [41]:
skull base as in the case of a preauricular subtem-
poral approach provides excellent visualization • Orbital apex involvement
of the lateral part of the infratemporal fossa, • Infratemporal fossa involvement
para-sellar, cavernous sinus and lesions located • Erosion of pterygoid plates
lateral to the cavernous internal carotid artery. • Cavernous sinus involvement
Craniofacial resection pertains to a combination • Intradural/brain parenchymal involvement
of transfacial or transpalatal approach to the para- • Involvement of nasopharynx and sphenoid
nasal sinus and a bicoronal incision with frontal sinus
craniotomy for the intracranial component. • Cranial nerve involvement other than I, II and
Choosing the best approach requires detailed pre- infraorbital nerve
operative radiological assessment and an under- • Encasement of internal carotid artery
standing of tumour biology.
Tumour extension to the above-mentioned
sites are technically resectable. Resection can be
7.4.1 Indications for Open attempted in case of benign tumours like naso-
Approaches pharyngeal angiofibroma and inverted papilloma,
and similarly, low-grade sinonasal malignancies
These vary for inflammatory disease and for neo- like olfactory neuroblastoma (Hyams grade 1 and
plastic disease. For inflammatory disease, mere 2), epithelial–myoepithelial carcinoma, bipheno-
drainage of sinus contents and partial removal of typic sinonasal sarcoma and adenoid cystic carci-
polypoid mucosa is appropriate and the contrain- noma [42]. It is to be noted that although adenoid
dications to endoscopic approaches are few. cystic carcinoma is a high-grade malignancy, it
Frontal sinus disease extending beyond the mid- has a protracted course with disease recurrence
pupillary line can however be a relative contrain- and metastasis occurring after as long as 10 years,
dication as it can be inaccessible even with the justifying the radical resection. Moreover, many
modified Lothrop technique. The prime focus of of these tumours are relatively non-responsive to
radiation or chemotherapy. Therefore, radical biopsy should be avoided as this may lead to
surgical excision followed by adjuvant therapy tumour seeding in the biopsy tract.
offers the best chance of cure [43, 44]. • Preoperative digital subtraction angiography
with or without embolization can be consid-
ered for vascular lesions (angiofibroma,
7.4.3 Preoperative Work-Up hemangiopericytoma and vasoformative
tumours). This is also indicated in cases where
Before embarking on the surgical aspects of radiology shows encasement, narrowing or
treating sinonasal tumours, detailed preoperative irregularity of the internal carotid artery.
evaluation is of paramount importance. This Information gathered from DSA and cerebral
broadly includes radiologically mapping the cross-circulation will guide the management
tumour followed by biopsy from representative of carotid artery involvement.
areas and screening for distant metastasis in case
of malignant tumours:
• Contrast-enhanced computed tomography 7.4.4 Classification of Approaches
(CECT) should preferably be high-resolu- to Nose and PNS
tion 1 mm cuts in the axial, coronal and sagit-
tal planes. This provides information with 1. Soft Tissue Approaches (Surgical Incisions
regard to bony involvement, intraorbital Pertaining to the Nose and PNS) (Fig. 7.22)
extension, skull base erosion, major vessel • Moure’s Lateral Rhinotomy Incision
encasement. • Modified Moure’s incision.
• MRI provides information complimentary to • Weber–Ferguson incision.
that of CECT with better soft tissue delinea- • Modified Weber–Ferguson incision.
tion. Hyperintense signal in any of the para- • Lynch–Howarth extension to Moure’s
nasal sinuses on T2 will differentiate incision.
accumulated secretions from tumour. Invasion • Weber–Ferguson with subcilliary
of periorbita can be identified on T1-weighted Dieffenbach Extension.
contrast sequences. Fat suppression allows • Midfacial degloving.
one to establish orbital fat involvement. This • *Classical Moure’s and Weber–Ferguson
facilitates preoperative decision-making with incisions provide excellent exposure but a
regard to management of the orbit. Perineural facial scar. Modifications were introduced
invasion can be inferred from a widened or to incorporate the concept of nasal and
destroyed of neural foramina on a CT scan. facial aesthetic subunits.
This can be confirmed on fat-suppressed • *Lip-split in a Weber–Ferguson incision
contrast-enhanced T1-weighted sequences as can be avoided in case of small tumours of
enhancement along the course of the nerve or the lateral wall of the nasal cavity.
atrophy of the muscles seen as hyperintensity 2. Bony Approaches:
on T2-weighted sequences. MRI provides • Maxillary swing
detailed information with regard to the extent • Le Fort I osteotomy
of intracranial invasion. Extensive intraparen- • Transpalatal Approach
chymal invasion with surrounding oedema • Denker’s Approach
usually precludes curative-intent treatment. • Facial Translocation
• Histopathological information is obtained by
means of an endoscopic biopsy. Radiology
should precede biopsy as this helps to under- 7.4.5 Soft Tissue Approaches
take a directed biopsy, and also the tissue
oedema consequent to a biopsy may lead to 1. Moure’s Lateral Rhinotomy incision is use-
overestimation of tumour extent if radiology ful for excision of tumours located in the
is undertaken after. Open biopsy or sublabial nasal cavity, maxillary sinus, ethmoid sinus
a b
Fig. 7.22 Surgical incisions pertaining to the nose and modified lateral rhinotomy, Weber–Ferguson–Longmire
PNS. (a) Weber–Ferguson–Longmire incision, (b) lateral with subcilliary Dieffenbach Extension (Courtesy—Dr.
rhinotomy, lateral rhinotomy with lip splitting incision, Harsha Yadav, JR, ENT, AIIMS, New Delhi, India)
and orbit. Lynch–Howarth extension is help- process. Entry into the nasal cavity is facili-
ful to access the frontal sinus. Weber– tated by the use of a Kerrison rongeur to
Ferguson with or without lip-split provides remove the bone at the naso maxillary suture
access to the lateral extension of the tumour line. Soft tissue connecting the nasal mucosa
to the pterygopalatine fossa or the infratem- to the vestibule can be divided at the pyriform
poral fossa. Soft tissue approaches can be aperture to complete exposure.
part of more extensive procedures like Complications:
medial maxillectomy, orbital exenteration • Bleeding and haematoma can occur from
and craniofacial resection the external carotid system, mainly the
Limitations internal maxillary artery. This complication
The lateral rhinotomy approach is best suited can be minimized by either preoperative
for midline tumours with minimal parame- embolization or by identifying and ligating
dian extension. Therefore, exposure to the the internal maxillary artery preemptively.
contralateral side or infratemporal fossa • Suture line dehiscence can occur especially
extension form an important limitation of this if acute angulations are created while
approach. designing the incision. One should always
Technique place incisions on a bony framework espe-
After making the incision, the flap is elevated cially near the medial canthus.
in a subperiosteal plane. Close to the orbit, the 2. Midfacial Degloving (Figs. 7.14 and 7.23)
flap is elevated superficial to the orbicularis This approach provides excellent exposure
oculi muscle. This is done to prevent ectro- without the need for a facial incision. With
pion. Lateral limit of dissection for Moure’s regard to the indications, it serves as an alterna-
Lateral Rhinotomy approach is the infraor- tive to the lateral rhinotomy. Additionally,
bital foramen and the nerve. Modifications tumours crossing the midline can also be
can be made to this step to include skin or approached. This technique can only be
subcutaneous tissue if involved by the disease extended to lesions situated inferior to the infra-
Indications
Tumour extending to the following anatomical
sites can be accessed using maxillary swing:
• Nasopharynx
• Infratemporal fossa
• Sphenoid sinus
• Pterygoid plates
• Cavernous sinus, clivus and foramen
magnum
Limitations
This approach is ideally suited for midline and
paramedian lesions. Therefore, one should not
consider maxillary swing in case of tumour
extension posterior to the carotid artery or
extension to the contralateral skull base.
Technique
The soft tissue approach can either be a
Weber–Ferguson or a midfacial degloving.
Fig. 7.23 Midfacial degloving (Courtesy—Dr. Harsha One should be careful in not elevating beyond
Yadav (JR (ENT), AIIMS, New Delhi) what is required to place the osteotomies to
prevent devascularization of the osteoplastic
orbital foramen. Moreover, skin and orbital flap. Preplating is performed at the following
invasion are not suitable for this technique. sites of osteotomy:
Technique • Frontal process of maxilla extending from
Midfacial degloving entails elevation of the the pyriform aperture to the inferior orbital
midface in a subperiosteal plane. To accom- fissure
plish this, a sublabial incision is made from • Zygomatic process of the maxilla to the
one maxillary tuberosity to the other. To inferior orbital fissure
elevate the cartilaginous external nasal Palatal incision is the modified Owen’s
framework off the pyriform aperture, a com- incision placed close to the alveolar process.
plete transfixion incision and an intercarti- Mucoperiosteal flap is elevated based on the
laginous incision is made. Once the vestibule contralateral greater palatine artery. Midline
is freed from the pyriform aperture, the flap osteotomy is performed over the hard palate.
elevation is completed till the infraorbital The last osteotomy is placed between the
foramen. maxillary tuberosity and the attachment of
Complications the pterygoid plates using a curved osteo-
A complication unique to this approach is tome. After completion of the osteotomies,
vestibular stenosis. the entire maxilla with the overlying skin and
soft tissue can be swung laterally exposing
the pterygomaxillary fissure and the infra-
7.4.6 Bony Approaches temporal fossa.
Complications
1. Maxillary Swing (Fig. 7.24, Fig. 6.16 (Chap. 6)) • Palatal fistula: This complication can be
Displacing the maxilla anteriorly as an osteo- minimized by avoiding the superimposi-
plastic flap with the overlying skin and soft tion of the mucosal and the hard palatal
tissue based on the greater palatine artery incision. One way to go about this is the
exposes the skull base posterior to the poste- modified Owen’s incision and placement
rior wall of the maxilla. of a palatal prosthesis to keep the muco-
a b
Infra temporal fossa
contents
Maxilla left
side
Fig. 7.24 Left maxillary swing. (a) Miniplates are fixed Delhi, India), (b) Maxilla swung on left side which allows
at the site of osteotomies (Courtesy—Dr. Kuldeep Thakur, exposure of infratemporal fossa contents (Courtesy—Dr.
MCh student (Head and Neck cancer), AIIMS, New Harsha Yadav (JR (ENT), AIIMS, New Delhi)
Fig. 7.25 Le Fort I Osteotomy (Courtesy—Dr. Harsha Yadav (JR (ENT), AIIMS, New Delhi)
periosteal flap in close proximity to the Le Fort I fracture displacing the palate
bone. inferiorly.
• Dental malocclusion: Preplating prior to Indications
osteotomy helps in maintaining postopera- This is a strictly midline approach for selected
tive occlusion. cases of nasopharyngeal angiofibroma, clival
2. Le Fort I Osteotomy (Fig. 7.25) chordoma and nasopharyngeal carcinoma. If
Following a sublabial incision, a transverse combined with medial maxillectomy, it can
facial osteotomy is created along the lines of provide some paramedian extension also.
Limitations Essentially a medial maxillectomy is under-

Exposure anterior to the pituitary and poste- taken via the sublabial route.
rior to the carotid artery is not possible with 5. Preauricular Subtemporal Approach ((Fig.
this approach. 6.17, Chap. 6), Figs. 7.13 and 7.26)
Complication Unlike maxillary swing which provides a
The risk of devascularization of the alveolar direct anterior approach to the infratemporal
ridge leading to palatal necrosis is a potential fossa, preauricular subtemporal offers a lat-
complication. eral approach to the same. It is indicated in
3. Transpalatal Approach case of tumour involvement lateral and poste-
This is another midline approach with the fol- rior to cavernous part of ICA. One can
lowing variants: approach the entire skull base from the naso-
• Palatal Retraction—Retracting the soft pharynx to the petrous apex and clivus with
palate anteriorly provides exposure for minimal brain retraction.
adenoidectomy, biopsy and excision of 6. Facial Translocation Approach
small tumours from the nasopharynx. This approach is based on the concept of
• Palatal Split—Vertical division of the soft “Modular-Disassembly” of facial subunits by
palate allows exposure from the lower Janecka et al. [45]. This means that the face is
third of clivus to C2. Can be used for basi- divided into subunits each with its own neuro-
lar artery aneurysm. vascular supply. It is divided into:
• Palatal Drop—Owen’s inverted U inci- (a) Limited facial translocation
sion is placed on the palate about 1 cm (b) Standard facial translocation
medial to the alveolar ridge, separating the (c) Extended facial translocation
hard and soft palate for choanal atresia and An example of standard facial translocation is
angiofibroma. provided here. To approach the nasopharynx
• Sardana’s Approach—S-shaped incision as well as infratemporal fossa and middle cra-
with three segments, a peroral palatal drop nial fossa, the entire maxilla, lateral orbital
approach (Owen’s incision), an ipsilateral wall and zygoma can be swung laterally as
sublabial incision and a connecting one single unit.
U-shaped incision curving behind the max- 7. Maxillectomy
illary tuberosity and connecting the previ- Maxillectomy can be classified as either total
ous two incisions. Especially indicated for if all six walls are removed or partial if it
tumours extending from the nasopharynx involves preservation of any of the six walls.
to the infratemporal fossa via the pterygo- Examples of partial maxillectomy include:
maxillary fissure. medial maxillectomy, subtotal maxillectomy
Limitation (preserving orbital floor) and palate preserv-
The transpalatal approach and its modification ing maxillectomy. Sometimes orbital exen-
allow excision of midline tumours from the teration is performed along with total
nasopharynx to C2. Exposure anterior to cho- maxillectomy. In this case, the appropriate
ana and sphenoid sinus, lateral to Eustachian term would be a radical maxillectomy.
tube and posterior to foramen magnum and (a) Total maxillectomy (Fig. 7.27)
brainstem are not accessible. Indicated in malignancy arising from the
Complication maxillary sinus, invasive fungal disease
Palatal fistula is a potential complication. causing destruction of the maxillary
4. Denker’s Approach sinus. The soft tissue approach preceding
Trans-naso-maxillary approach—Involves a a maxillectomy can either be a Weber–
large Caldwell–Luc antrostomy through sub- Ferguson incision or a sublabial incision.
labial route followed by removal of lateral It involves excision of the maxillary
nasal wall and frontal process of maxilla. sinus, one half of the hard palate, floor of
the orbit, palatine bone, lateral wall of (iv) Inferolaterally—The maxilla is sep-
nose and the inferior turbinate. The fol- arated from the pterygoid plates.
lowing osteotomies are performed to • May be accompanied by eth-
mobilize the maxilla: moidectomy or sphenoidotomy
(i) Superomedially—Nasal process of (b) Partial Maxillectomy: Medial maxillec-
maxilla. tomy: with or without ethmoidectomy.
(ii) Superolaterally—Between maxilla Involves resection of medial wall of max-
and zygomatic arch. illary sinus from the floor of orbit to floor
(iii) Inferiorly—Between lateral incisor of nasal cavity. The most common nasal
and canine till midline of palate. pathology where this is indicated is
inverted papilloma.
Osteotomies:
(i) Supromedially—From pyriform
aperture towards inferior orbital fis-
sure, inferiorly and parallel to
fronto-ethmoidal suture line
(ii) Laterally—Vertically along anterior
wall of maxilla towards inferior
orbital fissure along floor of orbit
(iii) Inferiorly—Above the alveolar arch
(iv) Infero-medially—Parallel to floor of
nasal cavity floor inferior to inferior
turbinate
8. Craniofacial Resection (Fig. 7.28)
Involves resection of intracranial as well as
extra-cranial parts of a sinonasal tumour
Fig. 7.26 Left side marked Preauricular Subtemporal extending to the anterior skull base. Paranasal
Approach sinuses are approached either by a lateral rhi-
Fig. 7.27 Maxillectomy specimen. Cuts are made the same as maxillary swing but anterior soft tissue flap is separated
from underlying bone as showed in Fig. 6.16 of Chap. 6.
a b
Fig. 7.28 Craniofacial resection
notomy or a midfacial degloving. Tumour brain retraction produces significant periop-

may also be approached by a nasal endoscopic erative morbidity.
approach. For the purpose of anterior skull
base exposure, a bifrontal craniotomy is per-
formed using a bicoronal incision. Cheesman 7.5 art E: Open Anterior Skull
P
and Reddy [46] have classified craniofacial Base Approaches:
resection into three types: Indications
• Type I: It is an extended medial maxillec- and Complications
tomy with limited resection of the anterior
part of the skull base without resorting to a The anterior cranial base has an endocranial surface,
craniotomy. which faces the brain, and an exocranial surface,
• Type II: Here the intracranial component is which faces the nasal cavity and sinuses, orbits,
approached through a window craniotomy. pharynx, infratemporal and pterygopalatine fossae,
• Type III: This is the traditional craniofacial and the parapharyngeal and infrapetrosal spaces.
resection where bicoronal incision is made Canals, foramina and fissures through which numer-
followed by bifrontal craniotomy. ous neural and vascular structures passes connect
9. Transbasal Approach both the surfaces. On the endocranial side, the bor-
The difficulties and potential complications der between the anterior and middle cranial bases is
related to a craniofacial resection are miti- the sphenoid ridge joined medially by the chiasmatic
gated to a certain extent by the transbasal sulcus. On the exocranium side, the anterior and
approach. The soft tissue approach can be middle cranial bases are divided at the level of a
either a bicoronal incision or a brow incision transverse line extending through the pterygomaxil-
or a spectacle incision. Instead of performing lary fissures and the pterygopalatine fossae at the
a bifrontal craniotomy, the frontonasal unit is upper level and the posterior edge of the alveolar
elevated as a free bone flap. The advantages in process of the maxilla at a lower level. Medially, this
doing so are limited brain retraction while corresponds to the anterior part of the attachment of
approaching lesions, extending posteriorly the vomer to the sphenoid bone.
towards the clivus. If approached through tra- The pathological conditions affecting the
ditional craniofacial resection, the resulting anterior cranial base are highly heterogeneous
groups. They can be classified according to the imaging (MRI) with contrast scan. The diagnostic
site of tumour origin as described below: cerebral angiography (DSA) is indicated in
selected cases to obtain information regarding vas-
1. Basal neurovascular structures and cularity of the lesion and possible involvement of
meninges surrounding major neurovascular bundle. Elective
• Meningiomas: Olfactory groove, Planum preoperative angiographic embolization is advised
Sphenoidale, Tuberculum sella in highly vascular cases to reduce intraoperative
• Schwannomas blood loss. Quantitative assessment of visual acu-
• Pituitary adenoma ity and visual field charting is required to docu-
• Craniopharyngiomas ment the preoperative status of vision. Endocrine
• Paraganglioma work-up is for tumours extending to the sellar/
• Hemangiopericytoma suprasellar region. The approaches for anterior
2. Cranial base skull base are tabulated in Fig. 7.29 [47, 48].
• Chordoma Transcranial approaches indicated for lesions
• Chondrosarcoma restricted to the intracranial compartment. They
• Osteosarcoma are divided into anterior and anterolateral
• Plasmacytoma approaches depending upon the tumour exten-
• Metastasis sions [49–51]:
3. Subcranial with upward extension
• Sinonasal carcinomas 1. Anterior:
• Olfactory neuroblastoma • Bifrontal craniotomy
• Juvenile angiofibroma • Unifrontal craniotomy
• Nasopharyngeal carcinoma • Transbasal craniotomy
• Adenoid cystic carcinoma Anterior craniotomy approaches are indi-
• Primary sarcomas cated for midline lesions like meningiomas of
olfactory groove, planum sphenoidale, tubercu-
Anosmia, frontal lobe dysfunction, increased lum sella, esthesioneuroblastomas without lat-
intracranial pressure, nasal obstruction, CSF rhi- eral extensions. Large midline lesions are
norrhoea, epistaxis, visual changes and endocrine approached using bifrontal craniotomy whereas
dysfunction are the list of symptoms with intra- small lesions can be approached using either
cranial connection of mass lesion of the nose and unifrontal/bifrontal craniotomy. The incision is
paranasal sinuses. bicoronal or unilateral frontal curvilinear inci-
sion. Following the incision, a bifrontal (large
lesions) or unifrontal (small lesions) craniotomy
7.5.1 Diagnostic Work-Up is performed. Dura is opened based on superior
sagittal sinus (SSS) and the sinus ligated and
The clinical examination is focused on complete cut. Sinus ligation is done in large lesions
evaluation with special attention to the head and involving the cribriform plate. Smaller lesions
neck region. Supplemental information regarding may not require sinus ligation (Fig. 7.30).
the extent of the tumour can be obtained by oph- 2. Anterolateral—Five types of anterolateral
thalmoscopy, indirect laryngoscopy or flexible approaches are described:
fibreoptic nasopharyngoscopy. The imaging bat- (a) Fronto-orbital
tery includes contrast-enhancing computerized (b) Fronto-temporal craniotomy
tomography (CECT) scan, magnetic resonance (c) Pterional craniotomy (Frontosphenotemporal)
• Lateral rhinotomy
• Weber-Ferguson
• Lynch incision
• Dieffenbach incision
Transfacial • Subciliary/Midcilary
• Midfacial degloving
(MFD)
Subcranial
Craniofacial Bifrontal craniotomy with subfrontal approach

• Unilateral frontal craniotomy with subfrontal
approach
• Pterionalapproach
Approaches Transcranial
• Fronto-orbital approach
to Anterior
• Frontotemporal-orbitozygomatic (FTOZ)
Skull Base
approach
Lesions
Subcranialor craniofacial with ipsilateral /bilateral partial

maxillectomy (Extension to Medial or superior maxillary walls
and periorbita)
• Subcranial–MFD (Benign tumours extending to the maxillary
sinus compartment ±Pterygopalatine fossa or nasopharynx)
• Craniofacial with Weber-Fergusson incision (Malignant
tumours extending to the inferior/ anterior/lateral/posterior
Combined maxillary walls)
Approaches • Subcranialor craniofacial with pterional (Extension to the
lateral skull base, cavernous sinus, middle fossa or
Infratemporal fossa)
• Subcranial-LeFortI (Extension to the lower clival region)
• Subcranialor transcranial with transorbital (Orbital apex or
intraorbitalextension)
• Transcranial-transfacial-transorbital (for Malignant tumours
extending to the maxillary sinus with intra-orbital extension)
Fig. 7.29 Approaches to anterior skull base
(d) Fronto-temporo-orbito-zygomatic suprasellar and para-sellar lesions. FTOZ is an

(FTOZ): An extension of pterional extension of the pterional craniotomy with
craniotomy additional removal of orbit and zygomatic
(e) Supraorbital keyhole craniotomy bones (Fig. 7.31). FTOZ is useful for lesions
Fronto-orbital is useful for lesions with orbital involving cavernous sinus and suprasellar
extensions. Fronto-temporal craniotomy is lesions reaching up to the third ventricle.
used for lesions with lateral and middle cra- Supraorbital keyhole is the mini frontolat-
nial fossa extensions. Pterional craniotomy is eral craniotomy (Fig. 7.32). It starts with an
the workhorse of neurosurgery as most of the eyebrow incision and it is cosmetically accept-
lesions can be approached with this able, includes frontal-orbital and part of the
craniotomy. zygomatic process. The indications are ante-
It is for midline lesions of anterior as well as rior skull base lesions, sellar suprasellar
middle fossa lesions like meningiomas, sellar/ lesions and aneurysms of anterior circulation.
a b
c d
Fig. 7.30 Stepwise demonstration of transbasal otomy with intact bilateral superior orbital walls and
approach: (a) Bicoronal skin incision and elevation of nasion, (d) Exposed bifrontal dura, spatula in midline
subgaleal flap separately for skull base carpeting later, (b) over SSS, bilateral orbit (Star), bilateral frontal sinus and
Burr holes on either side of SSS, (c) Single-piece crani- ethmoids (Donut) along with nasion
It is contraindicated in well-pneumatized are direct exposure of the anterior skull base from
frontal sinus and lesions involving cribriform anterior to posterior, allows simultaneous intra-
plate (relative contraindication). dural and extradural tumour removal from ante-
rior to posterior, does not require facial incisions
and minimal frontal lobe manipulation. The dis-
7.5.2 The Subcranial Approach advantage of this approach is osteonecrosis,
especially following radiotherapy (RT).
It is a single-stage procedure used for tumours
involving the anterior skull base [52, 53]. It
involves coronal incision and osteotomy of the 7.5.3 Reconstruction
naso-fronto-orbital bone segment. It allows
access to the intra- and extra-cranial compart- The aim is to create watertight dural closure and
ments of the anterior skull base. The advantages secure barrier between the nasal cavity and the
Fig. 7.31 Stepwise demonstration of FTOZ craniotomy. along the superior temporal line, (d) Single-piece crani-
(a) Positioning with malar eminence as the highest point, otomy with the temporalis muscle cuff, (e) Exposed orbit
(b) Curvilinear hairline incision, (c) Fronto-temporo (Star) and the fronto-temporal dura, (f) Bone fixed with
zygomatic bony exposure with cuff of muscle left attached miniplates and screws
Fig. 7.32 (a) Eyebrow incision shown as red, (b) eleva- dura, (E) after dural opening using suction and scissors
tion of periosteal flap (star) separately, suction pointing on and suction as dynamic retractors resting on the basifron-
the supraorbital frontal bone, (c) fashioning the craniot- tal lobe covered with cotton (star) and basal dura of ante-
omy (2.5 × 2.5 cms) using the footplate drill, (d) exposed rior cranial base (yellow asterisk)
cranial cavity. It can be done by curetting of turbinate’s anterior attachment and is lateral to
mucosa of frontal, ethmoidal and sphenoidal the agger nasi cells. The anterior attachment of
sinus and packed with fat. The dura defects the uncinate process is regarded as the posterior
should be closed primarily with sutures or with a limit of bone removal. The lacrimal sac and
fascial graft. Basal repair performed by placing a nasolacrimal duct slopes down backward and
pedicled galea aponeurotica-pericranial-frontalis inward. Chronic dacryocystitis is more com-
muscle flap based on the supraorbital–supra- mon in females than males because of the nar-
trochlear vessels along the anterior cranial fossa row nasolacrimal duct in women. On blinking
base (Fig. 7.28a). Further posterior reinforce- the orbicularis muscle alternate contraction and
ment of fascia lata graft with temporalis muscle relaxation creates negative pressure in the lacri-
rotation is required to obliterate the dead space. mal sac; this tear pump helps in sucking tears
Bony segments secured in their respective ana- into the sac. Capillary action carries most of the
tomical positions using sutures or miniplates + tears (70%) into the lower punctum and cana-
autologous temporal or frontal bone to reinforce liculus, while the rest is carried through the
the skull base bony reconstruction. Additionally, upper punctum and canaliculus.
musculocutaneous and free flaps based on the As demonstrated on Scintillography, the trans-
pectoralis major and trapezius as well as free fer of fluid from the canaliculi to the sac is an
omental flaps for basal repair. active process, while the flow of tears into the
nasolacrimal duct is the passive process.
7.5.4 Complications
7.6.1 Pathology—Dacryocystitis
Transcranial surgery has a long list of complications
such as cerebral edema, frontal lobe signs (mainly The most common cause is blockage of the naso-
due to retraction)—deficits of speech, memory, lacrimal duct, leading to inflammation of the sac.
cognitive and intellectual function, seizures, CSF It occurs due to:
leak, subdural or extradural haematoma, pneumo-
cephalus, CNS Infections like meningitis and brain • Structural limitation—congenital incomplete
abscess, vascular complications like carotid, ante- canalization (Hasner’s valve), narrow osseous
rior/middle cerebral artery injuries, hormonal dys- nasolacrimal duct, grossly deviated nasal
function and cranial nerve deficits [54]. septum, inferior turbinate hypertrophy, polyp
or tumour.
• Infection from surrounding structures—nasal
7.6 art F: Lacrimal Sac Anatomy
P infection, ethmoidal inflammation, conjunc-
and DCR tival infection, long-standing nasal packs.
• General infection—Influenza, chickenpox.
The lacrimal gland has a tubule-acinar structure
and secretes serous tears in superior fornix. The
secretomotor fibres are from the VII nerve 7.6.2 Preoperative Tests/
through the pterygopalatine ganglion. The lac- Investigations
rimal system starts from the lacrimal puncta
and consists of vertical and horizontal canalic- 1. ROPLAS—“Regurgitation on pressure over
uli (upper and lower), a common canaliculus, the lacrimal sac” area—the positive test indi-
lacrimal sac and nasolacrimal duct. Lacrimal cates the blockage of the nasolacrimal duct
sac is 12–15 mm long, situated in lacrimal fossa (Fig. 7.33).
formed by frontal process of maxilla and lacri- 2. Jones dye test—Fluorescein dye is instilled in
mal bone, anterior to posterior. The superior the eye. The presence of dye in the nasal
border of the lacrimal sac is above the middle cavity in 5 minutes is considered as normal
tivity of CT and MRI can be improved by

injection of contrast (Dacrocystrography). In
dacroscintigraphy, technetium 99 is placed on
the ocular surface. The canaliculi and sac are
visible within 10–15 s. The dye appears in the
nasal cavity after 10–30 min intervals.
Dacroscintigraphy is not useful because of
poor resolution and poor anatomical detailing.
The indications for dacryocystorhinostomy

(DCR) is obstruction of the nasolacrimal duct not
Fig. 7.33 Positive ROPLAS test on right side
responding to conservative treatment (like hot
compresses, massage, probing and intubation) in
functioining lacrimal pump system in the children [57], dacryocystitis with NLD
nasal cavity is considered as normal function- obstruction, mucocele with NLD obstruction,

ing lacrimal pump system [55]. congenital fistula and posttraumatic NLD
(a) Positive primary Jones test—no obstruction with epiphora. DCR can be done by
obstruction. endoscopic or open approach. ENT surgeons are
(b) If dye is not detected in the nose, syring- more familiar with endoscopic DCR. The advan-
ing is done and then fluorescein detected, tages of Endoscopic DCR are scarless surgery,
is labelled positive secondary Jones test, preservation of orbicularis oculi pump mecha-
which signifies functional obstruction in nism. It also allows simultaneous correction of
the nasolacrimal duct. intranasal pathology and results of endoscopic
(c) If no fluorescein is detected in the nose DCR are comparable with external DCR [58].
even after syringing, it is labelled nega- The prerequisite for success endo DCR is correct
tive secondary Jones test, which signifies identification of lacrimal sac and prevention of
stenosis of puncta or canalicular system. restenosis. Pre-existing anatomical variations
3. Probing—4% lignocaine drops are instilled in such as concha bullosa, septal deviation, agger
the eye. The punctum is dilated with nasi cells and lateralization of uncinate process
Nettleship’s punctual dilator and Bowman’s can increase the risk of failure as they require
probe. Soft block indicates a canalicular or more excision of mucosa for exposure. Bony
common canalicular block whereas hard stop window can be mal-positioned or incomplete due
indicates that the probe is in the lacrimal sac to anatomical variations [59].
and is touching the bone.
4. Syringing—the punctum is cannulated with a 7.6.2.1 Surgical Technique
soft cannula and saline is injected. No regurgita- for Endoscopic DCR
tion is considered as normal functioning drain- The key landmark is the ridge formed by the
age system. Canalicular block is considered frontal process of maxilla at the anterior attach-
when the fluid is regurgitated from the same ment of the middle turbinate, anterior to uncinate
punctum. Regurgitation through the opposite process, on the lateral nasal wall [60]. The sac is
punctum is either due to common canalicular located at and anterior to the axilla of middle tur-
blockage or NLD blockage. In NLD blockage binate or maxillary line in around 95% of cases
fluid is mixed with mucoid or purulent secretion. (Fig. 7.34).
In common canalicular blockage, fluid is clear. The flap elevation is started with two separate
5. Radiology—T2-weighted images of MRI is incisions 8 mm above and below the axilla of
helpful in detecting obstruction site exactly middle turbinate or it can be started with a verti-
within nasolacrimal duct and thus planning for cal curved anterior incision given 1 to 1.5 cm to
correct endoscopic procedure [56]. The sensi- the base of uncinate process vertically down till
the anterior end of the middle turbinate than two

horizontal incision (Fig. 7.35).
The overlying mucosa is separated using a
blunt dissector and this strip of mucosa is removed
using a pair of through-cut forceps. The Kerrison’s ML
bone punch is hooked against the posterior part of
the anterior lacrimal crest (Fig. 7.36) and bone
removed working from posterior thin bone to ante-
rior thick bone. A wide bony window is made of
the size of approximately 12–15 mm (Fig. 7.36). MT
Bone can also be removed by drilling, chisel and
hammer or laser. The use of powered instruments
has not shown an added advantage on surgical suc-
cess with cold instruments [61, 62]. Periosteum
and sac wall incised vertically using sickle knife or
12 number blade, pus drained, suction cleaning
done (Fig. 7.36). The whole of the medial wall of
Fig. 7.34 Relationship of sac with maxillary line (ML)
the sac can be removed or anterior-based flap can and anterior end of the middle turbinate (MT) (Courtesy—
be created to minimize mucosal trauma. Nasal Dr. Hitesh Verma, Associate Professor, AIIMS, New
mucosal flap can be joined with posterior wall of Delhi, India)
a b c
d e f
ML
Flap
Fig. 7.35 The surgical steps of flap elevation. (a) local horizontal incision, (f) posterior-based flap. Maxillary line
infiltration, (b) site of upper incision, (c) site of lower (ML) (Courtesy—Dr. Hitesh Verma, Associate Professor,
incision, (d) two horizontal incision lines, (e) joining of AIIMS, New Delhi, India)
a b
c d
Fig. 7.36 (a) Kerrison’s punch is engaged for bone out after puncturing of sac (Courtesy—Dr. Hitesh Verma,
removal, (b) lacrimal sac exposure, (c) sharp instrument is Associate Professor, AIIMS, New Delhi, India)
projected over lacrimal sac, (d) straw colour fluid coming
sac window and anterior-based sac flap can be used by most of the surgeon. Silicon tube stenting
joined with nasal mucosa to reduce the chances of in selected cases [65], covering of exposed bone
granulation formation, scarring and risk of reste- with nasal or lacrimal sac mucosal [66] applica-
nosis. Nasal mucosal flap can be double posterior tion of Mitomycin C [67] are the techniques to
based or bipedicled to cover a major area of prevent restenosis. Silicon tube with metal probes
exposed bone to reduce granulation formation [63, at both ends is placed through upper and lower
64]. Tissue glue can be applied at mucosal junc- punctum and pulled out of the sac into the nose
tion to prevent retraction and separation of approx- and knot tied to secure it. The tube is removed
imated flaps. after 6 weeks by cutting the loop at the medial
Grommet, t sheet, hydrogel, otogenic T tube, canthus. Stenting is indicated when the surgeon
proline and silicone tube are the materials men- is suspecting poor outcomes of surgery like
tioned in literature for stenting. Silicone tube is excessive mucosal trauma, significant flap
d amage, poor anatomy of the sac, revision cases, identified. Periosteum is cut and lacrimal sac is
etc. [68] The meta-analysis showed that silicone lifted from lacrimal fossa. Bony window is cre-
stenting is not affecting the surgical success and ated with burr or chisel hammer and widened
postoperative complications rate [69]. with Kerrison punch. The punctum is cannu-
lated and the sac is tented medially. Sharp scis-
Points to Remember Poor localization of sac, sors are used to create openings and flaps in the
incomplete osteotomy, inadequate opening on medial sac wall and nasal mucosa.
medial wall of sac, significant iatrogenic mucosal Corresponding cut ends of sac wall and mucosa
injury and circumferential cicatrization are the sutured together to create a new pathway for
most common causes of failure [70]. The surgical drainage and wound closed in layers. The
success can be improved by proper tissue han- advantages are direct visualization, the cre-
dling, good flaps approximation with good cavity ation of an adequate bony window and suturing
care (Fig. 7.37). of mucosa. The disadvantages are scar and dis-
ruption of the pump mechanism.
Follow-Up Any nasal pack placed should be
removed after 24–48 h. Medical management is Recent Development
indicated for a week. Look for any regurgitation • Intranasal laser Dacryocystorhinostomy—
from punctum, crusting, granulations, stenosis at KTP-YAG laser helps in precise coagulation
rhinostomy site or displacement of tube at weekly and vaporization of soft tissue, and thus blood
intervals for a month. loss and scarring are minimal.
• Transcanalicular laser-assisted
Surgical Technique of External DCR Dacryocystorhinostomy—The passing of a
A curvilinear skin incision is made at the level laser probe through the upper punctum and
of the medial canthus. Orbicularis oculi muscle canaliculi down the nasolacrimal duct and fir-
is separated and the anterior lacrimal crest is ing the laser to open up the sac wall.
Methylcellulose viscous is used along to dilate
the sac and lubricate the passage of laser fibre.
The advantages are fast technique, laser
passed towards the nose, so no risk of injury to
the eye. The disadvantages are that the mem-
brane formation may occur due to charring
and cause blockage, sump syndrome may not
be addressed, there is a risk of canalicular
injury and success rate is low due to small-
sized window placed at a higher level [71].
• Balloon Dacryoplasty—It is indicated in chil-
dren with failed probing or silicone intuba-
tion. In this, the nasolacrimal duct is dilated in
its distal portion using a balloon catheter
inserted through the upper punctum. The bal-
loon is inflated by injecting water and is
retained for one and a half minutes. After
deflation, it is withdrawn and again inflated
for half a minute at the junction of the lacrimal
sac and nasolacrimal duct.
• Ultrasonic endoscopic dacryocystorhinos-
Fig. 7.37 Wide-open nasolacrimal sac (courtesy—Dr.
Karan Agarwal, skull base fellow, AIIMS, New Delhi,
tomy is a new emerging technique. It utilizes
India) specific ultrasonic vibrations with irrigation to
emulsify and cut bone tissue with precision 7.7.1 Aetiology

and is less damaging to the surrounding soft
tissue [72]. Almost one-third of the cases do not have any pre-
• Microcanalicular endoscopes allow high- disposing factor. In others, the cause of obstruction
resolution dacryoendoscopy, giving a direct, may be inflammation, polyps, trauma, surgery or
clear view of luminal obstruction, better mass lesion [77]. Cystic degeneration of glandular
understanding and decision-making for tissue has been postulated to account for muco-
probing or DCR. But, due to the small cele, but a classical double wall is invariably not
diametre of dacryoendoscope, image quality found in these lesions [78]. Various bone-resorb-
is limited [73]. ing factors like PGE2, leukotrienes, IL-1, TNFa
have been found in mucoceles [79, 80]. So, it can
Limitations of EndoDCR be assumed that in mucocele, obstruction is fol-
In patients with epiphora due to lacrimal system lowed by some other event to initiate the produc-
dysfunction above the sac, like canalicular steno- tion of these bones resorbing cytokines resulting in
sis, Dacryocystorhinostomy is not useful. These bony expansion. The extended endoscopic proce-
patients need Conjunctivodacryocystorhinostomy dures and obliteration of sinuses have more
with insertion of Lester Jones glass bypass tube chances of mucocele formation [81].
[74]. Elderly patients and patients with proximal
obstruction of lacrimal system have a poor prog-
nosis with endoscopic DCR [75]. 7.7.2 Pathology
Histopathologically, mucoceles have pseudo-

7.7 Part G: Sinus Mucocele stratified ciliated columnar epithelium. Chronic
cases may show squamous metaplasia. Additional
Mucoceles are epithelial lined, mucus contain- findings may include cholesterol granuloma,
ing sacs filling any of the paranasal sinuses [76]. haemorrhage, fibrosis and granulation tissue.
They are caused by obstruction of the sinus
ostium or obstruction of a mucous secreting
gland in the lining of the sinus. In paranasal 7.7.3 Clinical Features
sinuses, they most commonly involve frontal
and ethmoid sinuses. They result from obstruc- Mucoceles are most common in the third or fourth
tion to the drainage pathway of the sinus. The decade of life with a slight male predilection.
common presenting symptoms are nasal Fronto-ethmoidal region is involved in almost
obstruction, swelling, visual abnormalities, 90% of cases followed by ethmoids, sphenoid and
headache and neurological effects. Significant maxillary sinus. Symptoms vary depending on the
morbidity is usually secondary to ophthalmo- location of the mucocele and may be classified as
logical or neurological involvement. Computed rhinological, neurologic or most frequently oph-
tomography is the radiological investigation of thalmologic. Fronto-ethmoidal mucoceles present
choice. It shows expansile, homogenous mass, with proptosis, hypophthalmos, diplopia and peri-
with remodelling of the bony walls of the orbital swelling. Sphenoid mucocele may present
involved paranasal sinus. On magnetic reso- with occipitoparietal headache, visual distur-
nance scan, mucocele is iso-/hypointense on T1 bance, diplopia, ptosis. 3, 4, 6 cranial nerves may
and hyperintense on T2-weighted images. be involved. Pituitary may be involved rarely.
Surgical exploration is the standard treatment Nasal endoscopic examination may reveal a mass
with the endoscopic approach being preferred in the nasal cavity or a bulge in the region of the
nowadays. sinus drainage area.
7.7.4 Imaging illa) and cholesterol granuloma are the differen-

tials for mucocele.
Computed tomography (CT) is the most relevant
radiological investigation. It provides basic ana-
tomical detail of the mucocele, its relation with 7.7.5 Treatment
the surrounding structures and helps in surgical
planning. CT shows an expansile, homogenous Early surgical intervention is the treatment of
mass with remodelling of the surrounding bone choice. An endonasal endoscopic approach is
(Figs. 7.38 and 7.39). The appearance of muco- almost always feasible and involves wide marsu-
cele on magnetic resonance imaging (MRI) pialization (Figs. 7.41, 7.42, and 7.43). This has
depends on the contents. In general, mucoceles the advantage of no scar, no interference with
are hypo/iso-intense on T1W1 and hyperintense periorbital structures and excellent visualization.
on T2W2 (Fig. 7.40). MRI is superior to CT for It also provides better restoration of normal sinus
the evaluation of intracranial and orbital exten- function. Virtually all ethmoidal, sphenoidal,
sion [82]. frontal and maxillary mucoceles can be managed
Benign and malignant neoplasms of sinonasal endoscopically [83–88]. However, the bone
origin, fungal sinusitis, odontogenic cyst (max- remodelling after endoscopic surgery may take a
long time to recover. So, it is essential to counsel
the patient that cosmetic results may not be
achieved immediately.
External approaches may include a Lynch–
Howarth, Caldwell–Luc or osteoplastic flap
approach. These may be relevant in cases with a
history of previous surgery with significant scar-
ring or in presence of significant pathology in the
frontal region [89]. Both external and endonasal
approaches may be combined when endonasal
approach is not possible.
7.7.6 Results
The overall recurrence rates are reported to be

less than 10%. Periodic nasal endoscopy in the
office is recommended to assess the patency of
Fig. 7.38 Coronal CT scan showing mucocele left ostium. Visual outcomes are usually good after
fronto-ethmoid region with erosion of lamina papyracea early surgical intervention (Fig. 7.44).
Fig. 7.39 Coronal CT scan showing mucocele involving posterior ethmoid and sphenoid sinus with erosion of sphe-
noid walls
Fig. 7.40 T2 MRI demonstrating hyperintense signal in sphenoid sinus consistent with mucocele
Fig. 7.43 View of sphenoid sinus showing expansion of

its walls and erosion of skull base
Fig. 7.41 Endoscopic view of sphenoid mucocele after

sphenoidotomy showing mucoid contents 7.7.7 Complications
Haemorrhage, cerebrospinal fluid rhinorrhea and

injury to the orbit can occur at surgical explora-
tion. These complications have become uncom-
mon with the advent of endoscopic techniques.
7.8 art H: Choanal Atresia

