101 CT Abdomen Solutions

101 CT Abdomen Solutions
Hariqbal Singh MD DMRD

Professor and Head
Department of Radiology
Shrimati Kashibai Navale Medical College
Pune, Maharashtra, India
Yasmeen Khan DMRE

Consultant
Department of Radiology
Shrimati Kashibai Navale Medical College
Pune, Maharashtra, India
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First Edition: 2016
ISBN: 978-93-5250-181-6
Printed at
Dedicated to
The unwearied, enduring, tolerant, and serene patients
who place themselves in the hands of
clinicians involved in research
in pursuit to alleviate their suffering
for restoration of health.
Radiology is a kindergarten
of logical rational coherent exploration and
balanced learning
and not dexterous adroit smugness
or learning egotism
cultivated by fake self-centeredness and egoism.
—Hariqbal Singh
Preface
The huge response received following the publication of 101 Chest X-ray Solutions
and 101 MRI Brain Solutions, prompted us to develop on 101 CT Abdomen
Solutions, which will hopefully be equally accepted by the readers. It provides
a large bank of CT images on abdomen with cases seen in routine practice to
more difficult cases of interest. With these images in mind, it will help the CT
practitioner to interpret the possible diagnosis on abdominal CT during routine
reporting practice. It will be an ideal reference for anyone involved with CT image
interpretation. In many images, small arrow point is used to show the lesion. This
is with an aim to provide better understanding for the reader. The importance of
having a good knowledge of anatomy cannot be undermined and this has guided
us to include a chapter on normal anatomy of Abdomen on CT imaging.
The book is meant for radiology residents, radiologists, general practitioners,
other specialists, CT technical staff and those who have a special interest in CT
imaging. It is meant for medical colleges and institutional libraries, departmental
and CT standalone unit libraries.
The book is a compilation of cases developed by unified, consistent and
cohesive endeavor of the panel of radiologists at Shrimati Kashibai Navale
Medical College, Pune, Maharashtra, India.
Hariqbal Singh
Yasmeen Khan
Acknowledgments
We thank Professor MN Navale, Founder President, Sinhgad Technical Educa

tion Society and Dr AV Bhore, Dean, Shrimati Kashibai Navale Medical College,
Pune, Maharashtra, India, for their kind acquiescence in this endeavor.
We are profusely extending our gratefulness to the consultants Varsha
Rangankar, Santosh Konde, Abhijit Pawar, Amol Sasane, Aditi Dongre, Pooja
Shah, Shripad Kamble, Patil Dharmendra, Varsha Sonawane, and Ajinkya Kolse
for their genuine help in building up this educational entity.
We are profusely gratified to the radiology residents Swati Shah, Vikram
Shende, Jarvis Pereira, Priya Bhole, Prasad Patil, Punit Agrawal, Swapnil Raut,
Amar Sangapwad and Prajakta Jagtap for their genuine help in correction of the
manuscript.
Our gratitude to Anna Bansode and Sachin Babar for their clerical help.
We are thankful and grateful to the God Almighty and mankind who have
allowed us to have this wonderful experience.
Contents
CT Anatomy: Abdomen and Pelvis1
SECTION 1 Esophagus
1. Hiatus Hernia 19
2. Esophageal Carcinoma 21
3. Leiomyomatosis of Esophagus 23
SECTION 2 Diaphragm
4. Eventration 27
5. Eventration of Diaphragm with Duplication of
Inferior Vena Cava 29
SECTION 3 Stomach
6. Gastrointestinal Stromal Tumor 33
7. Gastric Malignanacy 35
SECTION 4 Duodenum
8. Carcinoma Duodenum 41
SECTION 5 Small Bowel

9. Small Bowel Obstruction 45
10. Ileocecal Lymphoma 47
11. Small Bowel Gastrointestinal Stromal Tumor 49
12. Angiodysplasia of Jejunum 51
13. Ileal Carcinoma 53
14. Pneumatosis Intestinalis 55
15. Midgut Volvulus 57
SECTION 6 Appendix
16. Acute Appendicitis 61
17. Appendicular Abscess 63
SECTION 7 Colon
18. Intussusception 67
19. Nontoxic Megacolon 70
xii 101 CT Abdomen Solutions
20. Sigmoid Diverticulitis 72

21. Abdominal Koch’s 74
22. Carcinoma Sigmoid 77
SECTION 8 Rectum
23. Carcinoma Rectum 81
SECTION 9 Liver
24. Focal Fatty Liver 87
25. Simple Hepatic Cyst 89
26. Budd-Chiari Syndrome 91
27. Liver Laceration 94
28. Hepatic Abscess 97
29. Hepatic Hydatid Cyst 100
30. Hepatic Hemangioma 103
31. Focal Nodular Hyperplasia 106
32. Hepatic Adenoma 108
33. Hepatic Angiomyolipoma 110
34. Hepatocellular Carcinoma 112
35. Hepatic Metastases 115
36. Hepatoblastoma 118
37. Intrahepatic Cholangiocarcinoma 120
38. Extrahepatic Cholangiocarcinoma 123
39. Transient Hepatic Attenuation Difference 125
SECTION 10 Gallbladder
40. Choledochal Cyst 129
41. Acalculus Cholecystitis 131
42. Acute Calculus Cholecystitis 133
43. Emphysematous Cholecystitis 136
44. Choledocholithiasis 138
45. Porcelain Gallbladder 140
46. Carcinoma Gallbladder 142
SECTION 11 Pancreas
47. Acute Pancreatitis 147
48. Pancreatic Pseudocyst 149
49. Necrotizing Pancreatitis 153
50. Periampullary Carcinoma with Metastases 155
SECTION 12 Spleen
51. Splenunculus 161
52. Splenic Trauma 163
53. Splenic Abscess 166
Contents xiii
SECTION 13 Vascular
54. Superior Mesenteric Artery Syndrome 171
55. Superior Mesenteric Artery Thrombosis 173
56. Accessory Renal Artery Stenosis 176
57. Aneurysm of Abdominal Aorta 178
58. Inferior Vena Cava Thrombus 180
59. Aortic Thrombus 182
60. Portal Vein Thrombosis 184
SECTION 14 Adrenal
61. Adrenal Adenoma 189
62. Pheochromocytoma 192
63. Adrenal Metastases 194
SECTION 15 Renal
64. Renal Aplasia 199
65. Dysplastic Kidney 201
66. Polycystic Kidneys 203
67. Pelviureteric Junction Obstruction 205
68. Obstructive Uropathy 208
69. Emphysematous Pyelonephritis 215
70. Renal Vein Thrombosis 217
71. Renal Laceration 219
72. Renal Angiomyolipoma 221
73. Wilms’ Tumor 223
74. Renal Cell Carcinoma 226
SECTION 16 Urinary Bladder

75. Vesical Calculus 231
76. Urinary Bladder Diverticulum 233
77. Cystitis 235
78. Carcinoma Urinary Bladder 237
SECTION 17 Prostate
79. Carcinoma Prostate 243
SECTION 18 Scrotum
80. Hydrocele 247
81. Testicular Trauma 249
82. Seminoma 251
83. Undescended Testis 253
xiv 101 CT Abdomen Solutions
SECTION 19 Penis
84. Penile Carcinoma 257
SECTION 20 Uterus
85. Broad Ligament Fibroid 261
86. Hydrometrocolpos 263
87. Pyometra 265
88. Endometrial Carcinoma 267
89. Carcinoma Cervix 270
90. Vaginal Carcinoma 272
91. Ureterovaginal Fistula 274
92. Vulval Carcinoma 276
SECTION 21 Ovary
93. Ovarian Vein Thrombosis 281
94. Ovarian Tumor 283
SECTION 22 Abdominal Wall

95. Abdominal Wall Sarcoma 289
96. Abdominal Wall Hernia 291
SECTION 23 Miscellaneous
97. Inguinal Hernia 297
98. Omental Infarction 300
99. Primitive Neuroectodermal Tumor 302
100. Fetus-in-Fetu 304
101. Lymphangioma 306
Index309
Introduction
PHYSICAL PRINCIPLE OF CT SCAN IMAGING

CT was invented in 1972 by British engineer, Sir Godfrey Newbold Hounsfield
in Hayes, United Kingdom at EMI Central Research Laboratories using X-rays.
EMI laboratories is best known today for its music and recording business. About
the same time South Africa-born American physicist, Allan McLeod Cormack of
Tufts University in Massachusetts independently invented a similar process, and
both shared the 1979 Nobel Prize.
The first clinical CT scan was installed in 1974. The initial systems were
dedicated only to head scanning due to small gantry, but soon this was overcome
and whole body CT system with larger gantry, became available in 1976.
Basic principle is to obtain a tomogram having thickness in millimeters of
the region of interest using pencil beam X-radiation. The radiation transmitted
through the patient is counted by scintillation detector. This information when
fed in the computer is analyzed by mathematical algorithms and reconstructed
as a tomographic image by the computer so as to provide an insight into the
structure being studied (Table 1).
Developments in CT Technology
Conventional Axial CT (Table 1)
Table 1: Generations of CT scan
Generation Motion of X-ray Stationary detectors X-ray beam type
of CT scan tube-detector
system
First Translate-Rotate Two detectors Pencil beam
Second Translate-Rotate Multiple detectors up to 30 Narrow fan beam (10°)
Third Rotate-Rotate Multiple detectors up to 750 Wide fan beam (50°)
Fourth Rotate-Fixed Ring of 1500–4500 detectors Fan beam
Fifth Rotate-Fixed Two rings of 1500–4500 Fan beam
detectors with two tubes
Spiral/Helical CT
Spiral CT uses the conventional technology in conjunction with slip ring
technology, which simultaneously provides high voltage for X-ray tube, low
voltage for control unit and transmits digital data from detector array. Slip ring
is a circular instrument with sliding bushes that enables the gantry to rotate
continuously while the patient table moves into the gantry simultaneously, thus
three-dimensional volume rendered image can be obtained. The advantages
xvi 101 CT Abdomen Solutions
over the conventional scanner are the reduced scan time, reduced radiation
exposure and reduced contrast requirement with superior information.
Electron Beam CT (EBCT)

In EBCT, both the X-ray source and the detectors are stationary. High energy
focused electron beam is magnetically steered on the tungsten target to emit
X-rays, which pass through the subject on to the detectors and image is acquired.
EBCT is particularly used for faster imaging in cardiac studies.
Multislice/Multidetector CT (MDCT)
Spiral CT uses single row of detectors, resulting in a single slice per gantry
rotation. Multislice CT, multiple detector arrays are used resulting in multiple
slices per gantry rotation. In addition, fan beam geometry of spiral CT is replaced
by cone beam geometry.
The major advantages over spiral CT are improved spatial and temporal
resolution, reduced image noise, faster and longer anatomic coverage, and
increased concentration of intravenous contrast.
Dual Source CT
The dual energy technology of the new Flash CT provides higher contrast
between normal and abnormal tissues making it easier to see abnormalities while
reducing radiation. With its two rotating X-ray tubes, enhanced speed and power
allows children to be screened more effectively. It turns off the radiation when it
comes close to sensitive tissue areas of the body like thyroid, breasts, or eye lens.
Pediatric patients benefit because they do not need to hold breath or lay
completely still during the examination and they do not have to be sedated.
Hounsfield Units
CT numbers recognized by the computer are from (–) 1000 to (+) 1000, i.e. a range
of 2000 Hounsfield units which are present in the image as 2000 shades of gray,
but our eye cannot precisely discriminate between these 2000 different shades.
Hounsfield scale assigns attenuation value of water as zero (HU 0), and other
tissues their attenuation value as compared to water as given in Table 2.
Table 2: Attenuation value of various tissues on CT scan

Tissue Attenuation value in HU
Air (–)1000
Lung (–) 400 to (–) 800
Fat (–) 40 to (–) 100
Water 0
Fresh blood 55 to 65
Soft tissue 40 to 80
Bone 400 to 1000
Introduction xvii
Window Level (WL) and Window Width (WW)

To permit the viewer to understand the image, only a restricted number of HU are
put on view and this is accomplished by setting the WL and WW on the console
to a suitable range of Hounsfield units, depending on the tissue, for interpreting
the image. The expression WL represents the central Hounsfield value of all
the Hounsfield numbers within the WW. Tissues with CT numbers outside this
array are shown as either black or white. Both the WL and WW can be set on the
displayed image as desired by the viewer. On CT examination of the chest, a WW
of 300 to 350 and WL of 35 to 45 are chosen to image the mediastinum (soft tissue
window) whereas WW of 1500 and WL of 0 is used to assess the lung.
Image Reconstruction
The acquisition of volumetric data using spiral CT means that the images can be
postprocessed in ways appropriate to the clinical situation.
Multiplanar reformatting (MPR) is by taking standard axial images and
subject to the three-dimensional array of CT numbers obtained with a series of
contiguous slices; and can be viewed in sagittal, coronal, oblique and paraxial
planes (Figs 1A to C).
Three-Dimensional Imaging
Many fractures like fracture of the mandible associated with frontal bone with
or without walls of sinuses can be reconstructed into a 3-dimensional image
(Figs 2A to D).
CT Angiography
CT angiography (CTA) sequence is created subsequent to intravenous contrast,
images are acquired in the arterial phase and then reconstructed and exhibited in
2D or 3D format. This performance is used for imaging the aorta, renal, cerebral,
coronary and peripheral arteries (Figs 3 to 5).
CT is readily available in most hospitals and stand-alone CT centers. It is fast
imaging modality and provides with cross-sectional high-resolution images. Data
acquired on axial scans can be used for multiplanar and 3D reconstructions.
A B C
Figs 1A to C Bilateral renal cysts seen in axial section
(A) are reformatted into sagittal; (B) and coronal; (C) planes
xviii 101 CT Abdomen Solutions
A B
C D
Figs 2A to D Fracture of body of mandible and frontal bone with bilateral maxillary
hemosinus. D shows the 3D image of face including mandible
A B C
D E F
Figs 3A to F CT abdominal angiography
Introduction xix
Fig. 4 Volume rendered image—posterior coronal plane

shows coronary arteries
Fig. 5 Volume rendered image—posterior oblique coronal plane

shows coronary arteries
It detects subtle differences between body tissues. However, it uses X-rays which
have radiation hazards, CT need contrast media for enhanced soft tissue contrast.
Contrast is contraindicated in asthma, cardiac disease, renal and certain thyroid
conditions.
CT Anatomy: Abdomen and Pelvis
LIVER
Functional segmental anatomy of liver is based on distribution of three hepatic
veins. Middle hepatic vein divides the liver into right and left lobes. Left hepatic
vein divides the left lobe into medial and lateral parts. Right hepatic vein divides
the right lobe into the anterior and posterior parts. An imaginary transverse
line through the right and left portal vein divides these parts into anterior and
posterior segments which are numbered counterclockwise from the inferior vena
cava.
The Couinaud classification of liver anatomy divides the liver into eight
functionally indepedent segments. Each segment has its own vascular inflow,
outflow and biliary drainage. In the center of each segment there is a branch of
the portal vein, hepatic artery and bile duct. The numbering of the segments is in
a clockwise manner (Figs 1 and 2A to F).
Segment 1 (caudate lobe) is located posteriorly and extends between fissure of
the ligamentum venosum anteriorly and the inferior vena cava posteriorly.
The longitudinal plane of the right hepatic vein divides segment 8 from
segment 7 in the superior portion of the liver and in the inferior portion of the
liver segment 5 from segment 6.
Fig. 1 Anatomy of liver segments

2 101 CT Abdomen Solutions
B
Figs 2A and B
CT Anatomy: Abdomen and Pelvis 3
D
Figs 2C and D
F
Figs 2E and F
The longitudinal plane of the middle hepatic vein through the gallbladder
fossa separates segment 4a from segment 8 in the superior liver and segment 4b
from segment 5 in the inferior liver.
The longitudinal plane of the left hepatic vein and fissure of the ligamentum
teres separates segment 4a from segment 2 in the superior liver and segment 4b
from segment 3 in the inferior liver.
The axial plane of the left portal vein separates segment 4a superiorly from
segment 4b inferiorly and segment 2 superiorly from segment 3 inferiorly in the
left lobe.
The axial plane of the right portal vein separates segment 8 and segment 7
superiorly from segment 5 and segment 6 inferiorly in the right lobe.
Normal liver has a precontrast attenuation value of 45–65 HU and maximum
enhancement occurs at 50–60 seconds after administration of contrast. Normal
liver has a size up to 13 centimeters. Normal portal vein is 10–13 mm in diameter
(Figs 2G to N).
GALLBLADDER
Normal gallbladder is up to 10 cm long and 4 cm wide. It has a normal wall
thickness up to 3 mm. Gallbladder may have septae (Figs 2M and N). Bifid
appearance is due to longitudinal septum. Phrygian cap gallbladder is due to
kink or septum at the neck. Ectopic gallbladder can be seen beneath the left lobe
of liver or even in retro hepatic location. Floating gallbladder can result from
loose peritoneal attachments.
G
Fig. 2G
J
Figs 2H to J
M
Figs 2K to M
N
Fig. 2N
Normal cystic duct is 2 cm long and 2 mm wide. Maximum diameter of normal

common bile duct in an adult is 2–5 mm. Post cholecystectomy it can be up to
7 mm. Normal width increases by 1mm per decade in elderly over 60 years of age.
PANCREAS
It develops during the fourth week of gestation as the second endodermal
diverticulum from foregut. The dorsal diverticulum forms the dorsal pancreas.
Ventral diverticulum forms the ventral pancreas as well as the liver, gallbladder
and bile ducts.
The main pancreatic duct is known as the duct of Wirsung. The angle between
the pancreatic duct and common bile duct at their joining point is between 5°
and 30º. These ducts open into second part of duodenum through the ampulla of
Vater which has a sphincter called the sphincter of Oddi.
The entire length of pancreas is 10–15 cm. Pancreatic tail is up to 1.6 cm thick;
body is up to 1.1 cm thick and the head ranges from 1–2 cm in thickness (Figs 2L
to O).
Annular pancreas is a congenital anomaly in which the duodenum is enclosed
on all sides by pancreas as a result of abnormal migration of ventral pancreas.
SPLEEN
Spleen is formed during fifth week of gestational age from mesenchymal cells
between layers of dorsal mesogastrium. Accessory spleen can be seen in 10-
30% of patients. Spleen can even be attached to left testis or ovary as there is a
close relationship between the left gonadal anlage and the splenic precursor
mesenchymal cells (Splenogonadal fusion). It has a weight up to 200 g and a
length of 11 cm. The CT value of spleen is 5 HU less than the liver.
GASTROINTESTINAL SYSTEM
The gastrointestinal system originates from a pouch like extension of yolk sac
starting from 6 weeks of gestational age. The foregut is supplied by celiac artery,
midgut by superior mesenteric artery and the hindgut by inferior mesenteric
artery.
Upper gastrointestinal system starts from mouth and continues into oropharynx
which continues into esophagus. Esophagus is a 25 cm long tubular structure
which opens into the stomach via gastro esophageal junction. Parts of stomach
are the fundus, body, greater and lesser curvatures, antrum and pylorus. Walls are
3–5 mm thick except in pylorus where it can be up to 7 mm thick (Figs 2H to O).
Small intestine can be up to 6 m long and extends from pyloric orifice of
stomach up to ileocaecal valve. Duodenum is one feet long, jejunum is around
10 feet and ileum is upto 8 feet (Figs 2N to T). Fifteen centimeters long mesentery
is located between ileocaecal junction and ligament of Treitz. Circular folds of
small bowel are called as valvulae conniventes.
Rule of three for normal small bowel states that its walls are 3 mm thick,
valvulae conniventes are 3 mm thick, there are less than 3 air fluid levels and the
diameter is up to 3 cm.
Large intestine is 1.5 m long and extends from ileum to anus. Its parts are
caecum, ascending colon, hepatic flexure of colon, transverse colon, splenic
flexure, descending colon, sigmoid colon, rectum and anal canal (Figs 2O to T,
3A to C, 3E and 4).
Peritoneal spaces above transverse colon are:
• Spaces on the right
– Right subphrenic space
– Anterior and posterior right subhepatic space
O
Fig. 2O
R
Figs 2P to R
T
Figs 2S and T
Figs 2A to T Axial CT sections of abdomen
– Bare area of liver

– Lesser sac
• Spaces on the left
– Left subphrenic space
– Left subhepatic space
– Perisplenic space
Peritoneal spaces below transverse colon are:
• Superior and Inferior Ileocecal recesses
• Retrocecal space
• Right and left paracolic gutters
• Intersigmoid recess.
Two folds of peritoneum supporting a structure within the peritoneal cavity
together form a structure known as ligament.
C
Figs 3A to C
E
Figs 3D and E
Figs 3A to E Axial CT sections of female pelvis
Fig. 4 Axial CT section showing appendix

When two folds of peritoneum connect a portion of bowel to the retro

peritoneum it is known as mesentery. Ventral mesentery gives rise to falciform
ligament, gastrohepatic ligament and hepatoduodenal ligament. Dorsal
mesentery gives rise to gastro phrenic ligament, gastropancreatic ligament,
phrenicocolic ligament, gastrosplenic ligament, splenorenal ligament and
gastrocolic ligament. Dorsal mesentery also forms the small bowel mesentery
and transverse as well as sigmoid mesocolons.
Omentum is a structure connecting stomach to an additional structure. Lesser
omentum is formed by combination of hepatoduodenal and gastrohepatic
ligament. Greater omentum is an inferior continuation of gastrocolic ligament
and is composed of four layers of peritoneum resulting from double reflection of
dorsal mesogastrium.
Anterior right subhepatic space located posterior to porta hepatis
communicates with lesser sac through epiploic foramen also known as foramen
of Winslow.
UROGENITAL SYSTEM
• Kidneys arise from metanephros (of mesodermal origin) at fourth week of
intrauterine life. Bladder, urethra and prostate are formed from urogenital
sinus.
• Adult kidneys have a span of 7–12 cm. Renal arteries arise from abdominal
aorta at the level of L1-L2 vertebrae and then divide into following five
segmental branches: apical, anterior superior, anterior inferior, posterior and
basilar (Figs 2K to P).
• Renal arteries can be multiple, aberrant, accessory and even supplementary.
Single or multiple renal veins can exist (Fig. 2N).
• Retroperitoneum is the space between parietal peritoneum extending from
diaphragm to pelvic brim and fascia transversalis.
• Adrenal glands (suprarenal glands) are situated on the top of kidneys and are
3 cm long and 1 cm thick (Fig. 2L).
• Average size of testis is 2.5 × 3.0 × 3.5 cm. Epididymis has a head, body and a tail.
• Spermatic cord consists of testicular artery, cremasteric artery, pampiniform
plexus of veins, vas deferens, nerves and lymphatics.
• Gonadal artery arises from ventral surface of aorta slightly below the origin of
renal arteries. Occasionally it can arise from renal artery.
• Gonadal veins drain in the IVC or renal vein on right and in the renal vein on
left.
• Prostate has a normal size of 2.5 × 2.8 × 3.0 cm (Fig. 5). It is composed of an
outer part having a central and peripheral zone and an inner part made of
periurethral and transitional zone.
• Male urethra is 15-20 cm long and has a posterior part composed of prostatic
urethra and membranous urethra. The anterior part of urethra is composed of
bulbar and penile urethra.
Female urethra is 2.5–5 cm long (Figs 3C and D).
Adult uterus is 6–9 cm long, 2.5–4 cm anteroposterior and 3–4.5 cm transverse in
dimension. Endometrium is the innermost zone of uterus (Figs 3A and B). Serosa
is the outermost zone. Myometrium is the middle layer. CT scan usually does not
show them separately.
B
Figs 5A and B Axial CT sections of male pelvis
Fallopian tubes arise from upper and the outer aspect of uterus, and extend
between the folds of broad ligament towards the pelvic side walls to open just
above and anterior to ovaries located in ovarian fossa on each side.
Pelvic spaces formed due to relationship between urinary bladder, uterus and
rectum are:
• Recto uterine pouch of Douglas
• Uterovesicle pouch
• Rectovesicle recess.
Important Pelvic ligaments in relation to uterus are:
• Broad ligament—between uterus and pelvic sidewalls
• Round ligament—between uterus and labia majora
• Cardinal ligament/Mackenrodt’s ligament—between cervix and fascia of
obturator internus
• Uterosacral ligament—between uterus and sacrum
Adult ovaries measure 0.5–1.5 cm × 1.5–3.0 cm × 2–3 cm.
SECTION
1
Esophagus
1. Hiatus Hernia
2. Esophageal Carcinoma
3. Leiomyomatosis of Esophagus
CASE
1 Hiatus Hernia
CASE
A 43-year-old male with history of epigastric pain and burning sensation over a
period of 2–3 months was referred to department of radiology for CT thorax.
Radiological Findings on CT Examination

Contrast enhanced axial CT image (Fig. 1) at the level of heart shows presence
of portion of fundus of the stomach which is seen anterior and left lateral to the
Fig. 1
20 Section 1: Esophagus
esophagus. This is suggestive of upward displacement of the stomach through

the esophageal hiatus suggestive of hiatus hernia.
Comments and Explanation

Hiatus hernia is a condition in which there is upward displacement of the
gastroesophageal junction and/or the portion of the stomach through the
esophageal hiatus. Embryologic development of the diaphragm is a complex
process; a number of defects result in a variety of possible congenital hernias
through the diaphragm. A hernia may occur through a congenitally large
esophageal hiatus; however, acquired hernias through the esophageal hiatus are
more common.
Opinion
Hiatus hernia.
Clinical Discussion
Hiatus hernias are classified either as sliding hernias, paraesophageal (rolling)
hernias or mixed. Sliding hiatus hernias are the most common and account for
95% of the cases. In sliding hernia the gastroesophageal (GE) junction is >2 cm
above the diaphragm. In rolling hernia the GE junction is below diaphragm but
the gastric fundus protrudes through the hiatus. In mixed variety characters of
both the types of hernia are seen. Most hiatus hernias are found incidentally, and
they are usually discovered on routine chest radiographs or CT. Symptomatic,
patients may experience heartburn, dyspepsia, or epigastric pain. Rarely, the
patient may present with recurrent chest infections resulting from aspiration of
gastric contents. A paraesophageal or, rarely, a sliding hiatal hernia may present
with a volvulus or strangulation. Paraesophageal hernias are particularly likely
to incarcerate and cause symptoms of intermittent epigastric pain. Barrett
esophagus is commonly associated with hiatal hernia; patients with Barrett
esophagus may present with reflux symptoms or dysphagia. Large incarcerated
hiatal hernias may slowly bleed so that patients present with iron deficiency
anemia, rather than reflux symptom. Other complications include peptic
esophagitis from reflux, discrete marginal ulcer and strictures.
CASE
3 Leiomyomatosis of
Esophagus
CASE
A 25-year-old female patient with history of dysphagia was referred to radiology
department for CT scan thorax and abdomen.
Radiological Findings on CT Scan Examination

CT scan thorax and abdomen (Figs 1A to C) show diffuse circumferential
thickening of mid and lower esophageal wall extending up to the gastro-
esophageal junction and fundus of stomach. The entire eosophageal lumen is
dilated. Fat planes with the adjacent structures are preserved.
Gross specimen of the esophagus reveals circumferential thickening of
esophagus (Fig. 1D). Cut surface of the esophageal specimen shows abnormal
muscular thickening with intact mucosa (Fig. 1E). This turned out to be
esophageal leiomyomatosis on histopathologic examination.

Esophageal leiomyomatosis is a rare clinical entity characterized by proliferation
of smooth muscle cells in the esophageal wall, causing circumferential
thickening. Although it can occur at any age, it is more common in children and
young adults, and is more common in women. In pediatric patients, the usual
age at presentation is between 10 and 14 years. Chest X-ray, barium swallow,
endoscopy, CT scan, magnetic resonance imaging and EUS are commonly used
diagnostic modalities. A chest X-ray shows a mediastinal mass or widening of the
mediastinum. Barium swallow study reveals dilatation of the upper esophagus
and smooth tapering of the distal esophagus with decreased or absent esophageal
peristalsis, mimicking the appearance of achalasia. It is not easy to differentiate
these two entities, though the narrowed segment in achalasia is usually shorter
than in leiomyomatosis. The CT scan usually shows circumferential thickening
of the esophageal wall that extends to the cardia. This feature differentiates
esophageal leiomyomatosis from achalasia. It should also be differentiated from
diffuse circumferential thickening of the esophageal musculature that may occur
24 Section 1: Esophagus
B C
D E
Figs 1A to E
in neuromotor functional disorders. In addition it must be distinguished from

leiomyoma, which is a focal, encapsulated lesion and a true neoplasm. Another
differential diagnosis of circumferential wall thickening of esophagus is malignant
tumor. Upper endoscopy also is helpful because it may show irregularity of the
wall due to submucosal lesions that are mostly covered by normal mucosa.
Opinion
Esophageal leiomyomatosis.
Clinical Discussion
Esophageal leiomyomatosis is a rare, benign condition in which neoplastic
proliferation of smooth muscle causes marked circumferential thickening of
the esophageal wall, most commonly in the distal esophagus. Patients develop
symptoms because of encroachment of the lumen of the esophagus by thickened
and hypertrophied musculature. The most common presentation is dysphagia
for a long duration, regurgitation, dyspepsia, cough, dyspnea and weight
loss. Because of its rarity, the preoperative diagnosis is usually difficult. Early
evaluation with CT may be valuable in demonstrating the intramural location
and nature of the disease and differentiating this entity from achalasia and other
causes of dysphagia. The narrowed segment in patients with achalasia tends
to be shorter. No sarcomatous change in leiomyomatosis of the esophagus has
been reported. However, surgical removal of the lesion is nearly always indicated
in symptomatic patients. Surgical methods depend on the extent of the lesion.
An esophagectomy or esophagogastrectomy is usually curative and prognosis is
good.
SECTION
2
Diaphragm
4. Eventration
5. Eventration of Diaphragm with Duplication of Inferior Vena Cava
CASE
4 Eventration
CASE
A 15-year-old male with acute pain in abdomen was referred to the department
of radiology for CT scan chest and abdomen.