P
and Management
Nasal choana are the paired opening in the poste-

rior part of the nasal cavity which communicate
anterior nasal cavity with the nasopharynx. Each
choana is bounded superiorly by the inferior sur-
face of the sphenoid body, inferiorly by the hori-
Fig. 7.42 Endoscopic view after evacuation of sphenoid zontal portion of the palatine bone, laterally by
and wide sphenoidotomy medial pterygoid lamina and medially by vomer.
Fig. 7.44 Patient with left sphenoid mucocele exhibiting proptosis and ptosis (preoperative image). Ocular symptoms
in the immediate postoperative period
The absence of a normal opening is called atre- zontal processes of the palatine bone, incomplete
sia. Choanal atresia was first described by resorption of the nasopharyngeal mesoderm. The
Roederer in 1755. Choanal opening(s) may be most popular theory is the local misdirection of
occluded by soft tissue (membranous), bone or neural crest cell migration. The reason behind it,
both. Recent data based on CT shows mixed Treacher Collins syndrome which is caused by
bony and membranous atresia to be the most abnormal neural crest migration has a high rate of
common (70%) and pure bony to be forming the choanal atresia. Certain external factors like
almost 30% percentage of atresia. Pure membra- Retinoic acid deficiency [93] and the use of anti-
nous atresia is rarest in radiology [90]. The inci- thyroid drugs (methimazole, carbimazole, propyl-
dence of choanal atresia is 1:5000 to 1:8000 live thiouracil) during pregnancy are linked to choanal
births [91, 92]. It is more commonly encountered atresia [94].
in females (2:1). Choanal atresia may be unilat-
eral or bilateral; unilateral presentation being
more common than bilateral (65–70%). In unilat- 7.8.2 Patho-physiology
eral cases, right choana involvement is more
common than left. The closure part of the nasal Neonates are obligate nose breathers as the lar-
cavity is roomy. Choanal atresia is not interfering ynx is placed at a higher level which descends at
with the development of the face. Three-fourth 4–6 weeks of life and mouth breathing is estab-
cases of bilateral atresia are associated with other lished. In bilateral choanal atresia, neonate expe-
congenital anomalies like CHARGE syndrome, riences episodes of asphyxia and severe distress
Crouzon’s syndrome, Treacher Collins syn- with or without cyanosis in quiet respiration
drome, Polydactyly, craniosynostosis, cleft lip/ when the mouth is closed, especially during sleep
palate and nasal/palatal deformities. or feeding. Cyanosis is relieved by crying or
gasping when the child opens the mouth widely,
releasing air obstruction.
7.8.1 Aetiology
Various theories are proposed for the origin of 7.8.3 Clinical Presentation
choanal atresia. Some of the popular ones are the
persistence of the buccopharyngeal membrane, Clinical presentation in choanal atresia cases
persistence of the nasobuccal membrane of depends on the laterality, character and severity of
Hochstetter, medial outgrowth of vertical and hori- atresia. Bilateral choanal atresia is a life-threatening
condition. It may cause acute respiratory distress metallic tongue depressor just below the nos-
and cyanosis in a newborn. Distress and cyanosis tril may be used as the initial bedside test. No
are relieved with crying and there happens return of sound of breathing when the bell of the stetho-
cyanosis with rest (paradoxical cyanosis). Difficulty scope over nostril raised the possibility of
in feeding is obvious in these newborns. Unilateral atresia. A more frequently used screening test
choanal atresia presents later in life. Presenting is an attempt to pass an infant feeding tube or
complaints in unilateral cases are unilateral chronic suction catheter (6–8 F) through the nostril
nasal discharge with nasal obstruction and the child into the child’s oral cavity. Failure to pass the
shows thick nasal discharge on examination. A catheter into the oral cavity calls for transna-
child with unilateral choanal atresia presents rarely sal endoscopic examination. Cotton wisp test
with respiratory distress. and methylene blue dye test are the two other
Differential diagnosis includes pyriform aper- infrequently used screening tests.
ture stenosis, nasolacrimal duct cyst (dacryocys-
tocele), turbinate hypertrophy, septal dislocation Radiological Tests—Computed Tomography
and deviation, antrochoanal polyp, nasal neo- (non-contrast) is the radiological investigation of
plasm, meningocele, encephalocele. choice. One-mm thick coronal and axial cuts of
nose and paranasal sinuses in both bony and soft
tissue windows are requested (Fig. 7.46). The
7.8.4 Diagnosis and Evaluation indications of CT scan are to characterize the
type of atresia (bony/membranous/mixed), delin-
1. Clinical Tests/Examination—A confirmatory eate thickness of atresia, estimate mean choanal
diagnosis of choanal atresia is made only by air space and to differentiate from other causes of
transnasal endoscopic examination of the pos- nasal obstruction.
terior choana. Endoscopic examination with
2.7 mm rigid or flexible nasal endoscope after
nasal decongestion and mucous suctioning 7.8.5 Treatment
allows direct visualization of choanal atresia
(Fig. 7.45). Decreased fogging on placing a The treatment of choice is surgery. The timing or
urgency of surgery depends upon laterality. In
cases of bilateral choanal atresia, an immediate
Inferior turbinate preliminary airway management is warranted
followed by elective surgery. In unilateral atresia
Septum
Fig. 7.45 Left partial choanal atresia with roomy nasal

cavity (Courtesy—Dr. Hitesh Verma, Associate Professor, Fig. 7.46 Axial CT scan, unilateral left mixed choanal
AIIMS, New Delhi, India) atresia
cases, definitive surgery can be postponed to later hard palate and vomer which is at the
school-going age group. most infero-medial point of the atretic
plate. It is the safest site to enter into the
nasopharynx.
7.8.6 Preliminary Airway (e) Starting from this most infero-medial
Management portion of the atretic plate, bone is
removed sequentially, superiorly and lat-
Bilateral choanal atresia is an emergency requir- erally. Powered instruments are used for
ing immediate airway intervention. Inserting an the bone removal (microdebrider or dia-
oral airway is the best initial airway management mond drill). Spacious single neo-choana
in such cases. McGovern nipple is also a viable with removal of all intervening tissue and
option. It is an intraoral nipple with a large open- covering of bony defect with mucosal flap
ing made by cutting its end off and is secured in is the key to success (Fig. 7.47).
the mouth with ties around the infant’s head. If, The primary success rate is between 67 and
in spite of this, the patient fails to maintain an 88% (Mean = 85.3%) [99, 100]. Frequent
adequate airway, endotracheal intubation is the postoperative use of nasal saline irrigation
other alternative. If the patient is having associ- and periodic endoscopic surveillance or
ated comorbidities such as cardiopulmonary second-look procedure is required. If the nasal
instability and multilevel airway obstruction tra- passage is too narrow to pass both endoscope
cheostomy may be needed [95]. and drill, a 120° endoscope from nasopharyn-
geal side may be used for visualization
(Retropalatal approach). The rest of the proce-
7.8.7 Definitive Surgical dure is performed transnasally.
Management 2. Transpalatal Approach
This approach was first described by Owens.
Over the years, various surgical procedures have Greater palatine vessels-based, U-shaped
been proposed. An ideal surgical procedure mucosal flap is elevated posteriorly beyond
should maintain the patency of choana; it should the hard and soft palate junction. The palatine
not interfere with normal craniofacial develop- bones posterior to the greater palatine foram-
ment with minimal invasiveness and less risk of ina, the atresia plates, the posterior vomer and
recurrences. the medial pterygoid plates are carefully
drilled using a diamond burr [95]. It carries
7.8.7.1 Surgical Approaches the risk of significant complications including
1. Transnasal Endoscopic Approach palatal flap breakdown and fistula formation,
It is the most preferred surgical approach palatal muscle dysfunction, velopharyngeal
because of better surgical outcomes and fewer insufficiency and effect on maxillary growth
complication rates [96]. This approach was causing crossbite and high palatal arch defor-
first demonstrated by Stankiewicz and later mity. The transpalatal approach is not pre-
modified by other authors [97, 98]. This sur- ferred nowadays.
gery is completed in the following steps: 3. Transseptal Approach
(a) Adequate nasal decongestion. Described by Hall et al. and Osquthorpe et al.
(b) Rigid nasal endoscope (2.7 mm) is intro- in 1982, the transseptal approach is recom-
duced for visualization of atretic plate. mended in case of unilateral CA and in age
(c) A laterally based mucosal flap is raised to >8 years [101]. It permits better correction of
expose the bony part. any deviations of the septum, resection of the
(d) The best point of entry into nasopharynx posterior part of the vomer and preservation
is at the thinnest part of the atretic plate, of mucosal flaps for coverage of the bleeding
found usually at the junction between the area.
a b
c d
Fig. 7.47 Transnasal endoscopic approach for choanal middle turbinate, NF nasal floor, AP atretic plate, MF
atresia repair, from left nostril. Similar for the right side mucosal flap, NC neo choana
also S septum, I incision line, IT inferior turbinate, MT
4. Trans-antral Approach deformities of growing structures such as the

The trans-antral approach is only of historical maxilla and upper teeth.
interest. By providing adequate exposure to Sublabial-transseptal approach is also
the surgical field, this approach permits an described. Transnasal, transpalatal and
adequate and prompt control of any bleeding transseptal approaches are mostly used but
with a lesser risk of damaging the sphenopala- the Cochrane review has not shown advan-
tine arteries, veins and nerves. But this tage of one surgical approach over other
approach can significantly increase the risk of [102].
7.8.8 P
revention of Restenosis After is less likely required for older patients. Surgery
Surgery with navigation is preferred in syndromic
association.
Bilateral choanal atresia with purely bony atretic
plate, age less than 10 days, nasopharyngeal
reflux, gastroesophageal reflux and associated 7.8.9 Use of Laser in Surgery
malformations are the risk factors for restenosis.
Delayed surgery in bilateral atresia has a higher CO2 laser was used initially but ablation is not
failure rate [103]. Unilateral atresia can be possible when the bony atretic plate is thicker
delayed after at least 6 months of age and repair than 1 mm. Other types of laser used are KTP,
should be done by transnasal endoscopic Nd- YAG, holmium-YAG, contact diode laser but
approach [104]. The use of microbebrider, micro- they lack a significant advantage over
drills reduces the surrounding trauma which microdebrider.
reduces the risk of scarring. After a successful
repair, a close and long follow-up at 2, 4 and 8
weeks with endoscope-assisted cleaning of the 7.8.10 Syndromes Associated
nasal cavity and surgical site should help in with Choanal Atresia
reducing restenosis. Use of Mitomycin C (inhib-
its fibroblasts and angiogenesis), stents, mucosal CHARGE, Axenfeld–Rieger Syndrome—Type
flap preservation and serial balloon dilatations 1, Diamond–Blackfan Anaemia, DiGeorge
are still a matter of debate as systematic review Syndrome, Treacher Collins Syndrome, Apert
has depicted similar results even without using Syndrome, Crouzon Syndrome, Pfeiffer
them [105]. Customized endotracheal tube, naso- Syndrome, Marshall Syndrome, Raine Syndrome,
pharyngeal airway and Teflon sheet have been Fraser Syndrome, Pallister–Hall Syndrome,
used as stents for 48 h to 12 months in different Burn–McKeown Syndrome, Cat Eye Syndrome,
series (Fig. 7.48). Studies favour either no use of Fryns Syndrome, McKusick–Kaufman Syndrome
stents or use limited to bilateral choanal atresia. are associated with choanal atresia with variable
Today, the use of stents remains the surgeon’s frequency [91, 106].
choice in absence of proven advantage. Stenting
7.9 art I: Cerebrospinal Fluid

P
Rhinorrhea
Cerebrospinal fluid (CSF) leak occurs as a result

of an abnormal communication between the sub-
arachnoid space and a pneumatized area in the
skull base that includes the sinonasal tract. This
communication or fistula must involve a breach
of the arachnoid and dura matter, the bone of
skull base and the underlying mucosa. Spinal
fluid leak from the intracranial space to the nasal
respiratory tract is potentially very serious
because of the risk of an ascending infection
which could produce fulminant meningitis. CSF
rhinorrhea commonly occurs following head
trauma (fronto-basal skull fractures), as a result
Fig. 7.48 Postoperative stenting (Courtesy—Dr. Hitesh
of surgery, or destruction of lesions. In cases
Verma, Associate Professor, AIIMS, New Delhi, India) where a confirmatory test is needed, the beta-2
transferrin assay is the test of choice because of clear cells (<5/μL). CSF represents the end prod-
its high sensitivity and specificity. Various com- uct of the ultrafiltration of plasma across epithelial
binations of planar tomography and CT, contrast- cells in the choroid plexus lining the ventricles of
enhanced CT cisternography, and radionuclide the brain. Circulation of CSF is maintained by
cisternography, and, more recently, MR cister- the hydrostatic differences between its rate of
nography have been used in the diagnosis of CSF production and its rate of absorption. Normal
leak. MRI with NCCT is a very useful and spe- CSF pressure is approximately 10–15 mmHg,
cific diagnostic and localizing technique. and elevated pressure constitutes an intracranial
Traumatic CSF rhinorrhea is managed by con- pressure (ICP) greater than 20 mmHg.
servative measures in 70–80% of cases. In cases
of iatrogenic and spontaneous leaks, it is less
likely to heal with conservative measures. It is 7.9.2 Applied Anatomy
currently accepted that endoscopic intranasal
management of CSF rhinorrhea is the preferred The most common anatomic sites of spontaneous
method of surgical repair, with higher success cerebrospinal fluid (CSF) leaks are the areas of
rates and less morbidity than intracranial surgical congenital weakness of the anterior cranial fossa
repair. Uncomplicated CSF fistula, located at the and areas related to the type of surgery per-
posterior wall of frontal sinuses can be repaired formed. The lateral lamella of the cribriform
extradurally with osteoplastic frontal sinusotomy. plate appears to be involved in approximately
Intracranial approaches should be reserved for 40% of the cases, the frontal sinus in 15%
more complicated CSF rhinorrhea. The timing whereas sella turcica and sphenoid sinus are
for surgery and CSF drainage procedures must be involved in 15%. Common sites of injury second-
decided with great care and with a clear strategy. ary to endoscopic sinus surgery include the lat-
This chapter reviewed the applied anatomy and eral lamella of the cribriform plate and the
physiology, causes, diagnosis and treatment of posterior ethmoid roof near the anterior and
CSF leakage. medial sphenoid wall. Rarely, the leak can origi-
nate in the middle or posterior cranial fossa and
can reach the nasal cavity by way of the middle
7.9.1 Applied Physiology ear and eustachian tube. These patients typically
present with aural fullness due to a serous middle
The total volume of CSF in adults is 90–150 ml. ear effusion.
CSF is produced in the choroid plexus and epen-
dyma at a rate of 0.35 ml/min (500 ml/d). It is
absorbed in arachnoid villi, total volume turned 7.9.3 Classification
over 3–5 times per day. CSF circulates from the
lateral ventricle to the third ventricle via the It is classified by Ommaya et al. (1960) [107]. It
aqueduct of Sylvius. From the third ventricle, the is grossly divided into traumatic, non-traumatic
fluid circulates into the fourth ventricle and out and congenital types. Both entities can be further
into the subarachnoid space via the foramina of classified:
Magendie and Luschka. After circulating through (A) Traumatic
the subarachnoid space, CSF is reabsorbed via (i) Non-surgical
arachnoid villi. (ii) Surgical
CSF consists of a mixture of water, electro- (B) Non-traumatic
lytes (Na+, K+, Mg2+, Ca2+, Cl−, and HCO3−), glu- (i) Normal pressure
cose (60–80% of blood glucose), amino acids (ii) High pressure
and various proteins (22–38 mg/dL). CSF is (C) Congenital
colourless, clear and typically devoid of cells Traumatic CSF leak can be divided on the
such as polymorphonuclear cells and mononu- basis of aetiology:
(A) Trauma—it is the most common type and 7.9.4 Patient Evaluation
anterior cranial fossa is the most common
site (cribriform and roof of ethmoid). It is Presenting symptoms are clear, watery discharge
further classified into non-surgical and sur- from the nose (more on bending forward). The
gical. Non-surgical (accidental) accounts for fluid is non-sticky and has a salty taste in the
~80% of all CSF leaks result of blunt or pen- mouth. Patients are not able to sniff back the
etrating head trauma. 2–3% of major head fluid. The other presentation is the history of
trauma results in CSF leaks. CSF leak occurs recurrent meningitis. The history should be
in 15–30% of cases of skull base fracture. focused on duration, onset, associated symptoms.
Leak may be either immediate (within 48 h) History should also include the severity, laterality
or delayed and in ~95% of cases of delayed and quantity of rhinorrhea. The important ques-
leaks occur within 3 months. Surgical tions are history of trauma, symptoms of menin-
(Iatrogenic) CSF leak accounts for 16% of gitis, recent sinus surgery or neurosurgery. The
CSF leaks. Endoscopic sinus surgery is the physical examination includes complete ENT
most common cause (0.5% of ESS cases). examination, weight and BMI, site of leak by
The most common site of injury is the lateral banding forwards.
lamella of the cribriform plate.
(B) Non-traumatic—it is 4% of cases of CSF rhi-
norrhea. It can be further classified into high, 7.9.5 Differential Diagnosis
normal pressure leaks. High-pressure leak is
45% of non-traumatic cases. The patho- Autonomic dysfunction, allergic rhinitis, CSF
physiology is persistent high intracranial oto-rhinorrhoea are the differentials for CSF
pressure (ICP), that leads to remodelling and rhinorrhoea.
thinning of the skull base and creates com-
munication (theorized to be due to ischemia
from compression of vessels). The causes of 7.9.6 Investigations
high ICP are intracranial tumour growth
(typically pituitary tumours) and hydroceph- (A) Bed Side Test
alus secondary to obstruction of the normal 1. Halo or Ring Sign—blood will separate
pathway of CSF fluid drainage. Normal pres- out from CSF when nasal discharge is
sure leaks are 55% of non-traumatic cases. placed on a filter paper (central blood
The causes are true spontaneous leaks (usu- with clear ring). The ring sign is not spe-
ally seen in adults). Tumours and other cific to bloody CSF. Blood mixed with
osteolytic lesions of skull base erodes the water, saline, and other mucus will also
boundary of the nasal and cranial cavity form a ring sign.
(nasopharyngeal carcinoma, inverted papil- 2. Reservoir sign—Morning rise showed
loma, etc.) gush of CSF leak. It is because of fluid
(C) Congenital—It may be either increased ICP collection in paranasal sinuses.
or normal ICP. The reason for congenital 3. A handkerchief is not stiff when soaked
CSF leak is the failure of closure of the nor- with CSF fluid.
mal linings which separates the cranial and (B) Laboratory Tests
nasal cavity. It typically involves the fora- 1. Glucose testing—It is a rapid but highly
men cecum and fonticulus frontalis. The unreliable test. CSF glucose level is two-
persistent cricopharyngeal canal creates a third of blood glucose level. Glucose oxi-
vertical midline defect connecting the mid- dase paper colour is changed with
dle cranial fossa to the sphenoid. Primary glucose concentrations of 5+ mg/dL. In
empty sella syndrome is developed by con- recent trauma, the presence of blood
genital widening of the diaphragma sella. gives false-positive results. Recent men-
ingitis or other intracranial infections

cause a lower concentration of glucose in
CSF (false-negative). False-positive
results with lacrimal secretions or nasal
mucus. Negative glucose virtually elimi-
nates a diagnosis of CSF fluid.
2. Beta-trace protein—It is also known as
prostaglandin D synthase. It is synthe-
sized primarily in arachnoid cells, oligo-
dendrocytes and choroids plexus (CNS).
It is also found in human testis, heart and
serum. It is not routinely ordered as it
may be altered in many cases like renal
insufficiency, multiple sclerosis, cerebral
infarctions and some CNS tumours.
Fluid with a concentration >2.0 mg/L is
usually positive for CSF. Concentration Fig. 7.49 CT PNS showing left roof of ethmoid bony
<1.5 mg/L is not likely to contain defect post-trauma
CSF. Sensitivity and specificity are not
high as beta-2-transferrin. cate a dural tear. A deviated crista galli is
3. Beta-2-transferrin—It is currently the a radiological sign supporting primary
single best test for identifying the pres- CSF rhinorrhea. However, it may reveal
ence of CSF [108]. It is a protein pro- defects in the skull base that do not leak
duced by neuraminidase in CNS located or are not sites of active leaking, making
only within the CSF, perilymph and the diagnosis more difficult.
aqueous humour. The assay has a high CT Cisternography—It is more inva-
2.
sensitivity (94–100%) and specificity sive, not very frequently used. Intrathecal
(98–100%). It is rapid and is a non- contrast dye is injected and a CT scan is
invasive test and it requires only 0.5 cc of obtained. It is more accurate especially
fluid. It is stable at room temperature for those with active leaks (Fig. 7.50).
approximately 4 h, so immediate refrig- Sensitivity for detecting leaks drops from
eration following collection is recom- nearly 100% with active leaks to 60%
mended. Specimen should not be frozen. with intermittent leaks. It may miss crib-
If assay facility is available, one can get riform or ethmoid sinus defects. It can be
results within 3 h. Sensitivity is about associated with nausea, headaches and
100% with specificity of 95%. acute organic psychosyndromes.
(C) Imaging Studies Magnetic resonance imaging (MRI)—It
3.
1. High-Resolution CT Scans [109]—It is is not recommended as a first-line imaging
the imaging modality of choice for iden- modality unless an encephalocele is sus-
tifying a skull base defect associated pected. It demonstrates soft tissue abnor-
with a CSF leak (Fig. 7.49). It may dem- malities and pooling of CSF (high signal
onstrate skull base defects resulting from intensity on T2). It is not good at defining
accidental or iatrogenic trauma, and bony defects, unlike a CT scan. Contrast
underlying anatomic or developmental helps in the differentiation of sinus inflam-
abnormality, or an erosive lesion such as mation from CSF fluid. It is more expen-
neoplasm. It should have 1 mm cuts with sive and time-consuming.
axial, sagittal and coronal views. MR Cisternography—Avoidance of
4.
Pneumocephalus on a CT scan may indi- intrathecal injection of contrast is the key
I-131, Indium 111) is done and pledgets

placed at areas suspected of leak and
scintigrams of the skull are obtained.
Pledgets are then removed and measured
for radioactive tracer. The test is positive
only with active leak (70% detection
when active, 30–40% in inactive) and it
has poor localization. Radioactive iso-
tope is absorbed into the circulatory sys-
tem and deposited into normal tissues.
(D) Diagnostic Procedures
Intrathecal injection of Fluorescein dye:
Fig. 7.50 CT cisternography showing left lateral lamella
of cribriform plate defect It is good at locating active CSF leaks. After
lumbar puncture or drain placement, 10 ml
of CSF is withdrawn and about 0.1 ml of
10% fluorescein solution is mixed with
withdrawn CSF. The mixture is then re-
injected into the subarachnoid space over
10 min period. In most cases, dye can be
seen without filters. Smaller defects may
require filters or black light (yellow filter on
endoscope, blue on light source). It is impor-
tant to keep a low concentration of fluores-
cein; high doses can lead to severe side
effects (500 + mg) like seizure, pulmonary
edema, coma and death.
7.9.7 Treatment
(A) Medical Therapy

1. Conservative management: It has been
advocated in immediate-onset CSF rhi-
Fig. 7.51 MRI cisternography (T2 with Cg) in spontane-
ous CSF rhinorrhea, defect in left cribriform plate norrhea following accidental trauma. It
consists of a 7–10 day trial of bed rest
benefit of it. T2-weighted imaging can be with the head end elevation by 15–30
used to detect CSF in the sinonasal cavity degrees. The patient should avoid cough-
(Fig. 7.51). Pulse sequence can be ing, sneezing, nose-blowing and heavy
designed to enhance the detection proba- weight lifting. Stool softeners should be
bility. As with CT cisternography, false- used to decrease the strain associated
negative studies may result in intermittent with bowel movements. 75–80% of trau-
leaks. MR cisternography and HRCT of matic CSF leaks will spontaneously
nose PNS is the most accepted modality resolve with this management.
to diagnose the site of leak. 2. Lumbar drain [110]: Lumber drain can
5. Nuclear medicine tests (radionuclide be considered if CSF leak does not resolve
cisternography)—Intrathecal injection after 5–7 days of conservative manage-
of radioactive tracers (technetium-99, ment, mainly in large skull defects or iat-
rogenic CSF leaks. Continuous drainage with a better chance of patching a

is recommended over intermittent drain- defect in the face of increased ICP.
age (prevents spikes in CSF pressure). Disadvantages comprise increased mor-
The usual rate of drain is 10–15 cc/h. bidity, increased hospital time, injury to
Risks involve headaches, nausea and eme- the brain from retraction (haematoma,
sis, pneumocephalus, infection, coma. seizures, cognitive dysfunction and risk
3. Antibiotics: Role is controversial. The of permanent anosmia). It is not good for
reason for use is to prevent intracranial visualization of the sphenoid sinus.
infections. Brodie et al. concluded that Failure rates for this approach are 40%
there is no significant difference in the for the first attempt and 10% overall.
incidence of meningitis with prophylac- Extracranial Approach: It can be fur-
2.
tic antibiotic therapy [111]. It can be used ther divided into external and endo-
in iatrogenic CSF leak following skull scopic types.
base injuries during FESS. (a) External approach: These proce-
4. Diuretic: It is utilized in the presence of dures are infrequently chosen in cur-
a CSF leak with increased ICP [112]. rent practice, given the high success
Acetazolamide inhibits the conversion of rates and low morbidity associated
water and CO2 to bicarbonate and H+. with the endoscopic approach.
Loss of H+ slows the action of the Na+/ However, they should be part
K+ ATPase enzymes that are responsible of every skull base surgeon’s
for the production of CSF results in armamentarium.
decreased ICP. • External ethmoidectomy—
(B) Surgical Therapy Begins with the tarsorrhaphy on
1. Intracranial Approach: (mostly done the ipsilateral eye. Incision is
via frontal craniotomy, rarely middle or made halfway between the medial
posterior fossa) canthus and the midline of the
The indications include comminuted nose down to the bone. Lateral
skull fractures with displaced fragments elevation of the periosteum
requiring reduction, extensive skull base exposes the anterior lacrimal
fractures associated with intracranial ridge and the lacrimal fossa. The
haemorrhages or contusions that require lacrimal sac is elevated and
craniotomy for treatment [113]. It is also retracted out of the fossa. The
indicated when co-existing surgically anterior ethmoidal artery which
amenable mass lesion is laying inside the will be encountered 2–2.5 cm
cranium, more than 3 cm cranial defect, posterior to the lacrimal crest
multiple defects, multiple failed endo- should be ligated. The fronto-
scopic repairs and when site of leak is not ethmoid suture line marks the
visible by all investigations. Dural level of fovea ethmoidalis (dis-
defects may be closed primarily with or section should never be superior
without the use of grafts which could be to this line). The posterior
free or pedicled periosteal or dural flaps ethmoidal artery is found approx-
(Fig. 7.27a), muscle plugs, mobilized imately 1.2 cm posterior to the
portions of the falx cerebri, fascia grafts anterior ethmoidal artery in the
or many commercial grafts. It should be fronto-ethmoid suture line and
reinforced with fibrin glue. Advantages the optic nerve lies 5–6 mm pos-
include direct visualization of defect, terior to the posterior ethmoidal
inspection of adjacent cerebral cortex artery. A complete dissection of
the ethmoid labyrinth should be moidal angle. When needed, the

done and the skull base defect is pterygopalatine fossa can be
then identified. accessed via the posterior wall of
• Trans-ethmoidal sphenoidot- the maxillary sinus.
omy—First an external ethmoid- • Osteoplastic flap—Indicated for
ectomy is carried out as above, the defect in the posterior table of
the sphenoid sinus opening is the frontal sinus especially if
then identified and enlarged; the more than 2 cm and above the
anterior wall of the sinus is floor and lateral to the lamina
removed to reach the sella region. papyracea and is approached via
• Sublabial-transseptal sphe- coronal incision or eyebrow inci-
noidotomy—Can be carried out sion (Fig. 7.52).
using sublabial or transnasal inci- Endoscopic Approach: It is the
(b)
sion with exposure of pyriform most common and successful
aperture and nasal spine is made approach (90–95% success rate)
free. Left or right septal mucop- [114]. The advantages are better
erichondrial flap is elevated later- magnified visualization, angled visu-
ally and inferiorly along the nasal alization, no external incisions and
floor in the subperiosteal plane. minimized intranasal mucosal inju-
The cartilaginous septum is dislo- ries. It is of many types:
cated from the maxillary crest • Transfrontal approach (Lothrop
and the contralateral nasal floor or Draf III procedure)—It allows
mucoperiosteal flap is elevated. access to the floor and posterior
The contralateral nasal septum is wall of the frontal sinus. The
not elevated off the cartilage. The main advantage is it avoids oblit-
bony–cartilaginous junction is eration of the frontal sinus with
disarticulated and the opposite the osteoplastic flap. The frontal
posterior flap is elevated. The sinus outflow tract must be pre-
bony septum is removed to served to avoid mucocele. It is
expose the sphenoid rostrum, not effective for the defects in the
which is widely removed via most lateral or superior aspects of
osteotomies or a drill to expose the sinus. It begins by performing
the entire sinus. a complete ethmoidectomy fol-
• Trans-antral approach—It lowed by identification and dis-
offers wide access to the anterior section of frontal recess with
sphenoid, ethmoids, pterygopala- removal of superior septum and
tine fossa and maxilla. A gingivo- interfrontal septum.
buccal sulcus incision is made to • Transcribriform approach—
expose the anterior wall of the Exposes the medial anterior cra-
maxilla. The periosteum is ele- nial fossa from the medial aspect
vated superiorly as far as the of the middle turbinate to the
infraorbital nerve and canine olfactory groove (Fig. 7.53).
fossa osteotomy performed to Posteriorly, it extends to the ante-
enter into the maxillary sinus. The rior aspect of the planum sphe-
ethmoidal bone can then be noidale. Crita galli is exposed by
approached medially and superi- removal of the perpedicular plate
orly through the maxilloeth- of ethmoid bone. Care should be
Fig. 7.52 (a) Incision marking, (b) drilling the outline of with suturing, (f) obliteration of frontal sinuses
frontal sinus after marking with X-ray templet, (c) ante- (Courtesy—Dr. Hitesh Verma, Associate Professor,
rior frontal sinus wall is elevated, (d) view of frontal AIIMS, New Delhi, India)
sinus, (e) repair of dural defect with fascia lata and secured
a b c
Fig. 7.53 (a) Showing bony defect of left cribriform plate with dura exposed in spontaneous leak (black arrow), (b)
facia lata composite grafting, (c) showing fibrin glue/dura seal in situ
taken while doing dissection near dissection extends from the mid-
the olfactory groove. dle turbinate to the lamina papy-
• Transfovea approach—For get- racea. The frontal sinus marks the
ting access to the lateral aspect of anterior limit and the sphenoid
the anterior cranial fossa. The marks the posterior limit. In some
cases, the middle turbinate is access any defect in the middle

removed and the transfovea and fossa floor that occurs in this
transcribriform approaches are vicinity lateral to the Sternberg
combined. canal and the foramen rotundum.
• Transplanum approach—
Allows exposure of skull base The key to endoscopic repair of a CSF leak is
defects along the planum sphe- good visualization and exposure of the defect. If
noidale and those with significant an encephalocele is present, it should be cauter-
involvement of the suprasellar ized at its stalk with bipolar cautery prior to
region. Anterior and posterior reduction into the anterior cranial fossa to pre-
ethmoidectomy is performed vent intracranial haemorrhage. For good expo-
first, which provides access to the sure, the surgeon should elevate the surrounding
most anterior aspect of the pla- mucosa to provide 2–5 mm of bone exposure
num. The anterior seller wall is around the defect. Any mucosa remaining in the
taken down to provide posterior defect should be removed prior to repair to avoid
exposure. poor adhesion of graft with bed and to prevent
• Trans-sellar approach—The future mucocele formation.
route of choice can be medial or There are many types of grafts utilized, but it
lateral to middle turbinate for should be noted that the graft should be roughly
defects on the sella turcica. It is 30% larger than the defect to account for postop-
part of extended endoscopic pro- erative shrinkage. Types of grafting material uti-
cedure for pituitary lesion exci- lized are cartilage, bone (septum, mastoid tip,
sion. Complete ethmoidectomy is middle turbinate), mucoperichondrium, septal
followed by the opening of sphe- mucosa, turbinate mucosa and/or bone, fascia
noid sinus ostia. If bilateral (temporalis, fascia lata), abdominal fat, and pedi-
access is needed, the posterior cled septal or turbinate flaps. It should be noted
bony septum and the intersinus that pedicled flaps tend to tint, fold and contract
septum can be removed. when utilized.
• Transpterygoid approach—
First an endoscopic modified
medial maxillectomy is per- 7.9.8 Grafting Techniques
formed. The infraorbital nerve is
then identified and its trajectory 1. Overlay technique—a graft is placed directly
followed. A complete spheno- over the defect.
ethmoidectomy is then per- 2. Underlay technique—the graft is placed
formed. The crista ethmoidalis is between the dura and bony defect.
isolated and the main branch of 3. The combined technique utilizes both under-
the sphenopalatine artery (SPA) is lay and overlay grafts.
identified. The pterygopalatine 4. Bathplug technique, where a fat plug with a
ganglion which lies posterior to specifically secured vicryl suture into the
the SPA should be preserved. The intradural space [115].
fat in the pterygopalatine fossa
may be dissected or cauterized In addition to these techniques, we may rein-
until the pterygoid bones are iden- force the repair with fibrin glue to provide an
tified. Anterior wall of the lateral improved seal. The placement of absorbable (gel
recess of the sphenoid sinus, pter- foam) and/or non-absorbable packing can further
ygoid base is drilled. It is good to improve the seal. Non-absorbable pack removal
may lead to the displacement of the graft when optic nerve whereas indirect optic nerve injury
removed. In the face of increased ICP, it is rec- occurs due to blunt impact to head or face which
ommended that a multilayered graft be utilized. further sets a shearing force damaging the optic
The size of the defect also plays a role in the nerve or its blood supply. Direct and indirect
grafting technique utilized. If the defect is injuries both cause mechanical and ischemic
<2 mm, the type of grafting technique utilized damage to the optic nerve. CT scanning helps in
typically does not make much difference as most delineating fractures of bones and is critical for
techniques will be successful in repairing the surgical planning. MRI is superior in delineating
CSF leak. If the defect is 2–5 mm, one must note soft tissue involvement. Both corticosteroids and
whether comminuted bone segments or signifi- surgical decompression alone or in combination
cant dural injury is present. If they are not pres- helps in improving visual prognosis.
ent, the use of an overlay grafting technique is Orbital and Optic Nerve Anatomy [117]
sufficient. However, if either is present, one Optic nerve is 3–4 mm in diametre, 35–50 mm
should utilize a composite graft or a separately in length from retina to optic chiasma. It is basi-
harvested bone plus mucosa grafting technique cally divided into four segments. The first seg-
where the bone is placed in an underlay fashion ment named as intraocular segment is around
while the mucosa is placed in an overlay fashion. 1 mm in length. The second segment is intraor-
If the defect is >5 mm, the repair should be per- bital with 20–30 mm length, third and fourth seg-
formed with a composite graft or separate bone ments are intracanalicular (5–11 mm) and
plus mucosa grafting technique as described intracranial (3–16 mm), respectively, as depicted
above. Meningitis (0.3%), brain abscess (0.9%), in Fig. 7.54. The optic canal is approximately
subdural haematoma (0.3%), smell disorders 6.5 mm in diametre and 8–10 mm in length.
(0.6%), headache (0.3%) are the complications Figure 7.55 depicts relations of intracanalicular
of endoscopic technique (much lesser than crani- part of the optic nerve. Relations of intraorbital
otomy) [116]. part of optic nerve are shown in Fig. 7.56. Optic
Postoperative care includes bed rest with the canal contains optic nerve axons, their supportive
head of the bed set at 15–30 degrees for 3–5 days. glia, the ophthalmic artery and branches of the
The blood pressure should be maintained at a carotid sympathetic plexus of the autonomic ner-
normal level. Stool softeners and cough suppres- vous system. Axons of the optic nerve arise from
sants to prevent straining, coughing. The patients the ganglion cell layer of the retina and extend
should be advised to avoid blowing the nose and beyond chiasma and optic tracts just before syn-
any heavy lifting. If a lumbar drain is utilized apsing in the lateral geniculate body.
postoperatively, it should be left 3–5 days with a
maximum drainage of 10–15 cc/h. If non-
absorbable packing is utilized, antibiotics should
be given.
Intracular
7.10 P
art J: Optic Nerve Anatomy
and Management Intraorbital
Orbit is pyramidal in shape with apex posteriorly Intracanalicular

and base directed anteriorly. The optic canal rests
Intracanial
in the sphenoid bone and lies at the apex of the
orbit. Optic nerve injury is classically divided
into direct and indirect types. Direct optic nerve
injury is caused by penetrating injuries to the Fig. 7.54 Parts of optic nerve
Trochlear nerve Superior rectus
Frontal Levator palpebrae superioris

nerve Superior oblique
Medical rectus
Opthalmic nerve
superior
Opthalmic artery
opthalmic
vein Annulus of zinn
Lateral rectus
Inferior rectus
Oculomotor Inferior opthalmic vein

nerve
Nasociliary
nerve Abducens
nerve
Fig. 7.55 Relationship of intracanalicular segment of optic nerve
Lateral rectus
Optic nerve
Infratrochlear
nerve
Anterior
ethmoidal
artery
and nerve Opthalmic Posterior ethmoidal artery
artery and nerve
Medical
rectus
Fig. 7.56 Relationship of intraorbital part of optic nerve
The optic nerve is surrounded by pia, arach- supplied by arterial circle of Zinn–Haller with
noid and dura mater in its intraorbital and intra- contributions from posterior ciliary arteries, the
canalicular part which forms the optic sheath. In pial arterial network and the peripapillary choroi-
the intracanalicular part, the dura is fused to dal vasculature. Perforating branches derived
sphenoid periosteum and at the posterior end of from the ophthalmic artery supplies intraorbital
the optic canal, the optic nerve sheath is fused to part of the optic nerve and intracanalicular part is
dura lining calvaria. Thus, intracranial part lies in supplied by small pial branches from ophthalmic
subarachnoid space. Intraocular optic nerve is artery. On the other hand, intracranial part is sup-
plied by pial branches of the internal carotid, 2. Relative afferent pupillary defect is present
anterior cerebral and anterior communicating except in cases of symmetric B/L TON.
arteries. 3. Impairment of colour vision.
Traumatic optic nerve injury is basically of 4. Variable visual field defects.
two types: direct and indirect optic nerve injury.
Direct Optic Nerve injury is caused by penetrat- Optic disc appearance in anterior indirect
ing objects impinging directly on the optic nerve. TON is associated with disc swelling and retinal
Direct optic nerve injuries have a worst prognosis haemorrhages whereas in posterior indirect TON
than indirect optic nerve injuries. Indirect optic fundus looks normal. In direct TON, there could
nerve injuries are further divided based on ana- be avulsed optic nerve head or optic disc swelling
tomical site into anterior and posterior. Anterior with haemorrhages. CT findings can be sugges-
indirect optic nerve injuries are the injuries ante- tive of direct TON and excluding indirect
rior to where the central retinal artery enters the TON. Although both direct and indirect mecha-
optic nerve 8–12 mm posterior to insertion of nisms can cause optic nerve damage, a clear dis-
nerve into globe whereas posterior indirect optic tinction between the two is difficult.
nerve injuries are posterior to this site. Other causes of optic neuropathy include:
Initial ocular examination should be done
including visual acuity using Snellen’s chart, 1. Dysthyroid optic neuropathy is a consequence
colour vision and visual field charting [118]. of Graves orbitopathy that results in decreased
Swinging Flashlight test should be used to visual acuity, RAPD, disturbed colour vision,
elicit Relative Afferent Pupillary Defect optic disc abnormalities and visual field
(RAPD) which is positive in traumatic optic defects. Diagnosis and management requires
neuropathy but may be absent in bilateral a multidisciplinary approach. Mechanism of
cases. Ophthalmoscopic examination will help dysthyroid optic neuropathy appears to be
to evaluate the retinal and choroidal circula- caused by direct compression of the optic
tion, optic nerve head morphology and to rule nerve due to enlarged extraocular muscles,
out any intraocular foreign body. Visual evoked stretching caused by proptosis and inflamma-
potentials (VEP) are usually not required to tion. Treatment options are high dose i.v ste-
establish the diagnosis but may be used in roids followed by orbital decompression. The
questionable cases. Flash VEP amplitude ratio accepted dose regimen of these patients is
greater than 0.5 appears predictive of a favour- once per week dose of 500 mg i.v methylpred-
able, long-term visual outcome in unilateral nisolone for 6 weeks followed by 250 mg per
traumatic optic neuropathy. It has diagnostic week for another 6 weeks. Total cumulative
value in patients having suspicion of bilateral dose should not be more than 6–8 g [120].
optic neuropathy where RAPD may not be evi- 2. Fibrous dysplasia [121]—Clinical low vision
dent. Thin Section CT Scanning is the main with radiological proven optic nerve encase-
modality to see fractures of the optic canal and ment and documented progression of vision
to plan for any surgical intervention. MR imag- deterioration are the indications of optic nerve
ing is useful in chiasmal trauma and should be decompression in fibrous dysplasia.
done after the metallic orbital foreign body is 3. Benign intracranial hypertension—the role of
being ruled out. optic nerve fenestration can prevent further
Diagnosis of Indirect over Direct TON [119] visual loss in patients of BIH with rapidly
is made on the following findings: progressing vision loss but the risk of menin-
gitis is increased.
1. Variable visual loss ranging from normal to
no light perception in indirect TON; direct Treatment Options—There are two main
TON causes immediate and severe visual loss. modalities of treatment including medical ther-
apy and surgical decompression used alone or in patients with partial vision loss, surgical
combination: decompression was beneficial even when
(A) Medical therapy—Corticosteroids were
surgery was performed after 1 year of
considered as neuroprotective due to their onset of visual loss [126]. The surgical
antioxidant properties and inhibition of decompression can be done by endoscopic
free radical-induced lipid peroxidation. or external approaches:
This hypothesis was reinforced following 1. Endoscopic optic nerve decompression
National Acute Spinal Cord Injury Study 2 [127]—This technique is less invasive and
[NASCIS II]; a multicentre clinical trial provides good exposure to the optic canal
that evaluated patients with acute spinal and orbital apex. This procedure is done
cord injury concluded that the use of under general anaesthesia. Adequate
methylprednisolone (30 mg/kg loading nasal decongestion is achieved using
dose, followed by 5.4 mg/kg/h for 24 h) epinephrine and using a 4 mm 0 degree
started within 8 h of injury was associated rigid endoscope, standard spheno-
with a significant improvement in both ethmoidectomy is performed. Fracture of
motor and sensory function compared to lamina papyracea approximately 1 cm
patients treated with a placebo [122, 123]. anterior to the optic canal is done and then
There is no convincing evidence that ste- lamina papyracea is removed in a poste-
roids provide any additional benefit over rior direction to expose the annulus of
conservative management as there is high Zinn. Thin lamina is then replaced with a
rate of spontaneous visual recovery in thick bone of lesser wing of sphenoid near
TON [123]. optic canal, which is then removed after
(B) Surgical decompression—Due to the lack adequate thinning like eggshell. Removal
of Randomized controlled trials, the tim- of bone for a distance of 1 cm posterior to
ing and outcome of surgery is still contro- the face of the sphenoid sinus is usually
versial. In a recent meta-analysis, they sufficient. In acute conditions, incision of
divided patients into two groups based on the optic sheath is recommended in case
the timing of surgery, in which 57% of of intra-sheath haematoma or significant
patients in the early group (patients who papilledema. Optic sheath incision
had surgery in <3 days) had visual showed better results in delayed decom-
improvement and 51% in the late group pression. Optic sheath is then incised with
(>7 days) also improved. So, it concludes sickle knife in the superomedial quadrant
that even in delayed cases, surgical inter- to minimize risk of injury to ophthalmic
vention should be done [124, 125]. In artery (Fig. 7.57).
Fig. 7.57 Endoscopic optic nerve decompression. (a) Uncinectomy, (b) wide middle meatus antrostomy, ethmoidec-
tomy and sphenoidotomy, (c) drilling of sphenoid bone, (d) exposure of optic nerve (ON), (f) incision on optic sheath
d e
ON
Fig. 7.57 (continued)
2. Extra-nasal Trans-ethmoidal Approach There are other agents who have experimen-
[124]—This technique provides access tal importance and little clinical evidence to
to the ethmoid sinus and medial wall of support the effectiveness of these therapies
orbit. The incision is made along the [128]. These are:
medial canthus from the inferior margin
of medial aspect of the eyebrow and then 1. Crystallins—these are the heat shock proteins
the periosteum is elevated followed by which act as anti-inflammatory agents and are
removal of lacrimal bone and lamina neuroprotective.
papyracea. Following which, the medial 2. Erythropoietin—it increases retinal ganglion
wall of the apex of orbit, optic canal and cell somata and survival of axon.
optic foramen is drilled using diamond 3. Glutamate inhibitors—it acts as an excitatory
burr. Then thinned- out OC ring is neurotransmitter in the eye.
removed after tilting orbital contents to 4. Neurotropic factors—these factors help in the
the lateral side (Fig. 7.58). Endoscopic- survival of existing neurons and growth and
assisted medial transorbital approach is differentiation of newer ones. These include
also used to overcome drawbacks of fibroblast growth factor-2 (FGF-2), brain-
facial scar. derived neurotrophic factor (BDNF) and cili-
3. Transcranial approach [124]—This tech- ary neurotrophic factor (CNTF).
nique is more invasive than the endonasal 5. Tacrolimus—Protective role by inducing
approach as it requires brain retraction that fibroblastic apoptosis and prevents loss of
can lead to serious complications. It can myelin.
also alter cosmetic appearance as com- 6. Therapeutic hypothermia.
pared to the endonasal approach although 7. TNFα and NO synthase inhibitors—they
it provides a familiar view to neurosur- enhance retinal ganglion cell survival.
geons and achieve wider decompression. 8. Adipose tissue-derived stem cells are tried to
Recently minimally invasive approaches repair ischemic optic neuropathy and optic
like the supraorbital approach have been nerve injury in rat models and showed
introduced but lack clinical data. success.
a b c
ON
Fig. 7.58 External optic nerve decompression in fibrous (b) separation of orbital content from medial wall with
dysplasia. (a) Drilling of medial orbital wall right side to wider posterior view, (c) optic nerve decompression in
gain posterior access. Self-retaining retractor is placed, intracanalicular portion
7.11 P
art K: Skull Base the superficial temporal artery. The supraorbital
Reconstruction in Extended and supratrochlear artery based Pericranial flap
Endoscopic Approaches and the Palatal flap (Oliver flap) based on
descending palatine artery can also be used based
With widespread application of extended endo- on the location and size of the defect.
scopic skull base procedures, the need for a
robust reconstruction, preferably by the same
approach and from the tissue in the vicinity, was 7.11.1 Introduction
the need of the hour. This necessity gave rise to
the invention of the endonasal mucosal flaps. The Recent advances in vascular reconstruction tech-
endonasal flaps are designed based on the vascu- niques in skull base procedures have led to
larity of the nasal mucosa. The nasal mucosa of extended endonasal endoscopic procedures as the
both the septum as well as the lateral nasal wall is gold standard for anterior skull base pathologies
used along with its vascularity for the reconstruc- (Fig. 7.59). It reduces short- and long-term com-
tion of the defects. The choice of the endonasal plications like CSF leak (reduced from 20–30%
mucosal flap is dictated by the site and size of the to <5%) [129–131], meningitis and postoperative
skull base defect. The Hadad–Bassagasteguy flap mortality and morbidity [132, 133].
is the commonly used axial nasoseptal flap (NSF)
based on the posterior septal branch of the
Sphenopalatine artery. Flaps that can be har- 7.11.2 Principles of Skull Base
vested from the lateral nasal wall are the anteri- Reconstruction
orly based inferior turbinate endonasal flap which
is a random Pattern flap based on the anterior eth- Preoperative anticipation of area and size of the
moidal artery. The posteriorly based Inferior tur- defect, type of leak, type of reconstruction and
binate endonasal flap which is an axial flap based type of tissue available for reconstruction, sound
on the inferior conchal artery. The middle turbi- knowledge of nasal vascular anatomy and
nate flap which is again an axial flap based on the whether reconstruction is feasible as a part of the
middle turbinate artery. Regional flaps can also endoscopic procedure or not, is important.
be used for reconstruction like the temperopari- Attention to the flap harvesting, storage during
etal facial flap, based on the anterior branch of tumour resection, positioning (Avoid kinking of
contiguous areas involved plan more than one

flap. A free mucosal graft can be used as a sup-
plement for defect coverage along with vascular-
ized flap. Postoperative adequate bed rest, bowel
regime, head-end elevation, maintenance of air-
way pressure is important.
Nasal vascular anatomy (Fig. 7.61) About

40% have two branches of the posterior septal
artery at sphenopalatine foramen and 70% have
two branches of the posterior septal artery at the
level of sphenoid ostium (Fig. 7.61c). Mean dis-
tance from sphenoid ostium is 9.3 mm
(5–15 mm) [135, 136].
Fig. 7.59 Extended endonasal approach (1) transfrontal,
(2) trans-cribriform, (3) transplanum, (4) trans-sellar, (5)
trans-clival
7.11.3 Endonasal Mucosal Flaps
the pedicle) and fixation over the defect is para- 1. Nasoseptal flap (NSF)—(Hadad–
mount for the best outcome. Flaps should be peri- Bassagasteguy flap)—The NSF was designed
odically removed from its stored position to by Gustavo Hadad and Luis Bassagasteguy
reduce congestion. The flap should confound to from Argentina in 1996. It is an axial flap that
the complex skull base defect by making the sur- is based on the posterior septal branch of the
rounding bone surface smooth and filling dead Sphenopalatine artery (Fig. 7.62b). The flap
space with fat. Avoid burying of functional provides a large surface area and a wide arc of
mucosa as this can lead to mucocele formation in rotation which helps in covering defects from
the late postoperative period. Reconstruction the frontal region till the lower Clivus
should be robust and reliable enough to separate (Fig. 7.62c). The side from which it should be
the nasal cavity from the cranial cavity. Small harvested depends on anatomical variation
defects (CSF grades 0, 1, 2) are usually managed (deviated nasal septum and turbinate anoma-
with non-vascularized graft [134]. Large defects lies), side and extent of tumour, visualization
(CSF grade 3, 4), defects with high central pres- and space for instrumentation, surgeon prefer-
sure, post-radiotherapy and those who need post- ence, side and size of skull base defect. It is
operative radiotherapy will need vascular preferred to harvest the flap from the non-
reconstruction (Fig. 7.60 and Table 7.3). tumour side or from the side of the dural
Restoration of normal nasal and cranial physiol- defect. In paediatric patients (till 14 years),
ogy as much as possible should always be due to the differential growth rate of facial
attempted. Avoiding a tight nasal packing at the skeleton with the cranium, the use of NSF is
end of the procedure will help in retaining ade- limited [131]. Contraindications for an NSF
quate vascularity to the harvested vascular flaps. are if the tumour is involving the nasal septum
CSF diversion can be considered in selected or the sphenoidal rostrum and in patients in
cases, like those where there is a direct communi- whom there is a history of previous septal
cation of the defect with high-flow CSF pathways surgery.
(communication with the third ventricle). In Surgical Technique
cases of lesion crossing lateral to pterygoid plan, Adequate decongestion of the nasal mucosa
contralateral falp is indicated. Covering of two as in any other endonasal surgery is essential
contiguous areas of skull base defect is feasible before attempting any instrumentation and
with a single flap (NSF), when more than two this is an essential initial step. Exposure of
CLASSIFICATION OF FLAPS
Non vascularised graft

Mechanism of flap uptake
Fascial graft-Facialata, temporalis
fascia
Free mucasal graft Free graft
Fat
Cartilage Adherence (with fibrin)
Bone
Muscle Serum imbibtion 2-4 days
Allograft–acellular dermais,
Exograft-collagen matrix Inosculation
Tissure sealants
Titanium mesh
Collogen matrix is the most preferred Revascularisation
material for underlay
Neovascularisation
Vascularised flaps
Local–
Mechanism of flap uptake
• MSF (Nasoseptal artery)
• Middle turbinate flap (artery to
Depends on the blood supply of recipient
MT from SPA)
• Inferior turbinate flap
Anteriorly base endonasal
flap
(Random pattern based on Perfusion to the wound site
Anterior ethmoidal artery)
Posteriorly based endonasal Various stages of inflammation
flap
(Inferior conchal artery)
Regional- Neo-angiogenesis
• Pericranial flap (Trochlear and
supra-orbital artery) Remodelling
• Temperoparietal flap (STA)
• Palatal flap (Greater palatine artery)
Fig. 7.60 Classification and mechanism of uptake of graft and flap
Table 7.3 Intraoperative CSF leak grading system

Grade of leak Description
Grade 0 Absence of leak confirmed by Valsalva manoeuvre
Grade 1 Small “weeping” leak confirmed by Valsalva manoeuvre, without obvious or with only small
diaphragmatic defect
Grade 2 Moderate CSF leak, with obvious diaphragmatic defect
Grade 3 Large CSF leak, resulting from dural defect that comprises the entire diaphragm or planum
Grade 4 Large CSF leak, resulting from a dural defect of:
• Other single or multiple modules
• Trans-sellar module and an adjacent module
Sphenoethmoidal recess is the next step, and on the need, it can be extended superiorly till
this is done by lateralization of the middle tur- the dorsum of the nose or anteriorly till the
binate (or partial resection) followed by resec- mucocutaneous junction. The inferior incision
tion of lower one-third of superior turbinate. is made over the superior aspect of the poste-
This is followed by the exposure of mucosal rior choana and extends towards the posterior
bridge between sphenoidal ostium and upper part of septum and junction of septum and
choana. A fine tip mono-polar on 12–15 W nasal floor, based on the need it can involve
setting is preferred for mucosal incision. The the nasal floor or the inferior turbinate
superior incision of the NSF starts just below (Fig 7.62a). The anterior incision is made to
the sphenoidal ostium and followed anteriorly connect the superior and inferior incisions.
1 to 1.5 cm below the anterior skull base till The plane of dissection is in the sub-
the anterior end of the middle turbinate. Based mucoperichondrial over the cartilaginous
a b
Fig. 7.61 Nasal vascular anatomy (a) Medial Nasal wall, artery, (5) inferior branch of posterior septal artery, (6)
(b) Lateral Nasal wall, (c) Endoscopic Posterior nasal Superior labial branch of facial artery, (7) SPA (main
cavity. (1) Anterior ethmoidal artery, (2) Posterior eth- trunk), (8) Posterior lateral nasal artery, (9) Middle turbi-
moidal artery, (3) Nasoseptal branch of sphenopalatine nate artery, (10) Inferior turbinate artery, (11) Superior
artery (SPA), (4) Superior branch of posterior septal turbinate, (12) Middle turbinate, (13) Inferior turbinate
a b
Fig. 7.62 Nasoseptal flap (NSF), (a) Types of NSF, (b) (5) inferior incision, (6) reconstruction of posterior table
Incisions of NSF, (c) Uses of NSF. (1) Basic NSF, (2) of the frontal sinus, (7) reconstruction of planum and
anterior extension, (3) lateral extension (into floor with or sella, (8) reconstruction of clivus
without inferior turbinate mucosa), (4) superior incision,
nasal septum and sub-mucoperiosteal at its or nasal packing, which is removed after 2–3
bony part. days.
After harvesting, the flap is stored in the naso- 2. Rescue Nasoseptal Flap
pharynx or into the wide middle meatal The rescue NSF is useful in cases of unantici-
antrostomy. Repair is preferably multilayered, pated leaks [135]. The technique consists of
inlay with collagen graft (preferred) or syn- identification of sphenoid ostium followed by
thetic dural substitutes, autologous fascia, fat short mucosal incision (1–2 cm) from ostium
and onlay with vascularized flaps primarily to superior septum, and this is followed by an
covering the high-pressure areas and followed inferior incision made over superior choana
by layers of oxidized cellulose, tissue glue and vascular pedicle is dissected from anterior
and gel foam. Final support for the recon- sphenoid space. Total mucosal flap elevation
struction can be given using a Foley catheter can be done at the end of the procedure if
a b
Fig. 7.63 Inferior turbinate nasal flap. (a) Anteriorly based flap, (b) posteriorly based flap
needed. The major concern about the rescue

NSF is that the vascular pedicle is at risk
throughout the procedure.
3. Anteriorly Based Inferior turbinate endo-
nasal flap (Fig. 7.63a)
1
The anteriorly based inferior turbinate endo-
2
nasal flap is the random pattern flap based on
anterior ethmoidal artery [137]. The Mucosa
of the inferolateral nasal wall is used for the
reconstruction. This flap is useful in recon-
structing posterior frontal sinus defects.
4. Posteriorly Based Inferior turbinate endo-
nasal flap (Fig. 7.63b)
The posteriorly based inferior turbinate endo-
nasal flap is an axial flap based on the inferior
conchal artery. This artery enters 1–1.5 cm Fig. 7.64 Middle turbinate flap. (1) Anterior and medial
incision, (2) lateral incision
anterior to posterior end of inferior turbinate
from the lateral side of the inferior turbinate
[137]. This endonasal flap is useful in repair- junction area. The only contraindication
ing small sellar and clival defects. is any previous fronto-temporal proce-
5. Middle turbinate flap (Fig. 7.64) dures. Through a hemi-coronal incision,
The middle turbinate flap is an axial flap based flap is raised between the subcutaneous
on the middle turbinate artery [138]. This is tissue and superficial layer of the deep
useful in repairing cribriform area defects. temporal facia and transported via the
6. Regional flaps infratemporal fossa and the pterygopala-
(a) Temperoparietal facial flaps tine fossa [139].
The temperoparietal facial flap is based Pericranial flap (Fig. 7.30A)
(b)
on the anterior branch of the superficial The Pericranial flap derives its vascular
temporal artery. This regional flap is used supply from the supraorbital and supra-
for the reconstruction of defects from pla- trochlear artery. It is used for the closure
num sphenoidale till the cranial–vertebral of defects from cribriform area, the sella
and till the clivus. It cannot be harvested 8. Geltzeiler M, Turner M, Rimmer R, et al. Endoscopic
in patients who have undergone a previ- nasopharyngectomy combined with a nerve-
sparing transpterygoid approach. Laryngoscope.
ous fronto-temporal procedure. Through 2020;130:2343–8. https://doi.org/10.1002/lary.28479.
coronal incision or endoscope-assisted 9. Locatelli D, Pozzi F, Turri-Zanoni M, et al.
coronal incision pericranium flap is har- Transorbital endoscopic approaches to the skull base:
vested [140]. current concepts and future perspectives. J Neurosurg
Sci. 2016;60(4):514–25.
(c) Palatal flap (Oliver flap) 10. Kenyon B, Antisdel JL. Anatomic evaluation of endo-
The palatal flap or the Oliver flap is scopic transnasal transorbital approach to the lateral
based on the descending palatine artery. orbital apex. Am J Rhinol Allergy. 2014;28(1):82–5.
It is useful for defect repair in planum, https://doi.org/10.2500/ajra.2014.28.4000.
11. Kong DS, Young SM, Hong CK, et al. Clinical and oph-
sella and clivus regions. In patients with thalmological outcome of endoscopic transorbital surgery
previous palatal procedures, the flap for cranioorbital tumors. J Neurosurg. 2018;131(3):667–
cannot be used. The mucoperiosteal 75. https://doi.org/10.3171/2018.3.JNS173233.
flap from the hard palate with preserva- 12. Mehta GU, Raza SM. Endoscopic endonasal transpter-
ygoid approach to petrous pathologies: technique,
tion of one side greater palatine vessels limitations and alternative approaches. J Neurosurg
is harvested transported into nasal cav- Sci. 2018;62(3):339–46. https://doi.org/10.23736/
ity to reconstruct the skullbase defect S0390-5616.18.04302-3.
[141]. 13. Hardesty DA, Montaser AS, Carrau RL, Prevedello
DM. Limits of endoscopic endonasal transpterygoid
(d) Other less commonly used flaps for skull approach to cavernous sinus and Meckel’s cave.
base deconstruction are the occipital flap J Neurosurg Sci. 2018;62(3):332–8. https://doi.
and the buccal flap [142]. org/10.23736/S0390-5616.18.04330-8.
14. Park HH, Hong SD, Kim YH, et al. Endoscopic

transorbital and endonasal approach for trigeminal
schwannomas: a retrospective multicenter analysis
References (KOSEN-005) [published online ahead of print, 2019
Jun 21]. J Neurosurg. 2019:1–10. https://doi.org/10.3
1. De Lara D, Ditzel Filho LF, Prevedello DM, et al. 171/2019.3.JNS19492.
Endonasal endoscopic approaches to the paramedian 15. Battaglia P, Turri-Zanoni M, Dallan I, et al. Endoscopic
skull base. World Neurosurg. 2014;82(6 Suppl):S121–9. endonasal transpterygoid transmaxillary approach to
https://doi.org/10.1016/j.wneu.2014.07.036. the infratemporal and upper parapharyngeal tumors.
2. Kassam A, Snyderman CH, Mintz A, Gardner P, Otolaryngol Head Neck Surg. 2014;150(4):696–702.
Carrau RL. Expanded endonasal approach: the ros- https://doi.org/10.1177/0194599813520290.
trocaudal axis. Part I. Crista galli to the sella turcica. 16. Kasemsiri P, Carrau RL, Ditzel Filho LF, et al.

Neurosurg Focus. 2005;19(1):E3. Advantages and limitations of endoscopic endona-
3. Cappabianca P, Cavallo LM, de Divitiis E. Endoscopic sal approaches to the skull base. World Neurosurg.
endonasal transsphenoidal surgery. Neurosurgery. 2014;82(6 Suppl):S12–21. https://doi.org/10.1016/j.
2004;55(4):933–41. https://doi.org/10.1227/01. wneu.2014.07.022.
neu.0000137330.02549.0d. 17. Watanabe K, Zomorodi AR, Labidi M, Satoh S,

4. Goudakos JK, Markou KD, Georgalas C. Endoscopic Froelich S, Fukushima T. Visualization of dark side
versus microscopic trans-sphenoidal pituitary of skull base with surgical navigation and endoscopic
surgery: a systematic review and meta-analysis. assistance: extended petrous rhomboid and rhomboid
Clin Otolaryngol. 2011;36(3):212–20. https://doi. with maxillary nerve-mandibular nerve vidian corri-
org/10.1111/j.1749-4486.2011.02331.x. dor. World Neurosurg. 2019;129:e134–45. https://doi.
5. Aydin S, Cavallo LM, Messina A, et al. The endo- org/10.1016/j.wneu.2019.05.062.
scopic endonasal trans-sphenoidal approach to the sel- 18. Joo W, Funaki T, Yoshioka F, Rhoton AL Jr.

lar and suprasellar area. Anatomic study. J Neurosurg Microsurgical anatomy of the infratemporal
Sci. 2007;51(3):129–38. fossa. Clin Anat. 2013;26(4):455–69. https://doi.
6. Vescan AD, Snyderman CH, Carrau RL, et al. Vidian org/10.1002/ca.22202.
canal: analysis and relationship to the internal carotid 19. Fortes FS, Sennes LU, Carrau RL, et al. Endoscopic
artery. Laryngoscope. 2007;117(8):1338–42. https:// anatomy of the pterygopalatine fossa and the
doi.org/10.1097/MLG.0b013e31806146cd. transpterygoid approach: development of a surgical
7. Kassam A, Snyderman CH, Mintz A, Gardner P, instruction model. Laryngoscope. 2008;118(1):44–9.
Carrau RL. Expanded endonasal approach: the rostro- https://doi.org/10.1097/MLG.0b013e318155a492.
caudal axis. Part II. Posterior clinoids to the foramen 20. Arya S, Rane P, D’Cruz A. Infratemporal Fossa,

magnum. Neurosurg Focus. 2005;19(1):E4. Masticator space and parapharyngeal space: Can the
radiologist and surgeon speak the same language? tinomas. Surg Neurol. 1989;32(5):346–9. https://doi.
Otorhinolaryngol Clin. 2012;4(3):125–35. org/10.1016/0090-3019(89)90137-7.
21. Falcon RT, Rivera-Serrano CM, Miranda JF, et al. 33. Bronstein MD. Prolactinomas and pregnancy.
Endoscopic endonasal dissection of the infratem- Pituitary. 2005;8(1):31–8. https://doi.org/10.1007/
poral fossa: anatomic relationships and importance s11102-005-5083-4.
of eustachian tube in the endoscopic skull base sur- 34. Jallad RS, Musolino NR, Salgado LR, Bronstein
gery. Laryngoscope. 2011;121(1):31–41. https://doi. MD. Treatment of acromegaly: is there still a place
org/10.1002/lary.21341. for radiotherapy? Pituitary. 2007;10(1):53–9. https://
22. Hofstetter CP, Singh A, Anand VK, Kacker A,
doi.org/10.1007/s11102-007-0002-5.
Schwartz TH. The endoscopic, endonasal, trans- 35. Pivonello R, De Martino MC, De Leo M, Lombardi
maxillary transpterygoid approach to the pterygo- G, Colao A. Cushing’s Syndrome. Endocrinol Metab
palatine fossa, infratemporal fossa, petrous apex, and Clin N Am. 2008;37(1):135–149, ix. https://doi.
the Meckel cave. J Neurosurg. 2010;113(5):967–74. org/10.1016/j.ecl.2007.10.010.
https://doi.org/10.3171/2009.10.JNS09157. 36. Sindwani R, Woodard TD, Recinos PF. Endoscopic
23.
Kim SM, Paek SH, Lee JH. Infratemporal cranial base and pituitary surgery. Otolaryngol Clin
fossa approach: the modified zygomatico- N Am. 2016;49(1):xix–xx. https://doi.org/10.1016/j.
transmandibular approach. Maxillofac Plast Reconstr otc.2015.09.01.
Surg. 2019;41(1):3. https://doi.org/10.1186/ 37. Sethi DS, Leong JL. Endoscopic pituitary surgery.
s40902-018-0185-x. Otolaryngol Clin North Am. 2006;39(3):563. https://
24. Sekhar LN, Schramm VL Jr, Jones NF. Subtemporal- doi.org/10.1016/j.otc.2006.01.011.
preauricular infratemporal fossa approach to 38. Favier V, Boetto J, Cartier C, Segnarbieux F,
large lateral and posterior cranial base neoplasms. Crampette L. Endoscopic transnasal transseptal pitu-
J Neurosurg. 1987;67(4):488–99. https://doi. itary surgery. Eur Ann Otorhinolaryngol Head Neck
org/10.3171/jns.1987.67.4.0488. Dis. 2019;136(2):131–4. https://doi.org/10.1016/j.
25. Jain R, Keshri A, Manogaran R, Kumar R, Keeranghat anorl.2018.10.005.
P. Preauricular transzygomatic approach for infra- 39. de Almeida JR, Zanation AM, Snyderman CH, et al.
temporal fossa and surrounding skull base lesion: Defining the nasopalatine line: the limit for endonasal
an institutional experience. Ann Otol Neurotol. surgery of the spine. Laryngoscope. 2009;119(2):239–
2018;01(02):094–9. 44. https://doi.org/10.1002/lary.20108.
26. Parent AD, Brown B, Smith EE. Incidental pitu- 40. Yasuda A, Campero A, Martins C, Rhoton AL Jr, de

itary adenomas: a retrospective study. Surgery. Oliveira E, Ribas GC. Microsurgical anatomy and
1982;92(5):880–3. approaches to the cavernous sinus. Neurosurgery.
27.
Willemse RB, van Furth WR, Fokkens W, 2005;56(1 Suppl):4–27. https://doi.org/10.1227/01.
CG. Endoscopic approach to the sella. In: Georgalas neu.0000144208.42171.02.
C, Fokkens W, editors. Rhinology and skull base sur- 41. Donald PJ. Skull base surgery for malignancy:
gery from the lab to the operating room: an evidence- when not to operate. Eur Arch Otorhinolaryngol.
based approach. Thieme, New York. Stuttgart; 2013. 2007;264(7):713–7. https://doi.org/10.1007/
p. 738–57. s00405-007-0268-2.
28. Marcello D. Bronstein. Surgical indications for pitu- 42. Svane-Knudsen V, Jørgensen KE, Hansen O,
itarytumors. In: Stamm AIC, editor. Transnasal endo- Lindgren A, Marker P. Cancer of the nasal cavity and
scopic skull base and brain surgery tips and pearls. paranasal sinuses: a series of 115 patients. Rhinology.
New York: Thieme, Stuttgart; 2011. p. 224–7. 1998;36(1):12–4.
29. Teramoto A, Hirakawa K, Sanno N, Osamura 43. LoyAH, Reibel JF, Read PW, et al. Esthesioneuroblastoma:

Y. Incidental pituitary lesions in 1,000 unselected continued follow-up of a single institution’s experience.
autopsy specimens. Radiology. 1994;193(1):161–4. Arch Otolaryngol Head Neck Surg. 2006;132(2):134–8.
https://doi.org/10.1148/radiology.193.1.8090885. https://doi.org/10.1001/archotol.132.2.134.
30. Hall WA, Luciano MG, Doppman JL, Patronas
44. Lin EM, Sparano A, Spalding A, et al. Sinonasal
NJ, Oldfield EH. Pituitary magnetic reso- undifferentiated carcinoma: a 13-year experience
nance imaging in normal human volunteers: at a single institution. Skull Base. 2010;20(2):61–7.
occult adenomas in the general population. Ann https://doi.org/10.1055/s-0029-1236165.
Intern Med. 1994;120(10):817–20. https://doi. 45. Janecka IP, Sen CN, Sekhar LN, Arriaga M. Facial
org/10.7326/0003-4819-120-10-199405150-00001. translocation: a new approach to the cranial base.
31. Dekkers OM, Pereira AM, Romijn JA. Treatment and fol- Otolaryngol Head Neck Surg. 1990;103(3):413–9.
low-up of clinically nonfunctioning pituitary macroade- https://doi.org/10.1177/019459989010300312.
nomas. J Clin Endocrinol Metab. 2008;93(10):3717–26. 46. Cheesman AD, Reddy K. Craniofacial resection: a 10
https://doi.org/10.1210/jc.2008-0643. year experience. Proceedings of the 15th European
32. Bronstein MD, Musolino NR, Benabou S, Marino Rhinologic Congress; 1995.
R Jr. Cerebrospinal fluid rhinorrhea occurring in 47. Abu-Ghanem S, Fliss DM. Surgical approaches to
long-term bromocriptine treatment for macroprolac- resection of anterior skull base and paranasal sinuses
tumors. Balkan Med J. 2013;30(2):136–41. https:// 61. Herzallah I, Alzuraiqi B, Bawazeer N, et al. Endoscopic
doi.org/10.5152/balkanmedj.2013.9112. Dacryocystorhinostomy (DCR): a comparative study
48. Donald PJ. Frontobasal approach for trauma and
between powered and non- powered technique. J
tumor. Minim Invasive Neurosurg. 1994;37(2):37–41. Otolaryngol Head Neck Surg. 2015;44:56. https://doi.
https://doi.org/10.1055/s-2008-1053446. org/10.1186/s40463-015-0109-z.
49. Elbabaa SK, Al-Mefty O. Craniofacial approach for 62. Khalifa MA, Ragab SM, Saafan ME, El-Guindy

anterior skull-base lesions. Atlas Oral Maxillofac AS. Endoscopic dacryocystorhinostomy with double
Surg Clin North Am. 2010;18(2):151–60. https://doi. posteriorly based nasal and lacrimal flaps: a pro-
org/10.1016/j.cxom.2010.08.007. spective randomized controlled trial. Otolaryngol
50. Hendryk S, Czecior E, Misiołek M, Namysłowski Head Neck Surg. 2012;147(4):782–7. https://doi.
G, Mrówka R. Surgical strategies in the removal of org/10.1177/0194599812447759.
malignant tumors and benign lesions of the ante- 63. Mueller SK, Freitag SK, Lefebvre DR, Bleier

rior skull base. Neurosurg Rev. 2004;27(3):205–13. BS. Endoscopic DCR using bipedicled interlacing
https://doi.org/10.1007/s10143-004-0323-z. mucosal flaps. Laryngoscope. 2018;128(4):794–7.
51. McCutcheon IE, Blacklock JB, Weber RS, et al.
https://doi.org/10.1002/lary.26730.
Anterior transcranial (craniofacial) resection of 64. Tsirbas A, Wormald PJ. Endonasal dacryocysto-

tumors of the paranasal sinuses: surgical technique rhinostomy with mucosal flaps. Am J Ophthalmol.
and results. Neurosurgery. 1996;38(3):471–80. 2003;135(1):76–83. https://doi.org/10.1016/
https://doi.org/10.1097/00006123-199603000-00009. s0002-9394(02)01830-5.
52. Raveh J, Laedrach K, Speiser M, et al. The subcranial 65. Tabatabaie SZ, Heirati A, Rajabi MT, Kasaee A.

approach for fronto-orbital and anteroposterior skull- Silicone intubation with intraoperative mitomycin C
base tumors. Arch Otolaryngol Head Neck Surg. for nasolacrimal duct obstruction in adults: a prospec-
1993;119(4):385–93. https://doi.org/10.1001/archo tive, randomized, double-masked study. Ophthalmic
tol.1993.01880160029006. Plast Reconstr Surg. 2007;23(6):455–8. https://doi.
53. Spektor S, Valarezo J, Fliss DM, et al. Olfactory
org/10.1097/IOP.0b013e3181579795.
groove meningiomas from neurosurgical and ear, nose, 66. Tsirbas A, Davis G, Wormald PJ. Mechanical endo-
and throat perspectives: approaches, techniques, and nasal dacryocystorhinostomy versus external dac-
outcomes. Neurosurgery. 2005;57(4 Suppl):268–80. ryocystorhinostomy. Ophthalmic Plast Reconstr
https://doi.org/10.1227/01.neu.0000176409.70668. Surg. 2004;20(1):50–6. https://doi.org/10.1097/01.
eb. IOP.0000103006.49679.23.
54. Abergel A, Fliss DM, Margalit N, Gil Z. A prospec- 67. Selig YK, Biesman BS, Rebeiz EE. Topical applica-
tive evaluation of short-term health-related qual- tion of mitomycin-C in endoscopic dacryocystorhi-
ity of life in patients undergoing anterior skull base nostomy. Am J Rhinol. 2000;14(3):205–7. https://doi.
surgery. Skull Base. 2010;20(1):27–33. https://doi. org/10.2500/105065800782102672.
org/10.1055/s-0029-1242982. 68. Saeed BM. Endoscopic DCR without stents: clinical
55. Jones LT, Linn ML. The diagnosis of the causes of guidelines and procedure. Eur Arch Otorhinolaryngol.
epiphora. Am J Ophthalmol. 1969;67:751–4. 2012;269(2):545–9. https://doi.org/10.1007/
56. Somma F, d’Agostino V, Tortora F, et al. Magnetic s00405-011-1727-3.
resonance imaging in the pre-operative evaluation of 69. Kang MG, Shim WS, Shin DK, Kim JY, Lee JE, Jung
obstructive epiphora: true-FISP and VIBE vs gado- HJ. A systematic review of benefit of silicone intu-
linium. Radiol Med. 2017;122(2):123–30. https://doi. bation in endoscopic dacryocystorhinostomy. Clin
org/10.1007/s11547-016-0696-4. Exp Otorhinolaryngol. 2018;11(2):81–8. https://doi.
57. Savino G, Battendieri R, Traina S, et al. External org/10.21053/ceo.2018.00031.
vs. endonasal dacryocystorhinostomy: has the cur- 70. Dave TV, Mohammed FA, Ali MJ, Naik MN. Etiologic
rent view changed? Acta Otorhinolaryngol Ital. analysis of 100 anatomically failed dacryocysto-
2014;34(1):29–35. rhinostomies. Clin Ophthalmol. 2016;10:1419–22.
58. Rudert H, Maune S, Mahnke CG. Komplikationen https://doi.org/10.2147/OPTH.S113733.
der endonasalen Chirurgie der Nasennebenhöhlen. 71. Joshi RS. Conventional dacryocystorhinostomy in a
Inzidenz und Strategien zu ihrer Vermeidung failed Trans-canalicular laser-assisted dacryocysto-
[Complications of endonasal surgery of the parana- rhinostomy. Indian J Ophthalmol. 2011;59(5):383–5.
sal sinuses. Incidence and strategies for prevention]. https://doi.org/10.4103/0301-4738.83617.
Laryngorhinootologie. 1997;76(4):200–15. https:// 72. Sivak-Callcott JA, Linberg JV, Patel S. Ultrasonic

doi.org/10.1055/s-2007-997414. bone removal with the Sonopet Omni: a new
59. Hashemi SM, Eshaghian A. Limited approach in
instrument for orbital and lacrimal surgery. Arch
endoscopic dacryocystorhinostomy of pediatrics. Adv Ophthalmol. 2005;123(11):1595–7. https://doi.
Biomed Res. 2017;6:141. https://doi.org/10.4103/abr. org/10.1001/archopht.123.11.1595.
abr_375_14. 73. Kato K, Matsunaga K, Takashima Y, Kondo M.

60. Metson R. Endoscopic surgery for lacrimal obstruc- Probing of congenital nasolacrimal duct obstruction
tion. Otolaryngol Head Neck Surg. 1991;104(4):473– with dacryoendoscope. Clin Ophthalmol. 2014;8:977–
9. https://doi.org/10.1177/019459989110400408. 80. https://doi.org/10.2147/OPTH.S60377.
74. Lim C, Martin P, Benger R, Kourt G, Ghabrial

Laryngol Otol. 2004;118(5):352–6. https://doi.
R. Lacrimal canalicular bypass surgery with the Lester org/10.1258/002221504323086534.
Jones tube. Am J Ophthalmol. 2004;137(1):101–8. 88. Courson AM, Stankiewicz JA, Lal D. Contemporary
https://doi.org/10.1016/j.ajo.2003.08.002. management of frontal sinus mucoceles: a meta-
75. Nomura K, Arakawa K, Sugawara M, Hidaka
analysis. Laryngoscope. 2014;124(2):378–86. https://
H, Suzuki J, Katori Y. Factors influencing endo- doi.org/10.1002/lary.24309.
scopic dacryocystorhinostomy outcome. Eur Arch 89. Reale G, Ungari C, Riccardi E, et al. Fronto-

Otorhinolaryngol. 2017;274(7):2773–7. https://doi. ethmoidal osteoma. Open treatment. Ann Ital Chir.
org/10.1007/s00405-017-4541-8. 2014;85(3):214–8.
76. Kuczkowski J, Narozny W, Stankiewicz C, et al.
90. Brown OE, Pownell P, Manning SC. Choanal

Sluzowiaki zatok przynosowych [Mucoceles of the atresia: a new anatomic classification and clini-
paranasal sinuses]. Otolaryngol Pol. 2007;61(5):680– cal management applications. Laryngoscope.
6. https://doi.org/10.1016/S0030-6657(07)70506-1. 1996;106(1 Pt 1):97–101. https://doi.
77. Lund VJ. Anatomical considerations in the aetiol- org/10.1097/00005537-199601000-00019.
ogy of fronto-ethmoidal mucoceles. Rhinology. 91. Kurosaka H. Choanal atresia and stenosis: devel-

1987;25:83–8. opment and diseases of the nasal cavity. Wiley
78. Benkhatar H, Khettab I, Sultanik P, Laccourreye O, Interdiscip Rev Dev Biol. 2019;8(1):e336. https://doi.
Bonfils P. Mucocele development after endoscopic org/10.1002/wdev.336.
sinus surgery for nasal polyposis: a long-term analy- 92. Ramsden JD, Campisi P, Forte V. Choanal atre-

sis. Ear Nose Throat J. 2018;97(9):284–94. https:// sia and choanal stenosis. Otolaryngol Clin North
doi.org/10.1177/014556131809700918. Am. 2009;42(2):339. https://doi.org/10.1016/j.
79.
Lund VJ, Harvey W, Meghji S, Harris M. otc.2009.01.001.
Prostaglandin synthesis in the pathogenesis of 93. Dupé V, Matt N, Garnier JM, Chambon P, Mark M,
fronto-ethmoidal mucoceles. Acta Otolaryngologica. Ghyselinck NB. A newborn lethal defect due to inac-
1988;106:145–51. tivation of retinaldehyde dehydrogenase type 3 is pre-
80. Lund VJ, Henderson B, Song Y. Involvement of
vented by maternal retinoic acid treatment. Proc Natl
cytokines and vascular adhesion receptors in the Acad Sci U S A. 2003;100(24):14036–41. https://doi.
pathology of fronto-ethmoidal mucoceles. Acta org/10.1073/pnas.2336223100.
Otolaryngologica. 1993;113:540–6. 94. Barbero P, Valdez R, Rodríguez H, et al. Choanal
81. Hansen FS, van der Poel NA, Freling NJM, Fokkens atresia associated with maternal hyperthyroidism
WJ. Mucocele formation after frontal sinus oblit- treated with methimazole: a case-control study. Am
eration. Rhinology. 2018;56(2):106–10. https://doi. J Med Genet A. 2008;146A(18):2390–5. https://doi.
org/10.4193/Rhin17.187. org/10.1002/ajmg.a.32497.
82. Weissman JL, Tabor EK, Curtin HD. Magnetic reso- 95. Kwong KM. Current updates on choanal atresia.