Axial contrast-enhanced computed tomography (CECT) at chest level and sagittal
reconstruction of chest and abdomen shows eventration of right hemidiaphragm
with right kidney migrating into chest at D8 vertebral level under the diaphragm
(Figs 1A and B). Barium enema examination shows redundancy of the colon with
ascending colon and cecum extending into the right hemithorax underlying the
right hemidiaphragm (Fig. 1C). Upper GIT study (not in the figure) demonstrated
the stomach in normal position with duodenojejunal flexure on the right side as
a part of malrotation of right gut.
A B C
Figs 1A to C
28 Section 2: Diaphragm

Elevation of a single hemidiaphragm is usually secondary to adjacent pleural,
pulmonary, subphrenic disease or due to phrenic nerve palsy. Rarely it is related to
an intrinsic weakness of the diaphragm. In eventration weakened diaphragmatic
muscles results in the upward displacement of abdominal contents but its
incidence with malrotation of midgut is generally not seen. Occasionally it is
associated with superior renal ectopia as the kidney continues to migrate beyond
the normal renal fossa during development and ends up in the thorax as seen in
this case.
Opinion
Eventration of diaphragm.
Clinical Discussion
Diaphragmatic eventration refers to an abnormal contour of the diaphragmatic
dome and is typically due to incomplete muscularization of the diaphragm with
a thin membranous sheet replacing normal diaphragmatic muscle. Over a period
this region stretches and on inspiration does not contract normally. Usually it is
thought to be congenital. Commonly seen on right side. Elevation of the affected
portion of the diaphragm is usually seen as a smooth hump on the normal
contour of the hemidiaphragm.
CASE
Eventration of Diaphragm
5 with Duplication of
Inferior Vena Cava
CASE
A 20-year-old female with history of vomiting and acute pain in abdomen was
referred to the department of radiology for CT scan abdomen and pelvis.

CT abdomen shows elevated right dome of diaphragm which lies at the level
of D6, large and small bowel loops are seen closely abutting it (Figs 1A to E).
A B
C D E
Figs 1A to E
30 Section 2: Diaphragm
Duplication of IVC (white arrows) is seen as an incidental finding. In this the left
common iliac vein ascends as left IVC and the left renal vein (black arrow) drains
into it which crosses anterior to the aorta and joins the right IVC (Figs 1C and D).
The right IVC is larger in diameter than the left IVC (Fig. 1B).

Diaphragmatic eventration refers to an abnormal contour of the diaphragmatic
dome and is due to incomplete muscularization of the diaphragm with a thin
membranous sheet replacing normal diaphragmatic muscle. This has been
discussed in Case 04.
In double IVC, both left and right supracardinal veins persist. Duplication
of inferior vena cava is a rare vascular anomaly, but this abnormality needs to
be recognized, especially in association with renal anomalies like crossed fused
ectopia. The left common iliac vein ascends as duplicated left IVC and usually
drains into the left renal vein, which then crosses anterior to the aorta and joins
the right IVC in a normal fashion, i.e. incomplete double IVC. It is possible that
the left IVC does not drain into the left renal vein, but after receiving the left renal
vein it continues with a major preaortic trunk that travels obliquely and empties
into the right IVC, i.e. complete double IVC. The complete duplication of IVC
could be subclassified into three types: Type I or major duplication: comprises
two bilaterally symmetrical trunks and a preaortic trunk of the same caliber.
Type II or minor duplication: comprises two bilaterally symmetrical trunks, but
smaller than the preaortic trunk. Type III or asymmetric duplication: comprises
small left IVC, larger right IVC and even larger preaortic trunk.
Opinion
Eventration of diaphragm with duplication of IVC.
Clinical Discussion
An important differential for IVC duplication is transposition of IVC, in which
IVC continues on left side of aorta, where as in duplication, IVC is seen on both
sides of aorta.
SECTION
3
Stomach
6. Gastrointestinal Stromal Tumor
7. Gastric Malignanacy
CASE
6 Gastrointestinal
Stromal Tumor
CASE
A 45-year-old female patient with history of lump in right hypochondrium was
referred to radiology department for CT scan.
Radiological Findings on CT Scan

CT scan abdomen (Figs 1A and B) show a well defined soft tissue density mildly
enhancing lesion in lesser sac between the posterior margin of left lobe of liver
and lesser curvature of stomach. The lesion is infiltrating the lesser curvature of
stomach. In lower CT sections (Figs 1C and D) show a large exophytic lobulated
heterogeneously enhancing soft tissue density lesion involving the duodenum
and adjacent small bowel loops. It shows central cystic/necrotic component with
air fluid level. Both these lesions represent stromal tumors.
Figure 1B shows an ill defined heterogeneously enhancing lesion in segment
VII of right lobe of liver representing metastases.

The term stromal tumor was coined in 1983 by Clark and Mazur for smooth
muscle neoplasm of the gastrointestinal tract (GIT). Gastrointestinal stromal
tumors (GIST) are nonepithelial tumors arising from the interstitial cells of
Cajal. The clinical manifestations of GISTs depend on the location and size of
the tumors and are often nonspecific. Common symptoms include early satiety,
indigestion, bloating, vague abdominal pain, and a palpable mass. Occasionally,
gastrointestinal bleeding occurs with tumors involving the mucosa. Because of
these nonspecific clinical symptoms and the exophytic growth of the tumors,
GISTs are often not detected until late in their progression
Opinion
Gastrointestinal stromal tumor (GIST).
34 Section 3: Stomach
A B
C D
Figs 1A to D
Clinical Discussion
Gastrointestinal stromal tumors (GIST) can arise anywhere in the GI tract,
including the mesentery, omentum, and rarely retroperitoneum. Since most
of these tumors are submucosal in location, they usually attain a large size
without causing bowel obstruction. Many of these tumors have an exophytic
component as they arise from the muscularis propria. CT is the imaging modality
of choice for diagnosis and staging of GISTs at initial presentation and for
monitoring the disease during and after treatment. GISTs are typically large,
hypervascular, enhancing masses on contrast-enhanced CT scans and often
appear heterogeneous due to necrosis, hemorrhage, or cystic degeneration.
Fistulization to the gastrointestinal lumen are also common features of GISTs.
The masses usually displace adjacent organs and vessels. Direct invasion of
the adjacent structures is seen with advanced disease. Sometimes it can be
difficult to identify the origin of the mass because of its large size and prominent
extraluminal location. Calcification is uncommon. Differential includes
esophageal leiomyoma which is most commonly in the esophagus but is rare
in the remainder of the gastrointestinal tract. Most metastases of GISTs involve
the liver and peritoneum by hematogenous spread and peritoneal seeding,
respectively and less commonly metastases are found in the soft tissue, lungs,
and pleura. GISTs metastasizing to the lymph nodes are extremely rare.
CASE
7 Gastric Malignanacy
CASE
A 50-year-old male with complaints of hematemesis and weight loss was referred
to radiology department for CT scan abdomen.

Computed tomography (CT) scan abdomen (Fig. 1A) shows marked thickening
of the entire gastric wall with narrowing of gastric lumen in a case of gastric
lymphoma.
Other Cases of Carcinoma Stomach

Figure 1B CT scan abdomen in right lateral recumbent position of the patient
carcinoma of the pylorus shows circumferential thickening of pylorus with the
growth extending into antrum and duodenum. Prepyloric lymph node is seen
(arrow).
Figure 1C shows homogeneously enhancing circumferential thickening of
almost the entire stomach wall in a case of carcinoma of stomach. Few enlarged
lymph nodes are also present.
Figure 1D shows ascites and bilateral ovarian deposits (Krukenberg tumor) in
a previously operated case of carcinoma stomach.

Gastric malignancy continues to be one of the leading causes of cancer related
death. An important development in the epidemiology of gastric carcinoma
has been the recognition of the association with Helicobacter pylori infection.
Adenocarcinoma is by far the most common gastric malignancy, representing
over 95% of malignant tumors of the stomach. The remaining malignant tumors
include lymphoma, sarcoma, metastasis, and so on. CT is currently the staging
modality of choice because it can help identify the primary tumor, assess for
local spread, and detect nodal involvement and distant metastases. Detection
36 Section 3: Stomach
A B
C D
Figs 1A to D
of gastric carcinoma is improved by using thin-section sequences and helical or

multidetector-row CT. CT can show polypoid mass with or without ulceration
or focal wall thickening with mucosal irregularity. In linitus plastica the
stomach wall is diffusely thickened. The underlying cause is usually scirrhous
adenocarcinoma with diffuse submucosal infiltration, leading to thickening
and rigidity to the stomach wall. Metastases in cases of gastric carcinoma occur
along peritoneal ligaments and also to local lymph nodes. Lymphangitic spread
may occur to lungs. Hematogenous spread occurs in liver, adrenals, ovaries and
bones.
Opinion
Gastric Carcinoma.
Clinical Discussion
Gastric cancer is rare before 40 years of age, and its incidence peaks in the
seventh decade of life. Carcinoma stomach often produces no specific symptoms
when it is superficial although up to 50% of patients may have nonspecific
gastrointestinal complaints such as dyspepsia. Some patients may present with
anorexia and weight loss as well as abdominal pain that is vague and insidious
in nature. Nausea, vomiting, and early satiety may occur with bulky tumors that
Case 7: Gastric Malignanacy 37
obstruct the gastrointestinal lumen or infiltrative lesions that impair stomach

distension. Endoscopy is regarded as the most sensitive and specific diagnostic
method in patients suspected of harboring gastric cancer. Endoscopy allows direct
visualization of tumor location, the extent of mucosal involvement, and biopsy
for tissue diagnosis. But radiological methods are often the initial examination
that raises suspicion for gastric carcinoma, besides being used in the staging of
the disease. Double-contrast barium examinations have a sensitivity of 90–95%
in gastric cancer detection. Computed tomography (CT) scanning, magnetic
resonance imaging (MRI), and endoscopic ultrasonography (EUS) are used in
the staging, but not usually in the primary detection of gastric cancer.
SECTION
4
Duodenum
8. Carcinoma Duodenum
CASE
8 Carcinoma Duodenum
CASE
A 60-year-old male presented to the department of radiology with abdominal
pain and distension.

Axial post contrast CT images of abdomen (Fig. 1A) shows heterogeneously
enhancing mass lesion in second part of the duodenum with surrounding fat
stranding and loss of fat planes between the lesion and adjacent structures. Two
small hypodense lesions are seen in right lobe of liver (Fig. 1B). These findings
suggest duodenal carcinoma with hepatic metastases.

Adenocarcinoma is the most common primary malignant neoplasm of the
duodenum. It represents 0.3% of all gastrointestinal malignancies. It accounts
for 50–70% of small bowel adenocarcinomas occurring either in the duodenum
or proximal jejunum. There is an increased risk of carcinoma in patients with
familial adenomatous polyposis and adenomas in the duodenum. Small bowel
carcinomas may be associated with increased incidence of primary malignancies
at other locations. Disease progression may be assessed by lymph node
involvement and spread to the liver, spleen, lungs.
Opinion
Carcinoma duodenum with hepatic metastases.
Clinical Discussion
In general upper abdominal pain and weight loss are the symptoms, and usually
they are not suggestive of ulcer. In the late phases of the disease a variety of
symptoms and signs have been reported, commonly those of developing high
42 Section 4: Duodenum
B
Figs 1A and B
intestinal obstruction and jaundice, hematemesis, melaena, and occult blood in

the stool. A variety of other findings, such as low back pain and alteration in bowel
habit, have also been described. Grossly duodenal carcinomas have napkin ring
appearance or polypoidal fungating mass. Patients with familial adenomatous
polyposis and Gardeners syndrome are considered to have a higher likelihood
of developing duodenal cancer. Patients who have duodenal polyps without a
predisposing family history are also at an increased risk. Ultrasonography can
diagnose and assess vascularity of larger lesions but the smaller tumors (<2 cm)
may not be detected. CT is the modality of choice for staging of the disease by
identifying primary tumor, assessing local, nodal and distant spread. Duodenal
adenocarcinoma is associated with a delayed diagnosis and poor prognostic
and survival outcomes due to nonspecific clinical presentation. Metastasis,
poor tumor differentiation, increased depth of spread and pre-existing Crohn's
disease are associated with poor prognosis.
SECTION
5
Small Bowel
9. Small Bowel Obstruction
10. Ileocecal Lymphoma
11. Small Bowel Gastrointestinal Stromal Tumor
12. Angiodysplasia of Jejunum
13. Ileal Carcinoma
14. Pneumatosis Intestinalis
15. Midgut Volvulus
CASE
9 Small Bowel Obstruction
CASE
A 40-year-old male presented to the department of radiology with severe pain in
abdomen since two days.

Abdominal radiograph (Fig. 1A) shows radially arranged dilated small bowel
loops which is confirmed on the coronal reconstructed CT image of abdomen.
Dilatation and abrupt cut off of bowel loops is well seen on the reconstructed CT
image (Fig. 1B).These findings are suggestive of small bowel obstruction.
A B
Figs 1A and B
46 Section 5: Small Bowel

Small bowel obstruction is most commonly due to mechanical obstruction,
leading to dilated bowel loops and multiple air fluid levels. If an obstruction
cuts off the blood supply to the intestine, the condition is called strangulation.
Strangulation occurs in nearly 10 to 20% of cases with small-intestinal obstruction.
Usually, strangulation results when part of the intestine becomes trapped in an
abnormal opening (strangulated hernia), volvulus, or intussusception. Gangrene
can develop in as few as 6 hours. With gangrene, the intestinal wall is necrosed,
usually causing rupture, which leads to peritonitis, shock, and, if untreated,
death.
Opinion
Small Bowel obstruction.
Clinical Discussion
A small-bowel obstruction is caused by a variety of pathologic processes.
The leading cause of small bowel obstruction in industrialized countries is
postoperative adhesions (60%), followed by malignancy, Crohn disease, and
hernias. Intestinal obstruction usually causes cramping pain in the abdomen,
accompanied by bloating and anorexia. Vomiting is common with small-
intestinal obstruction but is less common and begins later with large-intestinal
obstruction. Complete obstruction causes severe constipation, whereas partial
obstruction may cause diarrhea. With strangulation, pain may become severe
and steady. Fever is common and is particularly likely if the intestinal wall
ruptures. In most of the cases abdominal radiograph will be helpful since it will
show dilated bowel loops and multiple air fluid levels. In complicated cases CT
abdomen will give the correct diagnosis. CT will help to determine cause and
complications due to obstruction.
CASE
10 Ileocecal Lymphoma
CASE
A 60-year-old male with history of abdominal distension and weight loss was
referred to the Department of Radiology for CT scan abdomen.

Figures 1A and B show a heterogeneously enhancing soft tissue density lesion
involving the cecum, ileocecal (I-C) junction and terminal ileum. Anteriorly fat
planes between this lesion and anterior abdominal wall are lost.
Gross specimen (Fig. 1C) shows a solid mass lesion involving the cecum, I-C
junction and terminal ileal loop. This turned out to be Non-Hodgkin’s lymphoma
on histopathologic examination.

The small bowel is the second most frequent site of gastrointestinal tract
involvement by lymphoma. Most cases of small bowel lymphoma are due to
Non-Hodgkin’s lymphoma. Lymphomas constitute approximately one-half
of all primary malignant small bowel tumors. The ileum is the most common
site of occurrence, the duodenum the least frequent. CT appearance of
lymphoma is variable. The typical appearance can be classified as aneurysmal,
constrictive, nodular and ulcerative infiltration. Definitive diagnosis is based on
histopathological examination from biopsy of the lesion.
Opinion
Ileocecal Non-Hodgkin’s Lymphoma.
Clinical Discussion
Non-Hodgkin lymphomas (NHLs) are tumors originating from lymphoid
tissues, mainly of lymph nodes. These tumors may result from chromosomal
B C
Figs 1A to C
translocations, infections, environmental factors, immunodeficiency states, and

chronic inflammation. The clinical manifestations of NHL vary with such factors
as the location of the lymphomatous process, the rate of tumor growth, and the
function of the organ being compromised or displaced by the malignant process.
Signs and symptoms of low-grade lymphomas include the following. Peripheral
adenopathy which is painless and can spontaneously regress. Primary extranodal
involvement. Bone marrow involvement is frequent may be associated with
cytopenias. Fatigue and weakness more common in advanced-stage disease.
Primary lymphoma criteria include:
• Confinement of disease to a small bowel segment
• Only regional lymphadenopathy
• No hepatic or splenic involvement except by direct tumor extension
• No palpable or mediastinal lymphadenopathy
• Normal peripheral blood smear and bone marrow biopsy.
CASE
Small Bowel
11 Gastrointestinal
Stromal Tumor
CASE
A 45-year-old male presented to the department of radiology with lump in left
hypochondriac region.

Axial and coronal reconstructed CT images of abdomen (Figs 1A and B) show
a well defined lobular heterogenously enhancing mass lesion arising from the
small intestine. The lesion is exophytic and no evidence of obvious obstruction
noted. Findings are suggestive of gastrointestinal stromal tumor (GIST).

Gastrointestinal stromal tumors are believed to arise from the interstitial
cells of Cajal with 95% staining positive for CD117 (c-KIT) and 70% for CD34.
A B
Figs 1A and B
The majority of GIST have a uniform appearance, falling into one of three
categories: spindle cell, epithelioid cell, and mixed cell. Because most of these
tumors are submucosal in location, they usually attain a large size without
causing bowel obstruction by the time of diagnosis. Many of these tumors
have an exophytic component as they arise from the muscularis propria. The
enhancement pattern can vary from homogenously enhancing to heterogenously
enhancing, with or without ulceration.
Opinion
Gastrointestinal stromal tumor (GIST).
Clinical Discussion
The clinical findings vary depending on the location and size of the tumor at
presentation. If the tumor is small, it may be only an incidental finding during
radiological imaging or surgery for some other cause, whereas a large exophytic
lesion may present as an abdominal mass due to its large size. Lesions in the
stomach, small bowel, or colon may present with gastrointestinal bleed in the
form of hematemesis, malena, or occult blood in stools; alternatively, there may
be abdominal pain, nausea, and vomiting. An esophageal GIST most commonly
presents with dysphagia. GISTs generally occur with equal frequency in both the
sexes. They are common in the fourth and fifth decades of life. GISTs can arise
anywhere along the GIT. In the esophagus, leiomyomas are more common than
GIST; however, in the stomach, small intestine, and colon, GISTs are the most
common mesenchymal tumors. For localizing the organ of origin and defining
the extent of the mass, 64-row multidetector computed tomography (MDCT)
with multiplanar reformations may be helpful. Metastases from GIST commonly
occur to the liver and peritoneal cavity via hematogenous spread and peritoneal
seeding and occasionally occur to soft tissues, lungs, and pleura. Tumors to
be considered in the differential diagnosis of GIST include adenocarcinoma,
lymphoma, peritoneal carcinomatosis, carcinoid and metastases. Imatinib is a
new chemotherapeutic agent used in the treatment of GIST. It is a molecularly
targeted tyrosine kinase receptor blocker. Response to imatinib is usually good,
with improved long-term survival. The imaging features in patients showing
response to imatinib include decrease in the density of the lesion, reduction in
enhancement, and reduction in the number of nodules and number of vessels.
CASE
12 Angiodysplasia of
Jejunum
CASE
A 70-year-old male with history of chronic per rectal bleeding and anemia was
referred to the department of radiology for CT scan abdomen.

Contrast enhanced CT abdomen coronal and sagittal reconstructions (Figs 1A
and B) show evidence of an intensely enhancing lesion involving the wall of
jejunum. Rest of the bowel loops and mesentery appear normal.
A B
Figs 1A and B

Angiodysplasia is a condition of unknown etiology in which microvascular
abnormalities are found in mucosa and submucosa of the bowel wall. The lesion
is predominantly found in caecum and right side of the colon. It is frequently
associated with acute or chronic intermittent blood loss. It is not associated with
family history or any other vascular abnormality. Endoscopy and angiography
are the most common methods of diagnosing angiodysplasia. Other diagnostic
tools include double-contrast barium enema, CT angiography, and radionuclide
scanning.
Opinion
Angiodysplasia of jejunum.
Clinical Discussion
Most patients found to have angiodysplasia are older than 60 years. No racial
predilection is there and it is seen in equal frequency in males and females. Many
patients with angiodysplasia are asymptomatic, and the lesions are incidentally
found during screening with colonoscopy. Hemorrhage from angiodysplasia is
episodic. Angiography will show a cluster of small arteries during the arterial
phase along the antimesenteric border of the colon. There will be accumulation
of contrast material in vascular spaces and intense opacification of the bowel
wall during the capillary phase followed by early opacification of dilated draining
veins that persists late into the venous phase. Clinical presentation and physical
examination are related to GI bleeding or its consequences. Angiodysplasia
can be seen in more than one location in GI tract. Depending upon the site
of the lesion the presentation varies. Patients having lesion in upper GI tract
may present with hemetemesis and if lesion is in lower GI tract then malena
is commoner presentation. Malena occurs in at least one fourth of patients
with colonic bleeding. Spontaneous cessation of bleeding (occurring in 90% of
patients) is the rule for angiodysplastic lesions located in any part of the GI tract.
CASE
13 Ileal Carcinoma
CASE
A 70-year-old male presented to the department of radiology with chronic
constipation and weight loss.

Axial and coronal reconstruction contrast enhanced CT images of abdomen (Figs
1A and B) show an enhancing mass in terminal ileum. The mass is seen to narrow
A B
Figs 1A and B
the lumen and there is evidence of dilatation of bowel proximal to the narrowing.
There is evidence of adjacent fat stranding and lymphadenopathy. Findings are
suggestive of ileal carcinoma.

Primary neoplasms of the small intestine are very rare, comprising approximately
1.6–6% of all tumors of the gastrointestinal tract, 60% of these tumors are
malignant and are most commonly seen in the 5th and 6th decades of life.
Adenocarcinoma is the most common malignant tumor of the small intestine. It
presents as enhancing mass lesion which can be either polypoidal or napkin ring.
Also it can present with obstruction and prestenotic dilatation of the bowel loops.
Opinion
Ileal adenocarcinoma.
Clinical Discussion
In general, small-bowel cancer prevalence is lower in Asia and in less industrialized
countries than in western countries. Men have higher rates of all types of small
bowel cancer than women. Most small bowel tumors are asymptomatic until the
late stages of disease. Symptoms when they occur include nonspecific abdominal
pain, weight loss, diarrhea, and constipation. Signs related to a complication
like bleeding, obstruction, or perforation may also be observed. Various genetic
disorders are also associated with an increased incidence of small bowel tumors
like Peutz Jhegers syndrome—hamartomatous polyps, Gardner’s syndrome—
adenoma, adenocarcinoma. Plain-film radiography can show a dilated proximal
jejunum and air-fluid levels if obstruction is present. A barium examination
will reveal annular narrowing or stricture formation, filling defects or polypoid
masses. The most typical radiological manifestation is a narrowed segment with
features of mucosal destruction, also known as the “apple core” sign. CT may
show an eccentric focal mass or a circumferential irregular thickening of the
small bowel wall. CT is the most effective technique for studying retroperitoneal
tumor extent and liver metastases. MRI may also help to demonstrate tumor
extension and metastatic disease.
CASE
14 Pneumatosis Intestinalis
CASE
A 40-year-old male patient with history of pain in abdomen since 7 days was
referred to radiology department for CT scan abdomen.

CT scan abdomen (Fig. 1) shows multiple air pockets in multiple segments of
small bowel wall.
Fig. 1

Gas in the bowel wall, or pneumatosis intestinalis, can occur as a primary isolated
entity or in conjunction with diseases of the gastrointestinal or respiratory
systems. In primary pneumatosis no disease process is present and it occurs
mainly in adults and involves the colon. It requires no treatment and resolves
spontaneously except in rare cases of hemorrhage, obstruction, or perforation.
Secondary pneumatosis intestinalis more commonly involves the small bowel
and is associated with a wide variety of conditions that affect the gastrointestinal
systems such as ischemia, obstruction, infection (particularly necrotizing
enterocolitis in infants), peptic ulcer disease, inflammatory bowel diseases,
endoscopy, colonoscopy, or surgery. Imaging modality of choice is CT, which will
show intramural gas, portal venous gas and pneumoperitoneum. Depending on
etiology bowel wall/mesenteric edema may be seen. Lung windows are used to
look for gas collections. CT with IV contrast is used to assess mesenteric vascular
patency.
Opinion
Pneumatosis intestinalis.
Clinical Discussion
Pneumatosis intestinalis is seen in the setting of intestinal ischemia and
infarction. Other etiologies like medications (steroids, chemotherapy,
immunosuppressants) and autoimmune disorders (SLE, scleroderma) cause
increased mucosal permeability which can lead to pneumatosis. Any form of
mucosal disruption like trauma, ulcers, irritable bowel disease, endoscopy and
surgical anastomoses can cause pneumatosis intestinalis. Clinical presentation
varies from abdominal pain/distention, fever, gastrointestinal bleed to sepsis. Gas
in the bowel wall in the neonatal period is diagnostic of necrotising enterocolitis.
CASE
15 Midgut Volvulus
CASE
A 25-year-old male patient with complaints of intermittent pain in abdomen
since one month was subjected to CT scan abdomen.

There is twisting of mesentery and few small bowel loops around the superior
mesenteric artery (Figs 1A and B). Jejunal loops appear edematous and most of
them are seen occupying the right side of abdomen (Fig. 1C). There is reversal
of superior mesenteric artery (SMA) and superior mesenteric vein (SMV)
relationship, i.e. SMV is to the left of SMA (arrows Fig. 1C). Cecum and ileocecal
junction is seen in midline in lower abdomen (arrow Fig. 1D).

The twisting of small bowel is normally prevented because of the normal broad
fixation of the mesentery. Narrow base of the mesentery allows the small bowel
and mesentery to twist and wrap around itself to create a distinctive ‘whirlpool’
appearance on CT scan. This pattern was first described by Fisher. Abnormal
orientation of the superior mesenteric artery and superior mesenteric vein
relationship is not entirely diagnostic of malrotation, it can be seen as a normal
variant in some patients and a proportion of patients with malrotation may have
a normal SMA-SMV relationship.
Opinion
Midgut volvulus.
Clinical Discussion
Derivatives of the midgut include the distal half of 2nd, 3rd and 4th part of
duodenum, jejunum, ileum, cecum, appendix, ascending colon and proximal
A B
C D
Figs 1A to D
two-thirds of the transverse colon. These structures are supplied by the superior
mesenteric artery, which also serves as the axis of midgut rotation. Midgut
volvulus is a complication of malrotation in which clockwise twisting of the
bowel around the superior mesenteric artery (SMA) axis occurs because of the
narrowed mesenteric attachment. In 20% it is associated with duodenal atresia
and annular pancreas. Congenital malrotation of the midgut often presents
within the first month of life. In adults recurrent episodes of colicky abdominal
pain, with vomiting over a period of months or years are typical. Ultrasound can
show distended proximal duodenum. Superior mesenteric vein to the left of
SMA. Thick-walled bowel loops inferior to duodenum and to the right of spine
associated with free peritoneal fluid. The degree of twisting can change due to
natural movement of bowel. Severe volvulus causes obstruction of SMV and SMA
which leads to bowel necrosis. Color Doppler shows mesenteric vessels moving
clockwise with caudal movement of transducer, this is called as clockwise
whirlpool sign. The CT whirlpool sign describes the swirling appearance of bowel
and mesentery twisted around the SMA axis.
SECTION
6
Appendix
16. Acute Appendicitis
17. Appendicular Abscess
CASE
16 Acute Appendicitis
CASE
A 40-year-old female with history of pain in right iliac fossa, fever, vomiting since
3 days was referred to the department of radiology for CT abdomen and pelvis.

Axial post contrast CT images show an enlarged long appendix with its tip in
midline in infraumbilical region. Its wall shows enhancement (Fig. 1A). There is
periappendiceal fat stranding and a small loculated collection adjacent to the tip
of appendix (arrow) (Fig. 1B).

Appendicitis essentially means inflammation of the appendix. It is a very common
condition in general radiology practice and is a major cause of abdominal
surgery in young patients. Appendicitis is typically caused by obstruction of the
appendiceal lumen, with resultant build up of fluid, secondary infection, venous
congestion, ischemia and necrosis. Ultrasound should be the investigation of
choice in young patients since it lacks ionizing radiation. The technique used is
A B
Figs 1A and B
62 Section 6: Appendix
known as graded compression and uses the linear probe, with gradual increasing
pressure exerted to displace the normal overlying bowel gas. Appendix is seen
as a blind ending noncompressible, tubular aperistaltic structure with diameter
> 6 mm. It shows a target appearance on transverse section. On Doppler there is
increased circumferential flow. Appendicolith is seen as an echogenic focus with
distal shadowing within the lumen of appendix. Thickening of adjacent bowel
wall, fluid collections, hypoechoic mass indicate perforation of appendix. Due to
its high sensitivity and specificity, CT is becoming the preferred imaging modality
for suspected acute appendicitis since it is less operator dependent than USG.
Concerns have grown over the possible adverse effects on patients from exposure
to radiation from CT scanning. Low-dose abdominal CT is preferred as it allows for
a 78% reduction in radiation exposure compared to traditional abdominopelvic
CT. It shows features like, dilated appendix with distended lumen (>6 mm
diameter), thickened and enhancing wall, thickening of the caecal apex (caecal
bar sign), periappendiceal inflammation, including stranding of the adjacent
fat and thickening of the lateroconal fascia or mesoappendix and extraluminal
fluid. Progression of the inflammatory process may lead to formation of sealed
abscess. An abscess with a well-defined border usually indicates chronicity and
the presence of air bubbles or air fluid levels inside indicates the presence of gas-
forming organisms or communication of the abscess with the bowel.
Opinion
Appendicitis.
Clinical Discussion
Acute appendicitis is the most common surgical abdominal emergency. It
is commonly seen in children and young adults with peak incidence in the
2nd to 3rd decades of life. Classically presentation consists of periumbilical
pain (referred) which within a day or later localizes to Mc Burney’s point and
is associated with fever, nausea and vomiting. Patient may have leukocytosis.
In most of the cases obstruction is important causative factor. Inflammation
of the appendix results from obstruction of its lumen from fecaliths, foreign
bodies, lymphoid hyperplasia, parasites, or tumors. The lumen of the appendix
becomes obstructed, leading to increased intraluminal pressure resulting in
inflammation, ischemia, and infection. The differential diagnosis of appendicitis
is often a clinical challenge because appendicitis can mimic several abdominal
conditions. Patients with many other disorders present with symptoms similar to
those of appendicitis, such as the following pelvic inflammatory disease, ovarian
cyst or torsion, mesenteric adenitis, diverticulitis, omental torsion, renal colic
and ectopic pregnancy. Recognized complications of acute appendicitis include
perforation, abscess formation and generalized peritonitis.
CASE
17 Appendicular Abscess
CASE
A 53-year-old male patient with history of fever and abdominal lump was
subjected to CT abdomen and pelvis.

Figure 1B CT abdomen and pelvis coronal reconstruction image shows enlarged
appendix with periappendiceal fat stranding. A loculated fluid collection with a
peripherally enhancing wall is seen in right iliac fossa adjacent to the appendix.
Air pocket is seen within it (Fig. 1A).

Abscess formation is the most common complication of appendicitis. Plain
radiograph may show free air, appendicolith in right iliac fossa and displacement
A B
Figs 1A and B
64 Section 6: Appendix
of cecal gas. Small bowel obstruction pattern may be seen. Ultrasound is primary
screening modality and may show hypoechoic fluid collection in the appendicular
region which may be well circumscribed and rounded or ill-defined and irregular
in appearance. Appendix may be visualized within the mass. CT is the examination
of choice and may show fluid collection with peripherally enhancing wall with or
without air within. Sometimes appendicolith may be seen.
Opinion
Appendicular abscess.
Clinical Discussion
An appendicular abscess is a complication of acute appendicitis. Patients with
appendicular abscess usually have a history of severe colicky pain in the right
lower abdomen (right iliac fossa) with a tender boggy swelling in this region.
Other symptoms may include vomiting, constipation or less frequently, diarrhea.
On examination the abdomen may be rigid and the swelling can be felt. When
the appendix becomes inflamed (appendicitis), complications arise if the
infection is not treated promptly. In some patients, appendicitis can lead to
gangrene of appendix. In most of these patients the intestinal coils and omentum
in the abdominal cavity tend to cover the inflamed gangrenous appendix. This
forms an appendicular mass. The continuing suppurative process inside the
appendicular mass can lead to the formation of an abscess. An abscess with a
well-defined border usually indicates chronicity and the presence of air bubbles
or air fluid levels inside indicates the presence of gas-forming organisms or
communication of the abscess with the bowel. Patients with abscess larger than
4 cm size and high fever are usually managed with drainage of abscess.
SECTION
7
Colon
18. Intussusception
19. Nontoxic Megacolon
20. Sigmoid Diverticulitis
21. Abdominal Koch’s
22. Carcinoma Sigmoid
CASE
18 Intussusception
CASE
A 30-year-old male patient came with history of pain in abdomen and vomiting
and was referred to radiology department for CT scan abdomen.

Contrast enhanced CT scan abdomen (Figs 1A and B) show intussusception
involving the transverse colon. No evidence of proximal bowel dilatation.
(Fig. 1A) shows classic bowel within bowel appearance of intussusception
involving the transverse colon.
B C
Figs 1A to C
68 Section 7: Colon

Intussusception involves the telescoping of a loop of bowel and its mesentery
(intussusceptum) into the lumen of contiguous bowel (intussuscipiens) because
of abnormal peristalsis related to a lead point mass. Intussusceptions are more
common in children. Intussusception is more common in children and is the
leading cause of bowel obstruction in this population. Intussusceptions in adults
are uncommon. Majority of adult intussusceptions involve a lead point mass, two-
thirds of which are neoplastic. Intussusceptions can be classified according to
their location—enteroenteric (small bowel only), ileocolic (prolapse of terminal
ileum into ascending colon), ileocecal (ileocecal valve or colon serves as the lead
point) and colocolic (large bowel only).
Opinion
Colocolic intussusception.
Clinical Discussion
In children cyclical colicky abdominal pain, vomiting, currant jelly stools (diarrhea
with mucus and blood) are the presenting features. Adults usually present with
intermittent crampy abdominal pain over days to months or there can be acute
obstruction with hours to days of abdominal distention, pain, and constipation.
Rarely patient can present with a palpable abdominal mass. Plain radiographs
are not sensitive or specific but can show soft tissue mass surrounded by a
crescent of gas and evidence of distal small bowel obstruction. Barium enema is
diagnostic and therapeutic. Barium is seen in the lumen of the intussusceptum
and in the intraluminal space giving a coiled spring appearance. Ultrasound
findings are (1) On transverse scan—“Doughnut sign” = concentric rings of
alternating hypoechoic and hyperechoic layers (intussuscepiens) with central
hyperechoic portion (mesentery of intussusceptum). (2) On longitudinal scan—
“Sandwich, pseudo-kidney or hayfork sign” = layering of hypoechoic bowel wall
and hyperechoic mesentery. Color Doppler demonstrates mesenteric vessels
dragged between entering and returning wall of intussusceptum. Absence of
blood flow within the intussusceptum suggests bowel necrosis. Presence of blood
flow within the intussusceptum is a good predictor of reducibility. Abdominal CT
is the most sensitive imaging modality for diagnosing intussusception. Three CT
patterns of intussusception have been described and are thought to correspond
to different stages of the process. They were initially described by Merine in 1987.
The target appearance occurs when an intraluminal soft-tissue mass and eccentric
fat density are seen as a result of the intussusceptum and the intussuscepting
mesentery. This pattern usually corresponds to an early intussusception with
only minimal obstruction, if any. These patients typically do not have signs of
ischemia at pathology. The reniform pattern is described as peripheral high
attenuation and lower attenuation centrally. This appearance is thought to result
from a thickened bowel wall surrounding the intussusceptum, probably resulting
from underlying ischemia. The sausage-shaped pattern results from alternating
areas of low and high attenuation related to the bowel wall, mesenteric fat and
fluid, intraluminal fluid, contrast material, or air. In adults with intussusception
Case 18: Intussusception 69
involving the colon, primary resection without reduction is recommended.

Reduction increases the risk of intraluminal seeding or venous embolization of
a possible tumor and can cause perforation and peritoneal soiling in cases of
bowel ischemia. However, for transient, otherwise asymptomatic enteroenteric
intussusceptions without a lead point, intervention is usually not necessary, as
these frequently resolve spontaneously.
CASE
19 Nontoxic Megacolon
CASE
A 50-year-old male presented to the department of radiology with distension of
abdomen.

Contrast enhanced CT images (coronal reconstruction and axial images at the
level of pelvis) (Figs 1A and B) shows dilatation of left half of the transverse
colon, descending colon and sigmoid colon. There is no evidence of pericolonic
fat stranding or wall thickening which suggests that there are no inflammatory
changes. The rectum is showing normal luminal diameter (Fig. 1C). Findings are
suggestive of nontoxic megacolon.

Megacolon is dilatation of colon > 6 cm. There is additional loss of haustral
markings. If it is associated with inflammation of colon or signs of peritonitis, it is
called as toxic megacolon. If there are no signs of inflammation and patient is only
having distension of abdomen then it is non toxic megacolon. The etiology of this
is not well understood. No large-scale studies have been conducted to determine
incidence of acquired megacolon. However, once present, the approximate risk
of a spontaneous perforation from nontoxic megacolon is 3%.
Opinion
Non toxic megacolon.
Clinical Discussion
Nontoxic megacolon is defined as severe dilatation of a segment or the entire
colon unaccompanied by signs or symptoms of colon toxicity. Mechanical
factors (volvulus, anastomosis, diverticulosis, carcinoma) are responsible for the
Case 19: Nontoxic Megacolon 71
A C
Figs 1A to C
nontoxic megacolon. It is seen sometimes secondary to acute pseudo-obstruction

(Ogilive’s syndrome, pancolonic megacolon, acute myxedemic ileus). The
approximate risk of a spontaneous perforation from nontoxic megacolon is
low. Colonoscopy should be considered as the initial treatment for nontoxic
megacolon prior to surgical intervention. Colonoscopic decompression can
successfully treat most of the pseudo-obstruction cases. However, in the cases
of obstruction due to volvulus, surgical intervention is necessary. Barium studies
should be avoided, due to the risk of perforation in these cases.
CASE
20 Sigmoid Diverticulitis
CASE
A 50-year-old male with complaints of pain in left iliac fossa since 4–5 days was
referred to the department of radiology.

Post contrast axial CT image (Fig. 1) shows evidence of multiple air filled
outpouchings involving the sigmoid colon suggesting multiple diverticuli.
Fig. 1
Case 20: Sigmoid Diverticulitis 73
There is thickening of the walls of these outpouchings and it shows contrast

enhancement. Also there is surrounding fat stranding. All these findings suggest
inflammation of these mentioned diverticuli suggestive of sigmoid diverticulitis.

Mucosal and submucosal herniation through the muscular layer of colon gives
rise to the diverticulum. It is commonly seen in the region of sigmoid colon.
Inflammatory changes of these diverticuli give rise to diverticulitis. Estimated to
occur in 10–15% of people with diverticulosis.
Opinion
Sigmoid diverticulitis.
Clinical Discussion
Diverticulitis is the most common complication of colonic diverticulosis. Most
commonly appear in the sigmoid colon. Obstruction at neck of colonic diverticula
by stool, inflammation, or food particles leads to bacterial overgrowth, vascular
compromise and microperforation which in turn lead to pericolic inflammation.
Symptoms of diverticulitis usually begin in the left iliac fossa with unremitting
pain and accompanying tenderness. An ill defined mass may also be palpable
representing the inflammatory phlegmon. On CT there is pericolic stranding,
often disproportionately prominent compared to the amount of bowel wall
thickening and segmental thickening of the bowel wall. Also there is enhancement
of the colonic wall. Complications include fistula formation, abscess formation,
adhesions, and pneumoperitoneum. Surgery is the treatment option for severe
cases of sigmoid diverticulitis.
CASE
21 Abdominal Koch’s
CASE
A 30-year-old male presented with fever, pain in abdomen and weight loss.
Patient was referred to radiology department for CT scan abdomen and pelvis.

Figures 1A to C are axial post contrast images of abdomen. Figure 1A shows
mesenteric fat stranding and lymphadenopathy. Colonic wall thickening is seen
A B
C D
Figs 1A to D
Case 21: Abdominal Koch’s 75
in Fig. 1B. Figure 1C shows matted bowel loops. Figure 1D is axial post contrast
image of thorax showing bilateral pleural effusions. All these findings indicate
abdominal tuberculosis.

Gastro-intestinal tuberculosis (GI TB) is a major health problem in many
underdeveloped countries. A recent significant increase has occurred in
developed countries, especially in association with HIV infection. It is a form
of chronic infection. It may affect peritoneum, mesentery, bowel, liver, spleen,
pancreas. The imaging findings depend upon the organ involvement and
virulence of the organism. On ultrasound (USG) pathologic lymph nodes may
appear as discrete nodular structures or appear as conglomerated masses. At
CT affected nodes may have low attenuation values or soft tissue density. On
contrast enhanced CT, they have typical peripheral enhancement with central
nonenhancing areas. This pattern reflects significant central liquefactive
or caseous necrosis and perinodal highly vascular inflammatory reaction.
Homogeneous nodal enhancement or calcifications may also be seen. Peritoneal
involvement is most commonly caused by rupture of an infected lymph node into
the peritoneal cavity. Hematogenous or lymphatic seeding may also occur. USG
shows the presence of free or loculated fluid, often with multiple mobile strands of
fibrin and echogenic debris. On CT, ascites has high attenuation values due to the
high protein content of the fluid. CT may also show regular or nodular peritoneal
and mesenteric thickening with increased mesenteric vascularity. Thickened
peritoneum usually shows contrast enhancement. Omental involvement may
appear as omental nodules, diffuse infiltration and thickening. Omental cake
may be seen. Bowel shows wall thickening. On CT, the most common findings
of intestinal involvement are circumferential wall thickening of the cecum and
terminal ileum and asymmetric thinking of the ileocecal junction. Associated
pulmonary infection can be depicted by pleural effusion, pulmonary cavitary
lesions and nodular opacities on CT Chest.
Opinion
Abdominal tuberculosis.
Clinical Discussion
Clinical features of intestinal TB include abdominal pain, weight loss, anemia,
and fever with night sweats. Patients may present with symptoms of obstruction,
right iliac fossa pain, or a palpable mass in the right iliac fossa. Hemorrhage
and perforation are recognized complications of intestinal TB, although free
perforation is less frequent than in Crohn’s disease. The peritoneum and ileocecal
region are commonly involved in majority of the cases by hematogenous spread
or through swallowing of infected sputum from primary tubercular infection.
The pulmonary tuberculosis may be apparent in about half of these cases. The
ileum is more commonly involved than the jejunum. Ileocecal involvement is
seen in 80–90% of patients with GI TB. This feature is attributed to the abundance
76 Section 7: Colon
of lymphoid tissue (Peyer’s patches) in the distal and terminal ileum. Barium
studies, CT scan, invasive procedures and serological tests now can help in timely
diagnosis and early institution of treatment of such cases so as to reduce morbidity
and mortality from this curable but potentially lethal disease. The treatment of
abdominal tuberculosis is on the same lines as for pulmonary tuberculosis.
CASE
22 Carcinoma Sigmoid
CASE
A 70-year-old male presented with painless bleeding per rectum and was referred
to Department of Radiology for CT scan abdomen.

Axial post contrast CT image at the level of pelvis shows circumferential irregular
intraluminal growth in the distal sigmoid colon that turned out to be carcinoma
(Fig. 1).
Fig. 1
78 Section 7: Colon

Colorectal carcinoma is common, accounting for 15% of all newly diagnosed
cancers, and tends to be a disease of the elderly, with the median age of diagnosis
between 60 and 80 years of age. Sigmoid colon is also involved in majority of cases.
The tumor shows irregular walls and may show polypoidal growth or napkin ring
growth pattern. Also it shows rapid spread to the surrounding in the form of fat
stranding and destruction of fat planes. Colorectal cancers, 98% of which are
adenocarcinomas, arise in majority of cases from pre-existing colonic adenomas
(neoplastic polyps), which progressively undergo malignant transformation as
they accumulate additional mutations.
Opinion
Sigmoid colon carcinoma.
Clinical Discussion
Clinical presentation is typically insidious, with altered bowel habit or iron
deficiency anemia from chronic occult blood loss and non specific symptoms
like fatigue and weight loss. Bowel obstruction, intussusception, heavy bleeding
and metastatic disease may also be the initial manifestation. Colon cancer is
now often detected during screening procedures. The incidence of colorectal
cancer is about equal for males and females. Age is a well-known risk factor for
colorectal cancer, as it is for many other solid tumors. The incidence of colorectal
cancer peaks at about age 65 years. Other common clinical presentations include
the following iron-deficiency anemia, rectal bleeding, abdominal pain, change in
bowel habits, intestinal obstruction or perforation. CT scan findings associated
with adenocarcinoma of colon include asymmetric bowel wall thickening with
contrast enhancement or the presence of a soft-tissue mass that frequently
leads to luminal narrowing or obstruction. Colorectal cancer may occasionally
be associated with a wide spectrum of colonic complications that cause acute
abdominal symptoms. Various complications such as obstruction, perforation,
abscess formation, acute appendicitis, ischemic colitis and intussusception can
occur in patients with colon cancer. Carcinomas of the transverse colon can
spread via direct extension to stomach. Common sites of metastatic involvement
include the liver, lungs, adrenal glands, peritoneum, and omentum. In females,
the ovary may be involved. Surgery and chemotherapy are the mainstay of the
treatment.
SECTION
8
Rectum
23. Carcinoma Rectum
CASE
23 Carcinoma Rectum
CASE
A 75-year-old male came with history of painless bleeding per rectum and weight
loss was referred to the department of radiology for CT scan abdomen.

Axial post contrast CT images (Figs 1A and B) show ill defined, irregular,
circumferential wall thickening of the rectum. The fat planes between rectal
mass and rectovesical space is disturbed suggesting spread. The mass shows
mild heterogeneous enhancement. Also there is evidence of involvement of few
perirectal lymph nodes. These findings suggest rectal carcinoma with perirectal
spread.
Axial post contrast CT images of another patient shows iso to hyperdense mass
involving the lumen of the rectum. Also there are multiple hypodense lesions in
both lobes of liver (Figs 1C and D). These findings suggest rectal carcinoma with
hepatic metastases.

Adenocarcinomas comprise the vast majority of colon and rectal cancers; more
rare rectal cancers include lymphoma, carcinoid, and sarcoma. On CT these
lesions are hypo to isodense with irregular margins and shows post contrast
enhancement. The growth can be circumferential or intraluminal. Like colon
cancer, rectal carcinoma also gives metastases to liver. Extrarectal tumor spread
is suggested by a loss of tissue fat planes between the rectum and surrounding
tissues, as well as perirectal fat stranding and nodularity. Invaded muscle may be
enlarged. CT is used for staging rectal carcinomas before treatment, for staging
of recurrent disease, and for detecting the presence of distant metastases after
surgery. CT detects hepatic metastases as well-defined areas of low density in the
portal venous phase, following injection of intravenous contrast medium. In the
early arterial phase, hepatic metastases may demonstrate rim enhancement or
become hyperdense or isodense in relation to normal liver.
82 Section 8: Rectum
C D
Figs 1A to D
Opinion
Rectal carcinoma.
Clinical Discussion
Rectal cancer is one of the most common tumor with a poor prognosis caused
by high risk of local recurrence and metastasis. It is commonly seen in age group
of 60 and above and has a male preponderance. Bleeding is the most common
symptom of rectal cancer, occurring in 60% of patients. Occult bleeding is
detected via a fecal occult blood test (FOBT) Abdominal pain is present in 20% of
the cases. Partial large-bowel obstruction may cause colicky abdominal pain and
Case 23: Carcinoma Rectum 83
bloating. Increased incidence of rectal carcinoma in western world is attributed

to consumption of low fiber diet, red meat, and chronic constipation. The local
recurrence is related to the extramural tumor spread into the mesorectum and
to the tumor distance from circumferential resection margin (CRM). Imaging
plays a crucial role in the preoperative management of rectal carcinoma because
traditional techniques usually performed to make diagnosis (colonoscopy and
digital rectal examination), do not adequately show important prognostic features
such as depth of tumor spread T stage) or the extent of lymph node involvement
(N stage). The mainstay of treatment is surgical excision; however pre-operative
down-staging with either radiotherapy alone or combined chemo-radiotherapy
is employed in T3 and/or N1 disease.
SECTION
9
Liver
24. Focal Fatty Liver
25. Simple Hepatic Cyst
26. Budd-Chiari Syndrome
27. Liver Laceration
28. Hepatic Abscess
29. Hepatic Hydatid Cyst
30. Hepatic Hemangioma
31. Focal Nodular Hyperplasia
32. Hepatic Adenoma
33. Hepatic Angiomyolipoma
34. Hepatocellular Carcinoma
35. Hepatic Metastases
36. Hepatoblastoma
37. Intrahepatic Cholangiocarcinoma
38. Extrahepatic Cholangiocarcinoma
39. Transient Hepatic Attenuation Difference
CASE
24 Focal Fatty Liver
CASE
A 52-year-old diabetic obese male was referred for CT abdomen as ultrasound
was suggestive of a focal hyperechoic area in the liver. CT abdomen was done to
rule out any focal liver lesion.

Non-enhanced CT (Fig. 1A) shows focal hypodense area in the liver. During the
contrast phase of enhancement (Figs 1B to D) the intrahepatic vessels, i.e. the
hepatic artery branches and portal vein follow the normal course in this hypodense
area without distortion or mass effect. This area shows less enhancement than
the rest of the liver on portal phase. This represent focal fatty infiltration of liver.

Focal fatty liver (FFL) is localized or patchy process of lipid accumulation in the
liver. It is likely to have different pathogenesis than nonalcoholic steatohepatitis
which is a diffuse process. FFL may result from altered venous flow to liver, tissue
hypoxia and malabsorption of lipoproteins. Focal fatty infiltration is distinguished
on CT from space occupying lesions as focal fatty infiltration does not cause any
mass effect or deformation of the organ. Typical location for focal fatty change
is medial segment of the left lobe of the liver either anterior to the porta hepatis
or adjacent to the falciform ligament. This distribution is the same as that seen
in focal fatty sparing and is related to variations in vascular supply. On NECT it
appears as a focal hypodense area which on CECT enhances less than the rest of
the liver without distortion of intrahepatic vessels or mass effect.
Opinion
Focal fatty infiltration of liver.
88 Section 9: Liver
A B
C D
Figs 1A to D
Clinical Discussion
Focal fatty infiltration of liver is commonly seen in patients with diabetes mellitus,
obesity, alcohol abuse, exogenous steroids, certain drugs, chemotherapy, and IV
hyperalimentation.
Treatment of the underlying cause will reverse the findings. Liver with fatty
change demonstrates increased echogenicity on ultrasound. The echogenic
walls of the portal veins and hepatic veins are lost, due to the increased liver
attenuation. MRI requires both in- and out-of-phase imaging and contrast to
adequately assess. Pseudolesion (focal sparing) is better seen on out-of-phase
imaging, but otherwise appears normal and similar to the rest of the liver on T2
and contrast enhanced sequences.
The diagnosis may be confirmed by biopsy and histopathology, however
diagnosis of fat on CT and MR if often diagnostic and often needs no confirmation.
CASE
25 Simple Hepatic Cyst
CASE
A 40-year-old male presented to the department of radiology with dull pain in
right hypochondriac region and was subjected to CT scan abdomen.

Axial plain (Fig. 1A) and post contrast (Fig. 1B) CT images of abdomen at the level
of liver shows a large, well defined, thin walled, cystic lesion seen in right lobe of
liver. The lesion shows smooth walls and there is no evidence of post contrast
enhancement. There is no evidence of septae or calcification. Findings suggest
simple hepatic cyst.

Simple hepatic cyst is seen in 5% of the population. There is slight female
predilection. These lesions may be isolated or multiple and vary from a few
millimeters to several centimeters in diameter. Simple hepatic cysts are benign
A B
Figs 1A and B
90 Section 9: Liver
developmental lesions that do not communicate with the biliary tree. They
result from isolated aberrant biliary ducts. The cyst contents are usually clear
serous fluid. They may cause obstruction or compression atrophy of the liver
parenchyma when they attain a large size.
Few close differential diagnosis of simple cysts are as follows:
• Benign developmental hepatic cyst: It is benign, congenital, and developmental
lesion which is derived from biliary endothelium that does not communicate
with the biliary tree.
• Von Meyenburg complex: It is benign malformation of the biliary tract that
originate from embryonic bile duct that fails to involute.
• Adult polycystic liver disease.
Opinion
Simple hepatic cyst.
Clinical Discussion
Simple hepatic cyst can occur anywhere in the liver, with greater predilection
towards the right lobe of the liver. Simple cysts generally are asymptomatic but
may produce dull right upper quadrant pain if large in size. Patients may present
with abdominal bloating and early satiety. Occasionally, a large cyst is palpable
as abdominal mass. Jaundice caused by bile duct obstruction is rare, as is cyst
rupture and acute torsion of a mobile cyst. Patients with cyst torsion may present
with an acute abdomen. When simple cysts rupture, patients may develop
secondary infection, leading to a presentation similar to a hepatic abscess with
abdominal pain, fever, and leukocytosis. The clinician has a number of options
for imaging the liver in patients with hepatic cysts. Ultrasonography is readily
available, noninvasive, and highly sensitive. Computed tomography scan is
also highly sensitive and is easier for most clinicians to interpret, particularly for
treatment planning. While planning for treatment of hepatic simple cysts, it needs
to be differentiated from cystic neoplasm. Cystic neoplasms tend to have thicker,
irregular, hypervascular walls, whereas simple cysts tend to be thin walled and
uniform. Simple cysts tend to have homogenous low-density interiors, whereas
neoplastic cysts usually have heterogeneous interiors with septa and papillary
extrusions.
CASE
26 Budd-Chiari Syndrome
CASE
A 33-year-old female patient came to the radiology department with history of
severe pain in abdomen and was subjected to CT abdomen.

Contrast enhanced CT abdomen (Figure 1) shows patchy nonenhancing
hypodense areas in both lobes of liver, predominantly affecting the right lobe.
There is nonvisualization of the right, middle and left hepatic veins. Portal vein,
portal radicles, IVC appear normal. On the basis of these findings the diagnosis of
Budd-Chiari syndrome needs to be considered.
Fig. 1
92 Section 9: Liver

Budd-Chiari syndrome is a condition caused by occlusion of the hepatic veins that
drain the liver. Caudate lobe hypertrophy is often present. Any obstruction of the
venous vasculature of the liver is referred to as Budd-Chiari syndrome, from the
venules to right atrium. This leads to increased portal vein and hepatic sinusoid
pressures as the blood flow stagnates. The increased portal pressure causes
increased filtration of vascular fluid with the formation of ascites in the abdomen
and collateral venous flow through alternative veins leading to esophageal, gastric
and rectal varices. Obstruction also causes centrilobular necrosis and peripheral
lobule fatty change due to ischemia. If this condition persists chronically what is
known as nutmeg liver will develop. Budd-Chiari syndrome is most commonly
diagnosed using ultrasound studies of the abdomen and retrograde angiography.
Ultrasound may show obliteration of hepatic veins, thrombosis or stenosis,
spiderweb vessels, large collateral vessels, or a hyperechoic cord replacing a
normal vein. Computed tomography (CT) or magnetic resonance imaging (MRI)
is sometimes employed although these methods are generally not as sensitive.
On CT there is inhomogeneous mottled liver with delayed enhancement in the
periphery of the liver and around the hepatic veins (nutmeg liver), peripheral
zones of the liver may appear hypoattenuating because of reversed portal venous
blood flow caudate lobe enlargement and increased contrast enhancement
compared with the remainder of the liver inability to identify hepatic veins.
Liver biopsy is nonspecific but sometimes necessary to differentiate between
Budd-Chiari syndrome and other causes of hepatomegaly and ascites, such as
galactosemia or Reye's syndrome.
Opinion
Budd-Chiari syndrome.
Clinical Discussion
It presents with the classical triad of abdominal pain, ascites and hepatomegaly.
The syndrome can be acute, chronic, or asymptomatic. The acute syndrome
presents with rapidly progressive severe upper abdominal pain, jaundice,
hepatomegaly, ascites, elevated liver enzymes, and eventually encephalopathy.
The fulminant syndrome presents early with encephalopathy and ascites. Severe
hepatic necrosis and lactic acidosis may be present as well. Patients may progress
to cirrhosis. It can be classified into primary and secondary types. (a) Primary
Budd-Chiari syndrome (75%): thrombosis of the hepatic vein (b) Secondary
Budd-Chiari syndrome (25%): compression of the hepatic vein by an outside
structure (e.g. a tumor). Hepatic vein thrombosis is associated with pregnancy,
postpartum state, use of oral contraceptives and hepatocellular carcinoma.
Budd-Chiari syndrome is also seen in infections such as tuberculosis, congenital
venous webs and occasionally in inferior vena caval stenosis. Often, the patient is
known to have a tendency towards thrombosis, although Budd-Chiari syndrome
can also be the first symptom of such a tendency. Examples of genetic tendencies
include protein C deficiency, protein S deficiency, the Factor V Leiden mutation,
hereditary anti-thrombin deficiency. An important nongenetic risk factor is
Case 26: Budd-Chiari Syndrome 93
the use of estrogen-containing (combined) forms of hormonal contraception.