nance imaging of the paranasal sinuses. Top Magn Front Pediatr. 2015;3:52. https://doi.org/10.3389/
Reson Imaging. 1990;2(4):27–38. fped.2015.00052.
83. Kennedy DW, Josephson JS, Zinreich SJ, Mattox DE, 96. Holtmann L, Stähr K, Kirchner J, Lang S, Mattheis
Goldsmith MM. Endoscopic sinus surgery for muco- S. Die endonasale endoskopische Resektion von
celes. Laryngoscope. 1989;99:885–95. Choanalatresien – wie groß ist der Langzeiterfolg?
84. Facon F, Nicollas R, Paris J, Dessi P. La chirurgie des [Endonasal endoscopic surgery of choanal atresia –
mucocèles sinusiennes: notre expérience à propos de long term results]. Laryngorhinootologie. 2018;
52 cas suivis à moyen terme [Surgery of mucocele of https://doi.org/10.1055/s-0044-101464.
the paranasal sinuses: report of 52 cases with a middle 97. Saraniti C, Santangelo M, Salvago P. Surgical

term follow up]. Rev Laryngol Otol Rhinol (Bord). treatment of choanal atresia with transnasal endo-
2008;129(3):167–73. scopic approach with stentless single side-hinged
85. Santos PLD, Chihara LL, Alcalde LFA, Masalskas flap technique: 5 year retrospective analysis. Braz
BF, Sant’Ana E, Faria PEP. Outcomes in surgical J Otorhinolaryngol. 2017;83(2):183–9. https://doi.
treatment of mucocele in frontal sinus. J Craniofac org/10.1016/j.bjorl.2016.03.009.
Surg. 2017;28(7):1702–8. https://doi.org/10.1097/ 98. Eladl HM, Khafagy YW. Endoscopic bilateral con-
SCS.0000000000003224. genital choanal atresia repair of 112 cases, evolv-
86. Venail F, Marlier F, Makeieff M, et al. Indications ing concept and technical experience. Int J Pediatr
des voies combinées (endoscopique et externe) dans Otorhinolaryngol. 2016;85:40–5. https://doi.
le traitement des mucocèles sinusiennes [Combined org/10.1016/j.ijporl.2016.03.011.
approach (endoscopic and external) for the treatment 99. De Freitas RP, Berkowitz RG. Bilateral choanal atre-
of sinusal mucoceles]. Rev Laryngol Otol Rhinol sia repair in neonates--a single surgeon experience.
(Bord). 2003;124(3):165–70. Int J Pediatr Otorhinolaryngol. 2012;76(6):873–8.
87.
Khong JJ, Malhotra R, Selva D, Wormald https://doi.org/10.1016/j.ijporl.2012.02.063.
PJ. Efficacy of endoscopic sinus surgery for parana- 100. Durmaz A, Tosun F, Yldrm N, Sahan M, Kvrakdal
sal sinus mucocele including modified endoscopic C, Gerek M. Transnasal endoscopic repair of cho-
Lothrop procedure for frontal sinus mucocele. J anal atresia: results of 13 cases and meta-analysis.
J Craniofac Surg. 2008;19(5):1270–4. https://doi. 113. Scholsem M, Scholtes F, Collignon F, et al. Surgical
org/10.1097/SCS.0b013e3181843564. management of anterior cranial base fractures with
101. Wormald PJ, Zhao YC, Valdes CJ, et al. The endo- cerebrospinal fluid fistulae: a single-institution expe-
scopic transseptal approach for choanal atresia rience. Neurosurgery. 2008;62(2):463–71. https://
repair. Int Forum Allergy Rhinol. 2016;6(6):654–60. doi.org/10.1227/01.neu.0000316014.97926.82.
https://doi.org/10.1002/alr.21716. 114. Briggs RJ, Wormald PJ. Endoscopic transnasal intra-
102. Cedin AC, Atallah AN, Andriolo RB, Cruz OL, dural repair of anterior skull base cerebrospinal fluid
Pignatari SN. Surgery for congenital choanal atresia. fistulae. J Clin Neurosci. 2004;11(6):597–9. https://
Cochrane Database Syst Rev. 2012;2:CD008993. doi.org/10.1016/j.jocn.2003.09.011.
https://doi.org/10.1002/14651858.CD008993.pub2. 115. Wormald PJ, McDonogh M. ‘Bath-plug’ technique
103. Murray S, Luo L, Quimby A, Barrowman N, Vaccani for the endoscopic management of cerebrospinal
JP, Caulley L. Immediate versus delayed surgery in fluid leaks. J Laryngol Otol. 1997;111(11):1042–6.
congenital choanal atresia: a systematic review. Int https://doi.org/10.1017/s0022215100139295.
J Pediatr Otorhinolaryngol. 2019;119:47–53. https:// 116. Hegazy HM, Carrau RL, Snyderman CH, Kassam
doi.org/10.1016/j.ijporl.2019.01.001. A, Zweig J. Transnasal endoscopic repair of
104. Moreddu E, Rizzi M, Adil E, et al. International cerebrospinal fluid rhinorrhea: a meta-analysis.
Pediatric Otolaryngology Group (IPOG) consensus Laryngoscope. 2000;110(7):1166–72. https://doi.
recommendations: diagnosis, pre-operative, opera- org/10.1097/00005537-200007000-00019.
tive and post-operative pediatric choanal atresia 117. Steinsapir KD, Goldberg RA. Traumatic optic neu-
care. Int J Pediatr Otorhinolaryngol. 2019;123:151– ropathy. Surv Ophthalmol. 1994;38(6):487–518.
5. https://doi.org/10.1016/j.ijporl.2019.05.010. https://doi.org/10.1016/0039-6257(94)90145-7.
105. Bedwell JR, Choi SS. Are stents necessary 118. Steinsapir KD, Goldberg RA. Traumatic optic neu-
after choanal atresia repair? Laryngoscope. ropathy: a critical update. Compr Ophthalmol Updat.
2012;122(11):2365–6. https://doi.org/10.1002/ 2005;6(1):11–21.
lary.23381. 119. Yu-Wai-Man P. Traumatic optic neuropathy-
106. Keller JL, Kacker A. Choanal atresia, CHARGE clinical features and management issues. Taiwan
association, and congenital nasal stenosis. J Ophthalmol. 2015;5(1):3–8. https://doi.
Otolaryngol Clin North Am. 2000;33(6):1343-viii. org/10.1016/j.tjo.2015.01.003.
https://doi.org/10.1016/s0030-6665(05)70285-1. 120. Saeed P, Tavakoli Rad S, Bisschop PHLT. Dysthyroid
107. Ommaya AK, Di Chiro G, Baldwin M, Pennybacker optic neuropathy. Ophthalmic Plast Reconstr Surg.
JB. Non-traumatic cerebrospinal fluid rhinorrhea. J 2018;34(4S Suppl 1):S60–7. https://doi.org/10.1097/
Neurol Neu-rosurg Psychiatry. 1968;31:214–25. IOP.0000000000001146.
108. Chan DT, Poon WS, IP CP, Chiu PW, goh KY. How 121. Abe T, Satoh K, Wada A. Optic nerve decompres-
useful is glucose detection in diagnosing cerebrospi- sion for orbitofrontal fibrous dysplasia: recent
nal fluid leak? The rational use of CT and Beta-2 development of surgical technique and equip-
transferrin assay in detection of cerebrospinal fluid ment. Skull Base. 2006;16(3):145–55. https://doi.
fistula. Asian J Surg. 2004;27(1):39–42. https://doi. org/10.1055/s-2006-949517.
org/10.1016/S1015-9584(09)60242-6. 122. Levin LA, Beck RW, Joseph MP, Seiff S, Kraker
109. Schuknecht B, Simmen D, Briner HR, Holzmann R. The treatment of traumatic optic neuropa-
D. Nontraumatic skull base defects with spontane- thy: the International Optic Nerve Trauma Study.
ous CSF rhinorrhea and arachnoid herniation: imag- Ophthalmology. 1999;106(7):1268–77. https://doi.
ing findings and correlation with endoscopic sinus org/10.1016/s0161-6420(99)00707-1.
surgery in 27 patients. AJNR Am J Neuroradiol. 123. Yu-Wai-Man P, Griffiths PG. Steroids for trau-
2008;29(3):542–9. https://doi.org/10.3174/ajnr. matic optic neuropathy. Cochrane Database
A0840. Syst Rev. 2013;6:CD006032. https://doi.
110. Casiano RR, Jassir D. Endoscopic cerebrospinal org/10.1002/14651858.CD006032.pub4.
fluid rhinorrhea repair: is a lumbar drain necessary? 124. Oh HJ, Yeo DG, Hwang SC. Surgical treatment for
Otolaryngol Head Neck Surg. 1999;121(6):745–50. traumatic optic neuropathy. Korean J Neurotrauma.
https://doi.org/10.1053/hn.1999.v121.a98754. 2018;14(2):55–60. https://doi.org/10.13004/
111. Brodie HA. Prophylactic antibiotics for post- kjnt.2018.14.2.55.
traumatic cerebrospinal fluid fistulae. A meta- 125. Dhaliwal SS, Sowerby LJ, Rotenberg BW. Timing
analysis. Arch Otolaryngol Head Neck Surg. of endoscopic surgical decompression in traumatic
1997;123(7):749–52. https://doi.org/10.1001/archo optic neuropathy: a systematic review of the litera-
tol.1997.01900070093016. ture. Int Forum Allergy Rhinol. 2016;6(6):661–7.
112. Chaaban MR, Illing E, Riley KO, Woodworth https://doi.org/10.1002/alr.21706.
BA. Acetazolamide for high intracranial pres- 126. Thakar A, Mahapatra AK, Tandon DA. Delayed
sure cerebrospinal fluid leaks. Int Forum Allergy optic nerve decompression for indirect optic nerve
Rhinol. 2013;3(9):718–21. https://doi.org/10.1002/ injury. Laryngoscope. 2003;113(1):112–9. https://
alr.21188. doi.org/10.1097/00005537-200301000-00021.
127. Metson R, Pletcher SD. Endoscopic orbital and 135. Pinheiro CD, Synderman CH. Nasoseptal flap. Adv
optic nerve decompression. Otolaryngol Clin N Otorhinolaryngol. 2013;74:42–55.
Am. 2006;39(3):551–ix. https://doi.org/10.1016/j. 136. Pinheiro-neto CD, Ramos HF, Peris-celda M,
otc.2006.01.004. Fernandez-miranda JC, Gardner PA, Snyderman
128. Kumaran AM, Sundar G, Chye LT. Traumatic CH, et al. Study of the nasoseptal flap for endoscopic
optic neuropathy: a review. Craniomaxillofac anterior cranial base reconstruction. Laryngoscope.
Trauma Reconstr. 2015;8(1):31–41. https://doi. 2011;121(12):2514–20.
org/10.1055/s-0034-1393734. 137. Stamm AC, editor. 44 Management of skull base
129. Harvey RJ, Nogueira JF, Schlosser RJ, Patel SJ, defects after extended endoscopic skull base surgery:
Vellutini E, Stamm AC. Closure of large skull base from free grafts to vascularized flaps. In: Transnasal
defects after endoscopic transnasal craniotomy. J endoscopic skull base and brain surgery. Stuttgart:
Neurosurg. 2009;111(2):371–9. Georg Thieme Verlag; 2011.
130. Kassam AB, Thomas A, Carrau RL, Snyderman 138. Georgalas C, Fokkens W, editors. Reconstruction of
CH, Vescan A, Prevedello D, et al. Endoscopic the skull base and management of skull base surgery
reconstruction of the cranial base using a pedicled complications. In: Rhinology and skull base surgery.
nasoseptal flap. Neurosurgery. 2008;63(1 Suppl Stuttgart: Georg Thieme Verlag; 2013.
1):ONS44–52; discussion ONS52–3 139. Fortes FSG, Carrau RL, Snyderman CH, Kassam
131. Shah RN, Surowitz JB, Patel MR, Huang BY, A, Prevedello D, Vescan A, et al. Transpterygoid
Snyderman CH, Carrau RL, et al. Endoscopic transposition of a temporoparietal fascia flap: a new
pedicled nasoseptal flap reconstruction for pediat- method for skull base reconstruction after endoscopic
ric skull base defects. Laryngoscope. 2009;119(6): expanded endonasal approaches. Laryngoscope.
1067–75. 2007;117(6):970–6.
132. Harvey RJ, Smith JE, Wise SK, Patel SJ, Frankel 140. Patel MR, Shah RN, Snyderman CH, Carrau RL,
BM, Schlosser RJ. Intracranial complications before Germanwala AV, Kassam AB, et al. Pericranial flap
and after endoscopic skull base reconstruction. Am J for endoscopic anterior skull-base reconstruction.
Rhinol. 2008;22(5):516–21. Neurosurgery. 2010;66(3):506–12.
133. Hadad G, Bassagasteguy L, Carrau RL, Mataza JC, 141. Oliver CL, Hackman TG, Carrau RL, Snyderman
Kassam A, Snyderman CH, et al. A novel recon- CH, Kassam AB, Prevedello DM, et al. Palatal flap
structive technique after endoscopic expanded endo- modifications allow pedicled reconstruction of the
nasal approaches: vascular pedicle nasoseptal flap. skull base. Laryngoscope. 2008;118(12):2102–6.
Laryngoscope. 2006;116(10):1882–6. 142. Patel MR, Taylor RJ, Hackman TG, Germanwala
134. Esposito F, Dusick JR, Fatemi N, Kelly DF. Graded AV, Sasaki-Adams D, Ewend MG, et al. Beyond the
repair of cranial base defects and cerebrospinal fluid nasoseptal flap: outcomes and pearls with secondary
leaks in transsphenoidal surgery. Oper Neurosurg. flaps in endoscopic endonasal skull base reconstruc-
2007;60(4 Suppl 2):295–304. tion. Laryngoscope. 2014;124(4):846–52.
Prevention and Management
of Complications 8
Anupam Kanodia,Hitesh Verma, Avni Jain,
Gopica Kalsotra, Sheetal Kumari,
Sonu Kumari Agrawal, Hitender Gautam,
Darwin Kaushal, Abhishek Gugliani,
and Jaini Lodha
Contents
8.1 Part A: Cavity Management 278
8.1.1 asal Packing Post-Surgery
N 279
8.1.2 Post-Operative Assessment of Surgical Outcomes 279
8.1.3 Nasal Douching 280
8.1.4 Post-Operative Complications and Their Management 281
8.1.5 Recent Advances 282
8.1.6 Other Therapies 282
8.2 Part B: Antifungal Therapy 282
8.2.2 Classification of Antifungals 283
8.2.3 Antifungal Agents Used for Treatment of Fungal Sinusitis 283
8.2.4 Antifungal Drug Resistance 286
8.2.5 Duration of Medical Therapy for Fungal Sinusitis 286
8.3 Part C: Fess Complications 287
8.3.1 asal Complications
N 287
8.3.2 Orbital Complications 291
8.3.3 Intracranial Complications 294
S. K. Agrawal · H. Gautam
A. Kanodia · H. Verma (*) Microbiology, AIIMS, New Delhi, India
e-mail: drhitesh10@gmail.com D. Kaushal · A. Gugliani
ENT, AIIMS, Jodhpur, Rajasthan, India
A. Jain
ENT, ESIC Medical College Faridabad, J. Lodha
Faridabad, Haryana, India ENT, Seven Hills Hospital,
Andheri East Mumbai, Maharashtra, India
G. Kalsotra · S. Kumari
ENT, GMC, Jammu, India
278 A. Kanodia et al.
8.4 art DA: Biofilms: Its Composition, Detection Methods and Role

P
in Human Infections (Microbiologist Aspect) 295
8.4.1 Introduction of Biofilms 296
8.4.2 Composition of Biofilms 296
8.4.3 Biofilms Formation 296
8.4.4 Biofilms and Antibiotic Resistance 297
8.4.5 Role of Biofilms in Human Infections 297
8.4.6 Biofilms Detection Methods 297
8.4.7 Methods to Control Biofilms 297
8.4.8 Future Aspects of Biofilm 298
8.5 art DB: Biofilms: Surgeon’s Aspect
P 299
8.5.1 Treatment 300
8.6 Part E: Empty Sinus Syndrome 301
8.6.3 Diagnosis 302
8.6.4 Management 302
8.6.5 Conclusion 303
References 303
8.1 Part A: Cavity Management
Performance of FESS for a patient suffering from

nasal polyposis or just chronic rhinosinusitis is
only half the work done. Post-operative manage-
ment of the patient is as important as the surgery
itself. A good follow-up with endoscopic suction
cleaning allows the cavity to heal with minimum
scarring and adhesion formation. An ideal post-
FESS nasal cavity is a cavity without scars or
adhesions; with all the diseased sinuses ade-
quately opened to allow medical therapy to pen-
etrate them. A good cavity care decreases the
chances of infection in the nasal cavity, prevents
scar formation and hastens normal healing by
enhancing mucosa to grow over the raw areas.
To achieve a healthy nasal cavity post-sur-
Fig. 8.1 Healed right nasal cavity with few adhesions
gery, the patient should be religiously followed-
up in the post-operative period (Fig. 8.1). The
first follow-up in the post-operative period is
pack removal. If absorbable nasal packing has may be asked to follow-up every 3–6 months
been used, then the first follow-up can be after subsequently.
3–7 days of surgery. However, if the conven- Saline irrigations are preferably continued
tional nasal pack has been placed, it should be lifelong [1, 2]. On follow-up visits, the patient
removed with in 2–3 days, using liberal saline undergoes nasal endoscopic evaluation of the
and glycerine irrigation. Following this, the cavity. Any blood clots, crusts or debris are
patient needs to follow-up every week for at least cleaned. Any swelling around the nose or eyes
1 month, thereafter if the cavity has healed, he needs to be examined, any deterioration in
8 Prevention and Management of Complications 279
vision or double vision needs to be evaluated and breathing gently through the nose. Apart
further. from saline irrigation, alkaline nasal douching
The cavity care is similar for patients who needs to be done twice or thrice a day. It helps in
undergo surgery for malignancy. However, dur- removal of any debris and prevents crust forma-
ing the follow-up visits, the operating surgeon tion. Steroids, when used topically and orally to
needs to clean the cavity endoscopically, simulta- block the pathway of inflammation, are beneficial
neously looking for any evidence of recurrence in polyp disease, including AFRS, as they reduce
of malignancy. the chances of recurrance [3].
Other important instructions are as follows:
8.1.1 Nasal Packing Post-Surgery (a) Avoid sneezing with mouth closed. Never
suppress sneeze/cough.
Nasal tampons with smooth and fine pores have (b) Do not blow your nose.
little tendency to adhere to tissues and hence (c) Do not bend, lift or strain after surgery.
cause decreased pain on removal. Cotton gauze (d) Avoid aspirin and other NSAIDs for seven to
strips cause the most discomfort, followed by the ten days after surgery. If required, take
non-coated polyvinyl acetal packs, followed by paracetamol.
the other types. Nasal packing should only be
(e) If the patient is on blood thinners, like
done when required and should be removed or Clopidogrel and Aspirin, consult a physician
replaced in 24–48 h depending on the extent of for best time to restart the medications.
surgery.
Pack removal can be done in the sitting posi-
tion, with the patient holding a bowl under his 8.1.2 Post-Operative Assessment
nose for holding the removed pack and to col- of Surgical Outcomes
lect the discharge that occurs subsequently.
Adequate lubrication of the pack needs to be Surgical outcomes can be measured subjectively
done with normal saline, glycerine and ligno- and objectively. SNOT 22 score is widely used
caine (2%). An analgesic can be administered 1 subjective scoring method for assesing CRS-
h prior to pack removal. Once the pack is ade- related disease s everity and quality of life [4].
quately softened, it may be pulled out very SNOT-20 and SNOT-22 are validated Quality of
slowly using the rotatory movement of the wrist Life (QoL) questionnaires, which are answered
and forearm. One pack should be removed at a by the patient. They contain 20 and 22 subjec-
time. After removal, topical nasal rinsing may tive measures respectively based on which qual-
be done using saline and glycerine. Xylo ity of life assessment can be done for sinonasal
metazoline may be added for better haemosta- conditions. They can be used to gauge the sub-
sis. Posterior pharyngeal wall needs evaluation jective improvement following sinonasal sur-
for any active bleeding. geries [5].
Patient needs to be observed for 30–60 min Objectively endoscopic assessment needs to
after complete pack removal for any residual be done using Lund Kennedy scores. The LK
anterior or posterior bleeding. Thereafter patient Endoscopy Score consists of five parameters
can be discharged. (polyposis, discharge, edema, scarring and crust-
Post pack removal, nasal saline mist sprays ing). Each parameter is given a score of 0, 1 or 2
should be used every 2–4 hours to prevent crust based on its severity [6]. Table 8.1 demonstrates
formation and clot deposition. Some bleeding the LK scoring system.
might happen from the nasal cavity while doing Although Lund Kennedy is the commonly
nasal cavity irrigation with saline. However, it is used scoring system, there is another scoring sys-
rarely significant. It can be controlled by local tem—Philpott Javer Endoscopic System which is
pressure, dabbing the nose with a cloth or a tissue used to grade AFRS (Tables 8.2 and 8.3) [7].
Table 8.1 Lund Kennedy endoscopic grading

Characteristics Score = 0 Score = 1 Score = 2
Polyposis None Confined to the middle meatus Beyond middle meatus
Discharge None Clear and thin Thick and mucopurulent
Crusting Absent Mild Severe
Scarring Absent Mild Severe
Edema Absent Mild Severe
Table 8.2 Philpott Javer endoscopic staging system • Hypertonic saline irrigation is also described.
Philpott Javer Endoscopic staging system for AFRS • A recent randomized controlled trial favours
Frontal 0–9 1 0–9 1 the use of Ringer’s lactate over hypertonic or
Ethmoid 0–9 1 0–9 1 isotonic saline [8].
Maxillary 0–9 1 0–9 1
Sphenoid 0–9 1 0–9 1 However, to date the alkaline nasal douche
Total 40 40 remains the preferred douching solution. Home-
Bilateral total 80 made alkaline solutions are equally effective
when compared to ready made dry preparations
Table 8.3 Philpott Javer endoscopic grading system [9].
Grading State of mucosa There are agents that can be used to prevent
0 No edema recurrent crusting, which are as follows:
1–3 Mucosal edema (mild/moderate/severe)
4–6 Polypoid edema (mild/moderate/severe) • Twenty-five percent glucose in glycerine has
7–9 Frank polyposis (mild/moderate/severe) been used locally for patients with atrophic
rhinitis to inhibit the growth of proteolytic
Table 8.4 Kupferberg staging system organisms. They can also be used by a person
Stage Endoscopic findings
who is having recurrent crusting, after having
0 (A/B) No mucosal edema done adequate nasal douching first.
I (A/B) Mucosal edema • Manuka honey has been used in the same role
II (A/B) Polypoidal edema as glucose-glycerine solution. Manuka honey
III (A/B) Sinus polyps is used as a topical antimicrobial agent in
A without allergic mucin, B with allergic mucin cases of chronic infections. In vitro studies
show it is effective against biofilm-producing
Another staging system that is used is bacteria and fungi. There is still no firm level I
Kupferberg staging system [7] (Table 8.4) evidence supporting the use of manuka honey,
The most commonly used staging system but the RCTs show marginal improvement in
remains Lund Kennedy staging system. acute exacerbations of chronic rhinosinusitis
[10]. There is however, no statistically signifi-
cant improvement in SNOT 22 scores proven
8.1.3 Nasal Douching as yet. However, it may have a role in recalci-
trant patients and needs further trials to prove
Traditionally, alkaline nasal douche has been pre- its value.
pared by taking a teaspoon of sodium bicarbon- • Steroid irrigations are the mainstay of topical
ate, sodium diborate and sodium chloride (in a treatment post endoscopic sinus surgery in
ratio of 1:1:2) and mixed in half a pint (280 ml) eosinophilic chronic rhinosinusitis (eCRS).
of lukewarm boiled water. The solution is stirred Eosinophilic CRS is defined histologically as
until all the salts have dissolved. Other agents are the presence of 10 eosinophils per high power
as follows: field. They are delivered in large volume posi-
tive pressure saline irrigations in a dilute form. tril. The solution is then allowed to passively
They do not cause HPA axis suppression [11]. drain through the same nostril. Later the same
process can be repeated with the other nostril.
However, topical steroids have limited role in One must ensure not to sniff large quantities
patients with AFRS. or to swallow the solution. The cupped hand
The following steroidal preparations can be can also be used in place of mug.
used for nasal irrigation for chronic rhinosinusitis • Using a battery-powered pump or a medical
and post-FESS cavity squeeze bottle, which allows the solution to
flow out from the other nostril, hence maxi-
• Fluticasone propionate mizing its effect [13].
• Beclomethasone
• Budesonide (Pulmicort) Large volume low-pressure irrigations are the
preferred method of douching when compared to
A comparative study by Neubauer et al. sniffing method, like medical squeeze bottle,
showed that Budesonide had greater improve- neti pots or bulb syringes [14]. There are various
ments in SNOT-22 scores and Lund—Kennedy methods of delivery- sprays, rinses and respules.
scores as compared to Fluticasone [12]. A clini- There is no level I evidence supporting the use of
cal trial at Yale University is currently comparing any of the three modalities. Please note, the posi-
the efficacy of Fluticasone and budesonide in tions for using nasal topical sprays, i.e. head
controlling the symptoms of chronic rhinosinus- back and head down positions are not described
itis. Nasal douching clears the mucus and crusts. for douching.
It also curbs the urge to pick the nose or blow the
crusts out. There is a lot of raw area after sinus
surgery, which leads to the collection of debris, 8.1.4 Post-Operative Complications
and the formation of crusting, which leads to and Their Management
increase in infection rate and synechiae forma-
tion. Nasal douching minimizes the collection of Recurrent crusting, occasional bleeding and syn-
debris and mucus and accelerates the healing of echiae formation are the most common post-
the raw area. operative problems faced by the patient and the
Following methods can be employed for nasal operating surgeon. Crusting can be prevented by
douching: proper nasal douching and weekly cavity clean-
ing. Bleeding can be prevented by the proper
• Pre-filled containers, neti pots or bulb syringes technique of saline irrigations and nasal douch-
may be used for nasal douching. While breathing, also by not allowing the cavity to dry up. The
ing through the mouth, the solution is intro- forceful blowing of the nose should be avoided.
duced in one nostril while tilting the head to Synechiae formation can be prevented by
the other side. This allows the solution to clear minimizing the mucosal trauma intraoperatively
both the nasal cavities and post-nasal space and being regular and thorough with cavity clean-
while it flows out through the other nostril. ing on post-operative visits. It is best to avoid the
The same procedure is to be repeated on the formation of synechiae in the first place. However,
other nostril. Gentle blowing of the nose can once they form, they can be released using sharp
be done after the procedure to remove any instruments or cautery under local or general
leftover soft crusts and debris. If it stings, one anaesthesia. The synechiae has a tendency to
may reduce the amount of salt in the solution. recur. To prevent their formation again, silastic
• ‘Sniffing method’: Taking the solution in a sheet, X-ray plate or non adhesive nasal pack can
wide-mouthed mug, one can sniff the solution be placed in the nasal cavity to prevent mucosal
from one nostril while blocking the other nos- approximation.
8.1.5 Recent Advances 10 mg OD—causes the significant improvement

in some patients. It is symbiotic with budesonide
Following novel therapies have been introduced irrigations. Betadine rinses, Itraconazole, aPDT
for improving SNOT 22 scores are the other therapies. Short course of systemic
steroids is good option for refractory cases.
(a) aPDT (Antimicrobial Photodynamic ther- Biologicals and cytokine therapy are in experi-
apy)—Non-invasive non-antibiotic broad- mental stage.
spectrum antimicrobial treatment. It has been Oral itraconazole is proven to be beneficial in
shown to be effective against biofilm-forming selected cases of AFRS. They are started at
microorganisms [15]. This works on a simple 200 mg BD and the responders are subsequently
principle, it introduces a non-toxic molecule tapered to the lowest effective dose within
that turns bactericidal on exposure to visible 2 months. Non-responders are given a trial of
light, by forming free radicals. 2 months after which the drug is stopped.
(b) Steroid saline irrigations—Can be started Itraconazole therapy requires regular monitoring

immediately post-operatively for cavity of liver function tests and cardiac function. The
cleaning purpose and to prevent recurrence EPOS 2012 paper does not recommend routine
of polyps. E.g., Budesonide preparation can use of systemic or topical antifungals like
be done as follows: amphotericin B for routine management of
2.5 mg/2 ml ampules are used; they are AFRS, as there is insufficient evidence support-
dissolved in 240 ml of water. Then nasal ing its use [3].
douching is done on either side thrice a day.
It can be reduced to twice a day after the first
week and once a day after the first month. 8.2 Part B: Antifungal Therapy
(c) Steroid stents—These stents are inserted in
nasal cavities to keep the sinus openings pat- 8.2.1 Introduction
ent. They gradually release a steroid that
reduces local inflammation in post-operative Surgical debridement is the preferred treatment
period. However, their role in decreasing the modality for fungal sinusitis. Antifungals with
symptoms and SNOT 22 scores in patients of surgical debridement are the treatment strategy
CRS remains doubtful [16]. for invasive fungal sinusitis. The incidence of
(d) Biologicals—omalizumab, dupilumab, invasive fungal infection increases because of
mepolizumab. They are experimental expen- widespread use of antibiotics, steroids and immu-
sive therapies. They have been successful in nosuppressant drugs. With the advancement in
about 40% of recalcitrant cases. knowledge and technology, the graph of organ
(e) Personalized therapies using cytokines. transplantation and intervention is raised.
(f) Immunotherapy—Allergen immunotherapy Antifungals are used by some clinicians in exten-
has been shown to decrease post-operative sive AFRS in pre-operative period or in follow-
exacerbations, decreases the need for revi- up period, when the surgeon is not sure for
sion surgery and lead to decreased depen- disease clearance or in patients with persistent
dence on steroids [17]. symptoms after surgery, to reduce the recurrence
rate. Fungal sinusitis occurs in different forms
and due to various pathogens, each requiring a
8.1.6 Other Therapies specific treatment regime aimed at the causative
pathogen. Antifungal agents have varying toxic-
The following therapies are described for AFRS ity and the benefit versus toxicity ratio needs to
patients that fail high concentration budesonide be weighed before starting treatment. The newer
and budesonide irrigations. Tab Montelukast antifungal agents that are less toxic are very
expensive. The management protocol for inva- orbital infections. Retrobulbar injection of
sive fungal sinusitis is antifungal treatment and amphotericin B is also used for the treatment
debridement of the involved part. of invasive sino-orbital Aspergillosis.
Amphotericin B binds to sterols, more prefer-
entially to ergosterol, which is a major com-
8.2.2 Classification of Antifungals [18] ponent of the fungal cell membrane. This
results in an increased permeability of the cell
1. Antibiotics: membrane, leading to leakage of intracellular
(a) Polyenes: Amphotericin B, Nystatin, components and eventually cell death [19,
Hamycin 20]. Owing to its lipophilic nature, amphoteri-
(b) Heterocyclic benzofuran: Griseofulvin cin B also binds to cholesterol in the mamma-
(c) Echinocandins: Caspofungin, Micafungin, lian cell membrane, but to a lesser degree,
Anidulafungin which probably accounts for its toxicity. Also,
2. Antimetabolite: Flucytosine (5-FC) its interaction with host cells can have a posi-
3. Azoles: tive effect by activation of macrophages
(a) Imidazoles: through an oxidation-dependent process.
(i) Topical: Clotrimazole, Econazole, Amphotericin B is available in four
Miconazole, Oxiconazole formulations:
(ii) Systemic: Ketoconazole (a) Amphotericin B Deoxycholate
(b)
Triazoles (systemic): Fluconazole, It is actually a colloidal suspension of
Itraconazole, Voriconazole, Posaconazole amphotericin B, in which deoxycholate
4. Allylamine: Terbinafine (bile salt) is used as solubilizing agent.
5. Other topical agents: Tolnaftate, Undecylenic This formulation has high toxicity. It has
acid, Benzoic acid, Quiniodochlor, Ciclopirox poor CNS penetration. The patient should
olamine, Butenafine, Sodium thiosulfate be hydrated with 500–1000 mL of saline
before starting the amphotericin infusion.
This supplements the sodium required to
8.2.3 Antifungal Agents Used maintain the intravascular volume and
for Treatment of Fungal inhibits the tubuloglomerular feedback
Sinusitis system, which reduces the risk of nephro-
toxicity. Continuous administration ver-
1. Amphotericin B sus 5 h administration of the drug is
Amphotericin B, is most commonly used controversial therapy, continuous infusion
polyene antifungal agent and it remains the have less toxicity profile whereas 5 h infu-
standard drug of choice for managing life- sion have more fungicidal effect. The
threatening systemic fungal infections [1]. It usual protocol is to administer test dose
was isolated by Gold et al. in 1955 from by diluting 10–15 mg of the drug in
Streptomyces nodosus. It is the standard drug 50–100 mL of 5% dextrose, and given
for all types of invasive fungal infections, slowly intravenously over 20 minutes. If
including invasive aspergillosis, zygomycosis there is no reaction, then the complete
and severe infections of blastomycosis, coc- dose can be administered. The standard
cidioidomycosis, sporotrichosis and histo- dose ranges from 0.25 to 1 mg/kg/day
plasmosis. Amphotericin B is also proved to given once daily, diluted in 5% dextrose,
be effective in the treatment of candidemia to be given slowly intravenously (over
and disseminated candidiasis. Local irrigation 2–6 h) [19, 21]. There are two ways to
of amphotericin B is reported to be controver- administer the drug. The first is to start
sial treatment to control of invasive sino- with a low dose and titrate gradually till
the maximum dose is achieved. This to 80% of patients. The contraindication

method is no longer recommended. The of amphotericin is acute renal failure.
second method which is preferred is to Symptoms are a result of electrolyte wast-
start with a standard dose as per patients’ ing (potassium and magnesium) due to
body weight and maintain the same till impaired urine concentrating ability [19,
total cumulative dose is achieved. The 21, 22]. It is also associated with renal
maximum daily dose in adults is 1.2 mg/ tubular acidosis. Nephrotoxicity can be
kg, and in children is 1.5 mg/kg but more minimized by 500–1000 mL of normal
than 1 mg/kg body weight increases the saline infusion before and after ampho-
chances of side effect drastically which in tericin B infusion. If serum creatinine
turn increases the treatment duration and rises above 3 mg/dL, it should be tempo-
hospital stay. The total cumulative dose rarily discontinued or substituted with a
ranges between 2 and 3 g given over lipid-based amphotericin formulation.
2–3 months. The renal function tests and Patients receiving a total dose greater
serum electrolytes should be monitored than 4–5 g of amphotericin B deoxycho-
twice weekly and complete haemogram late may have permanent renal dysfunc-
once weekly. As amphotericin B is sensi- tion. Amphotericin B has also been
tive to light, the infusion bottle and tubing reported to directly suppress erythropoi-
should be covered and protected from etin production leading to normochromic
sunlight, to maintain drug effectiveness. normocytic anaemia. Infrequently, neu-
The use of concomitant nephrotoxic drugs tropenia and thrombocytopenia may also
must be avoided. be seen [19, 21].
Amphotericin B is highly toxic and has (b) Lipid-Based Formulations of Ampho

various side effects. The immediate side tericin B
effects are infusion related and usually Recently, lipid-based formulations of
begin 1–1.5 h after starting the infusion. amphotericin B have been made available,
They are very common and occur in more using various lipid carriers. These lipid-
than half of the patients. It is probably due based formulations of the drug have fewer
to the release of cytokines (Interleukins side effects as compared to amphotericin
and tumour necrosis factor α). The B deoxycholate. They are selectively
infusion- related side effects commonly delivered into the reticuloendothelial sys-
include fever, chills, rigor, headache, nau- tem, such as the liver and spleen, and to a
sea, vomiting. Acute anaphylaxis may lesser extent, the lungs. There are three
rarely occur. These may be managed lipid preparations: amphotericin B colloid
symptomatically by premedication with dispersion (ABCD), amphotericin B lipid
paracetamol, antihistamines and anti- complex (ABLC) and liposomal ampho-
emetics. Hydrocortisone injection 0.6 mg/ tericin B (LAMB). Their standard doses
kg with the infusion may reduce the sever- are ABCD: 3–5 mg/kg, ABLC: 5 mg/kg
ity of the reaction. Thrombophlebitis is and LAMB: 1–5 mg/kg. The standard
also commonly seen with amphotericin cumulative dose is 5–7 g but it can
infusion. It can be reduced by slowing exceed further which is depends on clini-
down the rate of infusion of amphotericin cal condition and patient tolerance. The
B, adding small amount of heparin to the dose-related efficacy of lipid-based for-
infusion (1000 units/L), using a central mulations is lower than conventional
line, or by diluting the concentration of amphotericin B but, as higher doses can
the infused drug. Nephrotoxicity is be used, it makes them more efficacious.
another common side effect in patients Lipid-based formulations of ampho-
receiving amphotericin B, occurring in up tericin B are particularly used for the
treatment of invasive fungal infections in 800 mg, depending on the severity of infec-
patients intolerant of or refractory to tion. It is highly water soluble and its absorp-
Amphotericin B deoxycholate. LAMB is tion is not affected by the presence of food or
used as empiric therapy for fungal infec- gastric pH6. It has excellent activity against
tions in febrile neutropenic patients. It is most Candida species and is widely used for
also used in the treatment of patients with various fungal infections by Candida albi-
Aspergillus, Candida, Cryptococcus sp. cans. Fluconazole has better CNS penetration
infections refractory to or intolerant of than itraconazole. Itraconazole is very effec-
Amphotericin B deoxycholate. It is the tive against Aspergillus and black moulds,
drug of choice for rhinocerebral mucor- that typically cause fungal sinusitis. It is the
mycosis, which requires administration of drug of choice in these cases, unless there is
high dose of polyenes after debridement extensive bone invasion where initial therapy
[23]. Liposomal Amphotericin B also has is amphotericin B [23]. There have also been
better CNS penetration than Amphotericin reports of the efficacy of itraconazole for the
B deoxycholate or ABLC. treatment of allergic fungal rhinosinusitis and
It has multiple advantages over amphotericin B fungal ball. Both oral and intravenous prepa-
deoxycholate and is well tolerated by the rations are available. The daily dose is 100–
patient. It produces a milder reaction on infu- 400 mg/day depending on the indication. Its
sion, causes minimal anaemia and nephrotox- oral absorption and availability is highly vari-
icity. The only disadvantage of this drug is able and unpredictable. It is better absorbed
that it is expensive. Colloidal suspension cre- when administered with food or acidic bever-
ates more side effects than liposomal prepara- ages. The side effects of azoles are gastritis,
tion by upregulation of the inflammatory rash, headache, the elevation of liver enzymes,
gene. and aldosterone-like effects in high doses
2. Azoles (itraconazole). Hepatotoxicity, peripheral
Lately, azoles are gaining importance in neuropathy, pancreatitis and androgen related
the treatment of fungal rhinosinusitis as they side effects (alopecia, gynecomastia, loss of
are active against multiple fungal pathogens libido, etc.) are side effect of long-term use
without the serious side effects of amphoteri- [25].
cin B deoxycholate. They have also shown 3 . Newer Drugs
effectiveness in treatment of systemic myco- (a) Voriconazole: It is a synthetic derivative of
ses. Azoles inhibit cytochrome P450 enzyme fluconazole, a second-generation triazole.
and thus impair ergosterol synthesis, which is It is useful for the treatment of acute and
an essential component of the fungal cell chronic invasive aspergillosis. It is pre-
membrane [21, 24]. This leads to damage of ferred over amphotericin B where the
cell membrane of fungus by increasing its per- cause of fungal infection is not known.
meability and causing cell death. Both oral and intravenous preparations are
These drugs include imidazoles (clotrima- available and it is good alternative to
zole, miconazole, ketoconazole) and triazoles amphotericin B in invasive aspergillosis. It
(itraconazole, fluconazole). Ketoconazole, is given as loading dose of 6 mg/kg iv BD
given orally, has been used successfully for for 2 doses, followed by 3 mg/kg iv BD for
the treatment of invasive mycosis. However, 30 days. On signs of improvement, it can
its use has been mostly replaced by triazoles be changed to 200 mg BD orally to com-
owing to their superior efficacy, pharmacoki- plete 24 weeks [26]. The side effects
netics and safety profile. Fluconazole is avail- include mild elevation of liver enzymes
able in both oral and intravenous preparations. and transient visual disturbances. The lim-
The daily dose varies between 200 and iting factor is that the drug is expensive.
(b) Posaconazole: It is an azole, active against inducing drug resistance. Studies have shown that
yeasts and moulds including zygomyce- an increase in resistance to azole antifungal drugs
tes, aspergillosis, candida and cryptococ- may allow some cross-resistance to amphotericin
cal infection. It is used as salvage therapy B. The possible mechanism is azoles cause an
in invasive fungal sinusitis after failure or alteration in ergosterol synthesis which conse-
intolerance to other antifungals [27]. It is quently decreases the number of potential binding
available in oral preparations and the sites on the fungal cell membrane for amphoteri-
doses are 200 mg thrice daily as preven- cin B or multiple drug resistance (MDR) pumps.
tive management for invasive fungal In invasive mycoses, when the site of infection is
infection. The therapeutic doses are necrotic with poor vascularity, debulking surgery
800 mg daily in divided doses for invasive is essential to overcome antifungal resistance and
fungal infection. tissue samples should be evaluated for the sensi-
(c) Echinocandins: This class of antifungal tivity of drug against particular organism. A sub-
agents acts by inhibiting 1, 3 β-glucan optimal length of treatment, prolong drug
synthesis a critical component for mainte- exposure, repeated and prophylactic treatment
nance of fungal cell wall integrity [21]. It may also lead to drug resistance. Lastly, the
is approved for treatment of invasive underlying disease must be controlled or prevent
aspergillosis resistant to conventional fungal infections in high-risk patients. In vitro
antifungal and empirical management of assessment of drug susceptibility, newer drugs are
neutropenic patients suspected of having the alternatives in patients resistant to or not
fungal sinusitis. Drugs belonging to this responding to conventional treatment. Failure to
class are caspofungin, micafungin, treatment is defined as no improvement or wors-
anidulafungin. ening of clinical or radiological features in
7–14 days after starting standard antifungal
treatment.
8.2.4 Antifungal Drug Resistance
Drug resistence is the major cause of treatment 8.2.5 Duration of Medical Therapy
failure. This can occur in circumstances such as for Fungal Sinusitis
wrong diagnosis, multiple pathogens or immune
reconstitution inflammatory syndrome, seen in Treatment end point should be tailor made and
patients receiving immune-modulating therapies, multiple factors can be considered in each patient.
which may be confused with failure to control the Treatment should be continued till there is com-
fungal infection [27]. Also, in patients with severe plete resolution of all symptoms of fungal sinus-
immunosuppression, the antifungal cannot over- itis for at least 2 weeks, resolution of endoscopic
come the severe immunodeficiencies until the findings, resolution of radiological findings, neg-
host immunity is improved. Recent studies have ative fungal culture and biopsy the suspected
shown that early treatment of fungal infection area. Serum biomarkers such as galactomannan,
with a lower burden of organisms reduces treat- β-D-glycan and Aspergillus specific PCR can be
ment failure [28, 29]. Some fungal strains possess considered as end point for treatment as they
more virulent characteristics than others and have high negative predication value. Sometime
infection with such strains may have a poorer patient tolerance and co-morbidities are the
prognosis. Toxicity from polyenes (nephrotoxic- major limiting factor for complete treatment [32].
ity) and azoles (hepatitis) can be a cause of treat-
ment failure [30, 31]. Drug-drug interaction, 8.2.5.1 Combination of Antifungal
drug-target interaction, upregulation of drug Simultaneous administration of two or more anti-
transporters, biofilms and reduced cellular con- fungal drugs is a controversial topic in view of
centration can lead to morbidity and mortality by significant side effects, patient tolerance but it
has shown advantages against certain organism relationship to the orbit, anterior cranial fossa
and drug resistance. Flucytosine with amphoteri- and vascular structures, sinus surgery has many
cin B combination demonstrated survival benefit potential complications. Thorough knowledge of
in cases of Cryptococcal meningitis. Calcium— anatomy, detailed assessment of pre-operative
calcineurin signalling pathway plays a dominant imaging and advanced technology such as endo-
role in immunity. Synergistic action of calcineu- scopes, microdebrider and Image guidance with
rin inhibitors such as cyclosporine A, tacrolimus hypotensive anaesthesia can reduce the chance of
(FK 506) and pimecrolimus with azoles is help- complications drastically. Revision surgery,
ful to kill resistant fungi. Glucocorticoid (dexa- extensive nasal polyposis, dehiscence of sinuses
methasone, budesonide, hydrocortisone), lining wall, distorted anatomy are the common
antimetabolic agents (mycophenolic acid, reason behind complications. Normal anatomical
mizoribine), the target of rapamycin and few tra- various such as hypoplastic or extensive pneuma-
ditional Chinese medications (tetrandrine, arte- tized sinuses, long and high cribriform plate,
misinin, matrine) showed addictive effect with asymmetrical low lying ethmoidal roof are the
antifungal. These drugs are more studied with other factors. Dehiscent bony canal over optic
candida species. Hydrocortisone with amphoteri- nerve, internal carotid artery and anterior eth-
cin in human and rapamycin with azoles in rat moid artery can induce catastrophic
showed some synergistic effectiveness against complication.
Aspergillus infection [33]. Posterior choana, middle turbinate/ remnant
of it, sphenoid sinus, skull base, septum and
8.2.5.2 Recent Advances maxillary sinus roof are the stable intranasal

Urea derivative of amphotericin B is showed landmarks to be considered especially in revision
more potent outcome with less adverse effects in surgery. The factors with poorer outcomes
the animal model. Isavuconazole is potent orally include previous surgery, extensive disease, poor
and intravenously available azole and it is knowledge of anatomy and radiology. Outdated
approved by the US FDA for the invasive form of technology and the presence of risk factors such
aspergillosis and mucor infections. Fungal sphin- as smoking, asthma, aspirin sensitivity, allergies
golipid, calcineurin, Hsp 90, etc. are the newer and in immune deficiency, etc. are the other fac-
target sites for drugs. VT 1129, VT 1161 and VT tors for poor outcome. The list of complications
1598 are the newer tetrazoles and they claimed to is illustrated in Table 8.5. Nasal complications
be more specific for fungal cytochrome 51 and are the most common complications followed by
less for mammalian 450 cytochrome. orbital and intracranial complications.
Aminocandin (IP960 or HMR3270), CD 101,
enfumafungin, etc. are the newer echinocandins
against Aspergillus and candida species [34, 35]. 8.3.1 Nasal Complications
8.3.1.1 Adhesion (Synechiae)