Other risk factors include the antiphospholipid syndrome, aspergillosis, Behçet's
disease, dacarbazine, pregnancy, and trauma. Many patients have Budd-Chiari
syndrome as a complication of polycythemia vera. Patients suffering from
paroxysmal nocturnal hemoglobinuria (PNH) appear to be especially at risk
for Budd-Chiari syndrome, more than other forms of thrombophilia: up to 39%
develop venous thromboses and 12% may acquire Budd-Chiari.
CASE
27 Liver Laceration
CASE
A 43-year-old male came with history of trauma in a semiconscious state. CT
abdomen was done to rule out injury to the abdominal organs.

CT findings show contusions and lacerations in the liver which are seen on CECT
as irregular nonenhancing areas (Figs 1A and B). In case of severe trauma it can
result in diaphragmatic rupture with herniation of liver in the thorax as shown in
Figures 1C and D.

The liver is the second most commonly injured organ in abdominal trauma, first
being the spleen but damage to the liver is the most common cause of death after
abdominal injury. Trauma to the liver may result in subcapsular or intrahepatic
hematoma, contusion, vascular injury, or biliary disruption. The findings to look
for in abdominal trauma are Hemoperitoneum, Contrast blush consistent with
active extravasation, Laceration: linear shaped hypodense areas, Hematomas:
oval or round shaped areas, Contusions: vague ill-defined hypodense areas that
are less well perfused, pneumoperitoneum, devascularization of organs and
subcapsular hematomas.
Opinion
Hepatic trauma.
Clinical Discussion
Contrast-enhanced CT is accurate in localizing the site and extent of liver
injuries and associated trauma, providing vital information for treatment in
patients. CT scans can be used to monitor healing. Trauma to the liver may
Case 27: Liver Laceration 95
A B
C D
Figs 1A to D
result in subcapsular or intrahepatic hematoma, contusion, vascular injury,

or biliary disruption. CT has made a great impact on the diagnosis of patients
with liver trauma, and use of this technique has resulted in marked reduction
in the number of patients requiring surgery. CT can also detect injury to other
surrounding organs like pancreas, spleen, kidneys, etc.
CT criteria for the American Association of Surgery for Trauma (AAST) liver
injury grading system for liver trauma is as follows:
• Grade I: Hematoma: sub capsular, <10% surface area, Laceration: capsular
tear, < 1 cm depth.
• Grade II: Hematoma: sub capsular, 10–50% surface area, Hematoma:
intraparenchymal <10 cm diameter, Laceration: capsular tear, 1–3 cm depth
<10 cm length.
• Grade III: Hematoma: sub capsular, >50% surface area, or ruptured with
active bleeding, Hematoma: intraparenchymal >10 cm diameter, Laceration:
capsular tear, > 3 cm depth.
96 Section 9: Liver
• Grade IV: Hematoma: ruptured intraparenchymal with active bleeding,

Laceration: parenchymal disruption involving 25–75% hepatic lobes or
involves 1–3 Couinaud segments (within one lobe).
• Grade V: Laceration: parenchymal distruption involving >75% hepatic lobe
or involves > 3 Couinaud segments (within one lobe), Vascular: juxtahepatic
venous injuries (IVC, major hepatic vein).
• Grade VI: Vascular: hepatic avulsion.
Pooling of contrast material within the peritoneal cavity indicates active and
massive bleeding; patients with this finding may require emergency surgery.
Intrahepatic pooling of contrast material with an intact liver capsule indicates
a self-limiting hemorrhage. Vascular injury to the hepatic vein or IVC results
when a laceration or contusion extends upto them with hemorrhage seen in the
lesser sac or retrohepatic region. Pseudoaneurysms can be detected on dynamic
angiographic studies. Biliary injury is rare and may result in biliary peritonitis.
CASE
28 Hepatic Abscess
CASE
A 45-year-old male patient came with history of fever with chills and pain in right
hypochondrium since 5 days and was referred to radiology department for CT
scan abdomen and pelvis.
Radiological findings on CT scan

Figure 1 shows multiple well defined irregularly marginated hypodense lesions
of varying sizes in right lobe of liver. There is mild perilesional hypodensity in the
liver parenchyma suggestive of edema.
In another case plain CT abdomen (Fig. 2A) shows a large well defined
hypodense lesion with CT attenuation value 5–10 HU in the left lobe of liver. It
shows a thick peripherally enhancing wall. There is mild perilesional edema
(Fig. 2B).

Hepatic abscesses are localized collections of necrotic inflammatory tissue
caused by bacterial, parasitic or fungal agents. On ultrasound, large hepatic
abscesses have an appearance ranging from hypoechoic to hyperechoic, with
internal echoes and debris. Gas in hepatic abscesses causes high-intensity
linear echoes with acoustic shadowing or reverberation artifacts. On CT, amebic
abscesses usually appear as rounded, well-defined lesions with attenuation
values that indicate the presence of complex fluid (10–20 HU). An enhancing wall
and a peripheral zone of edema around the abscess are common characteristic
for this lesion. The central abscess cavity may show multiple septa, fluid-debris
levels and rarely, air bubbles. Pyogenic abscesses are usually multiple and may
be caused by hematogenous dissemination (of either gastrointestinal infection
via the portal vein or disseminated sepsis via the hepatic artery), ascending
cholangitis, or superinfection of necrotic tissue. Pyogenic abscesses may be
classified as either microabscesses (<2 cm) or macroabscesses (>2 cm). Pyogenic
micro abscesses may appear as multiple widely scattered lesions or as a cluster
98 Section 9: Liver
Fig. 1
of microabscesses that appear to coalesce focally (Cluster sign). It is likely that

clustering of pyogenic microabscesses represents an early stage in the evolution
of a large pyogenic abscess cavity. On contrast enhanced CT they appear as
multiple small, well-defined hypoattenuating lesions with rim enhancement
and perilesional edema. On contrast-enhanced CT, large abscesses are generally
unilocular well defined and hypoattenuating with smooth margins or complex
with internal septa and irregular margins. During arterial phase a double target
sign is seen, the area around the center which is not enhanced is stained while
the outermost layer shows hypodensity. In the portal to equilibrium phase a thick
ring like stain is seen owing to staining of the outermost layers. Fungal abscess
is caused by an opportunistic infection in immunocompromised patients. It
presents as microabscesses which show faint ring like enhancement in arterial
phase and hypodensity in the equilibrium phase.
Opinion
Hepatic abscess.
Case 28: Hepatic Abscess 99
A B
C
Figs 2A to C
Clinical Discussion
The typical presentation is right upper quadrant pain, fever and jaundice. Amebic
liver abscess is the most common extraintestinal complication of amebiasis and
commonly seen in a sub-diaphragmatic location and are likely to spread through
the diaphragm into the chest. As a general rule, bacterial and fungal abscesses
are often multiple, whereas amoebic abscesses are more frequently single.
The presentation of liver abscess is dependent on the way the bacteria have
entered the liver. Bacteria gets into the liver by four routes. The common route
is through the portal vein. As a result of abdominal infection the bacteria enter
through the slow flow portal system and they are layered within the vessel. In
sepsis the spread is via the arterial system as in patients with endocarditis and
there are multiple abscesses spread out through the periphery of the liver.
CASE
29 Hepatic Hydatid Cyst
CASE
A 56-year-old male patient with pain in abdomen was referred to radiology
department for CT scan.

Plain CT scan abdomen (Fig. 1A) shows a well defined cystic lesion in left lobe of
liver. Multiple small peripherally arranged cysts are seen within this lesion, these
represent daughter cysts. There is no calcification or solid component within this
lesion. Contrast enhanced CT scan shows cyst wall enhancement (Fig. 1B).

Hydatid cysts result from infection by the echinococcus worm, and can result
in cyst formation anywhere in the body. The ultrasonographic appearance of
hydatid cysts may vary. The cyst wall usually manifests as double echogenic
lines separated by a hypoechogenic layer. Multiple echogenic foci due to hydatid
sand may be seen. The cyst may appear as a well-defined fluid collection with a
A B
Figs 1A and B
Case 29: Hepatic Hydatid Cyst 101
localized split in the wall and “floating membranes” inside the cavity. Complete
detachment of the membranes inside the cyst has been referred to as the
ultrasound water lily sign. USG is the most sensitive modality for the detection
of membranes, septa, and hydatid sand within the cyst. Multivesicular cysts
manifest as well-defined fluid collections in a honeycomb pattern with multiple
septa representing the walls of the daughter cysts. Daughter cysts appear as cysts
within a cyst. Cyst calcification usually occurs in the cyst wall. When the cyst wall
is heavily calcified, only the anterior portion of the wall is visualized and appears
as a thick arch with a posterior concavity. CT may display the same findings as
USG. Cyst usually demonstrates fluid attenuation (3–30 HU). Calcification of
the cyst wall or internal septa is easily detected at CT. A hydatid cyst typically
demonstrates a high-attenuation wall at unenhanced CT even without
calcification. Detachment of the laminated membrane from the pericyst can
be visualized as linear areas of increased attenuation within the cyst. Daughter
cysts manifest as round structures located peripherally within the mother cyst.
Intrahepatic complications of hydatid cysts include cyst rupture and infection.
Cyst rupture results in free spillage of hydatid material into the peritoneal cavity,
pleural cavity, hollow viscera, abdominal wall, and so on. Both USG and CT
may demonstrate a cyst wall defect and passage of the cyst contents through the
defect in direct communication. Infection occurs only after rupture of both the
pericyst and endocyst which allows bacteria to pass easily into the cyst. CT is
the modality of choice for demonstrating cyst infection. Infected cysts may
manifest at CT as poorly defined masses, in contrast to the more clearly defined
masses seen in uncomplicated cases. Contrast-enhanced CT may reveal the
typical high-attenuation rim representing abscesses surrounding the lesion. CT
clearly depicts gas or air-fluid levels within the cyst. Involvement of the diaphragm
and thoracic cavity occurs in 0.6%–16% of cases of hepatic hydatid disease.
Transdiaphragmatic migration varies from simple adherence to the diaphragm
to rupture into the pleural cavity, seeding in the pulmonary parenchyma, and
chronic bronchial fistula. Peritoneal echinococcosis is almost always secondary
to hepatic disease. CT is the modality of choice in such cases as it allows imaging
of the entire abdomen and pelvis. Cysts may be multiple and located anywhere
in the peritoneal cavity.
Opinion
Hepatic hydatid cyst.
Clinical Discussion
Hepatic hydatid disease is a parasitic zoonosis caused by the echinococcus tape
worm. In the liver, two agents are recognized as causing disease in the
human: echinococcus granulosus and echinococcus alveolaris. Hydatid cyst
consists of 3 layers—endocyst (single layer lining the inner aspect of the cyst),
ectocyst (middle layer easily separable from the adventitia) and pericyst (outer
adventitia). Daughter vesicles (brood capsules) are small spheres that contain
the protoscolices and are formed from rests of the germinal layer. Before
becoming daughter cysts, these daughter vesicles are attached by a pedicle to the
germinal layer of the mother cyst. Hydatid cysts are slow growing at the rate of
102 Section 9: Liver
1–1.5 cm per year. Once the parasite passes through the intestinal wall to reach
the portal venous system or lymphatic system, the liver acts as the first line of
defense and is therefore the most frequently involved organ. The right lobe is the
most frequently involved portion of the liver. CT scanning has the advantage of
inspecting any organ, detecting smaller cysts when located outside the liver. MRI
may have some advantages over CT scanning in the evaluation of postsurgical
residual lesions, recurrences, and selected extrahepatic infections, such as
cardiac infections. It is also superior in identifying changes of the intrahepatic
and extrahepatic venous system and in identifying cysto-biliary fistulas.
CASE
30 Hepatic Hemangioma
CASE
A 50-year-old patient came with history of pain in abdomen and vomiting and
was referred to radiology department for CT scan.

Plain CT abdomen (Fig. 1A) shows a well defined hyperdense lesion in segment IV
of left lobe of liver. CT in arterial phase (Fig. 1B) shows peripheral discontinuous
nodular enhancement. Portal phase (Fig. 1C) and delayed image (Fig. 1D) show
gradual centripetal filling of the lesion. This lesion represents hemangioma.

It is the most common benign hepatic tumor in clinical practice. It is seen in all
age groups and has a female preponderance. It is detected in the absence of signs
and symptoms in almost all cases. They are lined by a single layer of endothelial
cells and are composed of large vascular channels filled with slowly moving blood.
When the tumor exceeds 4 cm, abdominal pain or discomfort or a palpable mass
may be present. Rupture occurs rarely. Hemangiomas are usually solitary but
are multiple in approximately 10% of cases. Their borders are clear, but they are
not encapsulated. As the hemangioma grows, various degenerative changes are
seen in its center, including old and new thrombus formation, necrosis, scarring,
hemorrhage, and calcification. When degeneration and fibrous changes become
more prominent, the lesion is referred to as a sclerosed hemangioma.
Opinion
Hepatic hemangioma.
A B
C D
Figs 1A to D
Clinical Discussion
Hemangioma occurs more commonly in women. These lesions tend to be
stable, but may enlarge during pregnancy or with estrogen administration.
Hemangiomas are usually asymptomatic and are discovered incidentally. Large
lesions can cause pain, nausea, or vomiting secondary to extrinsic compression
of adjacent bowel, rupture, hemorrhage, or thrombosis. On ultrasound they are
usually homogeneous well-defined hyperechoic masses with posterior acoustic
enhancement. In the background of fatty liver hemangiomas may appear
hypoechoic. Giant lesions can appear heterogeneous due to internal complex
composition. Calcification is rare and is seen usually in the central scar of a
giant hemangioma. On nonenhanced CT, hemangioma is depicted as a well-
demarcated hypodense lesion. It is sometimes round but more often oval or
irregular. Large lesions sometimes have a geographic (irregular) shape. In the
arterial phase of dynamic CT, peripheral discontinuous nodular enhancement
Case 30: Hepatic Hemangioma 105
is seen first, followed by gradual filling toward the center (centripetal filling) and
prolonged enhancement on the equilibrium phase—a pattern characteristic
of hemangioma. The density of hemangiomas reflects the vascular spaces,
and on precontrast, arterial and equilibrium phase dynamic CT, the fact that
the tumor’s density is similar to that of the aorta is useful diagnostic proof. In
small hemangioma containing small sinusoids, dynamic CT may show the
entire tumor to be enhanced from the early phase. The differential includes
hypervascular metastases but these wash out on delayed imaging, and remain
hypodense to the normal hepatic parenchyma whereas hemangiomas remain
hyperdense on delayed images. Large hemangiomas can have an atypical
appearance. Complete fill in is prevented in giant hemangiomas owing to central
fibrous scarring. Calcification and cystic degeneration are also found in some
cases. These lesions need to be differentiated from other lesions with a scar like
fibrolamellar carcinoma, focal nodular hyperplasia, and cholangiocarcinoma.
CASE
31 Focal Nodular
Hyperplasia
CASE
A 45-year-old woman with complaint of pain in right hypochondriac region came
for CT abdomen and pelvis.

Plain CT (Fig. 1A) shows isodense solid mass in liver with hypodense central scar.
On arterial phase (Fig. 1B) the lesion shows mild heterogeneous enhancement.
On portal and venous phases (Figs 1C and D) the hypodense central scar
A B
C D
Figs 1A to D
Case 31: Focal Nodular Hyperplasia 107
shows enhancement. This turned out to be focal nodular hyperplasia on

histopathological examination.

Focal nodular hyperplasia is benign lesion and does not require treatment unless
causing mass effect or pain. On ultrasound the lesions may be hypoechoic,
isoechoic, or slightly hyperechoic. Some lesions may show a hypoechoic halo
surrounding the lesion. This halo most likely represents compressed hepatic
parenchyma or vessels surrounding the lesion. Currently, multirow detector CT
does allow triphasic or even multiphasic dynamic contrast material–enhanced
imaging in relatively shorter scanning times. Typical FNH may have lobulated
contours on CT. On unenhanced CT, the lesions are either hypoattenuating or
isoattenuating to the surrounding liver. In the arterial phase, the lesions become
hyperattenuating due to the homogeneous intense enhancement of the entire
lesion, except the central scar. In the portal and later phases, the lesions become
more isoattenuating with the surrounding liver and the central scar may show
some enhancement. The delayed enhancement of the central scar at CT and
MR imaging relates to increased interstitial space and fluid content with slow
diffusion of contrast material into this space.
Opinion
Focal nodular hyperplasia.
Clinical Discussion
Focal nodular hyperplasia (FNH) is the second most common tumor of the liver,
after hepatic hemangioma. It is a benign hepatic tumor that likely represents
a local hyperplastic response of hepatocytes to a congenital arteriovenous
malformation. Though the use of contraceptives has not been implicated in
the pathogenesis of FNH, their use is associated with the risk of complications
with FNH. Use of contraceptives may be a factor in the development of FNH.
In symptomatic females, hemorrhagic foci or infarctions may occur within the
FNH. The rare complication is spontaneous rupture into the peritoneum. Most
patients are asymptomatic, and FNH is incidentally discovered during cross-
sectional imaging, angiography, radionuclide liver scanning, or surgery. In most
cases, FNH occurs as a solitary lesion (80–95%) measuring less than 5 cm in
diameter, but multiple lesions may occur. Although FNH usually has no clinical
significance, recognition of the radiologic characteristics of FNH is important
to avoid unnecessary surgery, biopsy, and follow-up imaging. Malignant
transformation of FNH has not been observed.
CASE
32 Hepatic Adenoma
CASE
A 40-year-old female patient came with complaints of pain in right hypo
chondriac region and was referred to radiology department for CT scan.

Plain CT (Fig. 1A) shows hyperdense mass in right lobe of liver. There is
homogeneous enhancement in the post contrast image (Fig. 1B) returning to
near isodensity on portal venous and delayed phase image (not shown in image).

The majority of hepatic adenomas contain fat and glycogen. In most cases,
nonenhanced CT depicts this tumor as a hypodense mass. Small tumors appear
A B
Figs 1A and B
Case 32: Hepatic Adenoma 109
homogeneous, but in general, the center shows inhomogeneous attenuation.

Coagulum or thrombus may be noted in relatively early stages of ruptured
hepatic adenoma as areas of hyperattenuation. In tumors with marked fatty
metamorphosis of hepatocytes, a fat-related hypodense area may be seen.
In addition, necrotic foci and scar tissue may appear as hypodense areas.
Calcification is seen within the tumor in some cases. In the arterial phase
of dynamic CT, moderate tumor enhancement is seen. In general they are
well marginated and iso attenuating to liver. On contrast administration they
demonstrate transient relatively homogeneous enhancement returning to
near isodensity on portal venous and delayed phase image. Unfortunately, this
homogeneous enhancement in the late arterial phase is not specific to adenomas,
since small HCC's, hemangiomas as well as hypervascular metastases and FNH
can demonstrate similar enhancement in the arterial phase. Malignant lesions
however have a tendency to loose their contrast faster than the surrounding liver,
so they may become relatively hypodense in later phases. The pathologic and
the imaging differentiation between hepatic adenoma and well-differentiated
HCC are not simple. Significant overlap is noted between the CT appearances
of adenoma, HCC, FNH, and hypervascular metastases, making a definitive
diagnosis based on CT imaging criteria alone difficult and often not possible.
Clinical correlation in such cases is most helpful. In otherwise healthy young
women using oral contraceptives, adenoma is favored.
Opinion
Hepatic adenoma.
Clinical Discussion
A hepatic adenoma is an uncommon benign liver tumor that is hormone induced.
It tends to occur in young women compared to FNH and most of whom have a
history of oral contraceptive use. Patients with hepatic adenoma usually present
with an abdominal mass or recurrent abdominal pain, but the presentation can
also present as acute abdomen owing to tumor rupture. In this case, the patient
may develop shock because of intraperitoneal bleeding. Hepatic adenoma
develops in noncirrhotic livers and is usually solitary but may occur in multiple
forms. Lesions protruding from the liver surface are common, with pedunculated
growth. The tumor border is clear and there is usually no capsule, although part
of the tumor or its entire circumference may be covered by a fibrous capsule in
some cases. In its core, bleeding, necrosis, and scar tissue are seen. They typically
measure 8–15 cm and consist of sheets of well-differentiated hepatocytes.
Adenomas are prone to central necrosis and hemorrhage because the vascular
supply is limited to the surface of the tumor. There is also association of the
tumor and glycogen storage disease. There is a very small risk of transformation
to hepatocellular carcinoma. In general adenomas are resected, both to eliminate
the risk of spontaneous rupture and to confirm the diagnosis. In inoperable cases,
hepatic arterial embolization may have a role.
CASE
33 Hepatic
Angiomyolipoma
CASE
A 50-year-old male patient with pain in right side of abdomen was referred to
radiology department for CT scan abdomen.

Plain CT abdomen (Fig. 1A) shows a well defined hypodense heterogeneous
lesion in right lobe of liver. It has small amount of fatty component. Contrast
enhanced CT scan (Fig. 1B) shows multiple enhancing vessels within this lesion.
Ultrasound (Fig. 1C) shows a well defined lobulated homogenously hyperechoic
lesion in right lobe of liver. These findings are suggestive of angiomyolipoma.

Angiomyolipoma (AML) is an uncommon benign hepatic mass lesion, containing
blood vessel (angioid), smooth muscle (myoid) and mature fat (lipoid)
components. The characteristic findings on any modality are the presence of
both fat and prominent vascularity in the same lesion. If the fatty component
predominates, it resembles lipomas but most of the time, a mixture of usual
solid soft tissue and fatty components will be seen. The drainage vein of AML is
the hepatic vein, and identifying a perfusing vein communicating with hepatic
vein from the tumor center can aid in differentiating AML from fat containing
hepatocellular carcinoma. On USG it appears hetero or homogeneous echogenic
(due to fat content) mass lesion in right hepatic lobe and could be indistinguishable
from hemangioma. Color Doppler sonography shows punctiform or filiform
vascular distribution pattern if the tumor has predominance of angiomatous
tissue. On nonenhanced CT, angiomyolipoma presents as well defined solid
heterogeneous mass containing hypodense areas. Due to presence of the vascular
component, marked enhancement in arterial phase is evident. Drainage is via
the hepatic veins and this is the main differentiating point from fat containing
hepatocellular carcinoma (HCC) that drains mainly in portal vein. It shows
significant enhancement in arterial phase. On portal phase the lesion becomes
hypoattenuated. Hypervascularity and tumor stain is seen on angiography.
Case 33: Hepatic Angiomyolipoma 111
A B
C
Figs 1A to C
Opinion
Hepatic angiomyolipomas.
Clinical Discussion
Most cases of angiomyolipoma are detected incidentally. Angiomyolipomas may
be single or multiple, round or lobulated fat containing mass lesions, seen more
commonly in the right lobe of liver. AMLs are usually found in the kidneys in
patients with tuberous sclerosis. Multiple hepatic AMLs associated with renal
AMLs should raise the suspicion for tuberous sclerosis. AMLs can be difficult to
diagnose on imaging studies as the proportion of vessels, muscle and fatty tissue
vary. Since hepatic AMLs usually follow benign clinical courses, the majority
of the cases can be conservatively treated. Careful follow-up of the tumor even
after the final diagnosis is necessary. We propose that tumor resection is indicated
in the following scenarios: (1) the patients show symptoms; (2) the tumor shows
an aggressive growth; (3) the tumor shows invasive growth into the vessels
evidenced by fine-needle biopsy or imaging studies; (4) the component of the
tumor shows atypical epithelioid pattern, high proliferation activity, and/or p53
immunoreactivity; and (5) a definitive diagnosis cannot be made by imaging and
pathological studies from malignant tumors.
CASE
34 Hepatocellular
Carcinoma
CASE
A 60-year-old male with right upper quadrant pain was referred to radiology

In Figure 1(A) plain CT abdomen shows mass in liver; (B) Arterial phase CT
shows enhancement in the mass. A hypodense scar is also seen (arrow); (C)
Venous phase CT shows enhancement in the mass as well as the scar (arrow); (D)
In delayed phase CT there is persistence of contrast in the scar. This differentiates
it from fibronodular hyperplasia.

Hepatocellular carcinoma (HCC) is the most common malignancy of liver.
The CT appearance of HCC is variable and depends not only on the size,
vascularity, histologic composition, and growth pattern of the tumor, but
on the CT technique used, most HCCs are hypoattenuating on precontrast
images, but a significant minority is isoattenuating to liver parenchyma prior
to IV contrast medium administration. Some of the isoattenuating lesions can
be identified on unenhanced images by the presence of a hypoattenuating
rim, which represents the tumor capsule, or by a focal bulge in the contour of
the liver. On rare occasions, the mass may extend exophytically beyond the
confines of the liver and stimulate an extra hepatic mass. Areas of necrosis or fatty
metamorphosis appear as hypoattenuating foci within the mass, whereas recent
hemorrhage may produce areas of hyper attenuation. Calcification is identified
in approximately 5–10% of HCCs. Precontrast images are important to identify
lesions that are hyper attenuating prior to contrast medium administration
(e.g. from hemorrhage or iron deposition) to avoid mistaking the increased
attenuation on post contrast images as lesion enhancement. On delayed images,
areas of fibrosis, including the capsule and septa, usually demonstrate prolonged
enhancement. Diffusely infiltrating HCCs are best seen during the late hepatic
Case 34: Hepatocellular Carcinoma 113
A B
C D
Figs 1A to D
arterial phase as ill-defined, vaguely nodular areas of hyper attenuation without

discrete margins, but such lesions may be difficult to detect during any phase of
enhancement. Contrast-enhanced CT is capable of demonstrating both vascular
invasion and arterioportal shunting associated with HCC. Portal or hepatic vein
tumor thrombus appears as a hypoattenuating filling defect within the expanded
vascular lumen. Intravascular tumor thrombus may show homogeneous or
streaky contrast enhancement, distinguishing it from bland thrombus. Signs of
arterioportal shunting include early or prolonged enhancement of the portal vein
and transient segmental, lobar or wedge-shaped hyper enhancement peripheral
to the tumor. Hepatocellular carcinoma may cause biliary ductal dilation by
compressive effect or, less commonly, by direct ductal invasion. Lesions that
occur in noncirrhotic livers tend to be larger and are more frequently solitary
than those occurring in cirrhotic livers.
Opinion
Hepatocellular carcinoma.
Clinical Discussion
Hepatocellular carcinoma is the fifth most common cancer in the world.
The various risk factors associated are infection with hepatitis virus infection
Hepatitis C, B, alcoholism and aflatoxin ingestion. The gross features of HCC

are classified into five major types: (1) small nodular with indistinct margin;
(2) simple nodular; (3) simple nodular with extra nodular growth; (4) confluent
multinodular; and (5) infiltrative. Patients with small, localized tumors usually
have no HCC-related symptoms. In the advanced terminal stage patients,
upper abdominal mass, abdominal pain, general malaise, anorexia, abdominal
fullness, weight loss, jaundice, ascites, edema, and gastrointestinal bleeding are
commonly present. The macro nodular cirrhosis is most often associated with
HCC rather than micro nodular HCC. Intraperitoneal bleeding (rupture) is one
of the most serious complications of advanced tumors, although it may occur in
smaller lesions as well. Most HCCs develop in cirrhotic livers. Therefore, it has
become possible to detect small, early-stage HCC in these high-risk patients. If
the lesion is small then resection is possible (partial hepatectomy) and may result
in cure. Liver transplantation is also a curative option.
CASE
35 Hepatic Metastases
CASE
A 60-year-old male, known case of mucinous carcinoma of transverse colon
came for CT abdomen and pelvis.

Figure 1A contrast CT abdomen shows differential enhancement in the left
lobe and an ill-defined low density mass which was hepatic metastases from
mucinous carcinoma of transverse colon. Enlarged liver shows multiple round
hypodense metastatic lesions in both the lobes (Figs 1B to D). Those of which are
more hypodense in center indicate onset of necrosis.

CT is the study of choice for evaluating liver metastases. On ultrasound, hepatic
metastases appear as well defined rounded hypoechoic lesions. Cystic, calcified,
infiltrative and echogenic appearances are all possible. In bull's eye, or target
metastases, the halo is most probably related to a combination of compressed
normal hepatic parenchyma around the mass and a zone of cancer cell
proliferation. Most liver metastases are hypovascular compared with surrounding
parenchyma and therefore most lesions appear either hypoattenuating or
isoattenuating relative to the surrounding normal liver on unenhanced CT.
Hypovascular lesions are more easily detected using contrast-enhancement.
On contrast-enhanced scans, liver metastases may display slight peripheral
enhancement with a hypoattenuating center. The margin of the lesions can
vary from well defined to ill defined. Hyperattenuating lesions are uncommon.
On the portal venous phase of scanning, some highly vascular primary tumors
such as renal cell carcinomas, pancreatic islet cell tumors, pheochromocytomas,
melanomas, and breast carcinomas, may appear as isoattenuating to normal liver.
Differential diagnosis include, multiple hemangiomas which can be mistaken for
metastases, focal nodular hyperplasia (FNH) may look like vascular metastases.
A B
C D
Figs 1A to D
Focal fatty sparing in a diffusely fatty liver can also look like metastases. MRI is
usually used as problem-solving rather than a primary technique in the diagnosis
of liver metastases. Most liver tumors, benign or malignant, appear as hypo
intense lesions on T1-weighted images and hyper intense lesions on T2-weighted
images. Gadolinium-enhanced MRI improves both the detection of focal liver
masses and the differentiation of benign from malignant lesions. Multiple hepatic
nodules of different sizes within the liver are nearly always due to metastases.
Opinion
Hepatic metastases.
Clinical Discussion
Metastasis is the most common neoplasm in an adult liver. The liver is a principle
target for gastrointestinal malignancies. The most common primary sites for
metastatic lesions to the liver in adults are colon, stomach, pancreas, breast,
lung, and eye. In children, most common primary sites for metastatic lesions to
the liver are neuroblastoma, Wilms’ tumor, and leukemia. Most liver metastases
are multiple. Multiple lesions often vary in size suggesting tumor seeding which
occurs episodically. About half of patients with liver metastases have clinical
Case 35: Hepatic Metastases 117
signs of hepatomegaly or ascites. Liver function tests tend to be insensitive and

nonspecific. Almost all tumors that metastasize to the liver also metastasize
elsewhere at the same time. Some tumors, such as colon carcinoma, carcinoid,
and hepatocellular carcinoma (HCC) may present with lesions confined to
the liver. The pathology of metastatic deposits in the liver closely resembles
the primary tumor, i.e. they are usually as vascular as their primary tumors. In
general, most metastases are hypovascular, but some primaries characteristically
have hypervascular metastases. The most common primary for hypervascular
metastases are carcinoids, leiomyosarcomas, neuroendocrine tumors, renal
carcinomas, thyroid carcinomas, choriocarcinomas occasionally pancreas,
ovary, or breast carcinomas. Blood flow increases in all metastases, even
hypovascular tumors. Neovascularity, vascular encasement, and arteriovenous
shunting are rare. Large metastases can outgrow their blood supply leading to
central necrosis.
CASE
36 Hepatoblastoma
CASE
A 12-year-old male child with history of anorexia, vomiting and jaundice was
referred to the department of radiology for CT abdomen and pelvis.

Figure 1 contrast enhanced CT scan abdomen is showing heterogeneous large
mass involving left lobe of liver with areas of necrosis and hemorrhage. There
Fig. 1
Case 36: Hepatoblastoma 119
is hypodense area with calcification in right lobe of liver. This turned out to be
hepatoblastoma on histopathological examination.

It is the most common malignant liver tumor in early childhood. On ultrasound,
hepatoblastomas appear as predominantly echogenic soft tissue mass. In larger
tumors heterogeneity and variable echogenicity is common. Even when large,
they tend to be relatively well defined. Intra-lesional calcifications may be visible
as areas of shadowing. On CT usually hepatoblastoma appears as a well defined
heterogeneous mass, which is usually hypoattenuating compared to surrounding
liver. Frequently there are areas of necrosis and hemorrhage. Chunky, dense
calcifications may also be seen. CT is also able to evaluate the lungs for metastases
and for nodal enlargement. MRI is superior to CT in defining tumor margins,
vessel involvement and adenopathy. On T1WI it is generally hypo intense. On
GAD, it shows heterogeneous enhancement. On T2WI it is generally hyper
intense compared to liver with areas of necrosis and hemorrhages are common.
Opinion
Hepatoblastoma.
Clinical Discussion
Hepatoblastoma primarily affects children from infancy to about 5 years of age.
It occurs more frequently in children who were born very prematurely (early)
with very low birth weights. Hepatoblastoma is a rare tumor that originates in
cells in the liver. Most hepatoblastoma tumors begin in the right lobe of the liver.
Hepatoblastoma cancer cells also can spread to other areas of the body. The most
common site of metastasis is the lungs. Although the exact cause of liver cancer
is unknown, there are a number of genetic conditions that are associated with
an increased risk for developing hepatoblastoma. They include: (1) Beckwith-
Wiedemann syndrome: this syndrome is characterized by a combination of
Wilms’ tumor, kidney failure, genitourinary malformations and gonadal (ovaries
or testes) abnormalities; (2) Familial adenomatous polyposis and; (3) Gardner
syndrome: this is a group of rare inherited diseases of the gastrointestinal tract;
(4) Fetal alcohol syndrome; (5) Prematurity and low fetal birth weight; (6) Glycogen
storage disease. Children who are exposed to hepatitis B infection at an early age,
or those who have biliary atresia, are also at increased risk for developing liver
cancer. The signs and symptoms of hepatoblastoma often depend on the size of
the tumor and whether it has spread to other parts of the body. Symptoms may
include a large mass in the abdomen, weight loss, decreased appetite, vomiting,
jaundice, itchy skin and anemia.
CASE
37 Intrahepatic
Cholangiocarcinoma
CASE
A 55-year-old male patient came with history of jaundice and pruritus since 15
days and was referred to radiology department for CT scan.

Venous phase CT (Fig. 1A) shows patent left portal vein and dilated
intrahepatic biliary radicals. No mass is seen. Delayed phase CT (Fig. 1B)
shows a vague minimally enhancing mass that was subsequently proven to be
a cholangiocarcinoma. Contrast CT (Fig. 1C) in another patient shows dilated
intrahepatic biliary radicals in left lobe. No obvious mass is seen. Delayed CT
(Fig. 1D) in same patient shows subtle enhancement in mass and thrombosed
portal vein.

Cholangiocarcinoma is a malignancy which originates from the intra or extra-
hepatic bile duct epithelium. Cholangiocarcinoma is divided into 3 geographic
regions—Intrahepatic (least common), Extrahepatic Perihilar (most common,
called the Klatskin tumor) and Distal Extrahepatic (Located from the upper border
of the pancreas to the ampulla). 95% are Ductal adenocarcinoma, the remainder
are squamous cell carcinoma. Intrahepatic cholangiocarcinoma is a carcinoma
arising from any portion of the intrahepatic bile duct epithelium. It is the second
most common primary intrahepatic malignancy after hepatocellular carcinoma.
Many patients present with unresectable or metastatic disease. Preliminary
evaluation with positron emission tomography (PET) has shown promise in
diagnosing underlying PSC. Small lesions (i.e. <1 cm) have been demonstrated.
PET is accurate for detecting nodular carcinomas, but the sensitivity diminishes
for infiltrating lesions. PET should be interpreted with caution in patients with
PSC and stents in place. PET/CT has been shown to be valuable in detecting
unsuspected distant metastasis.
Case 37: Intrahepatic Cholangiocarcinoma 121
A B
C D
Figs 1A to D
Opinion
Intra-hepatic cholangiocarcinoma.
Clinical Discussion
Cholangiocarcinoma is a biliary duct malignancy that may arise in the liver or in an
extrahepatic biliary location. The common manifestation are jaundice, pruritus,
weight loss and abdominal pain. The prevalence is higher in men than women.
The sixth decade of life is the most common time of presentation. Certain entities
have been associated with cholangiocarcinomas. These include infections (liver
flukes), chemicals (thorotrast), ulcerative colitis, primary sclerosing cholangitis
and Caroli disease. Initially, an ultrasound or CT may be ordered in symptomatic
patients. On ultrasound (USG), biliary duct dilatation is the most common
finding. The ability to delineate a mass is very variable on USG. Intrahepatic
cholangiocarcinomas can be difficult to depict on CT. If seen, the mass is round
or oval with segmental biliary dilatation. Delayed contrast enhancement is a
typical feature which can help in differentiation from hepatocellular carcinoma.
MRI has become the imaging modality of choice. It allows superior evaluation
of the liver parenchyma. The mass appears hypointense on T1 weighted images.
On T2 images, most masses are isointense or mildly hyperintense. Concentric
enhancement is present. Delayed enhancement is a typical feature. Using
MRCP, the biliary ducts can be evaluated. MR angiography is useful for staging
purposes to exclude vascular involvement. ERCP helps demonstrate the site of

biliary obstruction (benign and malignant appearing strictures) using retrograde
injection of contrast into the biliary system. Brushings and biopsies can be
obtained during the procedure. Stenting as a palliative measure can be offered
to help relieve the degree of obstruction. Cholangiocarcinomas tend to grow
slowly and to infiltrate the walls of the ducts, dissecting along tissue planes. Local
extension occurs into the liver, porta hepatis, and regional lymph nodes of the
celiac and pancreaticoduodenal chains. Life-threatening infection (cholangitis)
may occur that requires immediate antibiotic intervention and aggressive biliary
drainage.
CASE
38 Extrahepatic
Cholangiocarcinoma
CASE
Patient came with complain of pain in abdomen, clay colored stool, dark urine
since 1 month. Patient was subjected to CT scan abdomen.

The intra- and extrahepatic biliary tract and the gallbladder are distended. An
enhancing solid mass is seen in the distal end of common bile duct. The biopsy
confirmed it as cholangiocarcinoma (Figs 1A to C).
B C
Figs 1A to C

Cholangiocarcinoma is neoplasm originating from intra and extrahepatic bile
duct epithelium. Cholangiocarcinomas are classified according to their anatomic
location as intrahepatic and extrahepatic. The extrahepatic type including
cancers involving the confluence of the right and left hepatic ducts accounts for
80–90% and the intrahepatic type for 5–10% of all cholangiocarcinoma.
Opinion
Extrahepatic cholangiocarcinoma.
Clinical Discussion
Cholangiocarcinomas are malignancies of the biliary duct system that may
originate in the liver and extrahepatic bile ducts, which terminate at the
ampulla of Vater. Most cholangiocarcinomas remain clinically silent until the
advanced stages. Once patients become symptomatic, the clinical presentation
is dominated by location of tumor. Symptoms of cholangiocarcinoma include
jaundice, clay-colored stools, bilirubinuria (dark urine), pruritus, weight loss,
and abdominal pain. Jaundice is the most common manifestation of bile duct
cancer and, in general, is best detected in direct sunlight. The obstruction and
subsequent cholestasis tend to occur early if the tumor is located in the common
bile duct or common hepatic duct. Pruritus usually is preceded by jaundice.
Weight loss is a variable finding and may be present in one third of patients at
the time of diagnosis. Abdominal pain is relatively common in advanced disease
and often is described as a dull ache in the right upper quadrant. Complications
include infection, liver failure and spread of tumor to other organs. To afford
a chance at cure, complete surgical excision is needed. However, only 10% of
patients present early enough to be afforded curative resection. Nonsurgical
therapies include stenting and drainage to help improve obstructive symptoms.
Chemoradiation therapy is used successfully as adjuvant therapy and to help
reduce tumor size prior to surgery. The poorest survival rates are for those
individuals with nonresectable disease with palliative stent placement.
CASE
39 Transient Hepatic
Attenuation Difference
CASE
A 45-year-old male patient was referred to radiology department for CT scan
abdomen.

Figures 1A to D transient hepatic attenuation difference (THAD) is an attenuation
difference of the liver appearing during bolus-enhanced dynamic CT usually not
corresponding to any mass. It is generally seen as an area of high attenuation on
the hepatic arterial phase image (A and B) that returns to normal attenuation on
the portal venous phase (C and D) images.

The liver has a dual blood supply (70% portal vein, 30% hepatic artery) with
compensatory relationships: arterial flow increases when portal flow decreases.
Transient hepatic attenuation difference (THAD) is an attenuation difference of
the liver appearing during contrast enhanced dynamic CT and not corresponding
to mass.
Opinion
Transient hepatic attenuation difference.
Clinical Discussion
Transient hepatic attenuation difference (THAD) is generally seen as an
area of high attenuation on the hepatic arterial phase that returns to normal
attenuation on the portal venous phase images. According to morphology,
they can be divided into four groups (a) Lobar multisegmental; (b) Sectorial;
(c) Polymorphous; (d) Diffuse. (a) Lobar: They involve almost all segments
of one hepatic lobe and are usually caused by an increase in arterial inflow
A B
C D
Figs 1A to D
and therefore follow arterial distribution. They usually occur when a

hypervascular focal lesion like hepatocellular carcinoma, hemangioma, focal
nodular hyperplasia or hypervascular metastases leads to hyperperfusion of
the surrounding parenchyma (“siphoning effect”) in the absence of portal
hypoperfusion. They do not show a triangular shape or a straight border sign;
(b) Sectorial: They follow portal vein branches, are either wedge or fan-shaped
with at least one straight border sign (a clear separation line from the normally
attenuating parenchyma) when not associated with focal lesions. They can be
caused by portal or hepatic vein thrombosis, long-standing biliary obstruction,
or an arterioportal shunt. In such cases, THADs are always wedge-shaped with
a straight border sign; (c) Polymorphous: Usually does not follow the portal vein
branches and show various shapes and sizes without a straight border sign;
(d) Diffuse: Differences involve the entire hepatic parenchyma and may assume
a patchy, central peripheral or peribiliary pattern on the basis of location of
the portal blockade. Right heart failure and Budd-Chiari syndrome results in
a generalized central lobular enhancement during the arterial phase. When
obstruction takes place at the level of portal trunk, as in portal vein thrombosis
portal flow remains adequate for central zones of liver but not for the peripheral
ones. The arterial response produces enhancement of the peripheral subcapsular
hepatic parenchyma with relative hypodensity of the central perihilar area. This
CT pattern is called a “central-peripheral” phenomenon.
SECTION
10
Gallbladder
40. Choledochal Cyst
41. Acalculus Cholecystitis
42. Acute Calculus Cholecystitis
43. Emphysematous Cholecystitis
44. Choledocholithiasis
45. Porcelain Gallbladder
46. Carcinoma Gallbladder
CASE
40 Choledochal Cyst
CASE
A 1-year-old female patient with history of jaundice was referred to radiology
department for CT scan abdomen.

Figures 1A to E: (A) US shows the dilated, tortuous and ectatic left hepatic duct;
(B) CECT demonstrates a large cyst lying medial to gallbladder; (C) CECT shows
the dilated, tortuous and ectatic left hepatic duct (similar to USG Figure A) with
minimal dilatation of intrahepatic biliary radicles; (D) MRI cholangiography
shows the cyst medial to the gallbladder with dilated left hepatic duct;
(E) Photograph of resected specimen shows choledochal cyst, gallbladder and
the cystic duct.
A B C
D E
Figs 1A to E
130 Section 10: Gallbladder

Choledochal cysts are unusual congenital anomalies of the biliary tree
characterized by cystic dilation of the bile ducts. An anomalous junction of
the common bile duct and pancreatic duct proximal to the sphincter of Oddi
(outside of the duodenal wall) results in a long common channel of the common
bile duct and the pancreatic duct. Because of the long common channel,
pancreatic enzymes reflux into the common bile duct when the sphincter of Oddi
is contracted. This leads to injury of the biliary wall and results in dilation. This is
the major etiologic factor in the development of choledochal cysts.
Opinion
Choledochal cyst.
Clinical Discussion
Choledochal cysts are three times more common in females than males and usually
present in childhood. Children or adults with choledochal cysts often present
with abdominal pain, jaundice, or a palpable mass The Todani classification
system arranges them into 5 basic categories. Type I choledochal cyst is a focal,
saccular or fusiform dilation of the common bile duct, not extending into the
intrahepatic biliary ducts. Type II choledochal cyst is a true diverticulum of the
common bile duct. Type III choledochal cyst is also called a choledochocele. It
is a dilation of the most distal intraduodenal portion of the common bile duct.
Type IV choledochal cysts have multiple intra and extrahepatic biliary duct cysts.
Type V choledochal cysts refers to Caroli's disease in which there is saccular
dilation of the intrahepatic biliary ducts with sparing of the extrahepatic ducts.
In infancy, choledochal cysts can lead to biliary obstruction. USG shows a cystic
extrahepatic mass. CT shows a dilated cystic mass with distinct walls that is
separate from the gallbladder and may appear thickened if there is history of
chronic cholangitis. MRI/MRCP shows a large fusiform or extrahepatic mass
with strong signal on fluid sensitive sequences and can usually identify the
anatomy of the ductal structures. NM hepatobiliary scan shows photopenic
defect during initial images with later filling and stasis of radiotracer within cysts.
Cholelithiasis, choledocholithiasis, cystolithiasis, cholangitis, biliary cirrhosis,
portal hypertension and malignancy are all complications of choledochal cysts.
The risk of malignancy increases with age. Treatment is surgical excision with
Roux-en-Y hepaticojejunostomy.
CASE
41 Acalculus Cholecystitis
CASE
A middle age male presented to the department of radiology with pain in upper
right quadrant of abdomen with nausea and vomiting since last 3 days.

CT abdomen (Figs 1A and B) shows thickened edematous gallbladder wall which
reveals nodular enhancement. There is stranding of adjacent fat. No evidence of
calculus noted. This is suggestive of acalculus cholecystitis.

Acalculus cholecystitis is an acute necroinflammatory disease of the gallbladder
with absence of gallbladder calculi. The usual finding on imaging studies is a
distended acalculous gallbladder with thickened walls more than 3–4 mm with
or without pericholecystic fluid. The diagnosis of acute acalculous cholecystitis
with CT requires that 2 major diagnostic criteria be met or, alternatively, that
1 major criterion and 2 minor criteria be met. These criteria are as follows:
A B
Figs 1A and B
Major Criteria
• Gallbladder wall thickening greater than 3 mm
• Subserosal halo (i.e. gallbladder wall edema)
• Pericholecystic fatty inflammation
• Pericholecystic fluid (without ascites or hypoalbuminemia)
• Mucosal sloughing
• Intramural gas.
Minor Criteria
• Gallbladder distention (>5 cm transverse)
• High-attenuation bile (sludge).
Opinion
Acute acalculus cholecystitis.
Clinical Discussion
Acalculous cholecystitis is typically seen in patients who are hospitalized and
critically ill, though it may also be seen in the outpatient setting. It is a potentially
fatal form of acute cholecystitis that usually occurs in critically ill patients. The
disease may often go unrecognized due to the complexity of the patient’s medical
and surgical problems. It has also been found in association with total parenteral
nutrition, mechanical ventilation, and the use of narcotic analgesics, as well as
in major cardiovascular disorders, complicated diabetes mellitus, autoimmune
disease, AIDS and bile stasis. Complications include perforation or rupture.
Ischemia/reperfusion injury to the gallbladder is a central pathogenic feature.
CASE
42 Acute Calculus
Cholecystitis
CASE
A middle age man presented with complaints of abdominal pain for 4 days which
was localized to epigastric region with radiation to right upper quadrant.
Radiological Finding on CT Examination

CT scan shows multiple hyperdense calculi of varying sizes in gallbladder lumen.
There is pericholecystic collection (Fig. 1).
In another case CT images show distended gallbladder (GB) with multiple
hyperdense calculi and thickened wall especially in the region of fundus
Fig. 1
A B
Figs 2A and B
associated with soft tissue stranding in the adjacent greater omental fat in a case
of cholelithiasis with acute cholecystitis (Figs 2A and B).

Cholecystitis is inflammation of gallbladder. It may be associated with gallstones
or, less often, without gallstones (acalculous cholecystitis). It can be acute or
chronic. Acute calculus cholecystitis results from gallbladder stones. It occurs
when a stone blocks the cystic duct, which carries bile from the gallbladder.
Plain X-ray abdomen may show radio-opacities in right hypochondriac region.
Ultrasound shows an obstructing gallstone, dilatation of the GB, a positive
sonographic Murphy's sign (i.e. pain elicited by pressure over the sonographically
located gallbladder), pericholecystic fat inflammation or fluid and hyperemia of
the GB wall at power Doppler.
CT scan findings include gallstones within the GB, the cystic duct, or both;
more than 3 mm of focal or diffuse thickening of the GB wall in a noncontracted
GB; indistinct liver-GB interface; fluid in the GB fossa in the absence of ascites;
enlargement of the GB, with the transverse diameter measuring more than 5 cm;
infiltration of the surrounding fat; increased bile attenuation, caused by biliary
sludge.
Opinion
Acute calculus cholecystitis.
Clinical Discussion
Acute calculus cholecystitis is a common disease. A typical presentation is several
hours of progressively worsening right upper quadrant pain, followed by nausea
Case 42: Acute Calculus Cholecystitis 135
and vomiting. Often, the patient has had repeated similar episodes in the past.
These symptoms are caused by gallstone lodging in the neck of the GB or the cystic
duct, resulting in biliary stasis. Although the cause is not believed to be primarily
infectious, after the stone has caused biliary obstruction, superinfection is a
common occurrence without treatment. If the diagnosis is suspected clinically,
ultrasound is the imaging modality of choice.
CASE
43 Emphysematous
Cholecystitis
CASE
A 63-year-old diabetic male presented to the department of radiology with history
of right hypochondriac pain.

Contrast enhanced axial CT images at the level of pancreas show presence of
air in the gallbladder wall and lumen, common bile duct and pancreatic duct
(Fig. 1).
Fig. 1
Case 43: Emphysematous Cholecystitis 137

Emphysematous cholecystitis is an acute infection of the gallbladder wall caused
by gas-forming organisms that is considered a surgical emergency. Usually, the
diagnosis is made by the radiographic presence of air within the wall or lumen
of gallbladder. On USG intramural gas appears as an arclike echogenic interface
with posterior reverberation artefact. CT demonstrates emphysematous
changes in the gallbladder wall that are diagnostic of this condition and is highly
sensitive for tiny bubbles of air which may not be seen on ultrasonography. CT
is considered the most sensitive and specific imaging modality for identifying
gas within the gallbladder lumen or wall. The presence of pneumoperitoneum
indicates perforation. CT scanning can also provide precise information
regarding the location and extent of air and fluid collections, such as extension
into the pericholecystic tissues and the hepatic ducts. The radiologic differential
diagnosis is that presence of gas in the biliary tree, which may be due to a biliary-
enteric fistula, following ERCP; or may be due to cholangitis caused by gas-
forming organisms.
Opinion
Emphysematous cholecystitis.
Clinical Discussion
Emphysematous cholecystitis is an uncommon, insidious, and rapidly progressive
form of acute cholecystitis, characterized by early gangrene, perforation of the
gallbladder and high mortality. Most of the patients are males between 50 and 70
years of age and have underlying diabetes mellitus and peripheral atherosclerotic
disease. The most common clinical complaints initially are right upper quadrant
pain and fever. The insidious nature of this disease may mislead the clinician, and
the patient may unsuspectingly rapidly deteriorate with sudden cardiovascular
collapse and even death. Prompt surgical cholecystectomy, with excision of the
gallbladder is the mainstay of treatment because of the observation that septic
shock and death progresses quickly with this disease process, particularly in the
elderly and diabetic individuals.
CASE
44 Choledocholithiasis
CASE
A 48-year-old male patient presented to the department of radiology with
history of pain in right side of upper abdomen since one month with yellowish
discolouration of skin since 10 days for CT abdomen.

Plain CT images show massive dilatation of intrahepatic biliary radicals and
common bile duct (Figs 1A and B) secondary to an intraluminal calculus in distal
common bile duct (Figs 1C and D).
A B
C D
Figs 1A to D
Case 44: Choledocholithiasis 139
Comment and Explanation

Cholesterol or black pigment stones are more likely to form in the gallbladder,
while almost all brown pigment stones form in the bile duct. A classic ultrasound
finding with calcified stones is posterior acoustic shadowing, however, the
appearance of gallstones is based upon the location, size, and composition. The
best imaging tools to evaluate choledocholithiasis is ultrasound or magnetic
resonance cholangiopancreatography (MRCP). Conventional CT is useful for
detecting central round dense stone, target sign, surrounding hypodense mucosa,
calcified stone, hypodense bile surrounding calculus like a crescent, biliary
dilatation. MRCP shows filling defects within biliary tree on T2W images. There
are narrow differential for CBD calculus and depend on modality. Differentials
include cholangiocarcinoma, carcinoma of ampulla of Vater, pancreatic
carcinoma; parasites. Artefacts like air bubbles, susceptibility artefacts, flow
voids, vascular impression, and sphincter contractions can be mistaken as CBD
calculi.
Opinion
Choledocholithiasis.
Clinical Discussion
Stones within the bile duct may form either in situ or pass from the gallbladder,
and when recurrent tend to be pigment stones. Stone in bile duct does not cause
discomfort to patient but when blockage becomes severe patient may experience
abdominal pain in right upper abdomen, fever, nausea, vomiting and loss of
appetite. When a gallstone is stuck in the bile duct, the bile can become infected.
The presence of parasitic infection of Ascaris lumbricoides or Clonorchis sinensis
may result in formation of CBD stone due to ductal inflammation, proximal
stasis. It can move into the ductal system and then into the liver. It can become
a life-threatening infection. Possible complications include infection, biliary
cirrhosis, cholangitis, pancreatitis, gallbladder carcinoma, gallbladder polyp,
primary sclerosing cholangitis, and porcelain gallbladder.
CASE
45 Porcelain Gallbladder
CASE
A 40-year-old male patient with history of intense pain in the upper-right side of
the abdomen with nausea and vomiting, was referred to radiology department
for CT abdomen.

Plain CT abdomen (Fig. 1A) shows hyperdense appearance in the dependent
part of gallbladder due to multiple small calculi. There is calcification of the wall
(porcelain gallbladder). In right lateral decubitus position the calculi have shifted
to the now dependent position (Fig. 1B).
Comment and Explanation

Cholelithiasis is defined as calculi in gallbladder. Porcelain gallbladder means the
wall of the gallbladder has been calcified to hard bluish white texture resembling
A B
Figs 1A and B
Case 45: Porcelain Gallbladder 141
porcelain ceramic. This medical condition primarily results from a chronically

inflamed organ (Figs 1A and B).
Opinion
Cholelithiasis in porcelain gallbladder.
Clinical Discussion
Most people with cholelithiasis have no symptoms at all. A minority of patients
with gallstones develop symptoms: severe abdominal pain, nausea and vomiting,
and complete blockage of the bile ducts that may pose the risk of infection.
Extensive calcium encrustation of the gallbladder wall has been termed calcified
gallbladder, calcifying cholecystitis, or cholecystopathia chronica calcarea. The
term “porcelain gallbladder” has been used to emphasize the blue discoloration
and brittle consistency of the gallbladder wall at surgery. When complete wall
of gallbladder is calcified it is called porcelain gallbladder. Calcification in the
right upper quadrant of the abdomen has several causes. Porcelain gallbladder
must be differentiated from large solitary calcified gallstones, which are seldom
as large as porcelain gallbladders.
Calcification of the gallbladder wall or milk-of-calcium bile may have identical
appearances on sonograms; therefore, sometimes plain radiography is important
in distinguishing these entities.
Emphysematous cholecystitis can mimic porcelain gallbladder on
sonograms; however, their clinical presentation is distinct from that of porcelain
gallbladder. Complications include cholecystitis, Mirizzi syndrome, and
cholecystocholedochal fistula and gallstone ileus.
CASE
46 Carcinoma Gallbladder
CASE
A 70-year-old male with history of pain in abdomen, nausea and vomiting was

Contrast enhanced CT abdomen (Fig. 1) shows a lobulated soft tissue density
enhancing lesion seen in lumen extending to the neck of the gallbladder (white
arrow). Enlarged necrotic lymph nodes are seen in precaval and retrocaval
regions (black arrows).
Fig. 1
Case 46: Carcinoma Gallbladder 143
A B
Figs 2A and B
In another case CECT abdomen (Figs 2A and B) show a large heterogeneously

enhancing lesion replacing the entire gallbladder and infiltrating into the
adjacent liver parenchyma.