8.3 Part C: Fess Complications This is the most common complication of FESS
and it is seen in 4–35% of cases [36]. Synechiae
Functional Endoscopic sinus surgery is highly develop when two opposing raw mucosal sur-
sophisticated type of surgery that aims at main- faces remain in contact after the surgery. Gross
taining the physiological function and anatomical septal deviation, revision surgery, and middle tur-
structure. Powered instrumentations and stereo- binate instability is the major causes of synechiae
tactic image-guided surgery have improved effi- formation. The spacer should be placed under the
cacy and safety of this procedure and have vision to prevent instability of middle turbinate.
revolutionized endoscopic sinus surgery and Initially, micro fibrinous bands develop and
extended its applications. Because of the highly forms a scar tissue. Synechiae at maxillary ostia
variable individual anatomy and the intimate and ethmoid cavity have worse effect as it affects
Table 8.5 Complications of Endoscopic Sinus Surgery

Nasal complications Intracranial complications Orbital complications
• Synechiae (adhesion) • CSF Rhinorrhea • Orbital subcutaneous emphysema
• Haemorrhage • Meningitis • Fat prolapse
• Stenosis of ostium • Encephalocele • Extraocular muscle injury
• Mucocele/Pyocele • Orbital hematoma
• Olfactory impairment • Optic nerve injury
• Injury to NLD
Fig. 8.2 NCCT PNS orbit is showing synechiae in between inferior turbinate and septum
the drainage of maxillary, ethmoid sinuses. It also by spacer placement. Regular follow-up with
interferes in post-operative cavity cleaning. To operative surgeon and proper cavity care can pre-
prevent this, surgery should be performed with vent synechiae formation.
care. Any kind of injury to healthy mucosa should
be avoided. Loose hanging mucosa and bony 8.3.1.2 Haemorrhage
chips should be removed during surgery and in Nasal bleeding can be divided into bothersome
post-operative care. Irrigation of the cavity is mucosal ooze, bleeding from a named vessel and
required to minimizing the effect of heat injury. life-threatening haemorrhage from maxillary and
Absorbable and non-absorbable spacer is placed internal carotid artery. Surgeon’s scale is pro-
in between two raw surfaces to prevent approxi- posed to qualify amount of blood in field [41].
mation and adhesion. Meta-analysis, review arti- The scale is ranged from 0 to 5 where score 2
cles showed advantage of spacer placement means mild ooze and it requires minimal suction-
against synechiae formation [37–39]. ing. In score 3, the field is improved with suction-
Bolgerization and suture medialization of middle ing and in score 4, continue suctioning is required
turbinate are helpful in preventing synechiae for- to see the surgical field. In score 5, the surgical
mation when middle turbinate is destabilized field is not improved with continue suctioning.
(Fig. 8.2) [40]. Soft adhesion can be removed
easily but hard adhesion requires sharp instru- 1. Mucosal Ooze—It may limit the view of sur-
ments to break it and raw surfaces are seperated gical field which leads to increase operative
time. It also increases the risk of complica- rior branch of sphenopalatine artery is running
tions and may lead to termination of proce- just inferior to sphenoid ostium which can be
dure. Mucosal ooze can be reduced by injured by the inferior widening of ostium.
avoidance of NSAIDS, platelet inhibitors. Vessel injury can be avoided by separating the
Pre-operative antibiotics and oral steroid mucosa inferiorly before ostium widening.
reduces intraoperative bleeding by reducing The management of sphenopalatine bleeding
edema, exudates and blood vessels trauma by is mentioned in Chap. 9.
reducing the load of inflammatory mediators 3 . Internal Carotid Injury—Sellar type of pneu-
[42]. Oral steroids also enhance the effect of matization of the sphenoid sinus has thinnest
vasoconstrictors by increasing the spasticity bony wall over carotid or may even have
of smooth muscles. The doses were varied dehiscent carotid. Sometimes accessory sphe-
from 30–60 mg per day with 7 days duration noid septum is attached over the ICA bulge.
with or without tapering [43]. Pre-operative Anomalies and aneurysms of the artery also
steroid can generate serious side effects so it predispose to the internal carotid artery injury.
should be used cautiously [43, 44]. Pre- This can be avoided by pre-operative radio-
operative administration of tranexamic acid logical assessment and without pulling or
reduces periorbital edema and intraoperative avulsion of septas in the sphenoid sinus. The
bleeding [45, 46]. Hypotensive anaesthesia, management is mentioned in Chap. 9.
reverse Trendelenburg position, intraoperative
local infiltration in pterygopalatine fossa via 8.3.1.3 Sinus Ostium Stenosis
greater palatine or sphenopalatine foramen Sinus ostium stenosis is defined as loss of more
and application of cotton pledgets with vaso- than 50–60% of intraoperative size. Neo-
constrictor reduces mucosal ooze to some osteogenesis at the ostium level can lead to
extent [47]. stenosis (Fig. 8.3). Complex anatomy and narrow
2 . Bleeding from Named Vessel—Sphenopalatine outflow tract of frontal sinus make it as most vul-
artery is the major blood supply of the sinona- nerable sinus for recurrence of disease secondary
sal region. Anterior ethmoidal artery is the
branch of the ophthalmic artery. Anterior eth-
moid artery can be injured while removal of
antero-superior part of the anterior ethmoid
cell. Low lying anterior ethmoid artery is
found in cases with higher Keros, long cribri- FO
form plate, wide antero-posterior frontal
recess and presence of supraorbital recess
[48]. Abnormal course can be assessed by
proper pre-operative radiology. Injury to the
lateral part of the vessel can retract intra-
orbitally and creates complications by rising
intra-orbital pressure. Avoidance is the best
way to prevent complications and if the deal- MT
ing is required, it should be done in the middle
part of intranasal course of anterior ethmoid
artery so cauterization of injured vessel is pos-
sible. Once it retracts in orbit, external
approach is required to control bleeding and
the management of anterior ethmoid artery Fig. 8.3 Neo-osteogenesis with stenosis of left side fron-
bleeding is mentioned in Chap. 9. The poste- tal ostium (FO). MT middle turbinate)
to stenosis. It is found as high as 60% [49]. The headache, orbital symptoms and facial disfigur-
final size of the frontal ostium is defined around ing, etc. Extensive diseases have higher chances
1 year of post-surgery period. The preservation of of mucocele formation because of significant
normal ostium wall at least at one side, carpeting damage to normal mucociliary function while
of exposed bone by mucosal graft or flap, disease clearing. The measurements mentioned
Mitomycin C application, steroid releasing sinus in the mucosal ooze section and proper cavity
implants and proper cavity care can reduce the care are also applicable to minimize the chances
chances of stenosis [50–52]. of mucocele formation. In extended endoscopic
approaches, complete removal of mucosa under
8.3.1.4 Mucocele/Pyocele flap and the proper marking of mucosal surface
It is a late complication of endoscopic surgery. of the flap is required for prevention of iatro-
Mucocele appears after years of surgery. The genic mucocele [54]. The regular follow-up and
persistent mucosal inflammation and intraoper- interval MRI helps in early diagnosis [55].
ative trauma can lead to narrowing/obstruction Majority are manageable by endoscopic
of sinus cells outflow. The mucocele formation approach. Complicated mucoceles require
is ranged from 0 to 13% after endoscopic sur- urgent intervention. The detailed management
geries [53]. Frontal sinus is the most affected of mucoceles is mentioned in Chap. 7.
sinus because of its narrow drainage pathway.
Ethmoid and sphenoid are the next common 8.3.1.5 Nasolacrimal Duct Injury
sinuses in sequence. With the expansion in the Nasolacrimal duct is the continuation of nasolac-
list of endoscopic procedures, the chances of rimal sac in the lateral nasal wall. The course is
mucocele formation are increasing (Fig. 8.4). variable in the medial maxillary wall (Fig. 8.5).
Complete excision of mucosa is difficult in nar- The distance between the duct and anterior max-
row and hidden part of sinuses. Mucoceles may illary sinus wall is found less than 7 mm in
be incidental finding or it may present with approximately 88% of cases [56] whereas in

nasal endoscopic evaluation in cadavers, it runs
at and anterior to the maxillary line in 95% of
cases [57]. NLD can be injured while aggressive
removal of uncinate bone, anterior enlargement
of the maxillary ostium and in extended endo-
scopic approaches to pterygomaxillary fossa and
infratemporal fossa. Not all NLD injuries are pre-
sented with tearing. Proper pre-operative knowl-
edge of NLD course, anterior and posterior
nasolacrimal duct approach can reduce the injury
chances [58]. In extended endoscopic approaches,
sharp cut to NLD or DCR is advised.
Dacrocystostomy is the treatment option for
symptomatic cases. The details of the procedure
are mentioned in Chap. 8.
8.3.1.6 Empty Nose Syndrome

It is a late complication. It occurs after extensive
and usually recurrent sinus surgeries with the
Fig. 8.4 Right iatrogenic frontoethmoidal mucocele. removal of large areas of mucous membranes and
Hypodense area is the retained bone wax which is block-
ing the outflow tract of frontal sinus. Anterior wall of the resection of superior and middle turbinates.
frontal sinus is also breached which presented as fluctua- Patient will complain of paradox nasal obstruc-
tion swelling on the frontal sinus (Pott’s puffy tumour) tion in presence of objective wider nasal cavities
Fig. 8.5 Course of b

nasolacrimal duct canal. a
It is very much away
from anterior maxillary
sinus wall in (a) and in
(b), no gap in between
anterior maxillary wall
and NLD canal
and irritating crust formation. The etiology and crepitating are the clinical findings on eyelids. It
management of empty nose syndrome is men- is generally self-limiting and reabsorbs in short
tioned in last section. period. Patient should be advised to avoid activi-
ties like nose blowing, etc. Progressive emphy-
8.3.1.7 Olfactory Impairment sema can create acute compartment syndrome. It
It may occur due to avulsion of olfactory neuro- is painful condition that can present with restric-
epithelium from olfactory cleft or over resection tion of extraocular movement and impairment of
of superior turbinate. It can be prevented by vision. It requires urgent decompression of
avoiding unnecessary handling in the olfactory collected air to prevent permanent vision loss
cleft region and if required, sharp cutting instru- secondary to vascular compression and optic
ments should be used to prevent scarring. nerve stretching (Fig. 8.6) [59, 60].
8.3.2.2 Damage to Lamina Papyracea,

8.3.2 Orbital Complications Periorbita and Orbital Fat
Prolapse
The orbit comes in close relationship with all Median orbital wall is formed by frontal process of
paranasal sinuses. Periorbita is the only soft tis- maxilla, lacrimal bone and lamina payracea from
sue barrier in between orbit and paranasal sinuses. anterior to posterior direction. Lamina papyracea
Pre-operative radiology is helpful in accessing is the thinnest medial orbital bone and its thickness
bony anatomy, dehiscence’s of periorbital wall, reduces with age advancement. Predisposing fac-
fat prolapsed, optic nerve course. The incidence tors for fat prolapsed are dehiscent Lamina papy-
of orbital complications is ranged from 0.5 to racea, revision surgery, extensive disease, distorted
5%. The list of orbital complications is men- anatomy, excessive bleeding and hypoplastic
tioned in Table 8.5. Maxillary Sinus (Fig. 8.7). The preservation of
median bony wall and periorbita in dehiscent bony
8.3.2.1 Subcutaneous Emphysema wall is the key to prevent orbital complications.
It is characterized by the presence of air in orbital Fat is prolapsed when sickle knife inserted blindly
tissue. This occurs due to natural communica- while uncinectomy, dacrocystostomy and undue
tions or by accidental or iatrogenic breach of pulling of lateral attachment of middle turbinate.
partly wall. Orbital emphysema occurs due to Periorbita touching is painful under local anaes-
forceful nose blowing, sneezing and mask venti- thesia. Retrograde uncinectomy is the safer tech-
lation. It is mostly seen in eyelids with the normal nique [58]. Powered instruments have damaging
sclera and extraocular movement. Creaking and effect on orbital tissue than cold instruments by its
Fig. 8.6 Left side emphysema with normal-looking sclera. The right side picture is showing acute compartment
syndrome
Fig. 8.7 NCCT PNS orbit (axial cut) is depicting the showing extensive S/T/D in the left side of nasal cavity
dehiscence of lamina with prolapsed orbital fat. The and ethmoid sinus with pushed lamina papyracea
patient had history of trauma in childhood. Coronal cut is
suctioning effect [61]. The Stankiewicz pressure nent blindness, if orbit is not decompressed
test shows the movement of medial wall when within 100–120 min. The standard treatment
injury occurs to lamina papyracea and periorbita policy for intraoperatively diagnosed orbital
[62]. In doubtful cases, fat float test can be done. hematoma is urgent orbital and optic nerve
Surgery can be completed by avoiding manipula- decompression. When it is noticed in ward, the
tion of prolapsed fat, gentle bipolar of fat obstruct- surgical decision on the basis of intraocular pres-
ing the view and by avoid suctioning over it. Sinus sure (IOP) is controversial. The medical man-
ostium should be widened enough to prevent agement includes eye massaging, i/v mannitol,
obstruction of the drainage pathway by prolapsed i/v dexamethasone, and removal of nasal pack-
fat. Surgeon should avoid tight nasal packing. The ing. If IOP is above 30–35 mmHg and in patients
patient should be advised not to blow nose with IOP less than 20 with progressive proptosis,
post-operative. severe retro-orbital pain, RAPD, cherry red mac-
ula and no retinal artery pulsation, the manage-
8.3.2.3 Injury to Extraocular Muscles ment option is urgent canthotomy and or
The right eye injury is more common than the left cantholysis in ward after local infiltration.
eye probably due to right-handed surgeon’s Clamps are applied below and above lateral can-
majority. The medial rectus is the most vulnera- thus for devascularization. Canthotomy is full
ble extraocular muscle followed by inferior rec- thickness incision on lateral canthus towards the
tus and superior oblique. Strabismus and diplopia orbital rim. Cantholysis is the release of the lat-
are the leading clinical features. For contusions, eral canthal ligament. Both procedures allow
the treatment option is conservative treatment anterior prolapse of orbit and it can reduce pres-
(observation, antibiotics and steroids). If the sure by 10–15 mmHg. In progressive cases,
muscle is entrapped, the involved muscle should endoscopic or external orbital decompression
be released. Gross divergent squint and absent with multiple parallel incisions on periorbita to
adduction are the sign of muscle transaction. suppress the effect of raised IOP [63, 64]. Some
ENT surgeon may seek the advice of ophthal- surgeons performed canthal procedures and
mologist. The various management options orbital wall decompression in one go [65].
include hang back suture (strabismus reduction),
botulinum toxin in contra muscle, the recession 8.3.2.5 Injury to Optic Nerve
of lateral rectus and transposition [63, 64]. The optic nerve runs in the lateral relationship of
the posterior ethmoid and sphenoid sinus. The
8.3.2.4 Orbital Hematoma various predisposing factors for direct optic nerve
The orbit is the close compartment. The Normal injury are the presence of Onodi cell, dehiscent
intraocular pressure (IOP) is 10–20 mmHg. optic nerve canal and attachment of accessory
Orbital hematoma is the post septal accumula- sphenoid septum with the optic canal [66].
tion of blood. It accounts 0.05–0.5% of endo- Indirect damage can occur by compromising the
scopic surgery. The clinical features are blood supply of optic nerve [63, 64]. It is seen in
progressive proptosis, severe retrobulbar pain orbital hematoma. Altered visual reflex is the
and visual impairment. The signs are raised IOP sign of abnormality of function of optic nerve.
and alter pupillary reflex. The intraoperative fea- Pre-operative radiological assessment of the
tures are dilated fixed pupil and bradycardia. It is course of optic nerve can minimize the chances
of two types, slow venous type and fast arterial of injury. Intraoperative diagnosed optic nerve
type. In the slow venous type, intra-orbital veins injury should be managed by orbital and optic
are injured. Fast arterial type is mostly iatrogenic nerve decompression. Post-operatively diag-
and ethmoidal arteries are injured. Increased ten- nosed cases are managed by mega doses of i/v
sion in globe can cause irreversible visual steroids (Methylprednisolone) and endoscopic
impairment by inducing optic nerve stretching optic nerve decompression. The prognosis is very
and vascular compression. It can lead to perma- poor even after all measures taken [67, 68].
8.3.3 Intracranial Complications tifying the outflow of watery fluid from skull base.
The preventive measures for failed dural repair in
8.3.3.1 CSF Fistula extended approaches is to avoid large surgical
Extended endoscopic approaches increase the defect, achieve adequate haemostasis before the
chances of CSF rhinorrhoea. Incidence varies from closure of defect with graft or flap, mucosa should
0.2 to 16% in literature [69]. The patients with high be replaced back over multilayer repair where sinus
BMI, revision surgery and history of radiotherapy obliteration is not planned, under vision nasal
are at more risk. It occurs due to damage to the packing and smooth extubation. Intraoperatively
skull base and dura. Lateral lamella of the cribri- diagnosed cases should be repaired in the same sit-
form plate, ethmoid roof are the most common site ting by experienced surgeon. In post-operative
for CSF leak in FESS but in extended approaches, diagnosed cases, conservative management
pituitary fossa is the most common site. Chances includes i/v mannitol, stool softener, cough sup-
are increased by dehiscence in skull base by nasal pressants, head end elevation and restricted move-
pathology like polyposis, tumour, etc. Inadequate ment, etc. The use of lumber drain is based on the
knowledge of radiology and undue manipulation of effect of conservative management and surgeon’s
structures attached with skull base like middle tur- choice [69]. The site of leak in persistent cases
binate, superior turbinate, etc. can lead to iatro- (1–2 weeks of conservative management) can diag-
genic skull base damage. It is safe to identify skull nose by either single imaging or by combining of
base first by posterior to anterior approach espe- different modalities such as NCCT PNS orbit with
cially in revision cases or in cases with distorted MR cisternography and intra-thecal or topical
anatomy and if there is non-availability of naviga- application of fluorescein dye (Fig. 8.8) [70, 71].
tion system. CSF rhinorrhoea is diagnosed by iden- Endoscopic multilayer closure of the defect is
Fig. 8.8 NCCT coronal cut- skull base is damaged at sphenoid sinus superior wall with pneumocephalus
advised and naso-septal flap is most commonly dizziness, visual alterations, confusion, behav-
used to repair skull base defect [72]. ioural and personality change. NCCT head is
good enough to pick air. Pneumocephalus
8.3.3.2 Meningitis requires no treatment in asymptomatic patients.
This is a relatively rare intracranial complica- Tension pneumocephalus requires prompt treat-
tion and incidence varies from less than 1 to ment, decompression of the aerocele followed by
10%. Extended endoscopic approaches have rel- the closure of the defect [76, 77].
atively higher risk of meningitis. Intraoperative
and post-operative CSF leak, perioperative lum-
ber drain, prolong surgery, revision surgery in 8.4 art DA: Biofilms: Its
P
short span, missed prophylactic antibiotics are Composition, Detection
the common reason for meningitis in the post- Methods and Role in Human
operative period. Recent systemic review and Infections (Microbiologist
meta-analysis are not supporting the utility of Aspect)
prophylactic lumber drain [73]. Sometimes, the
infection may spread along perivascular and Biofilms are defined as group of microbes in
vascular or perineural spaces of the olfactory which cells adhere to each other or substratum
fibres. The meningitis trend is decreasing in the irreversibly. Biofilms can be present everywhere
recent past because of improvement in endo- in the environment. These biofilms have the
scopic surgical expertise, advance instruments, potential to neutralize antibiotics and result in
better sealing materials and use of naso-septal prolonged treatment. Due to its resistant proper-
flap [74, 75]. ties to antimicrobials and infections associated
Patient presents with severe headache, high- with indwelling devices poses a problem for pub-
grade fever, nuchal rigidity, vomiting, cranial lic health. Biofilms formation is a multi-step pro-
nerve palsy, behavioural changes and seizures. cess in which adaptation occurs during a series of
Sometime dry cough, mild headache and raised events under diverse nutritional and environmen-
TLC count is the only feature because of ongoing tal conditions. Biofilms have been found to be
post-surgical medications. In such cases, CSF involved in a wide variety of microbial infections
fluid analysis is helpful in creating the diagnosis. in the body such as bacterial vaginosis, urinary
MR cisternography is good investigation in tract infections, catheter infections, middle-ear
doubtful cases of CSF leak. Treatment includes infections, the formation of dental plaque, gingi-
targeted broad-spectrum antibiotics for 2 weeks vitis, coating lenses and endocarditis, infection in
and closure of the defect in persistent CSF rhi- cystic fibrosis, and infections of indwelling
norrhoea patients. devices. The biofilms are significantly resistant to
antibiotics and infection associated with them is
8.3.3.3 Pneumocephalus difficult to eradicate. Microbiological diagnosis
It occurs due to the presence of air in the cranial is important for the diagnosis of biofilms. The
cavity due to communication between the extra- traditional methods like microscopy, culture
cranial and intracranial cavity. It is rare complica- techniques are not always suited for the under-
tion of sinus surgery. It is more common in standing of biofilm science and are less sensitive
patients with intraoperative and post-operative for detection. Therefore, there is need of newer
CSF leak. It is also common with extended endo- methods for the detection of biofilms. The use of
scopic approaches for the removal of intradural bacteriophages, enzymes, surface coating agents,
lesions. Post-operative pneumocephalus is asso- pilicides and quorum sensing inhibitors are some
ciated with greater risk of CSF leak and intracra- of the methods to control biofilm formation. It is
nial infection (Fig. 8.8). The mechanism is challenging in medical science to eradicate infec-
believed to be ‘ball valve’ mechanism or ‘inverted tions related to biofilm formation. This is due to
bottle’ mechanism. The patient can complain of the fact that mature biofilms exhibit tolerance
towards immune response and antibiotics. teins and nucleic acids. Water (97%) is the major
Further studies are required to know the mecha- component of biofilm which is responsible for
nism of antibiotics resistance and their gene the flow of nutrients inside the biofilm matrix.
expression biofilm for better health care The other component of biofilms are proteins
improvement. (<1–2%), DNA (<1%), polysaccharides (1–2%)
and RNA (<1%) [80]. Various components of
biofilms are shown in Table 8.6.
8.4.1 Introduction of Biofilms
Biofilms are defined as group of microbes in 8.4.3 Biofilms Formation

which cells adhere to each other or substratum
irreversibly. These sticked cells become embed- The formation of biofilm is a multi-step process
ded in extracellular polymeric substance (matrix) in which adaptation occurs during a series of
produced by microbes themselves. Biofilms can events under diverse conditions such as nutri-
be present everywhere in environment, industrial tional and environmental. During this process,
and hospital settings and may form on living or microbes transform from planktonic to the sessile
non-living surfaces [78]. The antibiotics and mode of growth. It is a complex process that
human immune system normally cannot access includes: (a) adherence to a surface (b) growth of
the bacterial biofilms. These biofilms have the colonies (formation of micro-colony and three-
potential to neutralize antibiotics and result in dimensional structure formation) (c) detachment
prolonged treatment. Due to its resistant proper- (dispersal) as shown in Fig. 8.9 [81].
ties to antimicrobials and infections related with
indwelling devices poses a problem for public 8.4.3.1 Attachment
health. Biofilm-forming capacity has been found When a microorganism cell reaches to surface,
in number of bacterial species such as the interface of solid–liquid can provide a suit-
Escherichia coli, Staphylococcus aureus, able environment for microbes to attach and
Pseudomonas aeruginosa, Staphylococcus epi- grow. Hydrophilic, rough and coated surfaces
dermidis, Enterobacter cloacae, Klebsiella will provide better environmental attachment and
pneumonia [79].
Table 8.6 Biofilm composition
Constituents Percentages of matrix
8.4.2 Composition of Biofilms Water Up to 97%
Microbial cells 2–5%
Biofilms are community of microbes that pro- Polysaccharides 1–2%
duce matrix (extracellular polymeric substances Nucleic acid (RNA and DNA) <1–2%
(EPS) which consist of exopolysaccharides, pro- Proteins <1–2%
Fig. 8.9 Showing steps

of biofilms formation STEP-1 STEP-2 STEP-3
Attachment Growth Detachment

formation of biofilm. Increase in temperature of 8.4.5 R

ole of Biofilms in Human
the water, flow velocity or nutrients, locomotor Infections
organelle can further increase the attachment
process. Biofilms have been found to be associated with
wide variety of microbial infections in the body.
8.4.3.2 Growth of Colonies Recently, it has been observed that biofilms can
After attachment, chemical signals lead to the also impair wound healing by reducing topical
process of multiplication of bacteria in the bio- antimicrobial activity in treating wounds.
films. The bacterial cell divisions occur within Association between various human infections
the embedded matrix by using such signals which and biofilms are shown in Table 8.7 [84, 85].
results in micro-colony formation. After the stage
of micro-colony formation, expression of certain
biofilms related genes helps in the formation of 8.4.6 Biofilms Detection Methods
matrix. The water-filled channel formation takes
place after EPS formation for the transport of The biofilms are significantly resistant to antibi-
nutrients within the biofilms. These water chan- otic and infection associated with them is diffi-
nels help in distributing nutrients and removing cult to eradicate. Microbiological diagnosis is
waste materials from the micro-colonies of the important for the diagnosis of biofilms. The tradi-
biofilms. tional methods like microscopy, culture tech-
niques are not always suited for the understanding
8.4.3.3 Detachment of biofilm science and are less sensitive for detec-
After micro-colonies formation, occasionally tion. Therefore, there is need of newer methods
under some mechanical stress bacteria are for the detection of biofilms. Proper sonication of
detached from the communities into the environ- indwelling devices from the patients can signifi-
ment. But in most cases, some microbes stop EPS cantly improve the detection of biofilms. The
production and are detached into environment. development of molecular and imaging tech-
The detachment of new formed cells from grow- niques leads to a better understanding of biofilm
ing cells or dispersion of biofilm communities science. Classical and newer biofilm detection
occurs through a mechanism called quorum methods are shown in Table 8.8 [86].
sensing.
8.4.7 Methods to Control Biofilms [87]

8.4.4 Biofilms and Antibiotic
Resistance (A)
Pilicides—Small synthetic compounds
inhibit the synthesis of pili which further
The key factors responsible for antimicrobial inhibit binding and colonization on epithe-
resistance may vary among different sitting. The lial cells.
following mechanisms have been explored for (B) Enzymes—The enzymes have the capability
high resistance nature of biofilms: (1) low pen- to degrade the biofilm matrix. Further, deg-
etration of antibiotics, (2) neutralization by radation of biofilm results in the release of
enzymes, (3) heterogeneous functions, (4) cells components that are easily clear by immune
slow growth rate, (5) existence of persistent systems.
cells, (6) biofilm phenotype and (7) efflux pump (C) Quorum sensing inhibitors—Using quorum
and membrane alteration as shown in Fig. 8.10 sensing inhibitors is another effective way in
[82, 83]. control of biofilm.
• The penetration or diffusion of antibiotics to biofilmis affected by EPS which act as physical
barrier
Low Penetration of Antibiotics • Matrix may also acts as hindrance for Immune system cells
• The presence of neutralizing enzymes degrade or inactivate antibiotics

Neutralization by Enzymes • These enzymes are proteins which confer resistance by mechanisms such as hydrolysis,
modification of antimicrobials by different biochemical reactions
• The biofilmsare heterogeneous nature both metabolically and structurally and both aerobic and
anaerobic process occur at the same time. So response against antibiotics may be different in
Heterogeneous functions different areas of the biofilms.
• On surface of biofilm there is a high level of activity of antibiotics while inside the biofilms,
slow or absent growth reduces the sensitivity to antimicrobials
• This process occurs due to limited availability of nutrients which confer resistance to antibiotics.
In case of biofilma gradient of nutrients resulting in metabolically active cell (periphery or
Cell slow growth surface layer) and inactive cells (within its interior) . Antibiotics like penicillin and ampicillin
only attack the cells when they are growing. However, other antibiotics such as β-lactams,
aminoglycosides, cephalosporin and fluoroquinolonesattack cells in stationary phase
• In stationary phase, the density of bacterial cells raised to maximum indicating the role of
persistent cells for survival
Existence of Persistent Cells • There are certain evidences for the existence of persistent cells in biofilm: a) Presence of a
biphasic dimension in biofilms b) presence of gene description function as a regulation, c)
bacteriostaticantimicrobial contribute to the growth of persistent cell d) reshaping of biofilm
into original form when the antimicrobial therapy is withdrawn
• The bacteria produce secondary metabolites during biofilmformation.Thesemetabolites acts as

Biofilm Phenotype signaling molecules, which enhances biofilm formation
• Biofilm phenotype is regarded as group of cells that confer no response to antimicrobials
treatment
• Efflux pumps show resistant to multiple antibiotics thus reducing these antibiotics
concentration,example-over expression of the efflux pumps have been observed in P.
Efflux pump and membrane aeruginosa biofilms
• Mutation in porinsencoding genes can result in low permeability for the passage of hydrophobic
alteration molecules
• The differential expression of porins coding genes, occur in biofilm, leading to antibiotic resistance
Fig. 8.10 Showing factors responsible for antibiotic resistance in biofilms
(D) Surface Coatings—Another effective way

8.4.8 Future Aspects of Biofilm
for the eradication of biofilm is coating the
indwelling devices with antimicrobials. It is challenging to eradicate infections related to
(E) Bacteriophages—It has been observed that biofilm formation in medical science. This is due
bacteriophages have the ability to inhibit or to the fact the mature biofilms exhibit tolerance
reduce formation of biofilm. Phage cocktail towards immune response and antibiotics.
can also be used for removal of biofilm. Further studies are required to know the mecha-
Table 8.7 Showing association between various human infections and biofilms
Condition Salient features
Acute wound Biofilm formation in wounds has been investigated in-vivo model (murine and porcine) for S.
aureus, P. aeruginosa and Streptococcus biofilm
Chronic In chronic wound, antibiotic treatment is considered to be effective in initial stages but after
wound formation of biofilm, antibiotic therapy is least effective. Because biofilm can be up to 1000 times
resistant to antimicrobials
Infectious The interaction between bacteria and mineral substances derived from urine results in formation of
kidney stones kidney stones, which are responsible for urinary tract infections. This result in the formation of
biofilm
Bacterial The interaction between bacteria and host components lead to formation of biofilm which is known
endocarditis as vegetation. This vegetation can cause disease by different mechanisms: Disrupting the function
of valve by creating leakage, turbulence, causes bloodstream infections or break down the
vegetation which is then carried into the circulation (embolization)
Infections in These patients are most commonly infected with P. aeruginosa. The permanent infections in such
Cystic cases with P. aeruginosa biofilm take place which last for the rest of the patient’s life
fibrosis
Other Biofilm
Diseases
Otitis media • The patient speech development and learning capability will be affected
with effusion
Acute • Necrosed bone produced favourable conditions for biofilm development
osteomyelitis
Table 8.8 Detection methods of biofilm

Classical methods Newer methods
are believed to be due to the formation and per-
Microtiter plate Photobioreactor sistence of biofilms [88, 89]. These biofilms are
assay highly resistant to treatment with antimicrobials
Tube adherence Ultrasound and are capable of shedding bacteria into the
method bloodstream which leads to recurrent bouts of
Congo red agar Sequencing Technologies infection [90]. It has been noted that the presence
method
of bacterial biofilms can be the reason for some
Biofilm bioreactor PCR techniques
Biofilm Ring test Spectrometry forms of recalcitrant chronic rhinosinusitis.
Confocal laser scanning Biofilms that form on the surface of airway
microscopy mucosa are known as mucosal biofilms. These
Fluorescent in situ hybridization are different from those that form on inert devices
Nuclear magnetic resonance because these have to overcome the normal air-
imaging
way mucociliary clearance [91]. Inadequate
doses of antibiotics for the treatment of rhinosi-
nism of antibiotics resistance and their gene nusitis can lead to biofilm formations and chronic
expression biofilm. For better health care infections. The most common cause of CRS
improvement, better understanding is needed for refractory to medical treatment is the opportunis-
the development of novel, effective control strat- tic infection with biofilm-forming Pseudomonas
egies against biofilm. aeruginosa. Also implicated are Staphylococcus
aureus, Streptococcus pneumoniae, Haemophilus
influenzae and Moraxella catarrhalis [92, 93].
8.5 art DB: Biofilms: Surgeon’s
P Fungal elements are also seen in biofilms.
Aspect Candida albicans is the most common cause of
biofilm formation among pathogenic fungi [94].
Biofilms are increasingly recognized as a cause In children suffering from chronic otitis media
for persistent otorhinolaryngologic infections. and CRS, adenoidectomy is considered benefi-
About 75% of the microbial infections in humans cial. Biofilm covered adenoids in nasopharynx of
children with chronic rhinosinusitis, biofilms act 3. Quorum sensing inhibitors shift the bacterial
as reservoir for reinfection. 95% of the adenoids phenotype from sessile to platonic form.
and 70% of tonsils removed from children suffer-
ing from CRS have been found to be covered Various antibiotics have been tested for topi-
with biofilms. cal treatment of biofilms.
It is a potential cause or persistent symptoms
in some patients after ESS [95]. Frontal recess • Mupirocin has been found effective against the
stents, stenting for choanal atresia, intranasal Staphylococcus aureus biofilms. It is effective
tubes are highly likely to be covered with bio- because of its broad spectrum of action.
films and this can worsen the prognosis of • Honey was effective against S. aureus and P.
surgery. aeruginosa biofilms in vitro. It was found to
eradicate 73% of MRSA biofilms and 91% of
pseudomonas biofilms [97].
8.5.1 Treatment
Surfactants break up the biofilm and allow the
Bacteria associated with biofilms behave differ- bacteria to be removed by irrigation.
ently from platonic bacteria, particularly in terms
of antibiotic sensitivity. Biofilm cells are about • Baby shampoo has been used as a chemical
500 times more resistant to antimicrobial agents surfactant to disrupt biofilms [98].
[87]. The structure of the biofilm along with the • Citric acid/zwitterionic surfactant solution by
extracellular matrix prevents the drug from means of pressurized jet lavage is effective in
reaching the cells. Systemic treatment may breaking up biofilms in vitro [99].
require very high doses of antibiotics which may • Surgical ventilation of the affected sinus helps
be intolerable and may not be effective at all. against biofilm infections. It increases the
Genetic resistance to antibiotics could be due oxygen tension and mechanically disrupts the
to decreased penetration, decreased metabolic biofilms [100].
activity of biofilms, increase in the number of
efflux pumps and presence of different subpopu- Quorum sensing inhibitors increase the suscep-
lations of bacteria within a biofilm [96]. tibility of the biofilms to antibiotics and phagocy-
Interfering in the various stages of biofilm forma- tosis. Systemic long-term low dose macrolide
tion like the interruption of quorum sensing or therapy has been found to decrease the virulence
the genes involved in cellular attachment can be of the bacteria and prevents the formation of bio-
used as a strategy to inhibit biofilm formation. films [101]. For medical indwelling devices, ion
Variety of techniques has been evaluated for bombarded silicone ventilation tubes have been
managing and treating biofilms including sur- found to be better than other silicone tubes.
gery, topical antimicrobials and adjuvant thera- Preventive Measures:
pies. Newer treatments are aimed at disrupting Biofilm can be prevented by vaccination
the life cycle of biofilms, preventing their attach- against organisms that can cause chronic infec-
ment on to the surfaces and to disrupt the quorum tions like pneumococci. Antibiotic prophylaxis
sensing. With topical treatment, there are three and aggressive antibiotic therapy can prevent bio-
strategies for eradication of biofilms. film formation.
Newer Advances:
1. Specific antibiotics against the causative
The detection of intercellular signalling sys-
microorganism. tem, lasR-lasI and rhlR-rhlI, involved in the
2. Mechanical force for the detachment of the development of P. aeruginosa biofilms, indicate
biofilm from the surface. E.g Surfactants, irri- signal manipulation as a possible target to control
gation, surgery. biofilms [102].
8.6 art E: Empty Sinus

P presence of paradoxical nasal obstruction, despite
Syndrome an objectively visible wide nasal cavity. It occurs
few months to years after partial/total resection
Empty Nose syndrome (ENS) is a distinct clini- of the turbinates and sometimes even after turbi-
cal entity, which has been highlighted, in the nate surface cauterization. The basic pathology
recent few years because of the increasing inci- of this condition stems from changes in nasal
dence of Turbinate Surgeries. Since there are no physiology after volume reduction of turbinates.
set diagnostic criteria, so the diagnosis of these Exact incidence is not known, because of the
patients is based on combination of clinical paucity of literature and poor reporting of this
examination, standardized questionnaires, CT entity.
scan and few objective tests. Treatment mainly There are various subtypes of ENS described
consists of medical measures, with the surgical by Houser SM [103], depending on the turbinate
options only to be offered once the medical man- tissue, which is involved.
agement fails and psychosomatic component is
ruled out. In ideally selected candidates, surgery (A) ENS—IT type (Inferior Turbinate), which
can provide extremely satisfying results by aug- occurs after various surgeries for Inferior
menting the volume of the lost tissues of the tur- turbinate (IT) reduction (Fig. 8.11a).
binates, thus channelling the airflow patterns. (B) ENS—MT type (Middle Turbinate)—
Research is underway worldwide to restore the Symptoms occur after excessive resection of
function of the turbinates by injecting Platelet- the middle turbinate (MT). In addition to
Rich plasma, Platelet-rich lipotransfer and extra- paradoxical nasal obstruction, patients have
cellular matrix components, which have shown pain on breathing.
initial promising results.
(C) ENS-both—Refers to patients who have
resection of both IT and MT tissues and lastly.
(D) ENS-Type—Patients who seem to have ade-
8.6.1 Introduction quate normal tissue volume of the turbinate,
yet they have ENS like symptoms. This is
Eugene Kern from Mayo clinic first described because of mucosal changes, which have
this entity in 1994. Empty Nose Syndrome (ENS) occurred because of surface cauterization
is an iatrogenic disorder characterized by the (Fig. 8.11b).
Fig. 8.11 (a) ENS is IT TYPE and (b) ENS is TYPE 1B