Carcinoma of gallbladder is the most common malignant tumor of biliary tract.
Ultrasound shows heterogeneous mass in sub hepatic space replacing the GB.
Gallbladder carcinoma may be seen as an intraluminal fungating mass with
diffuse thickening of wall with or without cholelithiasis. The tumor mass may
contain low-attenuation areas of necrosis. Use of contrast-enhanced CT is
extremely helpful for distinguishing complicated cholecystitis from gallbladder
carcinoma. The CT demonstration of associated lymphadenopathy, soft-tissue
extension into the liver, and evidence of hematogenous metastases favors
the diagnosis of gallbladder carcinoma. Additional CT findings can include
extrahepatic biliary duct obstruction due to metastasis to pericholedochal and
superior pancreaticoduodenal nodes, encasement of common bile duct, biliary
dilatation and involvement of adjacent structures like liver. The most common
mode by which gallbladder carcinoma spreads to adjacent organs is direct
extension, followed by lymphatic and vascular extension. Intraperitoneal and
intraductal spread of tumor also occur. The liver is the organ most frequently
involved by direct contiguous spread, followed by the colon, duodenum and
pancreas. Without other primary or secondary tumors, local recurrence or distant
metastases are visualized with positron emission tomography on the basis of
increased fluorodeoxyglucose uptake.
Opinion
Gallbladder carcinoma.
Clinical Discussion
The clinical features of gallbladder carcinoma include right upper quadrant pain,
anorexia, weight loss, and jaundice. Often, the patient’s condition is clinically
indistinguishable from that seen in acute or chronic cholecystitis. Although
the presence of cholelithiasis is not correlated with gallbladder carcinoma, the
prevalence of cholelithiasis in cases of gallbladder carcinoma has been previously
reported to be in the range of 80–90%. Porcelain gallbladder is complicated by
gallbladder carcinoma in up to 25% of cases. Over 90% of cases of gallbladder
cancer are adenocarcinoma. Unfortunately, due to the largely asymptomatic
nature of these tumors, presentation is typically late with the majority of tumors
being large, unresectable, with direct extension into adjacent structures or distant
metastases present at diagnosis. Curative resection is only possible for localized
early disease, which is usually found incidentally.
SECTION
11
Pancreas
47. Acute Pancreatitis
48. Pancreatic Pseudocyst
49. Necrotizing Pancreatitis
50. Periampullary Carcinoma with Metastases
CASE
47 Acute Pancreatitis
CASE
A 40-year-old male with severe epigastric pain and raised serum lipase levels was

CT abdomen reveals bilateral pleural effusions (Fig. 1A) and bulky edematous
pancreas (Fig. 1B). Thin walled encapsulated fluid collections are seen in the
region of stomach bed, anterior to pancreas extending inferior to tail of pancreas
and anterior to Gerota’s fascia (Figs 1B to D).
A B
C D
Figs 1A to D
148 Section 11: Pancreas

Acute pancreatitis is defined as an acute inflammatory process of the pancreas
with variable involvement of other regional tissues or remote organ systems.
Contrast enhanced CT is the standard imaging modality for evaluating acute
pancreatitis and its complications. Intra-abdominal fluid collections and
collections of necrotic tissue are common in acute pancreatitis. In the early
stage these collections do not have a wall or capsule. Preferred locations are the
omental bursa and the retroperitoneal space (anterior and posterior pararenal
space).These collections are the result of the release of activated pancreatic
enzymes namely lipase and amylase which cause necrosis of the surrounding
tissues. Abnormalities seen in pancreas include focal or diffuse parenchymal
enlargement, indistinctness of the margins of the gland due to inflammation
and surrounding retroperitoneal fat stranding. Infected necrosis of pancreatic
parenchyma and/or extrapancreatic fatty tissue can also be seen. Air bubbles are
seen in patients with infected necrosis.
Balthazar score is used in CT severity index (CTSI) for grading of acute
pancreatitis. It is as follows:
• Normal pancreas: Score 0
• Enlargement of pancreas: Score 1
• Inflammatory changes in pancreas and peripancreatic fat: Score 2
• Ill defined single fluid collection: Score 3
• Two or more poorly defined fluid collections: Score 4
The extent of pancreatic necrosis is graded as follows:
• Score 0: None
• Score 2: Less than/equal to 30%
• Score 4: > 30–50%
• Score 6: > 50%
Opinion
Acute pancreatitis.
Clinical Discussion
Gallstones and alcohol abuse are the most common causes of acute pancreatitis.
Other causes include blunt trauma to the abdomen, drug-induced, infectious
etiologies (e.g. mumps, cytomegalovirus) and congenital anomalies like pancreas
divisum. Local complications of acute pancreatitis include fluid collections,
pseudocyst formation, abscess, pancreatic necrosis and hemorrhage. Pseudocyst
is a collection of pancreatic juice enclosed by a wall of fibrous tissue. It requires 4
or more weeks to develop and there is often communication with the pancreatic
duct. Pancreatitis and pseudocysts can cause a number of vascular complications
such as vascular occlusion, pseudoaneurysm and spontaneous hemorrhage.
Pseudoaneurysm can occur in any vessel in the peripancreatic area but the most
common vessel is the splenic artery.
CASE
48 Pancreatic Pseudocyst
CASE
A 25-year-old male with history of pancreatitis was referred to radiology
department for CT scan abdomen.

Contrast enhanced CT scan abdomen shows a well defined cyst in the region of
body and tail of pancreas. It has a thin peripherally enhancing wall (Fig. 1A). No
septation or solid components seen within it, this represents a pseudocyst. The
head of the pancreas appears normal (Fig. 1B).
In Other Cases
• Contrast enhanced CT scan abdomen (Fig. 2A) shows peripherally enhancing
loculated collection in the retrocardiac region. Bilateral pleural effusion is
seen. Another well defined cystic lesion with a thin peripherally enhancing
wall is seen in left posterior pararenal space pushing the left kidney antero-
laterally. This represents a pseudocyst (Fig. 2B). Also a loculated mesenteric
collection is seen in left side of abdomen (Fig. 2C).
A B
Figs 1A and B
A B
C
Figs 2A to C
• Axial post contrast CT image of abdomen at the level of pancreas (Fig. 3)

shows a well defined cystic lesion arising from the anterior portion of body of
pancreas with irregular margin. There is evidence of air fluid level within it. This
represents an infected pseudocyst of pancreas. Also there is peripancreatic fat
stranding and the head of pancreas appears bulky.

Excessive alcohol consumption is most common cause of pancreatitis. Abdominal
CT scanning is an excellent choice for imaging of pancreatic pseudocysts.
Presentations attributed to pseudocyst include mass effect leading to biliary
obstruction or gastric outlet obstruction. Pseudocysts are fluid filled oval or
round collections with a relatively thick wall. They can be multiple and are most
commonly located in the pancreatic bed. However, they can be found anywhere
from the groin to the mediastinum and even in the neck, having ascended in
the retroperitoneum via the diaphragmatic hiatus into the mediastinum. CT
attenuation values may be greater than 20–30 Hounsfield units because of the
presence of necrotic pancreatic or peripancreatic debris. The presence of such
Case 48: Pancreatic Pseudocyst 151
Fig. 3
material in the pseudocyst makes its appearance more heterogeneous on CT

scans. Pancreatic pseudocysts have several features that help to distinguish
them from acute fluid collections on CT scans. Most prominent is the presence
of a well-defined, nonepithelial, fibrous wall around the collection. Pseudocysts
are round or ovoid in configuration with an enhancing wall whereas acute fluid
collections are not well defined. It develops in 4–6 weeks, usually decreases
in size over time, sometimes enlarges or become infected. When it becomes
infected there is evidence of air pockets or air fluid level within the cyst. The
major weakness of CT scanning is the inability to distinguish pseudocyst from
cystic neoplasms, especially mucinous cystadenomas and intraductal papillary
mucinous tumors (IPMT). The clinical history provides clue to a diagnosis other
than pancreatic pseudocyst. If the patient has had no prior history of pancreatitis
but has a cystic mass associated with the pancreas, an alternative diagnosis
should be considered.
Opinion
Pancreatic pseudocysts.
Clinical Discussion
Patient clinically presents as acute pain in epigastric region and high grade
fever. There is evidence of history of chronic alcoholism. Pancreatitis leads to
formation of pseudocysts. Pseudocyst gets infected and leads to formation of
air pockets within. Also peripancreatic fat stranding is seen. Infection occurs
either spontaneously or after therapeutic or diagnostic manipulations. While
infected pseudocyst can initially be treated with conservative means, a majority
of patients will require intervention. Traditionally, surgery has been the preferred
modality but endoscopic treatment is gaining acceptance. An external drainage
may be necessary in selected situations such as when there is evidence of gross
sepsis and the patient is too unstable to undergo surgical or endoscopic drainage.
CASE
49 Necrotizing Pancreatitis
CASE
A middle aged male presented to the department of radiology with history of
sudden pain in the upper abdomen which is worse when lying down but may
feel less intense when sitting up or bending over since 2 days. Patient also had
nausea, vomiting and fever since 4 days.

Axial post contrast CT image at the level of pancreas (Fig. 1) shows nonenhancing
hypodense area involving the body and tail of pancreas suggesting area of
Fig. 1
necrosis along with peripancreatic fat stranding. Findings suggest necrotizing

pancreatitis.

Necrotizing pancreatitis represents the severe form of pancreatitis. Pancreatic
necrosis is diagnosed radiographically by dynamic intravenous contrast-
enhanced computed tomography (CT) of the abdomen. Because the normal
pancreatic microcirculation is disrupted during acute necrotizing pancreatitis,
affected portions of the pancreas do not show normal contrast enhancement.
Contrast-enhanced abdominal CT is the gold standard for the noninvasive
diagnosis of pancreatic necrosis, with an accuracy of more than 90%.
Atlanta classification for acute pancreatitis was modified to update
the terminology and provide simple functional clinical and morphologic
classifications. The modification divides acute pancreatitis into interstitial
edematous pancreatitis and necrotizing pancreatitis, distinguish an early
phase (1st week) and a late phase (after the 1st week), and emphasize systemic
inflammatory response syndrome and multisystem organ failure. In the 1st week,
only clinical parameters are important for treatment planning. After the 1st week,
morphologic criteria defined on the basis of CT findings combined with clinical
parameters form basis for treatment. This revised classification introduces new
terminology for pancreatic fluid collections. Depending on presence or absence of
necrosis, acute collections in the first 4 weeks are called acute necrotic collections
or acute peripancreatic fluid collections. Once an enhancing capsule develops
with persistent peripancreatic fluid collections are referred to as pseudocysts;
and acute necrotic collections, as walled-off necroses.
Opinion
Necrotizing pancreatitis.
Clinical Discussion
Severe acute pancreatitis is usually a result of pancreatic glandular necrosis.
The morbidity and mortality associated with acute pancreatitis are substantially
higher when necrosis is present, especially when the area of necrosis is also
infected. It is important to identify patients with pancreatic necrosis so that
appropriate management can be undertaken. Advances in radiologic imaging
and aggressive medical management with emphasis on the prevention of
infection have allowed prompt identification of complications and improvement
in outcome for necrotizing pancreatitis patients. As long as acute necrotizing
pancreatitis remains sterile, the overall mortality is approximately 10%. The
mortality rate at least triples if there is infected necrosis. In addition, patients with
sterile necrosis and high severity of illness scores accompanied by multisystem
organ failure, shock, or renal insufficiency have significantly higher mortality.
Complications include pseudocyst of pancreas, pancreatic abscess and sepsis.
CASE
Periampullary
50 Carcinoma with
Metastases
CASE
A 48-year-old female with history of Whipple’s surgery for periampullary
carcinoma with referred to the Department of Radiology for a follow-up CT
scan.

Axial post contrast CT images of abdomen shows an ill defined, hypodense, non-
enhancing lesion in segment IV of liver (Fig. 1A) and another similar lesion is
seen in segment VII (Fig. 1B). Preaortic and aortocaval lymphadenopathy with
central necrosis (Fig. 1C). Figure 1D shows pancreatic duct stent and its drainage
into the jejunum (post Whipple’s surgery). In an operated case of periampullary
carcinoma lesions in liver and enlarged retroperitoneal lymph nodes represent
metastases.

Periampullary carcinomas arise within 2 cm of the major papilla in the duodenum
and include four different types of malignancies, namely, those originating from
(a) the ampulla of Vater itself; (b) the intrapancreatic distal bile duct; (c) the head
and uncinate process of the pancreas; and (d) the duodenum.
Accurate diagnosis and origin determination may influence treatment
planning and the prediction of prognosis. In comparison to pancreatic cancer,
distal bile duct cancer is more resectable. To improve survival, the radical
resection of pancreatic cancer should be more frequently combined with
chemoradiation therapy or more extensive regional lymphadenectomy than the
radical resection of nonpancreatic periampullary cancers. Aggressive resection is
indicated in ampullary or duodenal carcinoma, even in the presence of positive
lymph nodes at preoperative imaging.
Most complications of pancreatoduodenectomy are managed without
radiologic intervention, although many are demonstrated at imaging. These
complications include delayed gastric emptying, pancreatic fistula, wound
A B
C D
Figs 1A to D
infection, hemorrhage, and pancreatitis. Knowledge of the postoperative

anatomy, familiarity with the various CT appearances of a normal loop, and
careful evaluation of the loop and its surroundings usually allow definitive
diagnosis of the presence or absence of an adjacent abscess. Postoperative
abscesses may occur in the retroperitoneal surgical bed or in the peritoneum.
The peritoneum allows fluid to migrate easily, and collections can be found
remote from the surgical site. One additional interpretive pitfall is a collection
in the gallbladder fossa that may mimic the appearance of the gallbladder. This
finding should not be misinterpreted as the gallbladder because the gallbladder
is usually removed during pancreatoduodenectomy. The bile ducts are very
sensitive to ischemia, and violation of the integrity of the intrahepatic bile
ducts may result in hepatic abscess or intrahepatic biloma. Biliary obstruction
in a patient after pancreatoduodenectomy can result from recurrent tumor,
anastomotic stricture, or bile duct injury.
Opinion
Operated case of periampullary carcinoma with hepatic metastases and
retroperitoneal lymphadenopathy.
Case 50: Periampullary Carcinoma with Metastases 157
Clinical Discussion
Periampullary tumors, compared to others in the vicinity, are diagnosed and
possibly detected early on account of their anatomical location. However, there
is a lack of adequate data to support this hypothesis. Thus the main feature is
painless progressive jaundice and significant weight loss. Abdominal pain is seen
in advanced stages of the disease. Icterus, pruritus, hepatomegaly and a palpable
gallbladder are among the prominent clinical features. The combination of MRCP
with conventional T1- and T2-weighted MR imaging, including gadolinium-
enhanced dynamic MR imaging, is important for the evaluation of periampullary
disease in terms of both detection and evaluation of the extent of a periampullary
mass.
SECTION
12
Spleen
51. Splenunculus
52. Splenic Trauma
53. Splenic Abscess
CASE
51 Splenunculus
CASE
A 26-year-old male came for routine CT abdomen.

Plain and contrast enhanced CT images (Figs 1A and B) show a well defined oval
structure medial to the spleen. It shows density and enhancement similar to the
spleen on plain and post contrast images. This represents splenunculus.
A B
Figs 1A and B
162 Section 12: Spleen

Splenunculus is accessory spleen, generally lies along the splenic artery, near
the hilum, or in the omental ligaments around the spleen. Splenunculi occur in
normal people and sometimes enlarge following splenectomy.
Opinion
Splenunculus.
Clinical Discussion
Splenunculi are small nodules of spleen that are detached from the rest of the
organ. They are benign and asymptomatic, their importance mainly related
to the need to distinguish them from more sinister pathology. Splenunculi are
typically a few centimeters in diameter when identified, well circumscribed
rounded or ovoid nodules. Although most are located near the spleen, they have
been identified elsewhere in the abdominal cavity including—near the spleen
(the most common), gastrosplenic ligament, splenorenal ligament, pancreatic
tail, greater omentum, mesentery, stomach or bowel wall. They have density and
enhancing characteristics similar to the rest of the spleen on CT. General imaging
differential considerations include peritoneal metastases, enlarged lymph node
and tumor from the tail of pancreas.
CASE
52 Splenic Trauma
CASE
A 62-year-old male patient came with history of road traffic accident and pain in
left side of abdomen. CT was done to rule out abdominal organ injury.

There is crescentic hyperdense collection in perisplenic region on plain CT
indicating a subcapsular hematoma (Fig. 1A). The subcapsular hematoma is 2 cm
in thickness. Contrast enhanced CT (Fig. 1B) shows an irregular nonenhancing
area in the superior part of spleen extending from posterior to anterior aspect
indicating the splenic laceration. It is 3 cm deep from the capsule. Splenic CT
injury grading scale is GRADE II. In this case subcapsular hematoma was
also seen around the liver (Fig. 1C). Surgical emphysema is seen in left lateral
abdominal wall and fracture is seen in left 8th rib (Fig. 1D).

The major CT features of blunt splenic injuries are lacerations, subcapsular
and parenchymal hematomas, active hemorrhage, hemoperitoneum and
vascular injury. CT scanning can also provide an accurate appraisal of coexisting
abdominal injuries, such as injuries to the retroperitoneum, abdominal wall,
and can exclude the presence of lesions requiring surgery, such as bowel or
pancreatic injuries.
Opinion
Splenic laceration with splenic subcapsular hematoma, subcapsular hepatic
hematoma, surgical emphysema and rib fracture.
164 Section 12: Spleen
A B
C D
Figs 1A to D
Clinical Discussion
Spleen is the most frequently injured solid organ in blunt trauma to the
abdomen. Splenic injury is often associated with left rib fractures and other organ
injuries like kidney. CT is highly accurate in diagnosing splenic injury. Splenic
parenchyma should be assessed in portal venous phase as the heterogeneous
contrast-enhancement seen on arterial phase can mimic splenic laceration/
contusion. Arterial phase scanning is useful in assessing vascular injuries such
as pseudoaneurysm and AV fistula. CT scan findings that indicate splenic
injury include hemoperitoneum, subcapsular hematoma and laceration, active
bleeding and contained vascular injuries including arteriovenous fistula and
pseudoaneurysm. Hemoperitoneum refers to localized fluid collections around
the spleen with an elevated Hounsfield unit. Briskly bleeding splenic lacerations
may show blood density fluid throughout the abdomen. Subcapsular hematoma
is seen as a crescentic low attenuation area along the lateral margin which
flattens the normal convex margin of spleen. Intrasplenic hematoma is seen as
round to oval hypodense area. Linear hypodense area represents laceration.
Contrast blush or extravasation is defined as hyperdense areas within the splenic
parenchyma that represent traumatic disruption or pseudoaneurysm of the
splenic vasculature. Active extravasation of contrast implies ongoing bleeding
and need for urgent intervention.
Case 52: Splenic Trauma 165
Splenic CT Injury Grading Scale

• GRADE I: Laceration < 1 cm deep, subcapsular hematoma < 1 cm diameter
• GRADE II: Laceration 1–3 cm deep, subcapsular hematoma 1–3 cm diameter
• GRADE III: Laceration >3 cm deep, subcapsular hematoma >3 cm diameter,
parenchymal hematoma > 5 cm
• GRADE IV: Laceration involving segmental or hilar vessels, producing major
devascularization (> 25% of spleen)
• GRADE V: Shattered spleen or avulsed spleen with total devascularization.
CASE
53 Splenic Abscess
CASE
A 48-year-old female with history of pyrexia of unknown origin subjected to CT
abdomen and pelvis.

CT abdomen, coronal reconstruction shows splenomegaly (Fig. 1). There is a
well defined hypodense lesion with a thick peripherally enhancing wall and mild
perilesional edema in the upper pole of spleen suggestive of splenic abscess.
Fig. 1
Case 53: Splenic Abscess 167

Abscesses are localized collections of necrotic inflammatory tissue caused
by bacterial, parasitic or fungal agents. Ultrasonography abdomen shows
hypoechoic to heteroechoic collection with or without internal septae and air. CT
shows low attenuation, ill defined lesion with peripheral contrast enhancement.
It may rarely contain gas bubbles or air fluid level. MR imaging shows abscess as
a fluid intensity, low intensity on T1WI and high intensity on T2WI.
Opinion
Splenic abscess.
Clinical Discussion
Abscess of the spleen is a rather rare clinical entity. Patients with recognized risk
factors are immunocompromised, endocarditis, diabetes mellitus, immuno
suppression, trauma, drug abuse. They are more frequently detected in middle-
aged and older individuals, with no obvious preference for either sex. The
clinical manifestations of splenic abscesses usually include abdominal pain,
exclusively located or, at least, more intensely described in the upper-left-
quadrant area. Fever, nausea, vomiting and anorexia may be also present in
various combinations. Laboratory findings are consistent with the acute phase
of infection, but their exact nature is determined by the pathogen isolated from
the abscess. The most common pathogens detected include Staphylococcus and
Streptococcus. Due to the seriousness of the potential implications, including a
threat to life itself, the most usual treatment currently applied is splenectomy,
which is followed by rapid clinical improvement. Percutaneus imaging guided
drainage is minimally invasive procedure.
SECTION
13
Vascular
54. Superior Mesenteric Artery Syndrome
55. Superior Mesenteric Artery Thrombosis
56. Accessory Renal Artery Stenosis
57. Aneurysm of Abdominal Aorta
58. Inferior Vena Cava Thrombus
59. Aortic Thrombus
60. Portal Vein Thrombosis
CASE
54 Superior Mesenteric
Artery Syndrome
CASE
A 15-year-old female presented to the department of radiology with pain in
epigastric region and nausea since 2–3 months.

Axial and sagittal reconstructed images of contrast enhanced CT abdomen shows
reduced distance between aorta and superior mesenteric artery (SMA) and also
there is evidence of reduced angle between the aorta and SMA (Figs 1A to D).

Superior mesenteric artery syndrome is a condition in which the distance
between the aorta and SMA and the angle between them is reduced which leads
to the extrinsic vascular compression of third portion of duodenum and the
patient presents with abdominal cramps and repeated vomiting.
Opinion
Superior mesenteric artery syndrome.
Clinical Discussion
The superior mesenteric artery syndrome occurs in older children and
adolescents. Commonly females are affected by this. Transverse duodenum
courses caudal to the SMA origin, which normally forms an angle of 45° with
the aorta. Any factor which narrows the aortomesenteric angle to approximately
10–22° can compress the transverse duodenum, resulting in SMA syndrome.
Causes include weight loss, prolonged bed rest in the supine position, corrective
surgery for scoliosis, and congenital causes (high insertion of the duodenum at
the ligament of Treitz or low origin of the SMA). The patient often presents with
chronic upper abdominal symptoms such as epigastric pain, nausea, voluminous
172 Section 13: Vascular
A B
C D
Figs 1A to D
vomiting (bilious or partially digested food), postprandial discomfort, early satiety,

and sometimes, subacute small bowel obstruction. Diagnosis requires clinical
and imaging correlation. Diagnostic imaging studies include CT, fluoroscopic
upper GI studies, and abdominal ultrasound. Fluoroscopy is particularly useful,
providing real-time imaging during contrast transit. This will show dilation
of the first and second portions of the duodenum as it passes anterior to the
aorta. A partial or complete obstruction to flow may be present. There is often
hyperperistalsis in the proximal segments of duodenum. CT criteria for the
diagnosis of superior mesenteric artery syndrome include an aortomesenteric
angle of less than 22° and an aortomesenteric distance of less than 8–10 mm. CT
scan will show pronounced dilatation of the stomach and proximal duodenum
with vertical linear compression defect in the transverse duodenum, overlying
the spine, and abrupt caliber change distal to the compression defect. Initial
treatment is typically conservative and includes adequate nutrition, nasogastric
decompression, and proper positioning after eating. Enteral feeding via feeding
tube passed distal to the point of obstruction is often required. Surgery is indicated
when conservative measures are ineffective.
CASE
55 Superior Mesenteric
Artery Thrombosis
CASE
A 55-year-old female presented to the department of radiology with acute pain
in abdomen.

Contrast enhanced axial and sagittal CT images of abdomen show wall thickening
and eccentric thrombosis of superior mesenteric artery (Figs 1A and B).
A B
Figs 1A and B
In Other Cases
• Contrast enhanced CT abdomen shows complete occlusion of the SMA lumen
by thrombus seen just after its origin from abdominal aorta (Figs 2A and B).
• CT mesenteric angiography shows thrombus in proximal part of SMA starting
from its origin from abdominal aorta. The distal SMA is patent (Figs 3A and B).

Thrombosis of the superior mesenteric artery is most often associated with a
pre-existing atherosclerotic lesion that already compromises flow. The most
common pre-existing pathology found in patients with acute mesenteric
thrombosis is atherosclerosis. The atherosclerotic plaque, usually at the origin
of the SMA, grows over time. The SMA is the most common visceral branch to
thrombose. Complete block of superior mesenteric artery leads to necrosis of
bowel, perforation and then peritonitis with fatal consequences. CT angiography
is important for diagnosis and it shows complete nonvisualization of SMA. Also
it can depict the bowel viability and diagnose complications like perforation
and peritonitis. Findings on CT scan in acute SMA occlusion include lack of
enhancement of the lumen of SMA and its branches. Other findings which can
be seen in thrombosis are mesenteric fat stranding due to mesenteric ischemia.
Intense mucosal enhancement of bowel wall with thickening, bowel distension
with intraluminal fluid accumulation, portal venous gas, free fluid and free intra-
abdominal air.
A B
Figs 2A and B
Case 55: Superior Mesenteric Artery Thrombosis 175
A B
Figs 3A and B
Opinion
Superior mesenteric artery thrombosis.
Clinical Discussion
Patients with acute mesenteric artery thrombosis present with a long history of
weight loss, postprandial pain. Symptoms worsen over time. Patients complain
of severe, acute, unrelenting abdominal pain. They may also complain of
frank blood in their stools. Medical history may be significant for stroke, MI,
or peripheral artery disease. Patients may have a long history of smoking or
uncontrolled diabetes. Clinical presentation is variable and depends upon the
extent of luminal narrowing. A mesenteric arterial embolism results in a different
extension of the infarcted areas because the emboli can occlude the vessel
tree to different levels. The poor prognosis of patients with mesenteric arterial
occlusions is most likely due to the proximal location of the occlusion in the
vessel tree; this determines a more extensive bowel infarction and the need for
extended intestinal resection. The prerequisite for success of a revascularization
is prompt diagnosis.
CASE
56 Accessory Renal
Artery Stenosis
CASE
A 53-year-old male patient with history of hypertension presented for renal
angiogram to the department of radiology to rule out renal artery stenosis.

CT renal angiography (Fig. 1) reveals normal main renal arteries, an accessory
renal artery is present, and it has a right lateral origin from the aorta proximal to
the bifurcation which shows stenosis at its origin (arrow).
Fig. 1
Case 56: Accessory Renal Artery Stenosis 177

Accessory renal arteries are a common variant and are present in 25% of the
population. Most commonly accessory renal arteries arise from the abdominal
aorta and supply to the inferior pole of the kidney although they can rarely arise
from celiac trunk, mesenteric arteries or other abdominal arteries.
Opinion
Accessory renal artery stenosis.
Clinical Discussion
CT angiography with MIP and quantitative measurement of stenosis is an
accurate noninvasive technique in the diagnosis of renal artery stenosis.
Accessory renal arteries are reliably identified by means of CTA. CT can detect
stenosis in the mainstem artery or its intrarenal branches, with a high degree of
accuracy. It is an important pathological sign that radiologist has to evaluate and
assess because of its association with hypertension. Multidetector computed
tomographic angiography (MDCTA) help to correctly evaluate accessory renal
arteries in addition to renal arteries. Not all accessory renal artery stenosis are
associated with renovascular hypertension. In this case considering the age of the
patient it is less likely to be associated with hypertension as it is more likely to be
essential hypertension.
CASE
57 Aneurysm of
Abdominal Aorta
CASE
A 62-year-old male with intermittent claudication since one month and vague
abdominal pain in supine position relieved in lateral position, was subjected to
CT angiogram (abdomen and pelvis).

3D volume rendered images (Figs 1A and B) of CT angiogram shows focal
aneurysm; pedicle is seen to arise from the anterior aspect, just above the
bifurcation of abdominal aorta.
A B
Figs 1A and B
Case 57: Aneurysm of Abdominal Aorta 179

An abdominal aortic aneurysm (AAA) is defined as focal dilatation of the
abdominal aorta that is 50% greater than the proximal normal segment or
that is greater than 3 cm in maximum diameter. Majority of abdominal aortic
aneurysms originate below the renal arteries and can extend to involve the aortic
bifurcation and proximal iliac arteries. AAA’s are frequently asymptomatic and
discovered during radiologic or physical examinations performed for other
reasons. Approximately 50% of abdominal aortic aneurysms are visible on a
plain radiograph of the lateral lumbar spine due to calcification within its wall.
Ultrasound is noninvasive modality and provides accurate measurement of the
diameter of aorta, and can discern free intraperitoneal blood. Unfortunately,
US is not particularly helpful for assessment of aneurysmal rupture, nor it is
useful for imaging the thoracic or suprarenal aorta, because of interference
from overlying lung. CT scan accurately demonstrates dilation of the aorta and
involvement of major branch vessels proximally and distally. This information
helps in determining the appropriate intervention, which may be either surgical
or endovascular repair. “Crescent sign” i.e. peripheral high-attenuating crescent
in aneurysm wall, i.e. acute intramural hematoma is a sign of impending rupture.
CT also shows the other organs in the abdomen and demonstrates involvement
or displacement of organs. The location and number of the renal arteries, caliber
of the aneurysm, degree of calcification, lengths of the neck, iliac artery, and
presence of mural thrombus are readily assessed. CT angiography (CTA) allows
multiplanar assessment of the aneurysm and associated relevant vessels. CT is
also helpful in detecting complications like aneurysm rupture and dissection.
CT scan findings in case of aneurysm rupture include anterior displacement of
kidney, extravasation of contrast material, fluid collection/hematoma within
posterior pararenal and perirenal spaces, free intraperitoneal fluid.
Opinion
Aneurysm of abdominal aorta.
Clinical Discussion
Normal size of abdominal aorta >50 years of age is about 2 cm. Prevalence of
abdominal aortic aneurysm increases with age, atherosclerotic disease and white
race. Risk factors include male gender, age >75 years, prior vascular disease,
hypertension, cigarette smoking, family history and hypercholesterolemia.
Clinically most of the patients are asymptomatic but may complain of abdominal
mass and pain. When the triad of abdominal or flank pain, shock, and a pulsatile
abdominal mass are present, the diagnosis of ruptured AAA is relatively
straightforward. Abdominal aneurysms are complicated by rupture, distal
thromboembolism, infection, spontaneous occlusion of aorta. Patients with AAA
< 4 cm will need serial ultrasound evaluations every 6 months. If growth exceeds
0.5 cm in six months, the aneurysm becomes > 4 cm, symptoms related to the
aneurysm are present, or a complicated aneurysm is present, surgical repair is
usually indicated.
CASE
58 Inferior Vena Cava

Thrombus
CASE
A 43-year-old male patient presented with bilateral pedal edema and was referred
to radiology department for CT abdomen.

CT scan abdomen (Fig. 1) shows a large intraluminal filling defect in the entire
length of inferior vena cava (IVC) extending into both common iliac veins. Few
collateral vessels are seen in this reconstruction. Superior vena cava (SVC) and
pulmonary vessels are normal.
Fig. 1
Case 58: Inferior Vena Cava Thrombus 181

The most reliable, noninvasive method to establish a diagnosis of IVC anomalies
is CT scan with intravenous (IV) contrast or MRI. CT scan is a good imaging
modality for evaluating the retroperitoneal space. Another accurate, but more
invasive, imaging modality is venography, which is particularly useful if any
surgery is planned. A bland thrombus results from external compression
of the IVC by a neoplastic lesion, so the IVC is usually narrowed at the site of
thrombosis. In contrast, tumor thrombus expands the IVC. Tumor thrombus will
often show continuity with primary tumor. In arterial phase, neovascularity may
be appreciated in tumor thrombus.
Opinion
IVC thrombosis.
Clinical Discussion
Inferior vena cava thrombosis is an essential diagnosis while evaluating any
neoplastic lesion, or portal hypertension. Etiology includes hypercoagulable
state, IVC filters, catheters, extension from tumors like renal cell carcinoma,
leiomyosarcoma of IVC. The classic presentation of IVC thrombosis includes
bilateral lower extremity edema with dilated, visible superficial abdominal veins.
In addition, if the thrombus is confined to the cava and does not involve the iliac
or femoral system, the collateral pathways form along the posterior abdominal
wall. This scenario may have significant impact on surgical procedures involving
this anatomic region. Thrombosis occurring at the level of the renal veins raises
the possibility of renal cell carcinoma. Patient can present with bilateral pedal
edema or pulmonary embolism. Any neoplastic lesion can cause IVC thrombosis,
renal cell carcinoma is the most common malignancy to extend into IVC. Other
tumors that have a tendency for IVC thrombosis are hepatocellular carcinoma
and Wilms’ tumor.
CASE
59 Aortic Thrombus
CASE
A 55-year-old male with complaint of pain in abdomen since three days was
subjected to CT abdomen and pelvis.
Findings on CT Examination
CT aortography shows acute long segment thrombotic occlusion of infra-renal
abdominal aorta extending to bilateral common iliac arteries (Figs 1A, B and E).
Short segment occlusion of inferior mesenteric artery is seen (Fig. 1D). Bilateral
main renal arteries are normal in their course and calibre (Fig. 1C).
A B
C D E
Figs 1A to E
Case 59: Aortic Thrombus 183

Transabdominal USG allows for detailed depiction of intraluminal thrombus
(ILT) morphology. With the use of low-frequency (e.g. 4-MHz) probes, the
echogenic ILT will be delineated against the echo-free aortic lumen. USG can
show calcifications in the ILT as areas of hyperechogenicity accompanied by an
echo-free shadow artifact. Contrast-enhanced CT allows for a detailed depiction
of ILT morphology by delineating the low-attenuating ILT against the contrast
filled, high-attenuating aortic lumen. With contrast-enhanced CT, a halo-shaped
area of high attenuation in the thrombus—the “Crescent sign” can be visualized.
CT shows calcifications in the intraluminal thrombus better than any other
imaging method.
Opinion
Infrarenal aortic thrombus extending to bilateral common iliac and inferior
mesenteric artery.
Clinical Discussion
Atheromatous occlusion of the distal abdominal aorta at the bifurcation into the
common iliac arteries is called Leriche syndrome. Triad of symptoms includes
claudication in the legs or buttocks absent or diminished femoral pulses, erectile
dysfunction. Usually affects younger males 30–40 years of age. Risk factors
include cigarette smoking, hypercholesterolemia and diabetes. Development of
the disease is slow and collaterals develop, limb-threatening ischemic disease
does not tend to occur. Treatment options include aortoiliac bypass surgery or
kissing balloon angioplasty and stent implantation.
CASE
60 Portal Vein Thrombosis
CASE
A 30-year-old female with history of pain in abdomen, nausea and vomiting since
5 days was referred to the department of radiology for CT abdomen.

Contrast enhanced CT abdomen reveals failure of opacification following IV
contrast of main portal vein and splenic vein (Fig. 1A arrows), portal confluence
(Fig. 1B arrow) and superior mesenteric vein (Fig. 1C arrow). This is thrombosis of
portal vein, splenic vein and superior mesenteric vein with resultant differential
enhancement in right lobe of liver (Fig. 1D).
In another case of contrast enhanced CT abdomen there is failure of
opacification of left branch of portal vein because of thrombosis (Figs 2A and B
arrow). Multiple calculi are also seen in gallbladder (Fig. 2B).

The thrombus is observed as an echogenic lesion within the portal vein, though
a recently formed thrombus may be anechoic and is not seen on standard gray-
scale ultrasound. Contrast-enhanced CT scan has the advantage over ultrasound
in displaying varices and parenchymal hepatic abnormalities. Portal venous
phase of CT shows partial or complete nonopacification of portal vein or its
branches. MRI is helpful if hepatic parenchymal detail is required. MRI can also
quantitate portal and hepatic vessel flow, which is required in the planning of
interventions, such as shunt surgery, transjugular intrahepatic portosystemic
shunt (TIPS) or liver transplantation. Acute clot (< 5 weeks) appears hyperintense
on both T1- and T2-weighted images, whereas older clots appear hyperintense
only on T2-weighted images. Tumor thrombi can be differentiated from bland
thrombi because they appear more hyperintense on T2-weighted images and
enhance with contrast. Cavernous transformation of portal vein is a sequelae
of portal vein thrombosis and is replacement of portal vein by multiple venous
channels. This develops in patients whose portal vein does not recanalize or
Case 60: Portal Vein Thrombosis 185
A B
C D
Figs 1A to D
A B
Figs 2A and B
only partially re-canalises collateral veins dilate and become serpiginous. On

USG cavernous transformation appears as numerous tortuous vessels occupying
the portal vein bed. Triphasic CT can confirm the diagnosis by demonstrating
numerous vascular channels in the region of portal vein which enhance during
portal phase and not during arterial phase distinguishing it from arteriovenous
malformation.
Opinion
Portal vein thrombosis.
Clinical Discussion
Portal vein thrombosis is rare and clinically may be asymptomatic. Thrombus
may be acute or chronic. Local factors favoring or precipitating development of
portal vein thrombosis include local inflammatory lesions, neonatal omphalitis,
diverticulitis, appendicitis, pancreatitis, duodenal ulcer, cholecystitis, tuberculous
lymphadenitis, injury to the portal venous system, surgical portacaval shunting,
splenectomy, colectomy, gastrectomy, cancer of abdominal organs and cirrhosis.
Symptoms often presents as gastrointestinal bleeding, variceal bleeding,
ascites, and abdominal pain. Portal hypertension and mesenteric ischemia are
complications of portal vein thrombosis. Treatment options include systemic
anticoagulation, endovascular infusion of thrombolytic agents: percutaneous
transhepatic approach and surgical thrombectomy.
SECTION
14
Adrenal
61. Adrenal Adenoma
62. Pheochromocytoma
63. Adrenal Metastases
CASE
61 Adrenal Adenoma
CASE
A 50-year-old male referred to the department of radiology with vague dull
abdominal pain in left hypochondriac region for CT abdomen.

Pre and post contrast axial images of abdomen (Figs 1A and B) show normal right
adrenal gland. Left adrenal gland shows a nonenhancing, solid, well-defined iso
to hyperdense lesion, suggestive of left adrenal adenoma with no evidence of fat
stranding or infiltration of surrounding tissues.
A B
Figs 1A and B
190 Section 14: Adrenal

The majority of adrenal adenomas are nonfunctioning; in such cases patients are
asymptomatic. Patients with hyper functioning adrenal gland adenomas present
with manifestations of excess hormone secretion, such as Cushing’s syndrome
due to excess cortisol production, Conn’s syndrome (due to excess aldosterone
production) or sex-hormone related symptoms. Adenomas can be divided into
those that have typical or atypical appearances. Typical adenomas are small, less
than 3 cm and are of low density. They show homogeneous appearance. Atypical
adenomas are large, more than 3 cm and show hemorrhage, calcification,
necrosis and absence of fat. If greater than 6 cm chances of it being malignant
is 85%. CT is a well established modality for investigating adrenal masses and
uses the fact that the majority of adenomas have high lipid content. Noncontrast
CT is performed and the CT number (Hounsfield units (HU)) of the mass is
measured. If the CT value is ≤10 HU it is considered to be a benign adenoma
on the basis of its fat content. If the CT value is >10 HU, enhanced 60 seconds
and a 15 minutes delayed postcontrast CT are obtained, and the enhancement
washout is calculated. The percentage of absolute enhancement washout can be
thus calculated:
enhanced attenuation value – delayed attenuation value × 100
% washout =
enhanced attenuation value – nonenhanced
attenuation value
The enhanced attenuation value is the attenuation value of the mass in HU,
60 seconds after contrast administration. The delayed attenuation value is the
attenuation value of the mass in HU, 10–15 minutes after contrast administration.
If the enhancement washout is >50%, the diagnosis of a benign lipid poor
adenoma is made. If the washout is <50%, the mass is considered indeterminate,
and a biopsy may be necessary to make a diagnosis. Metastatic deposits are usually
larger and more heterogeneous than adenomas and do not have intracellular fat.
Frequently in clinical practice, only postcontrast images are available. In these
patients, the percentage ‘relative’ enhancement washout can be thus calculated:
enhanced attenuation value – delayed
% relative washout = attenuation value × 100
enhanced attenuation value
At 15 minutes, if a relative enhancement washout of 40% or higher is achieved,

this has a sensitivity of 96–100% and a specificity of 100% for the diagnosis of
an adenoma. Therefore a combination of unenhanced CT and enhancement
washout characteristics correctly separates most adrenal masses as adenomas
or metastases. Adrenal cortical adenoma is a common benign tumor arising
from the cortex of the adrenal gland. It commonly occurs in adults, but it can
be found in persons of any age. Adenomas typically demonstrate rapid washout,
which is defined as an absolute percentage washout (APW) of more than 60% and
a relative percentage washout (RPW) of more than 40% on delayed images. The
majority of lesions are nonfunctioning. Although CT does not allow differentiation
of functioning from nonfunctioning masses, the presence of contralateral
adrenal atrophy suggests that a lesion may be functioning, because pituitary
adrenocorticotropic hormone secretion is suppressed by elevated cortisol levels.
Case 61: Adrenal Adenoma 191
Opinion
Adrenal adenoma.
Clinical Discussion
Nonfunctioning adrenal adenomas are asymptomatic. However the functioning
adrenal adenoma presents with pheochromocytoma like symptoms which
include episodic attacks, palpitations, sweating, headaches, and abdominal pain,
as well as labile hypertension. Vital signs may include findings of hypertension,
postural hypotension, and tachycardia. Hypertensive retinopathy is present.
Skin findings present as hirsutism. General signs include central obesity and
gynecomastia. Adrenal adenoma can be diagnosed using chemical shift MRI.
The characterization of a lesion as an adenoma relies on the ratio of a decreased
relative signal intensity from in phase to opposed phase images and the ratio of
adrenal mass and various organs on T2-weighted and chemical shift images.
Small adrenal mass with manifestations of hormonal excess need resection, as
do large (> 3 to 5 cm) nonfunctioning adrenal mass lesions as they are considered
potentially malignant.
CASE
62 Pheochromocytoma
CASE
A 14-year-old hypertensive male child with complaints of giddiness was subjected
to CT abdomen and pelvis.
Radiological Finding on CT Examination

CT abdomen shows a well defined round, hypodense lesion seen superior to the
left renal hilum (Figs 1A to C), the lesion shows heterogeneous enhancement and
is seen separate from left kidney, pancreas and left renal vessel.
A B
C
Figs 1A to C
Case 62: Pheochromocytoma 193

Adrenal tumors tend to be large at presentation. On CT examination lesions have
a precontrast attenuation >10 HU. Most lesions vigorously enhance (>80 HU)
and have less than 60% washout of contrast on delayed images. There may be
areas of necrosis and cystic change. Up to 7% demonstrate areas of calcification.
On T1WI pheochromocytoma appears slightly hypointense to the remainder of
the adrenal and appears heterogeneous if necrotic or hemorrhagic. On T2WI it
appears hyperintense (lighted bulb sign) and enhances heterogeneously. MRI
is preferred for detection of extra-adrenal pheochromocytoma. Differential
diagnosis includes adrenal adenomas, adrenal carcinomas and adrenal
metastases.
Opinion
Adrenal pheochromocytoma.
Clinical Discussion
Pheochromocytomas are rare, catecholamine secreting, neuroendocrine
tumor usually found in medulla of the adrenal gland originating in the
chromaffin cells. Extra-adrenal tumors are called paraganglioneuromas. Most
pheochromocytomas produce epinephrine and norepinephrine. Sometimes
dopamine is secreted. About 10% tumors are malignant and occur at any age with
peak in 3rd to 5th decades, with no sex predilection.
Locations of extra adrenal pheochromocytomas include the organ of
Zuckerkandl which is close to the origin of the inferior mesenteric artery,
bladder wall, heart, mediastinum, and carotid and glomus jugulare bodies.
Patients complain of headache, palpitations and diaphoresis with hypertension,
weakness, nausea, tremors, anxiety and weight loss. Pheochromocytomas
are associated with von Hippel-Lindau disease, neurofibromatosis, multiple
endocrine neoplasia (MEN) 2A (Sipple syndrome) and 2B, tuberous sclerosis,
Sturge-Weber syndrome. Plasma metanephrine and urine catecholamine,
creatinine, vanilmandelic acid and metanephrine levels after 24 hours are useful
for diagnosis. Resection of tumor is a treatment of choice.
CASE
63 Adrenal Metastases
CASE
A 55-year-old female with complaints of cough and breathlessness was subjected
to high-resolution computed tomography (HRCT) chest.

Large enhancing lobulated mass lesion seen in right upper lobe in paratracheal
region with nonenhancing necrotic areas. The lesion closely abuts the right main
bronchus, upper lobe bronchus, superior vena cava and extends to precarinal
region with loss of fat planes. These findings are suggestive of bronchogenic
carcinoma (Fig. 1A). Multiple small rounded metastatic nodules seen in bilateral
lungs (Fig. 1B). A well defined lobulated peripherally enhancing soft tissue
density lesion in left adrenal gland is suggestive of adrenal metastases (Fig. 1C).

Primary tumors that metastasize to the adrenal glands are lung carcinoma,
colorectal carcinoma, breast carcinoma, pancreatic carcinoma, renal cell
carcinoma, hepatocellular carcinoma, malignant melanoma. CT is the
investigation of choice for evaluation of adrenal metastasis and most of the
lesions show percentage enhancement of washout, similar to that of lipid-poor
adrenal adenoma. On MR it appears as T1 hypointense and T2 hyperintense
lesion and shows progressive enhancement on post contrast scan. A diagnosis
of adrenal metastasis is important in examining patients with cancer because
the metastasis indicates inoperable stage IV disease (except in ipsilateral renal
cancer). Adrenal metastases have no specific imaging features. Statistically most
nonadenomas are metastases.
Opinion
Primary lung carcinoma with pulmonary and adrenal metastasis.
Case 63: Adrenal Metastases 195
A B
C
Figs 1A to C
Clinical Discussion
A patient may develop symptoms related to insufficient production of steroid
hormones by the involved adrenal glands (adrenal insufficiency or Addisonian
state). Adrenal insufficiency is characterized by weakness, low blood pressure,
low blood sugar, low blood sodium and high potassium levels, and darkening
of the skin. The most effective treatment for adrenal metastases is to treat the
primary cancer, usually with chemotherapy and/or radiation therapy. If adrenal
insufficiency is present, then steroid hormone replacement should be given.
For patients in whom the adrenal is the only site of metastatic disease and the
primary cancer is well controlled, the adrenal metastasis may be treated by either
radiation therapy or surgical removal. In these cases, adrenalectomy can often be
done using minimally invasive technique.
SECTION
15
Renal
64. Renal Aplasia
65. Dysplastic Kidney
66. Polycystic Kidneys
67. Pelviureteric Junction Obstruction
68. Obstructive Uropathy
69. Emphysematous Pyelonephritis
70. Renal Vein Thrombosis
71. Renal Laceration
72. Renal Angiomyolipoma
73. Wilms’ Tumor
74. Renal Cell Carcinoma
CASE
64 Renal Aplasia
CASE
A 35-year-old male presented to the department of radiology as part of routine
health check up.

Axial post contrast CT image of abdomen (Fig. 1) shows absence of left kidney
in left renal fossa. The left renal fossa shows bowel loops. Right kidney appears
normal. No ectopic kidney was seen. Findings suggest left renal aplasia.
Fig. 1
200 Section 15: Renal

Renal agenesis refers to a congenital absence of one or both kidneys. If bilateral,
the condition is fatal, whereas if unilateral, patients can have a normal life
expectancy. If one kidney is absent the other kidney is hypertrophied since it
takes over the function. Patients are asymptomatic and diagnosed only when
they are screened for some other purpose.
Opinion
Unilateral renal agenesis.
Clinical Discussion
Embryologically renal agenesis results from a failure of the proper development
of the metanephros (precursor of adult kidney) resulting in complete absence
of a renal structure. Abnormalities in the mesonephros may result not only in
renal agenesis (due to absence of induction of the metanephros by the ureteral
bud) but also internal genital malformations [due to failure of the Wolffian and
Müllerian duct to develop or to involute (according to sex)]. There have been
reports of ipsilateral genital abnormalities in 20–70% of cases of renal agenesis.
While the incidence of unilateral renal agenesis is not known it is likely 4–20
times more common than bilateral renal agenesis. Unilateral renal agenesis may
have other associated birth defects like Müllerian duct anomalies, utero-vaginal
aplasia and Potter syndrome.
CASE
65 Dysplastic Kidney
CASE
A 7-year-old female child with pain in left lumbar region was referred to radiology
department for CT abdomen.

Contrast enhanced CT (Figs 1A to C) shows normal sized right kidney with good
excretion of contrast, left kidney is small and dysplastic with multiple well defined
cysts of various sizes. There is no evidence of contrast excretion in left kidney.
USG shows multiple well defined noncommunicating cysts of various sizes and
lack of normal corticomedullary differentiation of left kidney (Fig. 1D).
A B
C D
Figs 1A to D

Multicystic dysplastic kidney (MCDK) is a type of pediatric cystic renal disease.
It results in multiple small cysts being formed in utero in the affected kidney.
MCDK develops in utero and the diagnosis is often made either antenatally or in
the early neonatal period on ultrasound. The vast majority of cases are sporadic
and nonfamilial. Rarely autosomal dominant forms are seen. Associated
contralateral renal tract abnormalities are common and include vesicoureteric
reflux, pelviureteric junction obstruction, horseshoe kidney, ureterocele, and
renal hypoplasia. Bilateral MCDK is seen in 19% and contralateral agenesis is
seen in 11% patients.
Opinion
Multicystic dysplastic kidney.
Clinical Discussion
The diagnosis of MCDK is often made antenatally with multiple small cysts
becoming evident as early as the 15th weeks of gestation. Patient may present
with recurrent urinary tract infection, intermittent abdominal pain and
sometimes failure to thrive. On USG the kidney shows multiple cysts which are
mostly randomly positioned, but may sometimes be peripheral, variable in size
and noncommunicating. Sometimes artifacts may make noncommunicating
cysts appear to be communicating. The parenchyma is seen in small islands
between the cysts and the outline of the kidney tends to be lost. The central sinus
complex is absent. Particularly useful, the hydronephrotic form to assess for
associated obstructive uropathy. DTPA scan may show some flow to the kidney
and possible cortical uptake, but no excretion. The MCDK can be distinguished
from hydronephrosis by observing that the fluid filled cysts do not communicate,
whereas in hydronephrosis the fluid filled, dilated calyces can be seen to
communicate with the renal pelvis and infundibula. Voiding cystourethrogram
should be performed to rule out vesicoureteral reflux on the contralateral side,
to prevent progressive damage to the functioning kidney. Currently most cases
of unilateral MCDK are managed non surgically and are followed with serial
USG. The affected kidney may remain unchanged but it frequently undergoes
spontaneous regression.
CASE
66 Polycystic Kidneys
CASE
A 40-year-old male presented to the department of radiology with pain in
abdomen and raised serum creatinine level, was subjected to CT abdomen.

Coronal post contrast reconstructed CT image (Fig. 1) show multiple well defined
cysts of varying sizes in both kidneys. The normal renal parenchyma interspaced
between the cysts and shows adequate contrast enhancement. Multiple cysts are
also seen in liver. These findings are suggestive of bilateral polycystic kidneys.
Fig. 1

Adult polycystic kidney disease, which affects approximately 1 in 1000 people, is
transmitted as an autosomal dominant trait. Cysts arise from the nephrons and
collecting tubules; microdissection reveals that the cysts communicate directly
with the nephrons and collecting tubules. Islands of normal parenchymal renal
tissue are interspaced between the cysts. Ultrasound is an excellent choice for
repeated imaging as it is relatively inexpensive and lacks ionising radiation. Simple
renal cysts will appear rounded, anechoic with well-defined imperceptible walls
and posterior acoustic enhancement with very thin regular and imperceptible,
wall. CT is sensitive to characterize the diagnosis of renal cysts. Simple cysts
appear as structures with near water attenuation.
Cysts which have had internal complications may be hyperattenuating,
with internal nonenhancing septations or calcifications. A complex cystic mass
with solid components or thick septa which enhance should be viewed with
suspicion, and presence of a renal cell carcinoma suspected. Calcification may
develop. Renal cell carcinomas in contrast, although usually cystic in the setting
of autosomal dominant polycystic kidney disease (ADPKD), will have solid
components of thick septa with blood flow. Autosomal dominant polycystic
kidney disease (ADPKD) is an inherited condition that causes small, fluid-filled
sacs called cysts to develop in the kidneys. Although children are born with the
condition, ADPKD does not usually cause any noticeable problems until the cysts
grow large enough to affect the kidneys' functions. In most cases, this does not
occur until 30–60 years of age.
Opinion
Polycystic kidney disease.
Clinical Discussion
Clinical presentation is variable and includes dull flank pain, abdominal or
flank masses, hematuria and hypertension. A number of conditions are well
recognized as being associated with ADPKD like cerebral Berry’s aneurysm,
intracranial dolichoectasia, aortic dissection and colonic diverticulosis. The
kidneys are normal at birth, and with time develop multiple cysts. At the age of
30 years, approximately 68% of patients will have visible cysts by ultrasound.
Patients present with hypertension and progressive renal failure after their
third decade of life. Autosomal dominant polycystic kidney disease (ADPKD) is
uncommon in children and is rarely seen in neonates. Renal complications that
can occur are progression to end stage renal failure, recurrent urinary infection,
cyst, hemorrhage or infection resulting in acute pain and cyst rupture resulting in
retroperitoneal hemorrhage.
CASE
67 Pelviureteric Junction
Obstruction
CASE
A 35-year-old male with history of severe right flank pain was referred to
department of radiology for CT scan abdomen.

Axial and coronal reconstructed post contrast CT images of abdomen (Figs 1A and
B) shows calculus in right proximal ureter with gross dilatation of pelvicalyceal
A B
Figs 1A and B
Fig. 2
system and severe thinning of renal parenchyma. Findings suggest obstructive

uropathy.
In another patient post contrast CT coronal reconstructed image
(Fig. 2) shows bilateral dilatated pelvicalyceal system with abrupt narrowing at
pelviureteric junction in a case of bilateral pelviureteric junction obstruction.

Obstruction at the pelviureteric junction (PUJ) leads to proximal hydronephrosis.
The amount of obstruction governs the changes in renal pelvicalyceal system.
In complete obstruction there will be severe dilatation of pelvicalyceal system
with loss of renal parenchyma. Renal calculi is one of the most common causes
of pelviureteric junction obstruction. If the calculus remains impacted at that
site for a longer period leads to obstructive uropathy. Routinely intravenous
urogram (IVU) has been performed for assessing for PUJ obstruction. Ultrasound
will often show a dilated renal pelvis with a collapsed proximal ureter. CT
may show evidence of hydronephrosis with collapsed ureters and is useful for
assessing crossing vessels at the PUJ especially when surgical intervention is
planned. Scintigraphy can quantitate the degree of obstruction.99mTc MAG3 is
the agent of choice. Diuretic (Furosemide) renogram is performed to evaluate
between obstructive vs nonobstructive hydronephrosis. PUJ “obstruction” will
demonstrate excretion (downward slope on renogram) after administration
of diuretic from the collecting system. Whereas mechanical obstructive
hydronephrosis will demonstrate no downward slope on renogram, with retained
tracer in collecting system.
Case 67: Pelviureteric Junction Obstruction 207
Opinion
Pelviureteric junction obstruction with calculus.
Clinical Discussion
Pelviureteric junction (PUJ) obstruction is defined as an obstruction of the flow
of urine from the renal pelvis to the proximal ureter. The resultant back pressure
within the renal pelvis may lead to progressive renal damage and deterioration.
Congenital causes include abnormal muscle arrangement at PUJ, ischemic insult
to PUJ region, urothelial ureteric fold. Causes in adults include preceeding renal
pelvic trauma, obstructing calculus distal to PUJ, previous pyelitis with scarring,
intrinsic malignancy, extrinsic ureter compression of encasement, fibrosis,
malignancy. Patient is usually known case of renal calculus, in which the calculus
gets dislodged from kidney and gets stuck at the PUJ. Patient presents with severe
flank pain, hematuria. Pain radiates towards the thighs, scrotum or sometimes
to back. The pain increases on excess fluid intake due to fullness of pelvicalyceal
system. In these cases early diagnosis is necessary since once renal damage is
done, then removing the calculus won’t help kidney to gain function. Dynamic
contrast-enhanced magnetic resonance urography (MRU) is the latest imaging
modality used in assessing PUJ obstruction. In children, this study offers the
advantages of no radiation exposure and excellent anatomical and functional
details with a single study. The study also provides details of renal vasculature,
renal pelvis anatomy, location of crossing vessels, renal cortical scarring, and
ureteral fetal folds in the proximal ureter.
CASE
68 Obstructive Uropathy
CASE 1 RENAL PELVIC CALCULUS

A 35-year-old female presented to the department of radiology with pain in left
flank region and hematuria.

Plain radiograph (Fig. 1A) shows a calculus in left paravertebral region at the level
of L1-L2 intervertebral disc space.
Plain and post contrast axial CT image (Figs B and C) confirms the position of
calculus. The calculus is seen in left renal pelvis with dilatation of pelvicalyceal
system. Excretory phase shows contrast in dilated renal pelvis and calyces.
Contrast density obscures the calculus (Fig. 1D).

Renal pelvic calculus is due to minerals crystallizing out of urine in a normal
urinary tract. Over 90% of calculi are radiopaque on plain films and virtually all
are picked up on CT. They contain calcium salts, usually a mixture of oxalate and
phosphate, sometimes pure phosphate or oxalate. The hallmark of obstruction
on USG is the presence of hydronephrosis. Prominent anechoic structures
within the renal sinus represent a dilated pelvicalyceal system. Renal calculi may
be demonstrated as echogenic foci with or without shadowing, small ureteral
stones are extremely difficult to detect. Unenhanced helical CT has both a high
sensitivity and a high specificity in detecting ureteral calculi in the acute setting.
Dilatation of the pelvicalyceal system is seen on CT as anterior and medial bulging
of the renal pelvis, which is of low attenuation compared to the surrounding
renal parenchyma. Renal enlargement also may be observed in some patients.
Perinephric fat stranding, representing engorged lymphatics and/or edema, is
seen as linear wispy densities in the normally low-attenuation fat. Moderate-to-
severe perinephric stranding generally corresponds to the degree of obstruction
present.
Case 68: Obstructive Uropathy 209
A D
Figs 1A to D
Opinion
Left renal pelvic calculus.
Clinical Discussion
Acute onset of severe flank pain radiating to the groin, gross or microscopic
hematuria, nausea, and vomiting not associated with an acute abdomen are
symptoms that most likely indicate renal colic caused by an acute ureteral or
renal pelvic obstruction from a calculus. Location and quality of pain are related
to position of the stone within the urinary tract. Severity of pain is related to the
degree of obstruction, presence of ureteral spasm, and presence of any associated
infection.
Renal colic has been described as having 3 clinical phases. The first phase
is the acute or onset phase. The second phase is the constant phase. The third
phase is the abatement or relief phase.
Treatment for acute episode is with non-steroidal anti-inflammatory drugs
(NSAIDs). Definitive treatment is in the form of surgical removal of calculus or
extracorporeal shock wave lithotripsy (ESWL).
CASE 2 STAGHORN CALCULI

A 33-year-old male came to the radiology department with complaints of pain in
bilateral lumbar regions since 2 months.

Plain CT axial sections show bilateral renal calculi in the pelvicalyceal system
taking the shape of the pelvicalyceal system suggestive of staghorn calculi. There
is bilateral hydronephrosis with thinning of renal cortex. Small nonobstructive
left renal calyceal calculus is also seen (Figs 2A and B).