8.6.2 Pathophysiology
Extensive studies on understanding the pathophys-

iology of ENS have been done by Steven Houser
[103]. The perception of the nasal patency has an
underlying neuro-sensory mechanism. Activation
of trigeminal ‘cool’ thermoreceptors by nasal
mucosal cooling produces the sensation of nasal
patency. These receptors are located in abundance
in the inferior turbinate tissues, especially the
superficial mucosal layers, which if damaged
because of turbinate loss—produce sense of suf-
focation. Also, alteration in the airflow pattern is
causative for paradoxical nasal obstruction.
In addition to altering the receptors and the
airflow pattern, turbinate surgery also causes
nerve damage and aberrant growth of the nerves Fig. 8.12 Cotton Test
due to scarring [104, 105] which fails to carry the
message of nasal breathing, causing nasal with the cotton test (Fig. 8.12). In addition to this,
obstruction. patient’s symptoms can be gauged by administer-
ing modified SNOT 25 questionnaire and ENS6Q
questionnaire [107]. This also acts as a baseline
8.6.3 Diagnosis to compare the post-operative surgical outcome.
Another objective test to measure nasal obstruc-
There are no set criteria for the diagnosis of this tion by calculating the peak nasal inspiratory
condition. Combination of classical patient flow rate (PNIFR). Since patients with ENS have
symptoms, with history of prior surgeries clinches paradoxical nasal obstruction, their scores of
the diagnosis of ENS. The common nasal symp- PNIFR are always in the normal range. Thus the
toms include—paradoxical airway obstruction, protocol that can be handy for the diagnosis of
nose feels too open, sensation of suffocation, this entity includes the following
unable to feel the breathing from the nose, nasal
and pharyngeal dryness, dyspnea, hyposmia and 1. Thorough History taking with symptom

the common extra-nasal symptoms include facial evaluation
pain, headaches and excessive preoccupation of 2. History of prior nasal surgeries
the patient with the nasal issues affecting the 3. Nasal Endoscopy
quality of life, sleep patterns and causing severe 4. Cotton Test
depression and anxiety [106]. 5. CT—PNS (plain)
Nasal endoscopy reveals volume loss/scarring 6. Administering modified SNOT 25 question-
with pale and dry looking mucosa with occa- naire and ENS6Q questionnaire
sional crusting. Houser has devised the Cotton 7. Calculating the PNIFR
test, which serves dual purposes. It acts as a con- 8. Psychological evaluation to rule out psycho-
firmatory diagnosis for Empty nose Syndrome somatic disorder
and also aids in surgically planning the site of
sub-mucosal implantation. Moistened cotton
with isotonic sodium chloride solution is placed 8.6.4 Management
in the nasal cavity for 20–30 min and the patient
is asked to breathe comfortably and report the Since this is a recently recognized entity, defini-
change in symptoms [106]. Patients with ENS tive treatment options are still being explored.
will report marked improvement in symptoms Preventive strategies will go a long way to pre-
vent this condition. Utmost gentleness and care- References

fulness while handling the turbinate tissues is
essential and turbinectomy should be done only 1. Silva MP, Baroody FM. Allergic fungal rhi-
nosinusitis. Ann Allergy Asthma Immunol.
in malignant cases when required. Allergy and 2013;110(4):217–22. https://doi.org/10.1016/j.
other reversible factors should be taken care of in jaip.2016.03.010.
cases of turbinate hypertrophy, and if there is 2. Chakrabarti A, Denning DW, Ferguson BJ,
non-respondence to these, only sub-mucosal et al. Fungal rhinosinusitis. Laryngoscope.
2009;119(9):1809–18. https://doi.org/10.1002/
techniques should be used for turbinate lary.20520.
reductions. 3. Fokkens WJ, Lund VJ, Mullol J, et al. EPOS 2012:
Conventional medical management is the first European position paper on rhinosinusitis and
line of management. It comprises nasal moisturiza- nasal polyps 2012. A summary for otorhinolaryn-
gologists. Rhinology. 2012;50(1):1–12. https://doi.
tion with vaseline/lubricants, nasal irrigation and org/10.4193/Rhino50E2.
lavage, using cool mist humidifiers at home, 4. Kennedy JL, Hubbard MA, Huyett P, Patrie JT,
increased fluid intake, intermittent nose pinching Borish L, Payne SC. Sino-nasal outcome test
and cognitive behavioural therapy—for somatic (SNOT-22): a predictor of postsurgical improve-
ment in patients with chronic sinusitis. Ann Allergy
complaints. Surgical options if there is failed medi- Asthma Immunol. 2013;111(4):246–251.e2. https://
cal management, ENS6Q score >11 and positive doi.org/10.1016/j.anai.2013.06.033.
cotton test with ENS6Q score falling more than 7 5. Kosugi EM, Chen VG, da Fonseca VMG,
points [108]. Aim of the surgery is to restore the Pellogia Cursino MM, Mendes Neto JA, Gregório
LC. Translation, cross-cultural adaptation and vali-
nose geometry and function. Various reconstructive dation of SinoNasal Outcome Test (SNOT) - 22
options can be used to restore the geometric con- to Brazilian Portuguese. Braz J Otorhinolaryngol.
tours of the nasal passage like sub-mucosal implan- 2011;77(5):663–9. https://doi.org/10.1590/
tation of various alloplastic materials such as S1808-86942011000500021.
6. Lund VJ, Kennedy DW. Staging for rhinosinusitis.
hydroxyapatite, Teflon, Gore-Tex and Plastipore, Otolaryngol Head Neck Surg. 1997;117(3 Pt 2):S35–
Allograft materials like Alloderm, [109] Autologous 40. https://doi.org/10.1016/S0194-59989770005-6.
cartilage harvested from the septum or the concha 7. Philpott CM, Clark A, Javer AR. Allergic fungal
to create a neoturbinate [110]. rhinosinusitis – a new staging system. Rhinology.
2011;4:1–7. https://doi.org/10.4193/Rhino10.121.
Regenerative medicine options are being 8. Low T-HH, Woods CM, Ullah S, Carney AS. A
explored in few centres worldwide to restore the double-blind randomized controlled trial of normal
mucosal function by injecting adipose-derived saline, lactated Ringer’s, and hypertonic saline nasal
stem cells(ADSCs), Growth factors from PRP irrigation solution after endoscopic sinus surgery.
Am J Rhinol Allergy. 2014;28(3):225–31. https://
(Platelet-rich plasma), PRL (platelet-rich doi.org/10.2500/ajra.2014.28.4031.
lipotransfer) [111, 112] and a cell (extracellular 9. Lilic N, Waldvogel-Thurlow S, Douglas
matrix components) which is used by Dr. Subinoy RG. Physical characteristics of commercial and
Das (USA). home-made nasal lavage solutions. J Laryngol
Otol. 2014;128(S1):S40–3. https://doi.org/10.1017/
S0022215113001291.
10. Lee VS, Humphreys IM, Purcell PL, Davis
8.6.5 Conclusion GE. Manuka honey sinus irrigation for the treatment
of chronic rhinosinusitis: a randomized controlled
ENS is a complex condition difficult to anticipate trial. Int Forum Allergy Rhinol. 2017;7(4):365–72.
https://doi.org/10.1002/alr.21898.
and treat. It is essential to be empathetic while
11. Welch KC, Thaler ER, Doghramji LL, Palmer JN,
dealing with ENS patients. It is imperative to do Chiu AG. The effects of serum and urinary cor-
a detailed psychosomatic evaluation and offer a tisol levels of topical intranasal irrigations with
multimodality treatment to these patients. There budesonide added to saline in patients with recur-
rent polyposis after endoscopic sinus surgery. Am
are still unanswered questions as to why all
J Rhinol Allergy. 2010;24(1):26–8. https://doi.
patients after turbinectomies not suffer from org/10.2500/ajra.2010.24.3418.
ENS. Further studies and research are necessary 12. Neubauer PD, Schwam ZG, Manes RP. Comparison
to understand the disease better. of intranasal fluticasone spray, budesonide atomizer,
and budesonide respules in patients with chronic 27. Van Burik JA, Hare RS, Solomon HF, Corrado ML,
rhinosinusitis with polyposis after endoscopic sinus Kontoyiannis DP. Posaconazole is effective as sal-
surgery. Int Forum Allergy Rhinol. 2016;6(3):233–7. vage therapy in zygomycosis: a retrospective sum-
https://doi.org/10.1002/alr.21688. mary of 91 cases. Clin Infect Dis. 2006;42:e61–5.
13. Bartle J, Millington A. How to perform nasal douch- 28. Garey KW, Rege M, Pai MP, et al. Time to initiation
ing. Nurs Stand. 2017;31(49):41–5. https://doi. of fluconazole therapy impacts mortality in patients
org/10.7748/ns.2017.e10683. with candidemia: a multi-institutional study. Clin
14. Bastier P-L, Lechot A, Bordenave L, Durand M, Infect Dis. 2006;43:25–31.
de Gabory L. Nasal irrigation: from empiricism 29. Upton A, Kirby KA, Carpenter P, Boeckh M, Marr
to evidence-based medicine. A review. Eur Ann KA. Invasive aspergillosis following hematopoi-
Otorhinolaryngol Head Neck Dis. 2015;132(5):281– etic cell transplantation: outcomes and prognostic
5. https://doi.org/10.1016/j.anorl.2015.08.001. factors associated with mortality. Clin Infect Dis.
15. Biel MA, Pedigo L, Gibbs A, Loebel 2007;44:531–40.
N. Photodynamic therapy of antibiotic-resistant bio- 30. Mora-Duarte J, Betts R, Rotstein C, et al. Comparison
films in a maxillary sinus model. Int Forum Allergy of caspofungin and amphotericin B for invasive can-
Rhinol. 2013;3(6):468–73. https://doi.org/10.1002/ didiasis. N Engl J Med. 2002;347:2020–9.
alr.21134. 31. Herbrecht R, Denning DW, Patterson TF, et al.
16. Huang Z, Hwang P, Sun Y, Zhou B. Steroid-eluting Voriconazole versus amphotericin B for primary
sinus stents for improving symptoms in chronic therapy of invasive aspergillosis. N Engl J Med.
rhinosinusitis patients undergoing functional 2002;347:408–15.
endoscopic sinus surgery. Cochrane Database 32. Perlin DS, Rautemaa-Richardson R, Alastruey-
Syst Rev. 2015;6:CD010436. https://doi. Izquierdo A. The global problem of antifungal resis-
org/10.1002/14651858.CD010436.pub2. tance: prevalence, mechanisms, and management.
17. Gan EC, Thamboo A, Rudmik L, Hwang PH, Lancet Infect Dis. 2017;17(12):e383–92. https://doi.
Ferguson BJ, Javer AR. Medical management org/10.1016/S1473-3099(17)30316-X.
of allergic fungal rhinosinusitis following endo- 33. Zhang M, Yang X, Wang D, Yu C, Sun S. Antifungal
scopic sinus surgery: an evidence-based review activity of immunosuppressants used alone or in
and recommendations. Int Forum Allergy Rhinol. combination with fluconazole. J Appl Microbiol.
2014;4(9):702–15. https://doi.org/10.1002/ 2019;126(5):1304–17. https://doi.org/10.1111/
alr.21352. jam.14126.
18. Campoy S, Adrio JL. Antifungals. Biochem 34. Wiederhold NP. The antifungal arsenal: alternative
Pharmacol. 2017;133:86–96. https://doi. drugs and future targets. Int J Antimicrob Agents.
org/10.1016/j.bcp.2016.11.01. 2018;51(3):333–9. https://doi.org/10.1016/j.
19. Gallis HA, Drew RH, Pickard WW. Amphotericin ijantimicag.2017.09.002.
B: 30 years of clinical experience. Rev Infect Dis. 35. Robbins N, Wright GD, Cowen LE. Antifungal
1990;12:308–29. drugs: the current armamentarium and development
20. Carr M, Dismukes WE. Antifungal drugs. In: of new agents. Microbiol Spectr. 2016;4(5) https://
Gorbach SL, Bartless JG, Blacklow NR, editors. doi.org/10.1128/microbiolspec.FUNK-0002-2016.
Infectious diseases. Philadelphia: WB Saunders; 36. Saafan ME, Ragab SM, Albirmawy OA, Elsherif
1992. p. 306. HS. Powered versus conventional endoscopic
21. Groll AH, Piscitelli SC, Walsh TJ. Clinical phar- sinus surgery instruments in management of sino-
macology ofsystemic antifungal agents in clinical nasal polyposis. Eur Arch Otorhinolaryngol.
use, current investigational compounds and puta- 2013;270:149–55.
tive targets for antifungal drug development. Adv 37. Manji J, Habib AR, Amanian AA, Alsaleh S,
Pharmacol. 1998;44:343–501. Thamboo A, Javer AR. Potential risk factors asso-
22. Barton CH, Pahl M, Vaziri ND, et al. Renal magne- ciated with the development of synechiae follow-
sium wasting associated with amphotericin B ther- ing functional endoscopic sinus surgery. Eur Arch
apy. Am J Med. 1984;77:471–4. Otorhinolaryngol. 2018;275(5):1175–81. https://doi.
23. Luna B, Drew RH, Perfect JR. Agents for treatment org/10.1007/s00405-018-4936-1.
of invasive fungal infections. Otolaryngol Clin N 38. Lee JM, Grewal A. Middle meatal spacers for the
Am. 2000;33:277–99. prevention of synechiae following endoscopic sinus
24. Kauffman CA, Carver PL. Use of azoles for systemic surgery: a systematic review and meta-analysis
antifungal therapy. Adv Pharmacol. 1997;39:143–89. of randomized controlled trials. Int Forum Allerg
25. Sheehan DI, Hitchcock CA, Sibley CM. Current and Rhinol. 2012;2:477–86.
emerging azole antifungal agents. Clin Microbiol 39. Vlastarakos PV, Iacovou E, Fetta M, Tapis M,
Rev. 1999;12:40–79. Nikolopoulos TP. How effective is postopera-
26. Benitez LL, Carver PL. Adverse effects associated tive packing in FESS patients? A critical analy-
with long-term administration of azole antifun- sis of published interventional studies. Eur Arch
gal agents. Drugs. 2019;79(8):833–53. https://doi. Otorhinolaryngol. 2016;273(12):4061–71. https://
org/10.1007/s40265-019-01127-8. doi.org/10.1007/s00405-015-3863-7.
40. Friedman M, Landsberg R, Tanyeri H. Middle implant for the paranasal sinus ostia: a random-
turbinate medialization and preservation in endo- ized clinical trial. JAMA Otolaryngol Head Neck
scopic sinus surgery. Otolaryngol Head Neck Surg. Surg. 2018;144(1):28–35. https://doi.org/10.1001/
2000;123:76–80. jamaoto.2017.1859.
41. Boezaart AP, van der Merwe J, Coetzee 53. Benkhatar H, Khettab I, Sultanik P, Laccourreye O,
A. Comparison of sodium nitroprusside - and Bonfils P. Mucocele development after endoscopic
esmolol-induced controlled hypotension for func- sinus surgery for nasal polyposis: a long-term analy-
tional endoscopic sinus surgery. Can J Anaesth. sis. Ear Nose Throat J. 2018;97(9):284–94.
1995;42:373–6. 54. Vaezeafshar R, Hwang PH, Turner JH. Commentary
42. Mortuaire G, Bahij J, Maetz B, Chevalier on “How to avoid mucocele formation under pedicled
D. Lund-Mackay score is predictive of bleeding nasoseptal flap”. Am J Otolaryngol. 2014;35(4):547.
in ethmoidectomy for nasal polyposis. Rhinology. https://doi.org/10.1016/j.amjoto.2014.03.009.
2008;46(4):285–8. 55. Lee DH, Jang WY, Yoon TM, Lee JK, Jung S, Lim
43. Hwang SH, Seo JH, Joo YH, Kang JM. Does SC. Sphenoid sinus mucocele caused by compli-
the preoperative administration of steroids cations after transsphenoidal pituitary surgery. J
reduce intraoperative bleeding during endo- Craniofac Surg. 2018;29(7):1859–61. https://doi.
scopic surgery of nasal polyps? Otolaryngol Head org/10.1097/SCS.0000000000004693.
Neck Surg. 2016;155(6):949–55. https://doi. 56. Simmen D, Veerasigamani N, Briner HR, Jones N,
org/10.1177/0194599816663455. Schuknecht B. Anterior maxillary wall and lacrimal
44. Günel C, Başak HS, Bleier BS. Oral steroids and duct relationship - CT analysis for prelacrimal access
intraoperative bleeding during endoscopic sinus sur- to the maxillary sinus. Rhinology. 2017;55(2):170–
gery. B-ENT. 2015;11(2):123–8. 4. https://doi.org/10.4193/Rhin16.318.
45. de Vasconcellos SJA, do Nascimento-Júnior EM, 57. Ali MJ, Nayak JV, Vaezeafshar R, Li G, Psaltis
de Aguiar Menezes MV, Tavares Mendes ML, de AJ. Anatomic relationship of nasolacrimal duct
Souza Dantas R, Martins-Filho PRS. Preoperative and major lateral wall landmarks: cadaveric study
tranexamic acid for treatment of bleeding, edema, with surgical implications. Int Forum Allergy
and ecchymosis in patients undergoing rhinoplasty: Rhinol. 2014;4(8):684–8. https://doi.org/10.1002/
a systematic review and meta-analysis. JAMA alr.21345.
Otolaryngol Head Neck Surg. 2018;144(9):816–23. 58. Song XC, Sun Y, Zhang H, et al. Zhonghua Er Bi Yan
https://doi.org/10.1001/jamaoto.2018.1381. Hou Tou Jing Wai Ke Za Zhi. 2011;46(10):818–24.
46. Kang H, Hwang SH. Does topical application of 59. Rodriguez MJ, Dave SP, Astor FC. Periorbital emphy-
tranexamic acid reduce intraoperative bleeding in sema as a complication of functional endoscopic
sinus surgery during general anesthesia? Braz J sinus surgery. Ear Nose Throat J. 2009;88(4):888–9.
Otorhinolaryngol. 2020;86(1):111–8. https://doi. https://doi.org/10.1177/014556130908800414.
org/10.1016/j.bjorl.2019.08.006. 60. Shameer A, Pushker N, Lokdarshi G, Basheer S,
47. Ko MT, Chuang KC, Su CY. Multiple analyses of Bajaj MS. Emergency decompression of orbital
factors related to intraoperative blood loss and the emphysema with elevated intraorbital pressure.
role of reverse Trendelenburg position in endoscopic J Emerg Med. 2017;53(3):405–7. https://doi.
sinus surgery. Laryngoscope. 2008;118:1687–91. org/10.1016/j.jemermed.2016.10.021.
48. Abdullah B, Lim EH, Husain S, Snidvongs K, 61. Ikeda K, Ito S, Homma H, et al. Orbital injury in
Wang Y. Anatomical variations of anterior eth- endoscopic sinus surgery for sinonasal inflamma-
moidal artery and their significance in endoscopic tory disorders: Juntendo’s ten-year experience. Int J
sinus surgery: a systematic review. Surg Radiol Otolaryngol Head Neck Surg. 2017;6:65–70.
Anat. 2019;41(5):491–9. https://doi.org/10.1007/ 62. Stankiewicz JA. Blindness and intranasal endo-
s00276-018-2165-3. scopic ethmoidectomy: prevention and management.
49. Wynn R, Har-El G. Recurrence rates after endo- Otolaryngol Head Neck Surg. 1989;101(3):320–9.
scopic sinus surgery for massive sinus polyposis. https://doi.org/10.1177/019459988910100305.
Laryngoscope. 2004;114:811–3. 63. Khanna A, Sama A. Managing complications and
50. Zhang X, Ye T, Huang Z, et al. Clinical predic- revisions in sinus surgery. Curr Otorhinolaryngol
tors of frontal ostium restenosis after draf 3 pro- Rep. 2019;7:79–86. https://doi.org/10.1007/
cedure for refractory chronic rhinosinusitis. Am s40136-019-00231-3.
J Rhinol Allergy. 2018;32(4):287–93. https://doi. 64. Rene C, Rose GE, Lenthall R, Moseley I. Major
org/10.1177/1945892418773625. orbital complications of endoscopic sinus surgery.
51. Amonoo-Kuofi K, Lund VJ, Andrews P, Howard Br J Ophthalmol. 2001;85(5):598–603. https://doi.
DJ. The role of mitomycin C in surgery of the fron- org/10.1136/bjo.85.5.598.
tonasal recess: a prospective open pilot study. Am J 65. Mohammadi F, Rashan A, Psaltis A, et al. Intraocular
Rhinol. 2006;20(6):591–4. https://doi.org/10.2500/ pressure changes in emergent surgical decompres-
ajr.2006.20.2917. sion of orbital compartment syndrome. JAMA
52. Luong A, Ow RA, Singh A, et al. Safety and Otolaryngol Head Neck Surg. 2015;141(6):562–5.
effectiveness of a bioabsorbable steroid-releasing https://doi.org/10.1001/jamaoto.2015.0524.
66. Cetinkaya EA, Koc K, Kucuk MF, Koc P, Muluk NB, patterns following endonasal endoscopic skull base
Cingi C. Calculation of an optic nerve injury risk surgery as predictors of postoperative CSF leaks. J
profile before sphenoid sinus surgery. J Craniofac Neurosurg. 2014;121(4):961–75. https://doi.org/10.
Surg. 2017;28(1):e75–8. https://doi.org/10.1097/ 3171/2014.5.JNS132028.
SCS.0000000000003239. 78. Hall-Stoodley L, Costerton JW, Stoodley P. Bacterial
67. Kim JY, Kim HJ, Kim CH, Lee JG, Yoon JH. Optic biofilms: from the natural environment to infectious
nerve injury secondary to endoscopic sinus sur- diseases. Nat Rev Microbiol. 2004;2(2):95–108.
gery: an analysis of three cases. Yonsei Med https://doi.org/10.1038/nrmicro821.
J. 2005;46(2):300–4. https://doi.org/10.3349/ 79. Parsek MR, Singh PK. Bacterial biofilms: an emerg-
ymj.2005.46.2.300. ing link to disease pathogenesis. Annu Rev Microbiol.
68. Seredyka-Burduk M, Burduk PK, Wierzchowska 2003;57:677–701. https://doi.org/10.1146/annurev.
M, Kaluzny B, Malukiewicz G. Ophthalmic com- micro.57.030502.090720.
plications of endoscopic sinus surgery. Braz J 80. Fux CA, Costerton JW, Stewart PS, Stoodley
Otorhinolaryngol. 2017;83(3):318–23. https://doi. P. Survival strategies of infectious biofilms.
org/10.1016/j.bjorl.2016.04.006. Trends Microbiol. 2005;13(1):34–40. https://doi.
69. Kassam AB, Prevedello DM, Carrau RL, et al. org/10.1016/j.tim.2004.11.010.
Endoscopic endonasal skull base surgery: analysis 81. Costerton JW, Stewart PS, Greenberg EP. Bacterial
of complications in the authors’ initial 800 patients. biofilms: a common cause of persistent infections.
J Neurosurg. 2011;114(6):1544–68. https://doi. Science. 1999;284(5418):1318–22. https://doi.
org/10.3171/2010.10.JNS09406. org/10.1126/science.284.5418.1318.
70. Daele JJ, Goffart Y, Machiels S. Traumatic, iatro- 82. Nickel JC, Costerton JW. Bacterial localization
genic, and spontaneous cerebrospinal fluid (CSF) in antibiotic-refractory chronic bacterial pros-
leak: endoscopic repair. B-ENT. 2011;7(Suppl tatitis. Prostate. 1993;23(2):107–14. https://doi.
17):47–60. org/10.1002/pros.2990230204.
71. Liu HS, Chen YT, Wang D, et al. The use of topi- 83. Hogan D, Kolter R. Why are bacteria refrac-
cal intranasal fluorescein in endoscopic endona- tory to antimicrobials? Curr Opin Microbiol.
sal repair of cerebrospinal fluid rhinorrhea. Surg 2002;5(5):472–7. https://doi.org/10.1016/
Neurol. 2009;72(4):341–6. https://doi.org/10.1016/j. s1369-5274(02)00357-0.
surneu.2009.03.034. 84. Edwards R, Harding KG. Bacteria and wound heal-
72. Hadad G, Bassagasteguy L, Carrau RL, et al. A novel ing. Curr Opin Infect Dis. 2004;17(2):91–6. https://
reconstructive technique after endoscopic expanded doi.org/10.1097/00001432-200404000-00004.
endonasal approaches: vascular pedicle nasoseptal 85. Sims JN, Isokpehi RD, Cooper GA, et al. Visual
flap. Laryngoscope. 2006;116(10):1882–6. https:// analytics of surveillance data on foodborne vibriosis,
doi.org/10.1097/01.mlg.0000234933.37779.e4. United States, 1973-2010. Environ Health Insights.
73. D’Anza B, Tien D, Stokken JK, Recinos PF, 2011;5:71–85. https://doi.org/10.4137/EHI.S7806.
Woodard TR, Sindwani R. Role of lumbar drains 86. Azeredo J, Azevedo NF, Briandet R, et al. Critical
in contemporary endonasal skull base surgery: review on biofilm methods. Crit Rev Microbiol.
meta-analysis and systematic review. Am J Rhinol 2017;43(3):313–51. https://doi.org/10.1080/10408
Allergy. 2016;30:430–5. 41X.2016.1208146.
74. Conger A, Zhao F, Wang X, et al. Evolution of the 87. Xavier JB, Picioreanu C, Rani SA, van Loosdrecht
graded repair of CSF leaks and skull base defects MCM, Stewart PS. Biofilm-control strategies based
in endonasal endoscopic tumor surgery: trends in on enzymic disruption of the extracellular polymeric
repair failure and meningitis rates in 509 patients. substance matrix--a modelling study. Microbiology.
J Neurosurg. 2018;130(3):861–75. https://doi. 2005;151(Pt 12):3817–32. https://doi.org/10.1099/
org/10.3171/2017.11.JNS172141. mic.0.28165-0.
75. Borg A, Kirkman MA, Choi D. Endoscopic endo- 88. Davies D. Understanding biofilm resistance
nasal anterior skull base surgery: a systematic to antibacterial agents. Nat Rev Drug Discov.
review of complications during the past 65 years. 2003;2(2):114–22. https://doi.org/10.1038/nrd1008.
World Neurosurg. 2016;95:383–91. https://doi. 89. Richards JJ, Melander C. Controlling bacterial bio-
org/10.1016/j.wneu.2015.12.105. films. Chembiochem. 2009;10(14):2287–94. https://
76. Shelesko EV, Kapitanov DN, Kravchuk AD, doi.org/10.1002/cbic.200900317.
Okhlopkov VA, Zaytsev OS, Chernikova NA. 90. Vlastarakos PV, Nikolopoulos TP, Maragoudakis
Taktika lecheniia defektov osnovaniia cherepa, P, Tzagaroulakis A, Ferekidis E. Biofilms in ear,
soprovozhdaiushchikhsia pnevmotsefalieĭ nose, and throat infections: how important are they?
[Management of complex skull base defects accom- Laryngoscope. 2007;117(4):668–73. https://doi.
panied by pneumocephalus]. Zh Vopr Neirokhir org/10.1097/MLG.0b013e318030e422.
Im N N Burdenko. 2019;83(2):85–92. https://doi. 91. Parsek MR, Greenberg EP. Quorum sensing signals
org/10.17116/neiro20198302185. in development of Pseudomonas aeruginosa bio-
77. Banu MA, Szentirmai O, Mascarenhas L, Salek films. Methods Enzymol. 1999;310:43–55. https://
AA, Anand VK, Schwartz TH. Pneumocephalus doi.org/10.1016/s0076-6879(99)10005-3.
92. Prince AA, Steiger JD, Khalid AN, et al. Prevalence biofilm. Science. 1998;280(5361):295–8. https://doi.
of biofilm-forming bacteria in chronic rhinosinus- org/10.1126/science.280.5361.295.
itis. Am J Rhinol. 2008;22(3):239–45. https://doi. 103. Sozansky J, Houser SM. Pathophysiology of empty
org/10.2500/ajr.2008.22.3180. nose syndrome. Laryngoscope. 2015;125(1):70–4.
93. Ramage G, Mowat E, Jones B, Williams C, Lopez- https://doi.org/10.1002/lary.24813.
Ribot J. Our current understanding of fungal bio- 104. Wu X, Myers AC, Goldstone AC, Togias A, Sanico
films. Crit Rev Microbiol. 2009;35(4):340–55. AM. Localization of nerve growth factor and its
https://doi.org/10.3109/10408410903241436. receptors in the human nasal mucosa. J Allergy
94. Le T, Psaltis A, Tan LW, Wormald PJ. The efficacy Clin Immunol. 2006;118(2):428–33. https://doi.
of topical antibiofilm agents in a sheep model of rhi- org/10.1016/j.jaci.2006.04.037.
nosinusitis. Am J Rhinol. 2008;22(6):560–7. https:// 105. Sofroniew MV, Howe CL, Mobley WC. Nerve
doi.org/10.2500/ajr.2008.22.3232. growth factor signaling, neuroprotection, and neu-
95. Costerton JW, Lewandowski Z, Caldwell DE, ral repair. Annu Rev Neurosci. 2001;24:1217–81.
Korber DR, Lappin-Scott HM. Microbial biofilms. https://doi.org/10.1146/annurev.neuro.24.1.1217.
Annu Rev Microbiol. 1995;49:711–45. https://doi. 106. Chhabra N, Houser SM. The diagnosis and manage-
org/10.1146/annurev.mi.49.100195.003431. ment of empty nose syndrome. Otolaryngol Clin N
96. Alandejani T, Marsan J, Ferris W, Slinger R, Chan Am. 2009;42(2):311–ix. https://doi.org/10.1016/j.
F. Effectiveness of honey on Staphylococcus aureus otc.2009.02.001.
and Pseudomonas aeruginosa biofilms. Otolaryngol 107. Velasquez N, Thamboo A, Habib AR, Huang Z,
Head Neck Surg. 2009;141(1):114–8. https://doi. Nayak JV. The Empty Nose Syndrome 6-Item
org/10.1016/j.otohns.2009.01.005. Questionnaire (ENS6Q): a validated 6-item question-
97. Chiu AG, Palmer JN, Woodworth BA, et al. Baby naire as a diagnostic aid for empty nose syndrome
shampoo nasal irrigations for the symptomatic post- patients. Int Forum Allergy Rhinol. 2017;7(1):64–
functional endoscopic sinus surgery patient. Am J 71. https://doi.org/10.1002/alr.21842.
Rhinol. 2008;22(1):34–7. https://doi.org/10.2500/ 108. Thamboo A, Velasquez N, Habib AR, Zarabanda D,
ajr.2008.22.3122. Paknezhad H, Nayak JV. Defining surgical criteria
98. Desrosiers M, Myntti M, James G. Methods for for empty nose syndrome: validation of the office-
removing bacterial biofilms: in vitro study using based cotton test and clinical interpretability of the
clinical chronic rhinosinusitis specimens. Am J validated empty nose syndrome 6-item question-
Rhinol. 2007;21(5):527–32. https://doi.org/10.2500/ naire. Laryngoscope. 2017;127(8):1746–52. https://
ajr.2007.21.3069. doi.org/10.1002/lary.26549.
99. Zhang Z, Han D, Zhang S, et al. Biofilms and mucosal 109. Houser SM. Surgical treatment for empty nose
healing in postsurgical patients with chronic rhino- syndrome. Arch Otolaryngol Head Neck Surg.
sinusitis. Am J Rhinol Allergy. 2009;23(5):506–11. 2007;133(9):858–63. https://doi.org/10.1001/
https://doi.org/10.2500/ajra.2009.23.3376. archotol.133.9.858.
100. Tré-Hardy M, Vanderbist F, Traore H, 110. Jang YJ, Kim JH, Song HY. Empty nose syndrome:
Devleeschouwer MJ. In vitro activity of a ntibiotic radiologic findings and treatment outcomes of
combinations against Pseudomonas aeruginosa bio- endonasal microplasty using cartilage implants.
film and planktonic cultures. Int J Antimicrob Agents. Laryngoscope. 2011;121(6):1308–12. https://doi.
2008;31(4):329–36. https://doi.org/10.1016/j. org/10.1002/lary.21734.
ijantimicag.2007.12.005. 111. Xu X, Li L, Wang C, et al. The expansion of autol-
101. Tatar EC, Unal FO, Tatar I, Celik HH, Gursel ogous adipose-derived stem cells in vitro for the
B. Investigation of surface changes in different functional reconstruction of nasal mucosal tissue.
types of ventilation tubes using scanning elec- Cell Biosci. 2015;5:54. https://doi.org/10.1186/
tron microscopy and correlation of findings with s13578-015-0045-7.
clinical follow-up. Int J Pediatr Otorhinolaryngol. 112. Friji MT, Gopalakrishnan S, Verma SK, Parida PK,
2006;70(3):411–7. https://doi.org/10.1016/j. Mohapatra DP. New regenerative approach to atro-
ijporl.2005.07.005. phic rhinitis using autologous lipoaspirate transfer
102. Davies DG, Parsek MR, Pearson JP, Iglewski BH, and platelet-rich plasma in five patients: our experi-
Costerton JW, Greenberg EP. The involvement of ence. Clin Otolaryngol. 2014;39(5):289–92. https://
cell-to-cell signals in the development of a bacterial doi.org/10.1111/coa.12269.
Septum, Adenoid, and Epistaxis
9
Ravneet Singh, Hitesh Verma, Shashikant Paul,
Sanjeev Bhagat, and Vishal Sharma
Contents
9.1 Part A: Nasal Septum, Septal Correction, and Septal Perforation 309
9.1.2 Anatomy 310
9.1.3 Development 311
9.1.4 Pathology 311
9.1.5 Classification of DNS 311
9.1.7 Nasal Septal Perforation 315
9.2 Part B: Adenoid Hypertrophy and Management 315
9.2.1 linical Grading of Adenoid
C 317
9.2.2 Radiological Staging 317
9.2.4 Indications 319
9.2.5 Surgical Techniques 319
9.2.6 Complications of Adenoidectomy 320
9.3 Part C: Epistaxis and Management 320
9.3.1 auses
C 321
9.3.2 Risk Factors 322
References 328
9.1 art A: Nasal Septum, Septal

P
Correction, and Septal
R. Singh Perforation
ENT, GMCH, Chandigarh, India
H. Verma (*) 9.1.1 Introduction
e-mail: drhitesh10@gmail.com The nasal septum is a midline structure that sepa-
S. Paul rates the nasal cavity into two parts and forms the
ENT, JIPMER, Pondicherry, India medial part of the nasal valve bilaterally. It
S. Bhagat · V. Sharma supports the nasal dorsum and maintains the

ENT, Rajindra Hospital Patiala, Patiala, Punjab, India nasal tip. It is formed from the posterior midline
310 R. Singh et al.
growth of the frontonasal process. Initially 3. Septum proper (Osseo-cartilaginous frame-

formed entirely of cartilage, it later ossifies to work)—This can be further divided into bony
form the perpendicular plate of ethmoid and and cartilaginous segments.
vomer. The nasal septum is easily deformed, and
a septal deviation can be seen in up to 80% of the The cartilaginous part is formed by the lamina
population but only a minority is symptomatic. quadrangularis (quadrilateral cartilage). The
Surgery is the only definitive treatment for symp- bony part is formed by the lamina perpendicu-
tomatic cases. SMR and Septoplasty are the two laris (the perpendicular plate of ethmoid) and the
classical techniques with a variety of modifica- vomer with minor contributions from crest of
tions described to tackle the various types of nasal bones, nasal spine of frontal bone, rostrum
deviations. Septal perforation is a through and of sphenoid, crest of palatine bones, the maxil-
through defect of the nasal septum, perforations lary crest, and the anterior nasal spine of the max-
can be asymptomatic or can cause severe distress illa. A widened region of the anterior nasal
to the patient depending upon the size and loca- septum containing an increased amount of venous
tion of the perforation. sinusoids is called the nasal septal swell body.
The concentration of sinusoids suggests that it
has the capacity to alter nasal airflow, like the
inferior turbinates.
9.1.2 Anatomy
9.1.2.1 Blood and Nerve Supply
The nasal septum is a midline structure formed Septum receives blood supply from both exter-
by several bony and cartilaginous sources. It can nal and internal carotid artery. The external
be divided into three parts: carotid artery supplies via the braches of facial
and internal maxillary artery and internal carotid
1. Columellar septum—it is the most anterior artery via the branches of the ophthalmic artery.
part and it forms by the medial crura of alar Kiesselbach’s plexus (Little’s area) is an area of
cartilages. anastomosis within the branches of internal and
2. Membranous septum—it is double layer of external carotid artery systems (Fig. 9.1). It lies
skin with no bony or cartilaginous support. in the anterior part of the septum and due to the
Fig. 9.1 Anterior and Anterior ethmoidal artery

posterior ethmoid
arteries are the braches Posterior ethmoidal artery
of ophthalmic artery.
Superior labial is the Kisselbach’s plexus
branch of facial artery.
Sphenopalatine and
greater palatine are the
branches of the internal
maxillary artery.
Kesselbach’s plexus
(little area) lies in the
anterior part of septum
Septal branch of
superior labial artery
Greater palatine artery

9 Septum, Adenoid, and Epistaxis 311
Fig. 9.2 The line

diagram is showing the
nerve supply of nasal Olfactory fibres
septum
Anterior ethmoidal nerve
Nasopalatine nerve
Greater palatine nerve
rich blood supply, is a common site of signifi- abnormal development of the nose, maxilla, and
cant bleeding. The posterior septal artery is a orbit. Septal deviation has been correlated with
branch of the sphenopalatine artery which sup- external nasal deformities as well as facial
plies the posteroinferior septum. The nasoseptal asymmetries as is evident in children with cleft
flap (Hadad-Bassagasteguy flap) is the work- palate. The deviation of the nasal septum has
horse for endoscopic skull base reconstruction, been shown to affect the thickness of the nasal
is based on this artery (Fig. 9.1). The nerve sup- bones as well as the size of the maxillary sinus
ply of the nasal septum is derived mainly from and its propensity for inflammation.
ophthalmic (Anterior ethmoidal nerve) and
maxillary (Greater palatine and Nasopalatine
nerves) divisions of the trigeminal nerve 9.1.4 Pathology
(Fig. 9.2).
Pathological deviation is described as a septum
deviation with nasal obstruction, i.e., a subjective
9.1.3 Development reduction of nasal breathing.
Etiology: Septal deviations can be caused by
The neonatal nose is completely cartilaginous, (Fig. 9.3) [1].
and the cartilaginous septum extends from the
columella to the sphenoid. The perpendicular • Trauma/injury
plate of ethmoid is formed by enchondral ossifi- • Mass lesions—polyposis, neoplasia
cation while the vomer is formed as a result of • Genetic factors
intramembranous ossification. Premaxillary bone • Congenital defects or
contributes to the nasal septum via the anterior • Growth differences of the facial bones sur-
nasal spine and the premaxillary wings. rounding the nasal septum
Vomeronasal cartilage is a small portion of carti-
lage that appears along the lower edge of the sep-
tal cartilage and is connected to a small blind 9.1.5 Classification of DNS
pouch called the Vomeronasal organ. The vom-
eronasal organ is vestigial in humans but func- Many classification systems have been proposed
tions as an accessory olfactory organ in some by authors according to severity, location, or type
mammals, amphibians, and reptiles. The carti- of deviation.
laginous nasal septum acts as a dominant growth
centre in the developing mid face. The expanding A. Cottle had classified septal deviations into
septum produces mechanical forces that facilitate three types according to severity:
the separation of facial sutures (Nasal septal trac- 1. Simple Deviations: mild deviation of nasal
tion model). Loss of septal cartilage can lead to septum without any nasal obstruction.
312 R. Singh et al.
• Type 7—Combination of previously

described septal deformity types.
9.1.6 Surgical Management
In patients with symptomatic septal deviation,

removal, or correction of the deformity can lead
to significant relief. It is vital to select the patients
carefully before undertaking surgery on the sep-
tum [2]. Classically there are two techniques
described:
Fig. 9.3 CT Scan Nose and PNS (Coronal view):
Deviation of the Nasal septum to the right side and 1 . Sub-mucosal Resection (SMR)
enlarged turbinates on the left sides 2. Septoplasty
This is the commonest and needs no While the basic principles of the surgery
treatment. remain the same, each surgery needs to be modi-
2. Obstruction: more severe deviation of the fied to tackle different types and degrees of devi-
nasal septum. On vasoconstriction, the ation and it may not confirm to the description of
turbinates shrink away from the septum any one technique described. This has led to the
and obstruction is relieved. Hence surgery surgery being commonly referred to as “Septal
is not indicated. correction.” With any septal surgery, it is impor-
3. Impaction: There is marked angulation of tant to remember that the dorsal and caudal ends
the septum and space is not increased even of the septum (Struts) need to be preserved or
on vasoconstriction. Surgery is indicated reconstructed, failing of which, an external nasal
in these patients. deformity can occur. Whenever the area of the
B. DNS can be classified according to the shape strut needs to be tackled, septoplasty is chosen
1. C-shaped over SMR.
2. S-shaped Indications:
3. Septal spur
4. Anterior dislocation 1 . Nasal airway obstruction.
C. Mladina Classification is a more comprehen- 2.
Chronic sinusitis secondary to septal
sive system based on the precise location of deviation.
the deviation. 3. Epistaxis by septal vessels.
• Type 1—Unilateral vertical ridge in the 4. Obstructive sleep apnea.
area of the nasal valve. 5. In conjunction with other nasal and sinus pro-
• Type 2—Similar to Type 1 but more severe cedures, such as cosmetic rhinoplasty, func-
obstruction and disturbance of the nasal tional endoscopic sinus surgery (FESS), and
valve. skull base surgery.
• Type 3—Unilateral vertical ridge at the 6. As an access procedure in Skull base surgery.
level of the head of the middle turbinate. 7. Rhinological headache, caused by the contact
• Type 4—Combination of type 3 with of the septum with the lateral nasal wall.
either type 1 or 2.
• Type 5—Horizontal septal crest in contact An ideal surgical correction should satisfy the
with the lateral nasal wall. following criteria:
• Type 6—Prominent maxillary crest con-
tralateral to the deviation with a septal 1 . Should relieve the nasal obstruction.
crest on the deviated side. 2. Should be conservative.
3 . Should not produce iatrogenic deformity. the location and extent of the deviation. The
4. Should not compromise the osteomeatal
bony osseo-cartilaginous junction is disarticu-
complex. lated to reach the opposite side of the bony sep-
5. Should relieve all the contact areas. tum. The mucoperiosteal flaps on both sides are
6. Must have the scope for a revision surgery if elevated. The quadrilateral cartilage is disarticu-
required later. lated from the maxillary crest. A piece cartilage
is removed to allow for the straightening and
Contraindications: lengthening of the quadrilateral cartilage.
Deviated part of the bone is also removed.
1. Acute URTI The rest of the cartilage is straightened in-
2. Bleeding/Clotting disorders situ by (Fig. 9.5):
3. Uncontrolled DM/HTN
9.1.6.1 Steps of Surgery

1. Sub-Mucosal Resection (SMR)
A Killian incision is placed- about 1 cm ceph-
alad from the caudal end of the septum.
Mucoperichondrial and the mucoperiosteal
flap is elevated on the side of the incision.
Cartilage is incised just posterior to the muco-
sal incision and flaps are elevated on the oppo- Elevation Removal of Flaps
of flaps deviated segment repositioned
site side. Septal cartilage removed leaving a
dorsal and caudal strut. The deviated part of
the bony septum is freed from its attachments
and removed. The flaps are replaced and
sutured at the incision site. Nasal packing,
nasal splints, or trans-septal suturing can be
used to support the flaps (Fig. 9.4).
2. Septoplasty Trans-septal Nasal
Hemi-transfixation incision is placed at the cau- suturing splints
dal end of the septum. The mucoperichondrial

Fig. 9.4 The line diagram is showing different stage of
flap is raised on the concave side. The degree of submucosal resection with suturing technique and nasal
mucoperichondrial flap elevation depends upon splint placement
Baten graft
Deviated septum
Anterior nasal spine
Excess septum excised Septum scored Septum sutured to

and straightened anterior nasal spine
Fig. 9.5 The diagram is depicting ways of septal correction in the septoplasty technique
314 R. Singh et al.
( a) Scoring of the cartilage. 6 . Rees: Relocate entire quadrangular cartilage.

(b) Scoring and suturing—sutures are tightened 7. Gubisch: Used in combination with closed

till septum is straight. rhinoplasty. Entire quadrangular cartilage is
(c) Scoring and splinting—a batten graft is used removed, and the septum is re-created by
to support the scored cartilage. using cartilage pieces.
Tackling the septal spur is performed by
mucoperichondrial flap elevation over the Endoscopic Septoplasty:
quadrilateral cartilage and the bony septum The advent of the endoscope ushered in a new
making an anterior tunnel over the spur. A era in nasal surgery. Endoscopes may be used in
subperiosteal tunnel is raised posterior to the nasal septal surgery as the primary or as an acces-
septal spur. The mucosa left attached to the sory tool. They are extremely useful in more
spur is then elevated by sharp dissection cephalic and isolated deviations which can be
(Fig. 9.6). directly visualized. It allows for localized inci-
sions to be made, obliterating the need for exces-
Modifications sive flap elevation. It can also be used along with
Historical Overview: a conventional technique to tackle the posterior
part of the septum which is not otherwise visible.
1. Metzenbaum (Swinging Door) technique:
It can be used along with endoscopic sinus and
Technique was used to correct the caudal skull base surgery and is also an effective teach-
deviation of septum. The deviated cartilage is ing tool for residents.
removed, the septum is swung into midline External Approach Septoplasty:
and inferior end of the cartilage is anchored This is a favorable approach for dorsal L-strut
with sutures to the anterior nasal spine. deformity and in complex septal reconstructive
2. Doorstop technique: The excess caudal nasal cases. Incision is made over the columella and
septum is transposed over the nasal spine and the anterior end of the septum is exposed. This
fixed. technique can be used along with a rhinoplasty
3. Peer: Complete removal of the caudally devi- procedure.
ated cartilage and reinsertion of the cartilage Extracorporeal Septoplasty:
as a free graft. Intact septum is excised and replaced by
4. Galloway: Single free autograft after removal either:
of entire nasal cartilage, fixed with traction
sutures. 1. Re-orientation: L-strut is harvested from the
5. Vilar Sancho: L shaped cartilage graft to sup- excised septum and it is reinserted in place.
port back and tip of nose. 2. Reconstruction: Pieces of the septum are

splinted against the perpendicular plate of the
ethmoid and then reinserted into its position.
Grooves are made onto the maxillary crest
and the anterior nasal spine where the septum
is secured.
Anterior tunnel A
Pediatric Septoplasty:
Septal spur The age and extent of septal surgery in the
Posterior B
pediatric population is still controversial.
tunnel Delaying surgery can affect nasal and facial
growth and lead to prolonged nasal obstruction.
Early intervention carries the risk of disturbance
Fig. 9.6 The figure is showing the creation of tunnel
anterior and posterior to spur follow by joining of both of the ossification centers leading to nasal and
tunnels so that chances of mucosal perforation is reduced facial deformity. A range of techniques from
closed reduction to the extracorporeal technique toplasty procedures (1.4–5%). Septal perfora-
has been used. Resection of the cartilage should tions may also be surgically created in complex
be conservative, and disruption of the endochon- nasal and skull base endoscopic surgeries to pro-
dral ossification plates needs to be avoided [3]. vide a bi-nostril approach.
Management:
Complications [4] Conservative/Medical—The aim is to reduce
1. Bleeding drying, crusting, and epistaxis. Alkaline nasal
2. Infection douches, saline sprays, and petroleum-based
3. Saddle deformity ointments are commonly used.
4. Columellar retraction Obturator—The principle of obturation is to
5. Supratip deformity cover the inflamed mucosal margin. It helps by
6. Adhesion controlling whistling and epistaxis.
7. Septal Perforation Surgical—Variety of techniques and materials
8. Septal hematoma/abscess has been described to close the perforation.
9. Sensory changes including upper dental

anesthesia • Free Grafts:
–– Autografts
–– Allografts
9.1.7 Nasal Septal Perforation • Pedicle Flaps:
–– Local nasal mucosal
It is defined by through and through defect of the –– Buccal mucosal
nasal septum which may be more than one in –– Composite cartilage and mucosa or carti-
number. It may be asymptomatic, especially if lage and skin
the perforation is small and located in the poste- • Rotation/advancement of mucoperichondrial
rior part of the septum. It can lead to crusting, or mucoperiosteal flaps.
blockage, epistaxis, whistling sound while inhal-
ing air, a feeling of dryness, emptiness in the The selection of surgical approach is based on
nose, or a general feeling of discomfort. Huge the size of perforation. Endonasal approach is
perforations may cause rhinolalia aperta [5]. good for small size perforation (5 mm to 1 cm).
Causes: Medium size perforation (1 to 2 cm) requires
wider exposure and approach is external rhino-
1. Traumatic causes—nasal surgery, nose pick- plasty. Large size (more than 2 cm) can be man-
ing, nasal packing for epistaxis, septal hema- aged by midfacial degloving approach.
toma/abscess, foreign body, etc. Factors that affect the outcome are:
2. Surface irritants—cocaine insufflation, heroin
inhalation, lime, cement, glass, salt, dust, 1. The amount of mucosa available in the nasal
nasal decongestants, etc. cavity can be mobilized.
3. Infections—syphilis, TB, typhoid, diphtheria, 2. The use of an interposition graft to support the
rhinoscleroma, leprosy, mucormycosis, asper- mucosal repair.
gillosis, etc.
4. Neoplastic—melanoma, adenocarcinoma,
squamous cell carcinoma, lymphoma, etc. 9.2 art B: Adenoid Hypertrophy
P
5. Inflammatory—sarcoidosis, Crohn’s disease, and Management
rheumatoid arthritis, SLE, dermatomyositis,
etc. William Meyer coined the term Adenoid for veg-
etations in the nasopharyngeal cavity in 1870. It
The prevalence after submucous resection is also called as pharyngeal tonsil. It forms the
operations is higher (17–25%) compared to sep- central part of the inner Waldeyer’s ring.
316 R. Singh et al.
Embryology The adenoid develops as a midline Blood Supply Arterial supply is mainly derived
structure by the fusion of two lateral primordial from ascending palatine artery, ascending pha-
that become visible during early fetal life. ryngeal artery, the pharyngeal branch of internal
Adenoid tissue is fully developed by the seventh maxillary artery, ascending cervical branch of
month of gestation and continues to grow until thyrocervical trunk. Venous drainage usually
the fifth year of life often causing some airway drains into the pharyngeal plexus, pterygoid
obstruction then it gradually atrophies with air- plexus of veins, and also into the internal jugular
way improvement. It is lined by respiratory cili- vein. Lymphatic drains to upper jugular nodes
ated epithelium. directly or via retropharyngeal nodes.
Function The function of adenoid is to produce Clinical Features Chronic nasal obstruction is the
antibodies like IgG and IgA. It also plays vital commonest symptom which leads to nasal dis-
role in the development of immunological mem- charge, sinusitis, open mouth breathing, an elon-
ory in younger children [6]. gated face, dental malocclusion [7]. Aural symptoms
include otitis media with or without effusion,
Etiology Adenoid hypertrophy is mainly caused decreased hearing, otalgia, etc. Other symptoms
by infections which includes include sleep apnea, hyposmia, failure to thrive,
excessive daytime sleepiness, impairment of cogni-
1. Coronavirus, Cytomegalovirus, EBV, HSV,
tive functions, poor school performance, and psy-
Rhinovirus, etc. chosocial problems [8]. Adenoid faces is the term
2. Infection—Alpha, Beta, Gamma Haemolytic used to denote certain features in prolonged cases
Streptococci, Haemophilus influenza, which include dull looks, pinched nostrils, open
Moraxella catarrhalis, Staphylococcus mouth, narrow maxillary arch, retracted upper lip,
aureus, Corynebacterium diphtheriae, etc. high arch palate (Fig. 9.7).
3. Infectious causes that can lead to adenoid

hypertrophy are GERD, allergy, etc. Diagnosis Clinical examination including exami-
4. Lymphoma, Sinonasal malignancy. nation of the external nose, anterior rhinoscopy,
Fig. 9.7 The clinical

photograph is showing
features of adenoid faces
(Courtesy—Dr. Hitesh
Verma, Associate
Professor, AIIMS, New
Delhi, India)
Fig. 9.9 Adenoid hypertrophy is assessing by measuring

Fig. 9.8 Endoscopic view is shwoing grade 2 adenoid distance at maximum convexity from skull base
hypertrophy (Courtesy—Dr. Hitesh Verma, Associate Professor,
oral and ear examination with the neck. Posterior
rhinoscopy is relatively uncomfortable for young
children. Hence imaging is helpful in making
diagnosis which includes lateral neck radiography. 9.2.2 Radiological Staging
Computerized scan or magnetic resonant imaging
is indicated in doubtful diagnosis. Nasal endos- 1. Johanneson proposed in the year 1968.

copy is the gold standard in the modern era for Adenoid hypertrophy is assessed by measur-
diagnosis and grading of adenoid hypertrophy ing the distance from skull base at maximum
(Fig. 9.8). Rhinomanometry and polysomnogra- convexity (Fig. 9.9).
phy are indicated in OSA patients. For reflex asso- 2. Cohen and Konak method: The airway-to-
ciated adenoid hypertrophy, pH monitoring is soft-palate ratio is a comparison between the
indicated. width of the airway immediately behind the
soft palate and the width of the soft palate
1 cm below the hard palate (Fig. 9.10).
9.2.1 Clinical Grading of Adenoid Patients then were categorized into one of
three groups:
Clinical grading system is based on part of cho- (A) Normal (airway-to-soft-palate ratio ≥1)
ana is fill by adenoid tissue on endoscopic (B) Mild-to-moderate hypertrophy (airway-
examination. to-soft-palate ratio between 0.5 and 1)
(C) Severe hypertrophy (airway-to-soft-
• Grade I—adenoid tissue filling one-third of palate ratio <0.5) [9]
the vertical portion of the choana. 2-A-N ratio: This ratio is calculated by mea-
• Grade II is when adenoid tissue filling one- suring the maximal thickness of adenoid tis-
third to two-thirds of the choana. sue and distance measured along the line from
• Grade III fills from two-third to nearly com- posterior–superior to spheno-occipital syn-
plete obstruction of the choana. chondrosis on skull base (Fig. 9.11) [10]. AN
• Grade IV there is complete choanal ratio greater than 0.80 can be the indicator of
obstruction. enlarged adenoids.
318 R. Singh et al.
3. Crepeau et al. [11] graded adenoid hypertrophy 9.2.3 Management

by measuring maximum thickness of adenoid
tissue and the shortest distance between the Medical Management Breathing exercises,
anterior aspect of adenoid with the posterior steam inhalation, regular nasal douches and
wall of maxillary antrum (Fig. 9.12). Valsalva or reverse Valsalva maneuver are the
conservative method. Lifestyle modification
such as regular exercise and avoidance of pre-
Fig. 9.10 The distance between point a to b is soft palate Fig. 9.12 The red line representing adenoid thickness
thickness and in between b to c is airway width and the blue line is showing distance between anterior
(Courtesy—Dr. Hitesh Verma, Associate Professor, aspects of the adenoid with choana. (Courtesy- Dr. Hitesh
AIIMS, New Delhi, India) Verma, Associate Professor, AIIMS, New Delhi, India)
a b
Nasal cavity
Fig. 9.11 The line diagram is showing assessment of the ing from point of maximum convexity to right angle point
nasopharynx (posterior–superior edge of the hard palate from the imaginary line from anterior border of basi-
to spheno-occipital synchondrosis on skull base—black sphenoid and basi-occipit. X-ray lateral view of the neck
line). Spheno-occipital synchondrosis point can also showing enlarged grade 3 adenoids (A-N radio) blocking
define by the uppermost point of posterior margin of the the nasopharyngeal airway (Courtesy—Dr. Hitesh Verma,
pterygoid plate (red line). Adenoid is measure by assess- Associate Professor, AIIMS, New Delhi, India)
served food for reflux induced adenoid hyper- C. Other—Suspected neoplasia, adenoid hyper-
trophy. The selection of pharmacotherapy is trophy associated with chronic sinusitis.
based on the history of the patient. Anti-
inflammatory treatment (antihistaminic, ste- Contraindications Cleft palate, velo-
roid nasal spray, etc.) is indicated in recurrent pharyngeal insufficiency, and bleeding diathesis.
or persistent rhinosinusitis. Steroid based nasal Systemic review in cases of palatal abnormality
spray is the usual prescription for allergic and showed partial adenoidectomy is safe and effec-
persistent nasal obstruction secondary to ade- tive procedure in problematic cases [12].
noid hypertrophy. Mometasone based nasal
spray is approved above 2 year of age whereas
the majority of other spray is approved above 9.2.5 Surgical Techniques
5 years of age. Decongestant nasal drops can
be advice for both acute and chronic cases for 1. Conservative (Cold) Technique: For cold
not more than 7 days. Antibiotics are reserved technique, the patient should be placed in
for patient with purulent nasal discharge and Rose’s position after induction of general
for complicated adenoiditis. Proton pump anesthesia and Boyles Davis mouth gag is
inhibitors and antacids are indicated in reflux applied for oropharyngeal exposure. Red
cases. Leukotriene receptor antagonist (monte- rubber tube or catheter can be used to retract
lukast) has shown to be effective in reducing the soft palate for better visualization of the
the size of adenoids and respiratory-related nasopharynx. The size of the adenoid can be
sleep disturbances in children with mild OSA. assessed either by nasopharyngeal mirror or
by digital palpation. Use of endoscopes
Surgical Management Adenoidectomy is increases visualization by both trans-nasal
mainly indicated when there is no response to and per-oral route. For the appropriate selec-
conservative treatment. But surgery should be tion of curette, the width of incisors needs to
done early in grade 3 and grade 4 obstruction be assessed. Curette is held in dagger-like
cases and also when adenoid hypertrophy fashion and placed high in the nasopharynx,
induces sequelae because of its mass effect. Up abutting the posterior aspect of the nasal sep-
to grade 2 adenoid hypertrophy, the surgical tum and neck is flexed in the neutral position
selection is based on the response to medical to avoid injury to posterior pharyngeal wall
management. and dens. Then adenoid pad can be curetted
with care taken not to penetrate deeply into
the prevertebral region. Care needs while
9.2.4 Indications removing tissue far laterally to avoid trauma
to eustachian tube. Endoscopic assessment
A. Infection—Purulent adenoiditis, adenoid can be done in between procedure to conform
hypertrophy associated with complications tissue excision and for prevention of injury to
such as otitis media with effusion, chronic normal structures. Packs can be placed into
recurrent otitis media, chronic otitis media the nasopharynx for hemostasis [13]. Other
with perforation. techniques include suction diathermy ablation
B. Obstruction—Adenoid hypertrophy associ- of the adenoid, radiofrequency adenoidec-
ated with excessive snoring and chronic tomy. Suction diathermy ablation is safe with
mouth breathing, sleep apnea or sleep distur- minimal blood loss however it is slow and has
bances, adenoid hypertrophy associated with the risk of cicatrization and burns to surround-
cor pulmonale, failure to thrive, dysphagia, ing tissue [14].
speech abnormalities, craniofacial growth 2. Endoscopic Powered Technique includes
abnormalities, occlusion abnormalities. adenoidectomy by microdebrider. Power-
320 R. Singh et al.
assisted adenoidectomy allows more pre- 4. Grisel syndrome

cise, rapid, safe, and it achieves complete 5. Velopharyngeal dysfunction
removal of adenoid tissue. It is especially 6. Regrowth of adenoids
useful in removing adenoid tissue that
extends through the choana and into the Bleeding is mainly reactionary with the rate
nasal cavity. It can be done with multiple of 0.7%. It can be managed by proper hemosta-
blades with different angles ranging from 30 sis. Rarely, post nasal packing is required.
to 90° either through the nasal cavity or Secondary hemorrhage is very rare. It may be
through the oral cavity. Due to the suction due to bleeding from the aberrant ascending
and shaving action of microdebrider, it can pharyngeal artery or by infection in the postop-
remove the tissue down to the less vascular erative cavity. Unusual reactionary or second-
fascial plane. Oscillation cutting action of ary bleeding raises the possibility of clotting or
the blade minimizes the bleeding [15]. coagulation defect. Nasopharyngeal blood clot
3. Coblation Adenoidectomy: It utilizes a sys- may get pooled in the nasopharynx during the
tem of radiofrequency bipolar electrical cur- procedure. Failure to clear this clot may cause
rent that passes through a medium of normal fatal acute airway obstruction which is called
saline, which results in the production of Coroner’s clot. Infection is relatively uncom-
plasma field of sodium ions. These ions break mon and rarely retropharyngeal and mediasti-
down intercellular bonds and effectively nal abscesses may occur. Grisel Syndrome is
vaporize tissue at a temperature of only non-traumatic atlantoaxial subluxation seen
60°C. The coblator consists of a handpiece more commonly with curette adenoidectomy.
with a suction irrigation tip that transmits the Velopharyngeal dysfunction is rare but can
radiofrequency current and dissects tissue. It cause significant problems with hypernasal
also has cautery for hemostasis. With this speech and swallowing. It is mandatory to
technique, separate suction cautery device is assess the palate and uvula for submucous cleft
not necessary. It also ensures the complete prior to surgery. Regrowth of adenoid is usu-
removal of adenoid tissue with minimal ally seen more commonly with curettage
bleeding. Coblation has advantages like very adenoidectomy.
limited depth of penetration, minimal collat-
eral tissue damage, localized effect, con-
trolled volumetric tissue removal, low surface 9.3 art C: Epistaxis
P
temperature. To reduce the operating dura- and Management
tion, the surgeon combines microdebrider
with coblator. Epistaxis, or bleeding from the nose, is the com-
Among all technique, simultaneous use of nasal monest emergency in ENT practice. It affects up
endoscopes reduces complication to great to 60% of the population in their lifetime, and in
extent and conventional technique is rapid as 6%, it requires medical attention. It can be life
compared to other techniques. Powered instru- threatening in elderly patients and can cause
ments are more precise, less traumatic to sur- major concern in parents of young children.
rounding structures [16]. Nasal cavity mucosa is supplied by the terminal
branches of the internal and external carotid
artery (Fig. 9.13). Nasal bleeding most com-
9.2.6 Complications monly occurs from Kiesselbach’s plexus or
of Adenoidectomy Little’s area, which is supplied by both systems.
Woodruff’s plexus lying in the posterior part of
1. Bleeding nasal cavity just inferior to posterior-most end of
2. Dental trauma the inferior turbinate. It is generally responsible
3. Infection for posterior epistaxis.
Fig. 9.13 The line diagram is showing the nasal cavity blood supply
9.3.1 Causes (c) Juvenile nasopharyngeal angiofibroma

(d) Squamous cell carcinoma
The etiology of epistaxis can be divided into (e) Inverted papilloma
local and general causes; however 80–90% of 4. Granulomatous disorder
cases are idiopathic. (a) Sarcoidosis
(b) Wegener’s granulomatosis
9.3.1.1 Local (c) Tuberculosis
1. Trauma 5. Structural
(a) Nasal fracture (a) Septal Spurs
(b) Nose picking (b) Septal perforation
(c) Foreign body 6. Iatrogenic
(d) Continuous positive airway pressure (a) Functional endoscopic sinus surgery
2. Inflammatory Conditions (b) Septoplasty
(a) Allergic rhinosinusitis (c) Turbinate reduction
(b) Bacterial rhinosinusitis (d) Nasogastric tube insertion
(c) Common cold (e) Nasotracheal intubation
3. Neoplasia 7. Drugs
(a) Septal and turbinate hemangioma (a) Nasal steroids
(b) Nasal papilloma (b) Cocaine abuse
322 R. Singh et al.
9.3.1.2 General 3. Anatomical abnormalities like septal devia-

1. Hematological tions and spurs are also responsible.
(a) Coagulopathies
(b) Thrombocytopenia
(c) Platelet dysfunction, e.g., Von Willebrand’s 9.3.3 Management
disease
(d) Hemophilia The initial most management is resuscitation. It
(e) Aplastic anemia includes correction of volume loss by intrave-
(f) Hereditary hemorrhagic telangiectasia/ nous fluid administration. Blood transfusion
Osler Weber Rendu disease should be considered if hemoglobin levels fall
2. Hypertension below 9 g/dl. Detailed history and examination is
3. Environmental factors helpful to diagnose the cause of bleeding. After
(a) Humidity primary resuscitation, necessary blood investiga-
(b) Altitude tion is advised on the basis of history. Blood
(c) Temperature grouping and cross-matching is must for moder-
(d) Pollution ate to severe epistaxis cases. For anterior epi-
4. Drugs staxis, the patient should be asked to pinch the
(a) Anticoagulants like heparin, warfarin lower cartilaginous part of the nose while leaning
(b) Antiplatelets like ecosprin, clopidogrel forward over a bowl as bleeding into the naso-
5. Organ failure pharynx is more uncomfortable. Also, the blood
(a) Uremia will not be swallowed causing subsequent nau-
(b) Cirrhosis sea. The treatment policy is followed in the form
6. Atherosclerosis of four line of management. First line of manage-
7. Alcoholism ment is indicated when the site of bleeding is vis-
ible either by anterior rhinoscopy or by nasal
Epistaxis can be classified on the basis of eti- endoscopy. Bleeding point can be cauterized by
ology. Epistaxis is called primary when no cause electric or by chemical application and it is
is identify whereas secondary when cause is known as the direct method. Chemical cautery
available. When the site of bleeding is visible on with silver nitrate is more useful for bleeding
anterior rhinoscopy or anterior to pyriform aper- points in anterior part of the nose. Bipolar or
ture, it is called anterior epistaxis. When the site monopolar suction cautery is an alternative if
of bleeding is not visible by anterior rhinoscopy bleeding is more posterior, rigorous, or if refrac-
or behind the pyriform aperture, it is called poste- tory to chemical cautery (Fig. 9.14) [18].
rior epistaxis. Simultaneous bilateral cautery on the nasal sep-
tum should be avoided to minimize the risk of
septal perforation.
9.3.2 Risk Factors When the site of bleeding is not visible or it is
generalized, then second line of management is
Risk factors for recurrent epistaxis include the applicable. It is an indirect method and nasal
following: packing is done to control bleeding. The different
kinds of packing materials are mentioned in
1. Hypertension and diabetes mellitus are minor Chap. 1. In this chapter, we are discussing pack-
risk factors for recurrent epistaxis as both these ing technique. Newer absorbable and non-
conditions are known to induce atherosclerotic absorbable packing materials are generally
changes in the vasculature system [17]. effective in low to moderate amount of epistaxis.
2. Congestive heart failure is the cause of recur- Absorbable packs offer greater patient comfort
rent epistaxis because of the increased venous and are more desirable in patients with thrombo-
pressure in the nasal vessels. cytopenia or coagulopathy. They create less
injury to the surrounding mucosa. Three fourth commercial packs can be kept for 4–5 days. The
inch width Roller Gauze is helpful in almost all alarming signs for toxic shock syndrome are
kind of anterior epistaxis. It is applicable when, purulent foul smelling discharge from pack,
newer packing material failed, in moderate to fever, tachycardia, etc. In such situation, the pack
severe epistaxis and recurrent epistaxis. Roller should be removed immediately and broad-
gauze is soaked in Vaseline or petroleum jelly to spectrum antibiotics should start.
prevent surrounding adhesion and to minimized Posterior Packing is indicated for posterior
insertional/removal trauma. Pack can be placed epistaxis. It can be achieved by high volume,
in vertical and horizontal manner (Fig. 9.15). low-pressure balloon packs. Brighton Balloon is
Horizontal manner is relatively easy and most specifically manufactured for epistaxis. It has a
followed. Gauze is generally kept for 48–72 h. If postnasal balloon and immobile anterior balloon
required for more than 72 h, then it should be that are independently inflated. Epistat Nasal
changed to prevent toxic shock syndrome. Newer Catheter has two independently inflatable bulbs
for precise control of bleeding. The hollow cath-
eter allows nasal breathing. Conventionally pos-
terior nasal pack is prepared with gauze material.
The volume of the nasopharynx should be kept in
mind while preparing it. Incisor width is the
rough estimation of nasopharynx width. Foley’s
catheter is generally available in operation
theaters. It is more in use for posterior packing.
Ten to fifteen ml of water is sufficient to obliter-
ate the nasopharynx. It can hinge over columella
with umbilical tap. Columella should be secured
to prevent necrosis. When both anterior and pos-
terior nasal packing is required, the posterior
should be placed first.
Studies have shown the benefit of warm water
irrigation in posterior epistaxis as compared to
nasal packing. A modified bladder catheter that
Fig. 9.14 The suction monopolar cautery is used to con- seals the choana can be inserted. Water at 50 °C
trol epistaxis is irrigated through the catheter with the help of a
a b
Fig. 9.15 The diagram is depicting the vertical and horizontal way of nasal cavity packing with gauze material
324 R. Singh et al.
caloric stimulator and will exit the catheter Ethmoid crest

through a hole proximal to the inflated balloon. It
is believed that the warm water causes edema of
the nasal mucosa thereby compressing the bleed-
ing vessels in addition to possibly stimulating the
coagulation cascade. Tranexamic acid and epsi-
lon aminocaproic acid are useful as adjuvant sys-
temic therapy for recurrent and refractory Sphenopalatine artery
epistaxis [19].
Fig. 9.16 The endoscopic picture is showing the rela-
tionship of the left sphenopalatine artery and ethmoid
9.3.4 Surgical Management crest
If all the above methods fail to control the bleed-

ing, definitive surgical procedures have to be per- 9.3.4.2 Anterior Ethmoidal Artery
formed. It is the third line of management. Ligation
Sphenopalatine is the major blood supply for Anterior ethmoid artery is branch of ophthal-
nasal mucosa [20]. It can ligate by endoscopic or mic artery. It enters into nasal cavity via ante-
by sub-labial transmaxillary approach. rior ethmoid foreman. It runs with in ethmoid
roof bone in 90% of cases. In 10% it runs deep
9.3.4.1 Endoscopic Sphenopalatine within nasal cavity just posterior to frontal
Artery (SPA) Ligation recess. Anterior Ethmoidal artery can be
The SPA is the last branch of the internal maxil- injured in naso-ethmoid fractures or during
lary artery and it enters the nasal cavity through sinus surgery. It can lead to severe epistaxis.
the sphenopalatine foramen. Foreman lies in the Injury to the artery can also lead to intraorbital
posterior lateral nasal wall in the posterior-most or intracranial bleeding [21]. Retro-orbital
part of the middle meatus, just inferior to the lat- hemorrhage is an emergency as it can lead to
eral attachment of middle turbinate. blindness. Its management requires ligation of
Sphenopalatine foramen is lying behind and infe- the artery either by an external approach or
rior to the ethmoid crest (Fig. 9.16). Clipping or endoscope approach. Open approach is pre-
diathermy of the sphenopalatine artery is cur- ferred over endoscopic approach in traumatic
rently the accepted treatment. 97% of individuals cases. Lynch Howarth’s incision is the incision
have two or more branches medial to the ethmoid made in the region of the medial cantus
crest. Failure to identify these branches can lead (Fig. 9.17). Lacrimal sac requires lifting from
to the recurrence of bleeding. If no bleeder iden- its bed for better access. Artery is locating
tified, SPA ligation can be done as it has the wid- 24 mm deep to the anterior lacrimal crest. In
est supply in the nasal cavity. endoscopic approach, cauterization of artery is
Sphenopalatine bleed can also control by done in its middle course so that if any bleed-
identification in pterygopalatine fossa by creating ing occurs while handling, can be managed by
window in posterior wall of maxilla by Caldwell- endoscopic route. Once it retract laterally in
Luc approach in difficult case scenario. orbit, the open approach is better.
External carotid artery

Fig. 9.17 Lynch incision is marked on the left side of
medial and supra canthal region (Courtesy—Dr. Hitesh
Verma, Associate Professor, AIIMS, New Delhi, India)
Fig. 9.18 The clinical photograph is showing the left
9.3.4.3 Maxillary Artery Ligation side of the external carotid artery and its branches
Internal maxillary artery runs behind maxilla in (Courtesy—Dr. Hitesh Verma, Associate Professor,
infratemporal fossa and pterygopalatine fossa.
It may bleed while handing of nasal tumor
extending in retromaxillary space via trans-
nasal approach. Caldwell-Luc approach, endo- Angiography assisted embolization is the
scopic Denker’s or posterior sub-labial fourth line of management. It is advocated in
approaches are useful to get access in retromax- patients of refractory epistaxis who are unfit for
illary space [22, 23]. surgery or in whom surgery has failed to stem
the bleeding. Technique entails cannulation of
9.3.4.4 External Carotid Artery the external carotid artery and location of the
Ligation bleeding point by water-soluble contrast. Coils,
External carotid artery ligation is advised in gel foam, and polyvinyl alcohol can then embo-
extreme cases and when intervention radiologist lize the causative artery [24]. The success rate
is not available. The horizontal incision is made has been reported to be as high as 87%, which is
at the level of the hyoid bone. Sternocleidomastoid similar to arterial ligation. Complication
muscle is retracted laterally. Carotid space is includes cerebrovascular accidents when mate-
entered and the external carotid artery is con- rial dislodges into the internal carotid system
formed with its branches in the neck. The exter- but it is relatively rare in recent scenario due to
nal carotid artery is ligated above its first branch upgradation of material, technique, and
(Fig. 9.18). expertise.
326 R. Singh et al.
9.3.4.5 Internal Carotid Bleeding congested. Steam inhalation, nasal douches, liq-
1. The carotid artery can injure by accidental uid paraffin nasal drops, and ointments are help-
trauma and during skull base surgery. It is rare ful in hydration of dehydrate nasal mucosa.
but life threatening. Proper identification of Topical tranexamic acid can be used in patients
sphenoid sinus ostia and sphenoid ostium taking anti-platelet drugs. Avoidance of warfarin,
should be widened in inferomedial direction aspirin, and other nonsteroidal anti-inflammatory
to prevent this catastrophe. If it occurs while drugs (NSAIDs) is required as these medications
surgery, immediate compression of the CCA can affect platelets function. The correction of
in the neck and tight packing of the sphenoid clotting factor derived from the liver, can be done
sinus is needed. Small rent can be managed by by administration of vitamin K injection. The
mashed muscle piece but it is challenging. choice of clotting factor correction is based on
Clipping of injured site and direct vessel clo- deficit parameter. Literature is controversial for
sure can be attempted if there is adequate prescribing prophylactic antibiotics in anterior
exposure of the vasculature during surgery nasal packing [27].
otherwise patient should be shifted to the
intervention radiology Department. 9.3.4.7 Hereditary Hemorrhagic
Endovascular occlusion or stenting is per- Telangiectasia
formed by localizing the site of injury. The It is an inherited autosomal dominant disorder
selection of technique is verified by balloon that is characterized by malformations of various
occlusion test to check the adequacy of col- blood vessels (vascular dysplasia), potentially
lateral circulation [25]. Flow diversion is indi- resulting in recurrent bleeding. The surgical man-
cated in complex and recurrent aneurysm agement varies from the coagulation of vessel by
cases. Silk flow, pipeline embolization, flow laser to complete closure of the nasal cavity (Fig.
redirection endoluminal devices are the recent 4.5, Chap. 4). In septal dermoplasty, the nasal
therapy for the persistent aneurysm. These mucosa is replaced with autologous skin grafts.
devices reconstruct the artery by creating The nasal cavity is closed by modified Young’s
thrombosis at the aneurysm site [26]. The operation and it is indicated in moderate to severe
pack should be removed after conformation epistaxis that has proved unresponsive to other
with angiography. treatment options. Antifibrinolytic drugs such as
tranexamic acid have been found to have mixed
9.3.4.6 Medical Management results in treating nosebleeds. Bevacizumab
for Epistaxis (Avastin) has been used experimentally to reduce
Topical decongestants like oxymetazoline can be the number and severity of nosebleeds in persons
useful in mild epistaxis and when the mucosa is with HHT [28].
Flow chart for Epistaxis management
• Single episode or recurrent bleeding

• Unilateral or bilateral
Initial • Anterior or posterior bleeding
assessment • Look for signs of hypovolemic shock like tachypnea, tachycardia or
and resuscitation hypotension
• History of known bleeding disorders like ITP, thrombocytopenia
• In severe bleeds, establish intravenous access, draw blood for cross
match and blood grouping
Evaluation by anterior rhinoscopy/endoscopy and suction
Anterior Bleeding
Posterior Bleeding
Bleeding point
visible
Silver nitrate Bleeding Bleeding Endoscopic

Medical
cautery/Electrocautery Stops Stops electrocautery if
management and
with bipolar or suction bleeding vessel is
Follow up
monopolar cautery identified
Bleeding Persists
Bleeding Persists
Remove pack after 48

Posterior nasal
Nasal packing with to 72 hrs.
packing; high
absorbable/non- Prolong pack required-
pressure, low volume
absorbable packs pack change and broad
packs
spectrum antibiotics
If bleeding persists
Fit for Surgery

tried Unfit for surgery/ recurrent bleeding/ all method
Ligation of source of bleeding CT angiography followed by

embolization of bleeding vessel
328 R. Singh et al.
References 16. Ferreira MS, Mangussi-Gomes J, Ximendes R, et al.

Comparison of three different adenoidectomy tech-
niques in children - has the conventional technique
1. Takahashi R. The formation of the nasal septum
been surpassed. Int J Pediatr Otorhinolaryngol.
and the etiology of septal deformity. The concept
2018;104:145–9.
of evolutionary paradox. Acta Otolaryngol Suppl.
17.
Payne SC, Feldstein D, Anne S, Tunkel
1987;443:1–160.
DE. Hypertension and epistaxis: why is there limited
2. Fettman N, Sanford T, Sindwani R. Surgical manage-
guidance in the nosebleed clinical practice guidelines?
ment of the deviated septum: techniques in septo-
Otolaryngol Head Neck Surg. 2020;162(1):33–4.
plasty. Otolaryngol Clin N Am. 2009;42:241–52.
18. Tunkel DE, Anne S, Payne SC, et al. Clinical Practice
3. Verwoerd CDA, Verwoerd-Verhoef HL. Rhinosurgery
Guideline: nosebleed (Epistaxis). Otolaryngol Head
in children: surgical and developmental aspects.
Neck Surg. 2020;162(1_Suppl):S1–S38.
In: Nolst Trenité GJ, editor. Rhinoplasty. 3rd ed.
19. Kamhieh Y, Fox H. Tranexamic acid in epi-

Amsterdam: The Hague; Kugler; 2005. p. 201–8.
staxis: a systematic review. Clin Otolaryngol.
4. Ketcham AS, Han JK. Complications and man-
2016;41(6):771–6.
agement of septoplasty. Otolaryngol Clin N Am.
20.
Kitamura T, Takenaka Y, Takeda K, et al.
2010;43:897–904.
Sphenopalatine artery surgery for refractory idio-
5. Kridel RW. Septal perforation repair. Otolaryngol
pathic epistaxis: systematic review and meta-analysis.
Clin N Am. 1999 Aug;32(4):695–724.
Laryngoscope. 2019;129(8):1731–6.
6. Wysocka J, Hassmann E, Lipska A, Musiatowicz
21. Turri-Zanoni M, Arosio AD, Stamm AC, et al.

M. Naïve and memory T- cells in hypertrophic
Septal branches of the anterior ethmoidal artery:
adenoids in children according to age. Int J Pediatr
anatomical considerations and clinical implications
Otorhinolaryngol. 2003;67:237–41.
in the management of refractory epistaxis. Eur Arch
7. Bluestone CD. Current indications for tonsillectomy
Otorhinolaryngol. 2018;275(6):1449–56.
and adenoidectomy. Ann Otol Rhinol Laryngol Suppl.
22. Polev GA, Carrau RL, Golbin DA, et al. Intraoral
1992;155:58.
Endoscopic Ligation of Maxillary Artery in
8. Peter JR. The adenoid and adenoidectomy. In:
the Infratemporal Fossa. J Craniofac Surg.
Michael G, George GB, Martin JB, Ray C, John H,
2019;30(1):137–40.
Nicholas SJ, et al., editors. Scott-Brown’s otolaryn-
23. Huyett P, Jankowitz BT, Wang EW, Snyderman

gology, vol. 1. 7th ed. London: Hodder Arnold; 2008.
CH. Endovascular embolization in the treat-
p. 1095–101.
ment of epistaxis. Otolaryngol Head Neck Surg.
9. Cohen D, Konak S. The evaluation of radiographs of
2019;160(5):822–8.
the nasopharynx. Clin Otolaryngol. 1985;10:73–8.
24. Cheng CL, Lee BJ, Chen WH, Hu SY. Epistaxis from
10. Fujioka M, Young L, Girdany B. Radiographic

ruptured pseudoaneurysm of the internal carotid
evaluation of adenoidal size in children: adenoidal-
artery. Br J Hosp Med (Lond). 2019;80(4):iv.
nasopharyngeal ratio. Am J Radiol. 1979;133:401–4.
25. Zhang Z, Lv X, Yang X, Shiqing MU, Wu Z, Shen C,
11. Crepeau J, Patriquin H, Poliquin J, Tetreault L. Radio-
et al. Endovascular management of giant aneurysms:
graphic evaluation of the symptom—producing ade-
an introspection. Neurol India. 2015;63:184–9.
noid. Otolaryngol Head Neck Surg. 1982;90:548–54.
26. Tran QK, Rehan MA, Haase DJ, et al. Prophylactic
12. Salna I, Jervis-Bardy J, Wabnitz D, et al. Partial ade-
antibiotics for anterior nasal packing in emergency
noidectomy in patients with palatal abnormalities. J
department: a systematic review and meta-analysis
Craniofac Surg. 2019 Jul;30(5):e454–60.
of clinically-significant infections. Am J Emerg Med.
13. Clemens J, McMurray JS, Willging JP. Electrocautery
2020;38(5):983–9.
verses curette adenoidectomy: comparison of post-
27. Hsu YP, Hsu CW, Bai CH, et al. Medical treat-

operative results. Int J Pediatr Otorhinolaryngol.
ment for epistaxis in hereditary hemorrhagic tel-
1998;43:115–22.
angiectasia: a meta-analysis. Otolaryngol Head
14. Owens D, Jaramillo M, Saunders M. Suction

Neck Surg. 2019;160(1):22–35. https://doi.
diathermy adenoid ablation. J Laryngol Otol.
org/10.1177/0194599818797316.
2005;119(1):34–5.
28. Stokes P, Rimmer J. Intranasal bevacizumab in the
15. Stanislaw P, Koltai PJ, Feustel PJ. Comparison of
treatment of HHT-related epistaxis: a systematic
power assisted adenoidectomy vs adenoid curette
review. Rhinology. 2018;56(1):3–10. https://doi.
adenoidectomy. Arch Otolaryngol Head Neck Surg.
org/10.4193/Rhin17.166.
2000;126(7):845–9.
Radiotherapy, Chemotherapy,
and Quality of Life 10
Bharti Devnani, Suman Bhasker, Raja Pramanik,
Surya Prakash Vadlamani, and Suresh Mani
Contents
10.1 art A: Radiation Therapy in Nasal Cavity, Paranasal Sinus, and
P
Nasopharyngeal Tumors 330
10.1.2 Radiation in Nasal Cavity Tumors 330
10.1.3 Indications of Radiotherapy in Paranasal Sinus Tumors 331
10.1.4 Radiation Therapy for Nasopharyngeal Cancer 331
10.1.5 External Beam Radiotherapy Planning 331
10.1.6 Time, Dose, and Fractionation 331
10.1.7 Techniques of Radiation 332
10.1.8 Radiation Toxicities 333
10.1.9 Radiotherapy in Specific Histological Subtype 333
10.1.10 Radiotherapy in Benign Tumors 334
10.1.11 Future Directions 334
10.2 art B: Chemotherapy Perspectives in Nasal and Paranasal Sinus
P
Tumors 334
10.2.1 Summary 334
10.2.2 Strategies for Chemotherapies in Head and Neck Cancers 335
10.2.3 Chemotherapy in Different Tumors of Nose and Paranasal Sinuses 335
10.3 art C: Perioperative and Postoperative Measures to Improve
P
Quality of Life After Nasal Surgery 338
10.3.1 Quality Indicators 339
10.3.2 Preoperative Measures 339
B. Devnani · S. Bhasker (*)

Radiotherapy, AIIMS, New Delhi, India
e-mail: drsumanbhasker@gmail.com
R. Pramanik · S. P. Vadlamani
Medical Oncology, Dr.B.R.A-IRCH, AIIMS,
New Delhi, India
S. Mani
ENT, CMC, Vellore, Tamil Nadu, India
330 B. Devnani et al.
10.3.3 Perioperative Measures 340

10.3.4 Postoperative Measures 340
10.3.5 Follow-Up 341
10.4 Conclusion 341
References 341
The decision needs to be made in a multidisci- tumor to adjacent critical structures. Radiation
plinary clinical team. Para-nasal sinus malignan- therapy (RT) plays a pivotal role in the multimo-
cies are rare aggressive tumors. Radiotherapy is dality treatment of these tumors. Technological
an integral part of management either as single advancements in the form of Intensity-modulated
modality or in combination. There is wide range radiotherapy (IMRT) has given an advantage of
of histo-pathological entities in this subtype with steep radiation dose gradients to achieve more
varying radiation sensitivity. Local failure is the conformal treatment and better sparing of normal
major pattern of relapse. Lymph nodal involve- tissues.
ment is less frequent in nasal and para-nasal sinus
malignancies although in cases of nasopharyngeal
cancers it is present in up-to 90 % of the cases. 10.1.2 Radiation in Nasal Cavity
Advent of advanced technologies in the form of Tumors
IMRT and particle therapy substantially improved
the clinical outcome. Conformal treatment pro- Radiation therapy is an important treatment
vides high rates of local control with decreased modality in the management of nasal cavity can-
toxicities. Margin positivity & extra-capsular cers. For small tumors of vestibule radical radio-
spread in Lymph nodes are the indication for che- therapy alone provides excellent cosmetic
motherapy. Chronic rhinosinusitis negatively outcomes, especially in small anterior septal
affects quality of life (QoL) by disturbing the tumors and nasal ala region tumors. In locally
physical, social, and emotional well-being of advanced tumors of the nasal cavity, RT can be
patients. It also reduces economic productivity used as an adjuvant treatment modality in the
and can increase the risk of depression and sleep postoperative setting or in the preoperative set-
dysfunction. EuroQol 5D, Rhinosinusitis out- ting to debulk the tumor in surgically challenging
come measures (RSOM), McGill Pain cases. Indications of postoperative RT include
Questionnaire, Short Form-36 Health Survey and advance stage T3 or T4 tumor, close or positive
Short Form-12 Health Survey Rhinosinusitis margin in early stage, high tumor grade, and
Disability Index, Chronic Sinusitis Survey Score, involvement of lymph nodes or perineural inva-
Sinonasal Outcome Test-20, -16, and -22 are the sion. In cases of unresectable disease, a com-
scoring systems used to assess the quality of life. bined modality approach with concurrent
chemotherapy and radiotherapy is advocated.
Palliative radiation is offered to control the symp-
10.1 P
art A: Radiation Therapy toms of pain, nasal obstruction, proptosis, epi-
in Nasal Cavity, Paranasal staxis and for tumor growth restrain in ulcerative
Sinus, and Nasopharyngeal or fungating lesions.
Tumors Radiation can be delivered by external beam
radiotherapy, brachytherapy, or a combination of
10.1.1 Introduction both. In a study by Allen et al. [1], 32 patients with
nasal cavity tumors were treated by a median
Management of sinonasal region tumors is chal- EBRT dose of radiation of 65 Gy. At a median
lenging in view of the close proximity of the follow-up of 11 years, 5-year locoregional control
10 Radiotherapy, Chemotherapy, and Quality of Life 331
was 81% and OS was 94%, with few serious cally limited to biopsy for histological confirma-
adverse events. Brachytherapy is used for small tion and in cases of salvage therapy. Early-stage
lesions using interstitial brachytherapy catheter nasopharyngeal cancer can be successfully
implants or intracavitary mold using 192Ir radioac- treated with RT alone. In a study by Chua et al.
tive sources. Anterio-inferior septal lesions [5], 10-year recurrence-free survival (RFS) was
(<1.5 cm) are suitable for interstitial brachyther- more than 96% with radiation therapy. Concurrent
apy [2]. Tumor volume is an important prognostic chemotherapy needs to be added with radiation in
factor for regional recurrence following brachy- case of locally advanced nasopharyngeal cancer
therapy. Tumor volume <2.3 cc is associated with (T3, T4, or N+ disease). A precision radiotherapy
a 3-year locoregional control of 96%. Nasal technique like IMRT is the standard of care to
Appearance and Function Evaluation achieve a higher therapeutic ratio. Particle beam
Questionnaire (NAFEQ) is a 14-questions ques- therapy with proton beam and carbon ion therapy
tionnaire to assess patient satisfaction with esthetic is an emerging modality due to its physical char-
and functional outcomes following brachytherapy. acteristics of the Bragg’s peak. Proton beam ther-
It consists of two parts, including seven questions apy is especially useful in cases of reradiation in
regarding nasal function and seven items to assess recurrent disease [5]. Radiation workflow is men-
satisfaction with nasal appearance. tioned in Fig. 10.1.
10.1.3 Indications of Radiotherapy 10.1.5 External Beam Radiotherapy

in Paranasal Sinus Tumors Planning
Surgery followed by postoperative radiation ther- Meticulous radiotherapy planning is very crucial
apy (PORT) is the mainstay of treatment in to achieve higher control rates. MRI of the naso-
advanced paranasal sinus tumors. Other indica- pharynx and neck is an important diagnostic
tions of PORT include high tumor grade or high- investigation and is very useful for radiation
risk histology, perineural invasion, planning as clivus and nerves are best seen on
lymphovascular space invasion, positive lymph MRI. Figure 10.2 shows the various steps of radi-
nodes, margin positivity, and inadequate resec- ation therapy workflow from preplanning to
tion or tumor spillage. Radical radiotherapy with delivery of radiation. Target volume delineation
chemotherapy is used in locally advanced T3, T4 involves contouring of tumor volumes and organs
tumors especially in ethmoid sinus tumors where at risk. Gross tumor volume (GTV) consists of
extensive surgery may lead to structural and the entire visible gross tumor clinically or radio-
functional deficit. Patients who are not fit for sur- logically. Clinical target volume (CTV) encom-
gery due to medical comorbidities are also candi- passes GTV, postoperative bed in cases of
dates for radiotherapy. In cases of borderline postoperative cases, regions of positive margin,
resectable tumors with anterior soft tissue or skin and regions with nodal extracapsular extension
infiltration, minimal preorbital invasion or ptery- and regions at higher risk of micrometastasis. A
gopalatine invasion preoperative radiation is indi- 3–5 mm margin is given to CTV to account for
cated [3, 4]. inter- and intrafraction set-up errors to create a
planning target volume (PTV) [6, 7].
10.1.4 Radiation Therapy

for Nasopharyngeal Cancer 10.1.6 Time, Dose, and Fractionation
Radiation therapy is the mainstay of treatment for A radiation dose of 70 Gy in 35 fractions deliv-
nasopharyngeal malignancies. Surgery is typi- ered over 7 weeks is recommended to gross
Fig. 10.1 Radiation
Consent and Preplanning
therapy workflow
Clinical history, Imaging, surgical details and
histopathology
Immobilisation
Supine with neck rest, Thermoplatic cast, Bite block
CT Simulation for 3D planning

Fluroscopic simulation and
Thin slices of 3-5mm for contouring and planning
2D Planning
Maxillary sinus-Anterio-
Lateral wedge pair technique
with Shielding of normal
Target volume Delineation tissues
Contouring of target volumes and organs at risk (OAR) Ethmoid-direct enface beam
or combination of beams
Physics Planning
Beam arrangement and energy selection to optimise the
dose delivery to target volumes and maximal sparing of
OARs
Plan Evaluation
Evaluation of dose volume histogram, dose
distribution
Quality Assurance
Safe fulfilment of dose prescription to improve
patient safety & quality of care
Execution and Verification

Safe delivery and cheking of set-up errors
On treatment monitoring
To check for interfraction errors, acute toxicities and
compliance
tumor volume along with a 50–60 Gy to the areas 10.1.7 Techniques of Radiation
of micrometastasis. In cases of pre-op RT where
debulking is the primary aim, an RT dose of In two-dimensional conventional radiotherapy,
50Gy/25# is given. There are different fraction- the volume of irradiated tissue is simply deter-
ation schedules for palliative RT ranging from mined by anatomical field borders that are based
8Gy in a single fraction to 30Gy in 10 fractions. on radiological bony landmarks. There are more
20 Gy over 5 fractions is one of the commonly chances of excess normal tissue toxicity and
followed palliative dose fractionations. beam arrangements are limited to orthogonal
Fig. 10.2 A case of esthesioneuroblastoma showing radiation dose distribution in targets and organs at risk (a) Sagittal
section (b) Axial section
placements with crude shielding techniques. The by saline nasal sprays. Nasal cavity synechiae is
advantage of conformal radiotherapy is a steep prevented by regular nasal dosches and by proper
dose gradient close to the target. Conformal cavity management. Xerostomia is a common
radiotherapy includes 3D-Conformal radiother- sequelae post RT and parotid sparing IMRT
apy (3D-CRT), Intensity-modulated radiotherapy should be used wherever feasible based on tumor
(IMRT), and Image-guided radiotherapy (IGRT) extension. Decaying of teeth commonly follows
techniques. 3D-CRT technique shapes the beams xerostomia for which prophylactic fluoride tooth-
based on 3D reconstructions of the tumor size paste should be prescribed and loose or decayed
and shape and the location of nearby normal tis- teeth should be removed prior to starting RT to
sues. IMRT changes the intensity of each small further prevent osteoradionecrosis. Ocular symp-
beamlet to obtain even more conformal dose dis- toms in the form of chronic keratitis can occur in
tribution and avoidance of normal tissue damage. the RT of paranasal sinus malignancies.
IMRT is the standard technique for definitive Sensorineural hearing loss is prominent with
radiation therapy for nasopharyngeal cancer. concurrent use of chemotherapy for which mean
IGRT is a method of radiation therapy that incor- cochlea dose should be kept below 48 Gy to min-
porates imaging techniques during each treat- imize damage. Carotid artery stenosis is a poten-
ment session. Conformal radiotherapy offers tially fatal complication in reradiation cases.
precise dose shaping, minimizes the dose to criti- Routine duplex ultrasound scanning can be done
cal normal tissues thereby decreasing the radia- in cases of higher-risk patients.
tion toxicities.
10.1.9 Radiotherapy in Specific

10.1.8 Radiation Toxicities Histological Subtype
Skin erythema, mucositis, dryness, dysgeusia, Squamous cell carcinoma is the most common
bleeding from the nose, and fatigue are some of histopathological type of nose and paranasal
the common acute radiation toxicities. Nasal cav- sinus tumor. The treatment policy is mentioned
ity mucositis and dryness of mucous membranes above. Esthesioneuroblastomas, Kadish A tumors
is common following RT and should be managed can be treated with the single modality treatment
in the form of primary RT alone. The rest of the cases of positive margins after surgery. Radiation
tumors can be best treated by a combination of therapy in chordoma is challenging due to the
surgery and radiotherapy. It tends to invade the intrinsic radio-resistance of these tumors coupled
cribriform plate and anterior cranial fossa, and with the increased sensitivity of the adjacent criti-
therefore, these regions should be encompassed cal neural structures. Charged particle therapy has
in the target volume. Elective nodal radiation is an established role and increases control rates. The
generally not required. In terms of radiotherapy role of radiation therapy for inverted papillomas is
techniques, it is evident that 3D radiotherapy sig- seen in patients with carcinoma in situ or invasive
nificantly improves local control compared to the features found after resection.
2D technique (74% vs. 59%).
Adenoid cystic carcinoma originates mostly
from the minor salivary glands. In view of the 10.1.11 Future Directions
highly neurotropic nature of adenoid cystic carci-
nomas, radiotherapy volumes must encompass Particle beam therapy with proton beam and car-
the afferent and efferent local nerves to the skull bon ion therapy is an emerging modality due to
base. Adenocarcinoma is a locally aggressive its physical characteristics of the Bragg’s peak.
tumor that occurs almost exclusively in the eth- There are ongoing randomized prospective trials
moid sinus. Conformal radiation should be used evaluating the efficacy of the same. Although
for this location of the tumor. Combination che- data for charged particles are encouraging, the
motherapy with cisplatin, fluorouracil, and leu- lack of widespread access and high cost associ-
covorin has been shown to be efficacious. Mucosal ated with these facilities limit their routine use.
melanoma of the paranasal sinuses is a rare form
of melanoma (0.2–4%) and is notoriously resis-
tant to conventional chemoradiotherapy. 10.2 P
art B: Chemotherapy
Hypofractionated RT, combined immuno-IMRT Perspectives in Nasal
that may potentially enhance the therapeutic ratio and Paranasal Sinus Tumors
is investigational. Radiotherapy is an important
role in the curative treatment of patients with 10.2.1 Summary
Nasal Natural Killer T Cell Lymphoma. Yang
et al. reported that definitive radiation therapy Cancers arising primarily from the nasal cavity
with or without chemotherapy was more effective and paranasal sinuses are fairly uncommon. The
than strategies that used induction or primary che- most common histology encountered is squa-
motherapy. RT dose of >50 Gy is recommended mous in nature, yet one is more likely to see other
in contrast to other lymphomas [8]. histologies like adenocarcinomas, lymphomas,
sarcomas, plasmacytomas, etc. (Fig. 10.3) in this
region than elsewhere in the head and neck,
10.1.10 Radiotherapy in Benign thereby making things challenging. Each of these
Tumors distinct etiologies needs to diagnose accurately
for optimal management. This requires an experi-
Radiotherapy is also helpful in some benign con- enced head–neck pathologist. The paradigm for
ditions especially in cases of medically inoperable the management of each of these tumors is histo-
or locally recurrent tumors. RT is used in advanced logically driven. For each histological type of
inoperable or recurrent tumors juvenile nasopha- tumor, the plan of management depends on the
ryngeal angiofibroma. Recommended RT dose is stage, location, age, comorbidities, performance
30–50 Gy @2 Gy per fraction. Local control rates status, and previous therapies received.
are around 85–100%. In cases of ameloblastoma, Traditionally treated by chemotherapy, surgery,
RT helps in achieving local control in cases of and radiotherapy, the advent of immunotherapy
multiple recurrences and preventing recurrences in and targeted therapy in these malignancies has
Fig. 10.3 Spectrum of

tumors in nose and PNS Squamous
Cell
Esthesioneuro Carcinoma
blastoma Melanoma
Lymphoma SNUC
Nasal/PNS
Cancers Adenoid
Adenocarc
Cystic
inoma
Carcinoma
Sarcoma RMS
INI
Defecient Plasmacytoma
Tumors
opened up new vistas in the management of squa- 3. Definitive or radical chemoradiotherapy:

mous cell head–neck carcinoma. The recent most CTRT done with a curative intent. Usually for
addition is the use of combined immunochemo- surgically inaccessible sites.
therapy as the first-line palliative therapy in 4. Palliative: Chemotherapy given in metastatic
recurrent metastatic settings. PDL1 combined disease with a noncurative intent, to palliate
positive score (CPS) has emerged as a predictive symptoms, prolong life with good quality.
biomarker in the clinic. For those R/M HNSCC, 5. Sequential therapy: Induction chemotherapy
where the combined positive score of PDL1 followed by definitive CTRT.
>20%, single-agent pembrolizumab has arrived
as the standard of care.
10.2.3 Chemotherapy in Different
Tumors of Nose and Paranasal
10.2.2 Strategies Sinuses
for Chemotherapies in Head
and Neck Cancers 1. Squamous Cell Carcinoma:
(a) Adjuvant setting: After surgery for SCC,
1. Neoadjuvant/induction: Chemotherapy adjuvant chemotherapy concurrent with
given prior to definitive surgical or radiation radiotherapy (CTRT) is indicated in the
therapy. following situations:
2. Adjuvant: Chemotherapy given after radical (i) Margin positivity.
curative surgery. Mostly given as concurrent (ii) Extracapsular spread in lymph
chemo + radiotherapy. nodes.
(iii) Two types of concurrent regimens are (d) Sequential setting: NACT followed by
used worldwide. The optimum cumu- definitive CTRT is occasionally used
lative dose of cisplatin is 200 mg/m2. in locally advanced tumors not amenable
The weekly cisplatin regime till to surgical resection.
7 weeks period and the dose is 40 mg/ (e) Palliative setting: Indications: Recurrent
m2. For a 3-weekly cisplatin regime, and metastatic HNSCC (not amenable to
the dose is 100 mg/m2 per dose and 3 salvage surgery or re-irradiation). The
doses advised at day 1, day 22, day extent of treatment is till progression of
43. Three-weekly cisplatin is associ- disease control by management.
ated with better locoregional control (i) Standard of care:
(LRC) but increased toxicity profile • Firs Line: KEYNOTE 048
[9]. In cisplatin-ineligible patients If rapid tumor response is not
(renal dysfunction, SN Hearing loss), needed, when PDL1 CPS is more
cetuximab is indicated only in trial than 20% than single-agent pembro-
settings. Carboplatin (50 mg/m2 or lizumab and when PDL1 CPS is less
AUC 1.5–2) is often used but is not than 20%, cisplatin+5FU+ pembro-
evidence-based [10]. lizumab is the combination of drug.
(b) Definitive setting: SCC may be defini- If rapid tumor response is needed,
tively treated with (concurrent chemora- the regimes are cisplatin +5FU+
diotherapy) CTRT. Dosage is cisplatin cetuximab (EXTREME trial) [12,
weekly at 40 mg/m2 for 7 doses along 13]/Cisplatin +5FU + pembroli-
with RT. Nimotuzumab (anti-EGFR anti- zumab (if PDL1 CPS >1%).
body) added to weekly cisplatin (30 mg/ • Second line:
m2) during CTRT improves DFS If immune-oncology is used as first
(disease- free survival) [11]. Cisplatin- line then cetuximab + chemo is the
ineligible patients may be treated with regime and if immune-oncology is
concurrent cetuximab (400 mg/m2 load- not used previously then nivolumab
ing 1 week before RT, then 250 mg/m2 (240 mg q 2 weeks)/pembroli-
weekly). zumab 200 mg iv q3 weekly is the
(c) Neoadjuvant setting: Chemotherapy treatment regime [14].
may be used in specific cases to downsize Other treatment options in resource
tumors and increase resectability (skin limited settings are CDDP +5FU,
involvement, low ITF, induration above Paclitaxel + Carboplatin, Single-
zygoma). Preferred regimens: agent Methotrexate i.v (40 mg/m2
(i) Three-drug regimen (q 3 weekly): weekly) and Oral metronomic ther-
DCF (Docetaxel 75 mg/m2D1, apy: Gefitinib (500 mg/day),
CDDP 75 mg/m2 day 1, 5FU- Erlotinib (150 mg/day), Oral weekly
750 mg/m2/day continue intravenous Methotrexate (15 mg/
infusion over 96 h from day 2–5). m2) + Celecoxib (200 mg BID) [15].
(ii) Two-drug regimen (q 3 weekly): 2 . Nasopharyngeal carcinoma:
CDDP+5FU (CDDP 75 mg/m2 D1, (a) Definitive treatment—Standard of care
5FU-750 mg/m2/day continue intra- for Stage II and above is Concurrent
venous infusion over 96 h from day CTRT (weekly CDDP) + 3 cycles of adju-
2–5). vant chemotherapy (3 weekly
(iii) Two-drug regimen (q 3 weekly):
CDDP+5FU).
T + P (Paclitaxel 175 mg/m2 day 1, (b) Neoadjuvant setting—In cases of T4 or
Carboplatin AUC6 day 1). bulky tumors, treatment may start with
NACT (e.g., 3 cycles of CDDP+ 5FU or (iii) In the third form of regime, 3 cycles
DCF) followed by CTRT. of SMILE regime followed by RT
(c) Palliative setting: Following regimens and then again 3 cycles of SMILE
may be used in cases of metastatic regime. The detail of the SMILE
disease: regime is:
(i) Gemcitabine (1 g/m2 on day 1, day
Methotrexate 2 g/m2 Day 1 (Leucovorin
8) + CDDP (80 mg/m2 day 1) (first
Rescue)
Line) [16] Ifosfamide 1500 mg/m2 Days 2 to 4
(ii) CDDP+ 5FU Etoposide 100 mg/m2 Days 2 to 4
(iii) Paclitaxel + Carboplatin Dexamethasone 40 mg PO Days 2 to 4
3 . Esthesioneuroblastoma: Doubtful role of or IV
adjuvant chemotherapy after craniofacial L-asparaginase 6000 units/ Days 8, 10, 12, 14, 16,
resection and RT. NACT (Cisplatin 30 mg/m2 m2 IM 18, 20
D1,2,3 + Etoposide 100 mg/m2 D1,2,3) is
often used in Kadish C, D tumors based on (b) Advanced stage (II non-contiguous, III,
institutional experiences to downsize the IV): the treatment policy is 6 cycles of the
tumor and make it amenable to resection. SMILE regime.
Cisplatin + Etoposide are used in palliative
therapy of relapsed or metastatic disease. 5. DLBCL (Diffuse Large B cell Lymphoma):
4. Adenoid cystic carcinoma: In the adjuvant For early-stage (I, II) non-bulky lesion,
setting, the treatment policy is the same as 3 cycles of R-CHOP+IFRT whereas for early
HNSCC. Wait and watch policy is indicated in bulky lesion (>7.5 cm), 6 cycles of R-CHOP
asymptomatic metastatic cases. For symptom- +IFRT. For advanced stage (III, IV), 6 cycles
atic disease, the options include CAP of R-CHOP regime (Table 10.1).
(Cisplatin [50 mg/m2, D1], doxorubicin 6. Sinonasal Adenocarcinoma: They may be
[50 mg/m2, D1], and cyclophosphamide salivary gland type, intestinal type (ITAC), or
[500 mg/m2, D1]) q 28 days. non-intestinal type. The treatment policy is
(a) NK-T Cell lymphoma: These tumors are similar to HNSCC.
resistant to CHOP chemotherapy due to the 7. Sarcoma (STS): Radiotherapy is the mainstay
expression of P-glycoprotein. Preferred reg- of treatment in all high-grade tumors. The role
imens in early stage (IE/IIE contiguous): of adjuvant chemotherapy in H&N sarcomas is
(i) Concurrent CTRT, where chemo- unknown. In metastatic disease, performance
therapy regime is DeVIC status and histology is the guide for the choice
[Dexamethasone, Etoposide, of drugs. Commonly used regimens are:
Ifosfamide, Carboplatin]).
(a) Doxorubicin-based chemotherapy (IA:
(ii) Another regime is radiotherapy fol- Ifosphamide+ doxorubicin)
lowed by 3 cycles of DeVIC/VIPD (b)
Angiosarcoma: weekly paclitaxel,
(etoposide, ifosfamide, cisplatin, Gemcitabine + Docetaxel, Pazopanib,
dexamethasone). Trabectedin
Table 10.1 The list of drugs comes under the R-CHOP regime, their doses, and the day of administration
R-CHOP Drug Dose Schedule
Rituximab 375 mg/m2 i.v Day 1
Cyclophosphamide 750 mg/m2 iv Day 1
Doxorubicin 50 mg/m2 iv Day 1
Vincristine 1.4 mg/m2 (2 mg max) iv Day 1
Prednisolone 100 mg po Day 1–5
Table 10.2 Risk categories, chemotherapy schedule, and doses

Risk category Chemotherapy schedule Drug regimen
Low risk VA:
Subset A VA X 15 cycles (45 weeks) V = Vincristine 1.5 mg/m2 (max 2 mg) q week
Subset B VAC × 14 cycles (40 weeks) A = Actinomycin-D (0.045 mg/kg) (Max 2.5 mg) q 3 week
Intermediate risk VAC × 14 cycles (40 weeks) VAC:
V = Vincristine 1.5 mg/m2 (max 2 mg)q week
A = Actinomycin-D (0.045 mg/kg) (Max 2.5 mg) q 3 week
C = Cyclophosphamide (1200 mg/m2 with Mesna) q 3 week
High risk VAC × 14 cycles (40 weeks) Same as intermediate risk regime

(c) Chondrosarcoma: Low grade (well- vant setting. In metastatic cases, treatment is
differentiated): no role. Poorly differenti- extrapolated from that of skin melanomas.
ated (doxorubicin-based chemotherapy) (a) BRAF V600E mutated: Dabrafenib,
8. Rhabdomyosarcoma: It usually occurs in
Vemurafenib
children. It commonly involves three sub- (b)
Kit mutated: Imatinib, dasatinib,
sides of head and neck region, orbit (25%) sorafenib
[favorable], Para-meningeal (paranasal (c) No mutation: Nivolumab, Nivolumab +
sinuses, nasopharynx, nasal cavity, middle Ipilimumab
ear, mastoid) (50%) [non-favorable], non- 11. SNUC (sinonasal undifferentiated
orbital non-para- meningeal (25%) [favor- Carcinoma): It has a very poor prognosis. It
able]. The choice of adjuvant therapy (RT/ has no clinical trial evidence. Trimodality
chemo) and selection of chemotherapy is therapy is the maximum surgical resection
based on various clinical factors such as followed by concurrent CTRT is standard.
TNM stage, clinical group after surgery, 12. INI-deficient carcinoma: It is a recently
site, size (>/<5 cm), age, histology (embryo- recognized entity (SMARCB1/INI deficient)
nal/alveolar), and FOXO1 fusion. Combining with a very poor prognosis. Surgery with
these information, we define three risk cate- adjuvant chemoradiation is used.
gories as in Table 10.2. 13. Plasmacytoma:
If it is a solitary disease, then radiotherapy
alone is sufficient. If multiple, then treatment
9. Osteosarcoma (OS): is the same as multiple myeloma: VRd
Head and Neck OS is notorious for local regime, 6 cycles followed by autologous
recurrence and less commonly distant metas- transplant (eligible pts) [V = Bortezomib
tases than limb OS. Adjuvant chemotherapy 2 mg subcutaneous injection on days 1, 8,
is given to all cases (although evidence exists 15, 22; R = Lenalidomide 25 mg once daily
only for extremity OS). Cisplatin + doxoru- from day 1 to day 15, d = Dexamethasone
bicin are most commonly used. Adjuvant RT 40 mg weekly].
is for R1 resections even after re-resection.
Cisplatin may be added concurrent to RT,
although evidence is limited. Regimens for 10.3 P
art C: Perioperative
metastatic disease: Cisplatin + doxorubicin, and Postoperative Measures
high-dose methotrexate, ifosphamide+ eto- to Improve Quality of Life
poside [17]. After Nasal Surgery
10. Mucosal Melanoma: It has a poorer prog-
nosis and response compared to skin mela- Chronic rhinosinusitis (CRS) is a common dis-
nomas. There is no established role of ease that can be managed either medically or sur-
chemotherapy or immunotherapy in an adju- gically with ongoing medical management.
Around 20–30% of patients who undergo sinus addition of two items of interest (nasal obstruc-
surgery for CRS do not experience significant tion and olfaction) formed the SNOT-22, which
improvement. Physical, social, emotional, psy- has been demonstrated to be reliable, valid, and
chological, sexual, cognitional, and economic responsive [19, 20]. In SNOT-22, the domains are
aspects of life can be integrated in a general term broke down into three sinus-specific symptom
of well-being and it is commonly known as domains (Rhinologic, Extra-rhinologic, and Ear/
health-related QoL (HRQoL). Chronic rhinosi- facial symptoms) and two general health-related
nusitis negatively affects quality of life (QoL), QoL domains (Psychological and Sleep
reduces economic productivity, and can increase dysfunction).
the risk of depression and sleep dysfunction. In
the last few decades, quality of life has repre-
sented the development of patient-oriented 10.3.2 Preoperative Measures
assessment of health status and it is being increas-
ingly perceived by researchers and physicians as There are no clinical trials of immediate preop-
a significant outcome measure. Questionnaires, erative medication. Many surgeons have pre-
visual scales, and grading systems are just some ferred to use oral steroids and antibiotics in the
of the instruments used in quantitatively measur- preoperative period to improve the outcome of
ing HRQoL. Many such instruments are available surgery. Oral systemic steroids (preferably
at present to measure the QoL in CRS. Functional Prednisolone) for 10−14 days preoperatively
outcome following sinus surgery is determined and 7−14 days postoperatively (1 mg/kg) follow
by preoperative, intraoperative, and p ostoperative by tapering of therapy in 1−2 weeks is the com-
management. Careful analysis of these measures monly followed therapy. The dose used is
results in an improvement in surgical outcome around 30 mg which is taken as a single daily
which in turn improves the quality of life. dose in the morning. Since there is no solid evi-
dence on which to base this choice of dose, the
clinical experience of the surgeon is used to
10.3.1 Quality Indicators inform this choice. The moderate dose chosen
(30 mg) is believed to be sufficient for effective
Generally, questionnaires allow the patient to rate clinical activity and to mitigate the potential
the impact of the disease alongside a number of undesirable short-term side effects associated
other areas of healthcare interest. Every question with higher doses (e.g., 50–60 mg). Topical cor-
is scored according to the severity or repercus- ticosteroids (commonly fluticasone propionate,
sion of the disease and individual domain scores mometasone furoate, ciclesonide, and flutica-
are combined to produce an overall score. sone furoate) are of use in the primary treatment
EuroQol 5D, Rhinosinusitis outcome measures of nasal polyps when they are of a small or
(RSOM), McGill Pain Questionnaire, Short medium size but surgery is generally required
Form-36 Health Survey and Short Form-12 for larger polyps because of the resultant nasal
Health Survey Rhinosinusitis Disability Index, obstruction and limited access for topical prepa-
Chronic Sinusitis Survey Score, Sinonasal rations. Maximal medical therapy for patients
Outcome Test-20, -16, and -22 are the most with nasal polyposis included prolonged trials
widely used specific questionnaires in clinical tri- of topical therapy for more than 3 months.
als. Of these, the 22-item Sinonasal Outcome Topical therapy was defined as intranasal ste-
Test (SNOT-22) has been widely adopted in clini- roids given twice daily and saline irrigations.
cal practice and has been proved to be the most No statement can be made regarding a specific
suitable sinonasal outcome scoring system [18]. length of treatment in CRS without polyposis
The SNOT-20 was developed from the 31-item and the decision should be individualized based
Rhinosinusitis Outcome Measure (RSOM-31) by on the degree of symptom relief, patient prefer-
removing 11 items thought to be redundant. The ence, and clinician experience.
Clinical experience suggests that oral antihis- rent sinusitis with prior sinus surgery having
tamines may provide symptomatic relief of poorer QoL and more radical surgery may require
excessive secretions and sneezing although there eradication of the disease. Failed endoscopic
are no clinical studies supporting the use of anti- sinus surgery continues to be a significant prob-
histamines in CRS. In the preoperative period, lem both in terms of its economic consequences
antibiotics may decrease inflammation by mini- and also with respect to significant patient quality
mizing infection and so improve the operative of life issues.
field. Culture-specific antibiotics may prevent Increased nasal hair density decreases the
antibiotic resistance in most of these cases. development of asthma in those who have sea-
Smoking can severely affect the outcome of sinus sonal rhinitis, possibly due to an increased capac-
surgery. Smoking causes increased scar tissue ity of the hair in the nostrils to filter out pollen
and poor healing that lead to failure of endo- and other allergens. Moffett’s solution is a popu-
scopic sinus surgery. Cessation of smoking lar choice for the preparation of the surgical field
3–4 weeks before surgery and avoidance of in sinonasal surgery due to its efficacy. It
smoking for an additional month after surgery is decreases intraoperative bleeding by vasocon-
an absolute must to achieve good results. There striction and allows improved operative access
are certain medications that can increase the risk and visualization by decongesting the nasal
of bleeding during and after sinus surgery. These mucosa. Cocaine also exerts its analgesic effects
medications include Aspirin, NSAIDs, anticoag- by blocking sodium channels along the axons of
ulants and they should be stopped at least 1 week sensory nerves, dampening pain signal genera-
prior to surgery. Vitamin E and herbal medicines tion and propagation but a long list of side effects
such as ginkgo biloba, ginseng, and garlic tablets limits its uses.
can also increase the risk of bleeding and should
be stopped prior to surgery.
Asthma, prior paranasal surgery, nasal polyps, 10.3.4 Postoperative Measures
aspirin-exacerbated respiratory disease, depression
or anxiety disorder, and poor preoperative QoL Antibiotics are widely used by surgeons both
have been linked with poorer QoL outcomes after before and after sinus surgery. Used following
ESS. Preoperative screening of undiagnosed psy- sinus surgery, they may facilitate healing by pre-
chological disorders may allow for improved patient venting infection. This generally pertains to mac-
counseling and psychology/psychiatry referral and rolide agents, which have been suggested to
initiation of complementary therapies [21]. possess significant anti-inflammatory attributes.
The most duration still recommend is 4–6 weeks
of uninterrupted therapy for CRS. Postoperative
10.3.3 Perioperative Measures fibrin clot debridement and granulation removal
are thought to be necessary to prevent scar tissue
Surgical technique has developed with improve- formation. This is achieved by postoperative
ments in instrumentation, optics, and mucosal office debridement and nasal douching [22].
preservation techniques. Psychological and sleep Postoperative daily use of nasal douching with
dysfunction were significantly more likely to hypertonic saline alone for a period of 6 months
have a greater relative influence on patients elect- has shown comparable outcomes in terms of symp-
ing surgical therapy than any of the sinus-specific tom scores and prevention of synechiae. The best
symptom domains (Rhinologic, Extra-nasal rhi- way of nasal irrigation should follow these steps:
nologic, Ear/facial symptoms). Surgical and
medical treatment modalities result in improve- 1. Stand with head over a sink and tilt head to
ment across all domains of SNOT-22 but subjects one side.
opting for surgical interventions experience 2. Using a squeeze bottle or bulb syringe, pour
greater relative improvement. Patients with recur- or squeeze the saline solution slowly into the
upper nostril, allow the solution to pour out of grades: mild (0–20 points), moderate (21–40
the other nostril and into the drain. points), and severe (41–60 points). Patients with
3. Breathe through the mouth, not the nose. younger age, accompanying asthma, severe
4. Repeat on the opposite side. eosinophilia, severe chronic rhinosinusitis, pol-
5. Try not to let the water go down the back of yps in the frontal sinus, and olfactory disorders in
the throat. the preoperative stage are adverse predictors.
6. Gently blow nose into a tissue to clear out any Such people should be carefully treated for a lon-
mucus. ger time after FESS [25–28].
Despite the widespread use of steam inhala-

tions and nasal decongestants, there is no avail- 10.4 Conclusion
able evidence as to their efficacy in improving
outcomes after sinus surgery. Despite significant Although rhinosinusitis is not a life-threatening
postoperative improvements, the elevated preva- condition, it impairs daily functioning and quality
lence of symptoms of psychological dysfunction of life (QoL). The measurement of sinus specific
following sinus surgery underscores the difficul- quality of life is perhaps the most commonly uti-
ties in treating patients with recalcitrant lized outcome measure for CRS. Surgical and med-
CRS. Causes for persistent psychological dys- ical treatment modalities result in improvement
function are likely multifactorial and include across all domains but subjects electing surgical
persistent sinonasal inflammation, unmeasured
interventions experience greater relative improve-
patient factors including healthcare satisfaction, ment. The decision to undergo surgical interven-
postoperative response shifts, and comorbid psy- tion is best predicted by health-related QoL
chological factors such as undiagnosed anxiety domains pertaining to psychological impairment
and depressive disorders. and sleep dysfunction. Previous sinus surgery,
asthma, smoking, and aspirin intolerance may
affect the results of surgical treatment. Functional
10.3.5 Follow-Up outcome following sinus surgery is determined by
preoperative, intraoperative, and postoperative
Early detection of worsening lesions in the sino- management which facilitates mucosal healing,
nasal area is of great importance in the successful minimizes scar tissue, and ensures rapid return of
treatment of chronic rhinosinusitis. Postoperative nasal mucosa to normal function. Adjuvant medi-
endoscopic evaluation is a simple and cost- cal therapy such as oral steroids, leukotriene antag-
effective method to assess the nasal mucosa fol- onists, immunotherapy, and monoclonal antibodies
lowing surgery. Several postoperative endoscopic also play a vital role in resulting overall improve-
scores have been developed such as the Lund and ment in the quality of life.
Kennedy score and its modification, Perioperative
Sinus Endoscopy scoring system and operating
score.
The operating score reflects the course follow- References
ing Functional Endoscopic Sinus Surgery
1. Allen MW, Schwartz DL, Rana V, et al. Long-term
(FESS). Patients with more severe operative find- radiotherapy outcomes for nasal cavity and septal
ings require longer postoperative treatment. The cancers. Int J Radiat Oncol Biol Phys. 2008;71:401–6.
operating score is based on the operative findings 2. Czerwinski MD, Van Leeuwen R, Kaanders J,
in the sinuses (sinus score) and olfactory clefts Zwijnenburg EM, Lipman D, Takes RP, et al. Image
guided brachytherapy for cancer of the nasal vesti-
(olfactory cleft score) on both sides [23, 24]. The bule: local control and cosmesis. Int J Radiat Oncol
operating score ranges from 0 to 60 points. Biol Phys. 2018;103:913–21.
According to the operating score, the severity of 3. Liang ZG, Kusumawidjaja G, Kazmi F, Wee JTS,
operative findings was classified in terms of three Chua MLK. Intensity-modulated radiotherapy for
paranasal sinuses and base of skull tumors. Oral in platinum-insensitive failures and/or early failures
Oncol. 2018;86:61–8. postmultimodality management in oral cancers.
4. Wang K, Zanation AM, Chera BS. The role of radia- Indian J Med Paediatr Oncol. 2015;36(3):161.
tion therapy in the management of sinonasal and ven- 16. Zhang L, Huang Y, Hong S, Yang Y, Yu G, Jia J, et al.
tral skull base malignancies. Otolaryngol Clin N Am. Gemcitabine plus cisplatin versus fluorouracil plus cis-
2017;50(2):419–32. platin in recurrent or metastatic nasopharyngeal carci-
5. Chua DT, Sham JS, Kwong DL, et al. Treatment noma: a multicentre, randomised, open-label, phase 3
outcome after radiotherapy alone for patients with trial. Lancet Lond Engl. 2016;388(10054):1883–92.
stage I-II nasopharyngeal carcinoma. Cancer. 17. Vermorken JB, Mesia R, Rivera F, et al. Platinum-
2003;98:74–80. based chemotherapy plus cetuximab in head and neck
6. Halperin EC, Brady LW, Wazer DE, Perez CA. Perez cancer. N Engl J Med. 2008;359:1116.
and Brady's principles and practice of radiation oncol- 18. Soler ZM, Jones R, Le P, et al. Sino-nasal out-

ogy. 7th ed. Philadelphia: Wolters Kluwer Health/ come test-22 outcomes after sinus surgery: a sys-
Lippincott Williams & Wilkins; 2018. tematic review and meta-analysis. Laryngoscope.
7. Lee NY, Lu JJ. Target volume delineation and field 2018;128(3):581–92.
setup-a practical guide for conformal and intensity- 19. Quintanilla-Dieck L, Litvack JR, Mace JC, Smith

modulated radiation therapy. Springer; 2015. TL. Comparison of disease-specific quality-of-life
8. Yang Y, Zhu Y, Cao JZ, et al. Risk-adapted therapy instruments in the assessment of chronic rhinosinus-
for early-stage extranodal nasal-type NK/T-cell lym- itis. Int Forum Allergy Rhinol. 2012;2(6):437–43.
phoma: analysis from a multicenter study. Blood. 20. Lehrer-Coriat E, Mariño-Sánchez F, Alobid I, Mullol
2015;126:1424–32. J. Quality of life measures in patients on rhinosinusitis
9. Noronha V, Joshi A, Patil VM, Agarwal J, Ghosh- trials. Clin Invest. 2013;3(3):251–63.
Laskar S, Budrukkar A, et al. Once-a-week versus 21. Levy JM, Mace JC, DeConde AS, Steele TO, Smith
once-every-3-weeks cisplatin chemoradiation for TL. Improvements in psychological dysfunction
locally advanced head and neck cancer: a phase III after endoscopic sinus surgery for patients with
Randomized Noninferiority Trial. J Clin Oncol Off J chronic rhinosinusitis. Int Forum Allergy Rhinol.
Am Soc Clin Oncol. 2018;36(11):1064–72. 2016;6(9):906–13.
10. Racadot S, Mercier M, Dussart S, Dessard-Diana B, 22. Alakarppa AI, Koskenkorva TJ, Koivunen PT, Alho
Bensadoun R-J, Martin M, et al. Randomized clinical O-P. Quality of life before and after sinonasal surgery:
trial of post-operative radiotherapy versus concomitant a population-based matched cohort study. Eur Arch
carboplatin and radiotherapy for head and neck can- Otorhinolaryngol. 2017;274:795–802.
cers with lymph node involvement. Radiother Oncol J 23. Kohli P, Naik AN, Farhood Z, Ong AA, et al. Olfactory
Eur Soc Ther Radiol Oncol. 2008;87(2):164–72. outcomes after endoscopic sinus surgery for chronic
11. Patil VM, Noronha V, Joshi A, Agarwal J, Laskar SG, rhinosinusitis: a meta-analysis. Otolaryngol Head
Budrukkar A, et al. Results of a randomized phase III Neck Surg. 2016;155(6):936–48.
study of nimotuzumab in combination with concur- 24. Bugten V, Nilsen AH, Thorstensen MW, Moxness

rent radiotherapy and cisplatin versus radiotherapy MHS, et al. Quality of life and symptoms before and
and cisplatin alone, in locally advanced squamous after nasal septoplasty compared with healthy indi-
cell carcinoma of the head and neck. J Clin Oncol. viduals. BMC Ear Nose Throat Disord. 2016;16:13.
2018;36(15_suppl):6000. 25. Alakärppä AI, Koskenkorva TJ, Koivunen PT, Alho
12. Vermorken JB, Mesia R, Rivera F, Remenar E,
O-P. Predictive factors of a beneficial quality of life
Kawecki A, Rottey S, et al. Platinum-based chemo- outcome in patients undergoing primary sinonasal
therapy plus cetuximab in head and neck cancer. N surgery: a population-based prospective cohort study.
Engl J Med. 2008;359(11):1116–27. Eur Arch Otorhinolaryngol. 2018;275:1139–47.
13.
Burtness B, Harrington KJ, Greil R, et al. 26. Le PT, Soler ZM, Jones R, Mattos JL, et al.

Pembrolizumab alone or with chemotherapy versus Systematic review and meta-analysis of SNOT-22
cetuximab with chemotherapy for recurrent or meta- outcomes after surgery for chronic rhinosinusitis
static squamous cell carcinoma of the head and neck with nasal polyposis. Otolaryngol Head Neck Surg.
(KEYNOTE-048): a randomised, open-label, phase 3 2018;159(3):414–23.
study. Lancet. 2019;394:1915. 27. Rosenfeld RM, Piccirillo JF, Chandrasekhar SS, et al.
14. Ferris RL, Blumenschein G, Fayette J, Guigay J,
Clinical practice guideline (update): adult sinusitis.
Colevas AD, Licitra L, et al. Nivolumab for recurrent Otolaryngol Head Neck Surg. 2015;152(2S):S1–S39.
squamous-cell carcinoma of the head and neck. N 28. Tsuzuki K, Hashimoto K, Okazaki K, et al. Post-
Engl J Med. 2016;375(19):1856–67. operative course prediction during endoscopic sinus
15. Patil VM, Noronha V, Joshi A, Pinninti R, Dhumal surgery in patients with chronic rhinosinusitis. J
S, Bhattacharjee A, et al. Metronomic chemotherapy Laryngol Otol. 2018;132:408–17.

Essentials of Rhinology (Hitesh Verma, Alok Thakar)

Uploaded by

Copyright:

Available Formats

Essentials of Rhinology (Hitesh Verma, Alok Thakar)

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Essentials of Rhinology (Hitesh Verma, Alok Thakar)

Uploaded by

Copyright:

Available Formats

Essentials of

ISBN 978-981-33-6283-3 ISBN 978-981-33-6284-0 (eBook)

The nose is an amazing organ. It undertakes humidification, filtration, and

New Delhi, India Hitesh Verma

1 Endoscopic Anatomy and Surgery ������������������������������������������������ 1

8 Prevention and Management of Complications���������������������������� 277

Hitesh Verma MBBS (SMS Medical College,

Alok Thakar MBBS (AIIMS), MS (AIIMS), DNB,

Abha Kumari ENT, Command Hospital, Kolkata, West Bengal, India

Ashu Seith Bhalla Radiology, AIIMS, New Delhi, India

Jaini Lodha ENT, Seven Hills Hospital, Andheri East Mumbai,

Prateek Sharma ENT, AIIMS, New Delhi, India

Smita Manchanda Radiology, AIIMS, New Delhi, India

1.4 Part D: FESS 16

1.1  art A: Anatomy of Nasal

1.1.1 Ethmoid Cells

Ethmoid air cells are 3–18 in number. It is broadly

1. Agger Nasi Cells

2. Frontal Cells nate. It extends posteriorly till the anterior

It is made up of the horizontal medial part (lam- 1.1.7 Sphenoid Sinus

Internal carotid artery Type 3 ON ICA

classified into four different types. Type 1 is

1.2  art B: Local Anesthesia

The detailed preoperative evaluation is very

intraoperative patient’s cooperation. Daycare 3. 1 cc of sodium bicarbonate in every 9 ml of

disorientation, seizure, loss of consciousness, soaked in 4% lignocaine solution with

Nerve blocks—It is required for the therapeu-

A. Frontal Nerve Block

Fig. 1.13 The site of local infiltration is corresponding to

sphenopalatine foramen region, near the

F. Maxillary Nerve Block 1.3 Part C: General Anesthesia

1.3.2 Anesthesia Technique explained to the patient in preoperative visit and

1.3.7 Postoperative Concerns

1. HRCT (nose and paranasal sinuses)- 1 mm cuts

5. Computer-aided surgery (CAS, or image

1. Extensive nasal polyposis

• Type-1 is Simple Drainage (DRAF1)—It is

Fig. 1.21 The figure is depicting sphenoid ostia in the

1. Ten–fifteen millimetre above the upper end of

Robot-Assisted Surgery (RAS) • Surgery is usually the first-line treatment for

Navigation and Image-Guided Surgery • Complicated sinusitis

1.4.6 Balloon Sinuplasty minimize complications and in patient admission.

1.5.1 Uses of Nasal Packing

Fig. 1.22 Anterior and

Figure 1.22 shows the preparation required for

available both with and without an external

Rapid Rhino Device Nasal device consisting of

Algosteril It is a calcium alginate nasal pack

Petroleum Jelly Impregnated Gauze

Balloon Catheter Device It is specially

environment for healing [31, 32]. It is available

Collagen Derived Products These are derived

Due to fragmentation, these absorbable nasal

10. DeMaria S Jr, Govindaraj S, Chinosorvatana N,

2.1  art A: External Nasal

The external nose is pyramidal in shape. The root

Fig. 2.1 The chart is EXTERNAL NASAL ANATOMY

Skin Frame Work Support tissues

cartilages bones muscles ligaments

Fig. 2.2 The clinical a b

New Delhi, India Hitesh Verma

1 Endoscopic Anatomy and Surgery �� 1

8 Prevention and Management of Complications�� 277

1.4 Part D: FESS 16

1.1 art A: Anatomy of Nasal

1.1.1 Ethmoid Cells

It is made up of the horizontal medial part (lam- 1.1.7 Sphenoid Sinus

1.2 art B: Local Anesthesia

F. Maxillary Nerve Block 1.3 Part C: General Anesthesia

1.3.2 Anesthesia Technique explained to the patient in preoperative visit and

1.3.7 Postoperative Concerns

1.4.6 Balloon Sinuplasty minimize complications and in patient admission.

1.5.1 Uses of Nasal Packing

2.1 art A: External Nasal

2.2 art B: Open and Close

3.4 Part D: Frontal Sinusitis 62

3.1 art A: Physiology of Nose

ing Kartagener syndrome. In addition, muco- 3.1.3.1 Measurement of Nasal

3.1.3.2 Important Objective Tests

3.1.3.3 References Values for Normal investigation is required for intracranial lesions.

3.3.6 Differential Diagnosis

3.3.8 Treatment risk of systemic side effects. As allergy can be asso-

3.4.4 Preoperative Workup

Parasagittal view helps in identifying the com- 3.4.4.1 Surgical Approaches

3.5 art E: Complications

3.5.3 Conclusion imal but if not addressed on time, may become

3.6 Part F: Allergic Rhinitis Chirurgical Society on 16 March 1819 “Case of a

certain benign things to prevent the onset of 3.7.3 Clinical Features

3.7.5 Treatment it is probably due to as an anti-

v idian nerve. In this selective and Pathophysiology of the non-invasive spectrum of

treatment in form of antifungal agents and exten- 3.9.1 Clinical Presentations

s pecific h istopathological feature. majority of dis- chronic inflammatory reaction, characterized by