Staghorn calculi are the result of recurrent infection and are thus more commonly
encountered in women, those with renal tract anomalies, spinal cord injuries,
neurogenic bladder or ileal ureteral diversion. The majority of staghorn calculi
are symptomatic, presenting with fever, hematuria, flank pain and potentially
septicemia and abscess formation. On X-ray the vast majority of staghorn calculi
are radiopaque and appear as branching calcific densities overlying the renal
outline and may mimic an excretory phase IVP. Lamination within the stone is
common. The collecting system is filled with a densely calcific mass producing
intense posterior acoustic shadowing on ultrasound. On CT, staghorn calculi
are radiopaque and conform to the renal pelvis and calyces, which are often
to some degree dilated. When viewed on bone windows they have a laminated
appearance, due to alternating bands of magnesium ammonium phosphate and
calcium phosphate.
Opinion
Bilateral staghorn calculi.
A B
Figs 2A and B
Clinical Discussion
Staghorn calculi represent a less-common nephrolithiasis subgroup so named
because the significant stone burden that fills the renal pelvis and calyces forms
a shape on radiographs that resembles a deer’s horns. Most staghorn stones in
Western society are composed of struvite and can cause significant morbidity
and mortality if left untreated; therefore, large struvite stones must typically be
removed. Unlike other urinary stones that commonly produce symptoms (e.g.
renal colic) that necessitate intervention, treatment of **struvite stones often
occurs in patients without classic signs of nephrolithiasis; this is because large
staghorn calculi may not cause acute renal or ureteral dilatation and resultant
pain.
Staghorn calculi need to be treated surgically (PCNL +/– ESWL) and the entire
stone removed, including small fragments, as otherwise these residual fragments
act as a reservoir for infection and recurrent stone formation. If left untreated,
staghorn calculi result in chronic infection and eventually may progress to
xanthogranulomatous pyelonephritis.
**Struviteis a phosphate mineral having the formula NH4MgPO4-6H2O. Struvite calculus

form in association with infection. In this urease enzyme is produced by some bacteria in
the urinary tract which helps with ammonium needed for this type of stone production.
These stones have speedy growth resulting in staghorn calculus.
CASE 3 URETERIC CALCULUS

A 40-year-old female patient came with the complaints of pain in both the lumbar
region radiating to groin accompanied with hematuria.

Plain CT KUB shows a hyperdense focus in the left lower ureter (Fig. 3A)
suggestive of lower ureteric calculus with dilatation of the pelvicalyceal system
and enlargement of the kidney.
In another patient plain CT scan abdomen (Figs 3B and C) show bilateral
hyperdense foci at the vesicoureteric junction with hydronephrosis suggestive of
bilateral vesicoureteric junction calculi.

X-ray kidney, ureters, and bladder (KUB) is not very sensitive in detecting calculi
as compared to USG and CT. Calculi may be present in 30% of the time when
X-ray KUB is negative. Ureteric calculi can be confused with phleboliths on
plain X-ray. Typically, phleboliths are round or oval, and they may demonstrate
a central lucency. However, they are often difficult to distinguish from ureteric
calculi. Phleboliths in the pelvis are usually located lower than and lateral to the
ureter. Ultrasound was the previous standard study for ureterolithiasis and is still
the best investigation if non-contrast computerized tomography (NCCT) is not
available. It provides information regarding site and degree of obstruction and
size of stone. Lately it has been replaced by CT. Pelvicaliectasis is noted proximal
A
Fig. 3A
C
Figs 3B and C
to the obstruction caused by the ureteric calculi. The twinkling artifact sign is seen
when color flow is put on the calculus. Absent ureteral jet on affected side may
be present with partially obstructing calculus. CT is a highly sensitive, specific
and accurate modality for detecting ureteric and vesicoureteric junction calculi.
Spiral CT is increasingly replacing IVU in the investigation of ureteric colic and
can be regarded as the investigation of choice. It is performed without injection
of contrast medium and provides rapid result. The study of choice is non-
enhanced abdominal and pelvic CT. In the presence of ureteral calculi, proximal
ureterectasis is the most commonly seen indirect sign. The other differential
for calculus within the ureter includes phlebolith. The presence of the comet
tail sign an adjacent eccentric, tapering soft tissue mass corresponding to the
noncalcified portion of a pelvic vein helps differentiate between ureteric calculus
and phlebolith. The other indirect signs of vesicoureteric junction calculi on CT
are ureterovesical junction edema, stranding of perinephric and paraureteric fat.
Opinion
Bilateral vesicoureteric junction calculi.
Clinical Discussion
Renal colic is characterized by acute colicky flank pain frequently radiating into
pelvis, groin and testis and hematuria. Ureteric calculi occur in 12% of the general
population. It is much more common in males with a male to female incidence of

4:1. The peak onset occurs in the 3rd decade. The various types of stones include
calcium oxalate, struvite, uric acid, calcium phosphate and cystine. Various
metabolic conditions that predispose to urinary stones are hypercalciuria,
hypoxaluria, hyperuricosuria, cystinuria, xanthinuria and nephrocalcinosis.
Most vessels are impacted at narrowest portions of the ureters which are uretero-
pelvic junction, iliac vessel crossing and vesicoureteric junction. The gold
standard imaging investigation is now CT-KUB with a sensitivity rate of 99%
for stones as small as 1 mm. Ultrasound is largely reserved for complications
such as pyonephrosis and hydronephrosis, which may require percutaneous
nephrostomy insertion.
CASE
69 Emphysematous
Pyelonephritis
CASE
A 50-year-old diabetic male presented to the department of radiology with flank
pain, fever since 4–5 days.

Axial post contrast CT image of the abdomen at the level of kidneys shows enlarged
left kidney. Multiple nonenhancing areas with air pockets are seen within the
left renal parenchyma (Fig. 1). Findings are suggestive of emphysematous
pyelonephritis.

Emphysematous pyelonephritis (EPN) is a life-threatening, fulminant, necro
tizing upper urinary tract infection associated with gas within the kidney. It is
rare, but the frequency is higher in patients who are immunocompromised,
especially patients with diabetes. Escherichia coli and Klebsiella pneumoniae
are the most common organisms isolated from urine culture. The diagnosis of
emphysematous pyelonephritis (EPN) is established radiologically. Without early
therapeutic intervention, the condition becomes rapidly progressive, generalizes
to fulminant sepsis, and carries a high mortality rate. CT is the modality of choice
for evaluating patients with emphysematous pyelonephritis. Findings include
parenchymal enlargement and destruction, small bubbly or linear streaks of
gas, fluid collections, gas-fluid levels, and focal tissue necrosis with or without
abscess.
Opinion
Emphysematous pyelonephritis.
Fig. 1
Clinical Discussion
The mean age of patients with EPN is reported as 55 years, with a range of 19–81
years. The condition is 6 times more common in women. Ninety-five percent
of patients have diabetes. In most patients, the diabetes is uncontrolled, with
high levels of glycosylated hemoglobin (72%) or high levels of blood sugar.
Patients typically present with fever, abdominal or flank pain, nausea and
vomiting, dyspnea, acute renal impairment, altered sensorium, shock, and
thrombocytopenia. Crepitus over the flank area may occur in advanced cases
of EPN. Two types of distribution of the gas have been found to correlate with
prognosis. Type 1 emphysematous pyelonephritis is characterized by renal
parenchymal destruction that manifests with either streaky or mottled areas of
gas. Intra- or extrarenal fluid collections are notably absent. In contradiction,
type 2 emphysematous pyelonephritis is characterized by renal or perirenal fluid
collections containing loculated gas or gas within the urinary collecting system.
Intravenous antibiotics are administered and percutaneous catheter drainage
of perirenal or retroperitoneal collections is done. Severe cases often warrant a
nephrectomy.
CASE
70 Renal Vein Thrombosis
CASE
A 40-year-old male with acute left flank pain and fever was subjected to CT
abdomen.

Axial post contrast CT image of abdomen at the level of kidneys shows enlarged left
kidney with multiple hypodense nonenhancing areas of collection with multiple
air pockets. Left renal vein is stretched and shows an intraluminal filling defect
(Fig. 1) suggestive of thrombosis. Findings are suggestive of emphysematous
pyelonephritis along with left renal vein thrombosis.
Fig. 1

Renal vein thrombosis (RVT) has numerous etiologies, but most commonly
occurs in patients with nephrotic syndrome. Dehydration and sepsis are common
underlying factors for renal vein thrombosis in children. In adults, renal vein
thrombosis can result from a variety of disorders include renal cell carcinoma,
nephrotic syndrome and collagen vascular disease. US is the initial study of choice
to exclude the presence of RVT. In an acute setting, US may reveal an edematous
and enlarged kidney with decreased echogenicity caused by diffuse edema, as
well as focal or diffuse disruption of parenchymal architecture and/or thrombus
in the renal vein. CT findings include decreased nephrographic attenuation, loss
of corticomedullary differentiation, a low-attenuating thrombus in the renal vein,
and renal enlargement with persistent parenchymal opacification. In the acute
stage of RVT, capsular venous collaterals and thickening of the Gerota’s fascia
are often observed. Acute renal vein thrombosis presents as absent nephrogram,
enlarged renal outline and stretched pelvicalyceal system.
Opinion
Emphysematous pyelonephritis with partially thrombosed left renal vein.
Clinical Discussion
The presentation of RVT is variable, and patients may be asymptomatic. When
RVT occurs as a result of malignancy, the signs of the renal malignancy like
hematuria and weight loss predominate. The more common chronic form of
RVT is generally overt. The less frequent acute form usually occurs in younger
patients, with flank pain and macroscopic hematuria, which can be severe in the
acute onset of thrombosis. When RVT is associated with infection then patients
present with pain, pyuria, and fever. RVT is seen in associated with antithrombin
III deficiency, protein C or S deficiency, antiphospholipid antibody syndrome,
pregnancy or estrogen therapy, renal vein invasion by malignant cells, postrenal
transplantation, Behçet syndrome, and extrinsic compression. CT currently is the
procedure of choice for diagnosing RVT. It depicts the occluded veins and renal
changes. Treatment of underlying cause is essential in treating the thrombosis
along with anticoagulation therapy. Surgery is rarely needed for treatment.
CASE
71 Renal Laceration
CASE
A 40-year-old male presented to the department of radiology with history of blunt
abdominal trauma.

Coronal post contrast reconstructed CT image of abdomen at the level of kidneys
show a large area of hypodensity in right kidney extending from its lateral border
to medial border horizontally. There is evidence of extravasation of contrast from
the middle and lower calyceal system. The interpolar region and lower pole of
right kidney appear hypodense suggesting large hematoma which is seen to
spread into the perirenal spaces (Fig. 1). This is suggestive of large renal tear
and Grade 4 renal injury according to American Association for the Surgery of
Trauma (AAST).

Renal trauma can result from direct blunt, penetrating and iatrogenic injury.
The mechanism of renal trauma is from deceleration injuries from collision of
the kidney with the vertebral column or thoracic cage. Renal laceration is seen
as irregular linear hypodense parenchymal areas. Most of these lacerations heal
on conservative management. Laceration with vascular injury or fracture kidney
requires operative intervention.
Opinion
Small renal laceration.
Clinical Discussion
Patients tend to present with microscopic or macroscopic hematuria and flank
and/or abdominal pain. In more severe cases, hypotension and shock may be
Fig. 1
present. Iatrogenic injuries can result from surgery, percutaneous renal biopsy,
nephrostomy and extracorporeal shock wave lithotripsy (ESWL). The mechanism
of injury is direct blow (>80%) frequently compressed and often lacerated by
lower ribs, and acceleration-deceleration injuries can produce renal artery tears.
It is associated with other organ injury in 20% of cases.
Renal injuries are graded by the American Association for the Surgery of
Trauma (AAST) on the basis of the depth of injury and the involvement of vessels
or the collecting system as follows:
• Grade 1: Hematuria with normal imaging studies, contusions, nonexpanding
subcapsular hematomas.
• Grade 2: Nonexpanding perinephric hematomas confined to the retro
peritoneum, superficial cortical lacerations less than 1 cm in depth without
collecting system injury.
• Grade 3: Renal lacerations greater than 1 cm in depth that do not involve the
collecting system.
• Grade 4: Renal lacerations extending through the kidney into the collecting
system, injuries involving the main renal artery or vein with contained
hemorrhage, segmental infarctions without associated lacerations, expanding
subcapsular hematomas compressing the kidney.
• Grade 5: Shattered or devascularized kidney, ureteropelvic avulsions,
complete laceration or thrombus of the main renal artery or vein.
CASE
72 Renal Angiomyolipoma
CASE
A 29-year-old female patient came with history of pain in abdomen and was
referred to radiology department for CT scan.

CT scan (Figs 1A to C) shows multiple well defined lesions containing fat, internal
septae and soft tissue components in both kidneys. The soft tissue components
show mild enhancement. The lesion at upper pole of left kidney has displaced the
pancreas and splenic vein anteriorly.
B C
Figs 1A to C

Renal angiomyolipomas (AML) are benign renal neoplasms. They are composed
of blood vessels (angio), plump spindle cells (myo) and adipose tissue (lipo).
On USG angiomyolipomas appear as well defined hyperechoic lesions, located
in the cortex with posterior acoustic shadowing. In the setting of tuberous
sclerosis, they may be so numerous that the entire kidney is affected, appearing
echogenic with loss of normal corticomedullary differentiation. On CT it appears
as well-marginated, cortical-based, heterogeneous tumor predominantly of fat
density (–20 to –40 HU) and shows variable enhancement due to smooth muscle
and vessels. Angiomyolipomas >4 cm bleed spontaneously in 60% cases. In
the setting of hemorrhage, or when lesions contain little fat, appearances may
be difficult to distinguish from a renal cell carcinoma. Isolated reports of renal
cell carcinoma with demonstrable fat content have appeared in the literature.
These renal carcinomas may entrap surrounding perinephric fat or undergo fatty
change because of metaplasia. Intratumoral fat is also reported in Wilms tumors,
oncocytoma, xanthogranulomatous pyelonephritis, renal and retroperitoneal
liposarcoma, and teratoma. Hemorrhagic shock can occur from bleeding into
angiomyolipoma or into retroperitoneum.
Opinion
Bilateral renal angiomyolipomas.
Clinical Discussion
The majority of angiomyolipomas are typically seen in adults in fifth decade of
life with a strong female predilection. Angiomyolipomas occur in 80% of patients
with tuberous sclerosis and are large, bilateral and usually multiple. Small lesions
are asymptomatic. Acute abdominal pain due to hemorrhage is the most common
presenting symptom. Patient may have a palpable mass with hematuria. Although
many angiomyolipomas do not show growth over time, those that occur with
the tuberous sclerosis complex are more likely to show progressive evolution
and are more likely to need intervention such as selective arterial embolization,
renal sparing surgery, or nephrectomy. The need for intervention, including
prophylactic embolization, should be predicated on the presence of rapid growth
or the development of symptoms related to retroperitoneal hemorrhage and
mass effect. Annual follow-up is required for lesions <4 cm. Larger tumors or
those that have been symptomatic can be electively embolized or resected with
a partial nephrectomy.
CASE
73 Wilms’ Tumor
CASE
A 6-year-old male child presented to the department of radiology with gradually
increasing lump in abdomen.

Axial post contrast CT images of abdomen (Figs 1A to D) at the level of kidneys
show a large well-defined enhancing soft tissue density lesion with few areas of
A B
C D
Figs 1A to D
necrosis, involving the right kidney, sparing its upper pole. Medially, the lesion
is seen to displace the pancreas and great vessels to left side with compression
of IVC. Cranially, the lesion is seen insinuating the inferior surface of liver and
inferiorly extends up to iliac crest. Findings are suggestive of Wilms’ Tumor.

Wilms’ tumor (nephroblastoma) accounts for 87% of pediatric renal masses and
arises from mesodermal precursors of the renal parenchyma (metanephros) and
occasionally is found to arise in the extrarenal retroperitoneum, presumably
within mesonephric remnants. Wilms’ tumor is the most common solid renal mass
and abdominal malignancy of childhood, with a prevalence of 1 case per 10,000
population. At USG, the mass has heterogeneous echogenicity, which represents
hemorrhage, fat, necrosis, or calcification. Examination of the inferior vena
cava is critical to detect tumor extension, which could necessitate modification
of the surgical approach. CT demonstrates the heterogeneous mass and nodal
metastases, as well as areas of calcification and fat. Intravenous administration
of contrast material is mandatory to detect nodal or hepatic metastases, tumor
extension into the renal vein or inferior vena cava, contralateral synchronous
tumor, and associated nephrogenic rests. Wilms’ tumor manifests as a solid
intrarenal mass with a pseudocapsule and distortion of the renal parenchyma
and collecting system. The tumor typically spreads by direct extension and
displaces adjacent structures but does not typically encase or elevate the aorta;
such encasement or elevation is a distinguishing characteristic of neuroblastoma.
Opinion
Wilms’ tumor.
Clinical Discussion
Wilms’ tumor is the most common abdominal malignancy of childhood. Both the
kidneys are affected synchronously or metachronously. Peak age of incidence is
2.5–3 years. There is no recognized gender predilection; however presentation is
a little later in females. Clinical presentation is typically with an asymptomatic
painless upper quadrant abdominal mass. Hematuria is seen in approximately
20% of cases and pain is uncommon. It has associations with multiple syndromes.
Wilms’ tumor staging is largely anatomical and relates to the invasion and spread
of the tumor.
The (post-surgical) staging of Wilms' tumor according to the North American
National Wilms' Tumor Study Group is summarized below:
• Stage I
– Confined to kidney
– Complete resection possible
• Stage II
– Local spread beyond kidney including renal vein involvement
– Complete resection possible
Case 73: Wilms’ Tumor 225
• Stage III
– Lymph-node involvement or
– Disease confined to the abdomen: For example, peritoneal spread, residual
tumor
– Complete resection NOT possible
• Stage IV
– Hematogenous metastases (typically lungs, liver, distant nodes)
• Stage V
– Bilateral renal involvement
– Each kidney should be staged individually
Unilateral Wilms’ tumor is generally treated with nephrectomy followed
by adjuvant chemotherapy. Presurgical treatment with chemotherapy may
be used to promote shrinkage of the tumor and improve outcome. In children
with bilateral Wilms’ tumor, preoperative chemotherapy is especially important
because each kidney is staged separately, and complete resolution of disease in
one kidney may allow surgery on the contralateral kidney with eventual cure.
CASE
74 Renal Cell Carcinoma
CASE
A 74-year-old male presented to the department of radiology with painless
hematuria and abdominal lump. Patient was subjected to CT scan abdomen and
pelvis.

CT abdomen shows evidence of iso to hypodense lesion one in both kidneys
which show heterogeneous enhancement with central hypodense necrotic areas.
Findings suggest bilateral renal cell carcinoma. Multiple well defined hypodense
lesions of various sizes are seen in liver. These represent metastases (Figs 1A and
B).
In another case axial plain and post contrast CT images of abdomen at the
level of kidneys show large, heterogeneously enhancing mass lesion in left renal
fossa with central hypodense area suggestive of necrosis (Figs 2A and B). Findings
suggest left renal cell carcinoma (RCC). Also chest radiograph and axial post-
contrast CT image of thorax shows multiple rounded mass lesions in bilateral
lungs suggestive of lung metastases (Figs 2C and D).
A B
Figs 1A and B
Case 74: Renal Cell Carcinoma 227
A B
C D
Figs 2A to D

Renal cell carcinoma (RCC) is the most common primary renal malignant
neoplasm in adults. It accounts for approximately 90% of renal tumors and 2%
of all adult malignancies. Risk factors include increased age, male sex, smoking,
cadmium, benzene, trichloroethylene, and asbestos exposure, excessive weight,
chronic dialysis use and several genetic syndromes (familial RCC, hereditary
papillary RCC, von Hippel-Lindau syndrome, and tuberous sclerosis). It presents
as painless hematuria. On CT examination it is iso to hypodense on plain CT and
shows heterogeneous enhancement on early arterial phase with necrosis within.
Opinion
Bilateral renal cell carcinoma with metastasis.
Clinical Discussion
Renal cell carcinoma patients are typically 50–70 years of age at presentation,
with a moderate male predilection of 2:1. Presentation is classically described as
the triad of macroscopic hematuria, flank pain, palpable flank mass. This triad
is however only found in 10–15% of patients, and increasingly the diagnosis is
being made on CT for assessment of hematuria alone or as an incidental finding.

However, clinical symptomatology may be quite nonspecific for example,
anorexia, tiredness, weight loss, or fever of unknown origin. Other presentations
include varicocele formation from tumor thrombus in the left renal vein or
the inferior vena cava. RCC may also present with a variety of paraneoplastic
syndromes, such as polycythemia secondary to excessive secretion of erythro
poietin, hypercalcemia secondary to factors regulating calcium, and hepatic
dysfunction.
RCCs can be staged by using the American Joint Committee on Cancer TNM
(T-Tumor, N-Node, M-Metastases) classification, as follows:
• Stage 1: RCCs are 7 cm or smaller and confined to the kidney.
• Stage 2: RCCs are larger than 7 cm but still organ confined.
• Stage 3: Tumors extend into the renal vein or vena cava, involve the ipsilateral
adrenal gland and/or perinephric fat, or have spread to local lymph nodes.
• Stage 4: Tumors extend beyond the Gerota fascia, have spread to local or
distant nodes, or have distant metastases.
Typically in renal cell carcinomas whenever feasible a radical nephrectomy
is performed, however in elderly patients or those with comorbidities, and
especially those with smaller tumors suggestive of papillary histology, then organ
sparing treatment can be done.
SECTION
16
Urinary Bladder
75. Vesical Calculus
76. Urinary Bladder Diverticulum
77. Cystitis
78. Carcinoma Urinary Bladder
CASE
75 Vesical Calculus
CASE
A 40-year-old male with history of burning micturition and pain in the suprapubic
region was referred to radiology department for CT abdomen and pelvis.

CT pelvis shows calcific lesion (CT value 730 HU) with irregular margins within
the urinary bladder diagnosed as vesical calculus (Fig. 1).
Fig. 1
232 Section 16: Urinary Bladder

Initial imaging choice is plain radiography of the kidneys, ureters, and bladder
(KUB) area or as the first film of intravenous pyelography (IVP), to detect
radiopaque stones. Pure uric acid and ammonium urate stones are radiolucent
but may be coated with a layer of opaque calcium sediment. Calculi with
laminations are common, with the layers stratified according to metabolic and
infectious status. Radiolucent calculi are seen as a filling defect in the bladder on
IVP. If the filling defect moves when the patient is repositioned, the presence of
a stone is likely possibility. Nonmobile filling defects could be calculi attached
to the bladder wall in a diverticulum, differential diagnosis includes urothelial
carcinoma, or clot. IVP may also be used to identify associated abnormalities, e.g.
upper urinary tract calculi, ureterocele, cystocele, enlarged prostate, and bladder
diverticula.
USG is widely available; being rapid modality is extensively used in the
diagnosis of bladder calculi. Sonograms typically show a classic hyperechoic
object with posterior shadowing, and they are effective in identifying both
radiolucent and radiopaque stones.
CT is usually performed for other reasons like abdominal pain, pelvic mass
or suspected abscess and may demonstrate bladder calculi even without
intravenous contrast. Unenhanced spiral CT scanning is highly sensitive and
specific in diagnosing calculi along the urinary tract. Even pure urate calculi can
be detected with this method. The stone may be obscured if contrast has been
administered.
Opinion
Vesical calculus.
Clinical Discussion
Vesical calculi are common in developing countries. It usually occurs in patients
who have urinary stasis, and recurrent bladder infections. It mostly affects
males over 50 who have bladder outlet obstruction due to enlarged prostate.
The chronic presence of bladder calculi has been associated with squamous
cell carcinoma. There may be pain, dysuria, increased frequency, hesitation,
terminal gross hematuria, suprapubic fullness. Most bladder stones form from a
nidus inside the bladder. They may be single or multiple. Causes include bladder
outlet obstruction, urinary infections, neurogenic bladder and schistosomiasis.
CASE
76 Urinary Bladder
Diverticulum
CASE
A 50-year-male patient with history of hematuria was referred to department of
radiology for CT abdomen and pelvis.

Plain X-ray abdomen shows staghorn calculus in right kidney and a large calculus
in bladder area (Fig. 1A). CT demonstrates a large posterior bladder diverticulum
with a large calculus (Fig. 1B). A large staghorn calculus is seen in right kidney
(Fig. 1C). Sagittal reconstructed CT image shows a posterior diverticulum filled
with urine and a large calculus within it (Fig. 1D).

A bladder diverticulum is an outpouching from the bladder wall, where mucosa
herniates through the bladder wall. They may be solitary or multiple in nature
and can vary considerably in size. Diverticula may be congenital or acquired.
Acquired diverticula are common, resulting from chronic bladder outlet
obstruction. Diverticula are often an incidental finding on imaging investigations,
including ultrasound, CT, MRI and IVU. They may be associated with a range of
complications including infection, reflux, stone formation and malignancy.
Opinion
Urinary bladder diverticulum with calculus.
Clinical Discussion
A Hutch diverticulum is a congenital bladder diverticulum seen at vesicoureteric
junction. Congenital bladder diverticulum, not associated with posterior urethral
valve are seen in boys. Patient presents with repeated urinary tract infection,
A C D
Figs 1A to D
incontinence or urinary retention. Micturating cystourethrogram (MCU) shows

contrast filled outpouchings arising from urinary bladder at vesicoureteric
junction, and often seen with vesico-ureteric reflux. On USG a round or oval
anechoic fluid collection is seen arising from base of urinary bladder or around
ureteric orifice. Incidentally detected diverticulum, does not require any therapy.
If associated with vesicoureteric reflux, recurrent urinary tract infection (UTI)
or obstruction, it should be excised. Differential diagnosis include bladder ears,
which protrude through internal inguinal ring. It is more often seen in children
than adults. Seen most often when bladder is maximally distended. Bladder ear
will empty when bladder is emptied whereas diverticula tend to fill when bladder
is emptied.
CASE
77 Cystitis
CASE
A 65-year-old male patient came to the radiology department with history of
burning micturition and was subjected to CT scan abdomen.

Figure 1 CT scan abdomen and pelvis shows thick irregular enhancing urinary
bladder wall s/o cystitis.
Fig. 1

Cystitis is inflammation of part or the entire urinary bladder wall. It may be
described as acute, chronic, hemorrhagic, bullous, emphysematous, polypoid.
USG shows thickening of the wall of the bladder when distended (>6 mm). CT
shows bladder wall thickening and perivesical edema. MR demonstrates mucosal
edema and inflammation as high signal intensity on T2WI, easily differentiated
from normal low-signal bladder wall. The common causes are infections,
bacterial, viral and fungal. Other causes included are indwelling catheter,
calculus, toxic and allergic etiologies.
Opinion
Cystitis.
Clinical Discussion
Acute cystitis may have a normal appearance; chronic usually appears as
thickened walls and diminishes filling capacity. Focal inflammation such
as bullous edema may be radiographically indistinguishable from bladder
carcinoma. Cystitis cystica is characterized by multiple fluid-filled submucosal
cysts. Most cases are associated with bladder infection. Cystitis glandularis is
a further progression of cystitis cystica with proliferation of mucous secreting
glands in the lamina propria. The cysts vary in size and may obstruct the ureteral
orifice. Cystitis glandularis may be a precursor of adenocarcinoma of the bladder.
Bullous edema of the bladder wall is usually associated with chronic irritation
from indwelling catheters. Grape-like cysts elevate the mucosa. Interstitial cystitis
is a chronic, idiopathic inflammation of the bladder found most often in women.
The bladder capacity is progressively diminished, and the bladder wall thickens
and becomes trabeculated and fibrotic. Hemorrhagic cystitis is characterized
by hemorrhage into the mucosa and submucosa. It is caused by bacterial or
adenovirus infection. Eosinophilic cystitis is an infiltration of the bladder wall by
eosinophils. The cause is uncertain. The bladder wall is greatly thickened and
frequently nodular. Emphysematous cystitis is a form of bladder inflammation
with gas within the bladder wall. It is associated with poorly controlled diabetes
mellitus, bladder outlet obstruction, and infection with Escherichia coli, which
ferment sugar in the urine to release carbon dioxide and hydrogen gasses. Gas
within the bladder lumen is seen with emphysematous cystitis, instrumentation,
and vesicocolic fistula.
CASE
78 Carcinoma Urinary
Bladder
CASE
A 75-year-old female patient came to the radiology department with painless
hematuria since 1 month.

Figures 1A to F scout image shows staghorn calculus in right renal pelvis. Plain
CT shows staghorn calculus with small renal calyceal calculi. A growth is seen
within the bladder on right side. Contrast CT shows uptake of contrast by renal
A B C
D E F
Figs 1A to F
A B
Figs 2A and B
parenchyma and excretion by both kidneys. Delayed contrast CT shows contrast

opacified right ureter coursing through the mass in urinary bladder.
In another case (Figs 2A and B) posterior and right lateral wall of urinary
bladder shows irregular wall thickening. Right vesicoureteric junction is involved.
Fat plane with rectum is however preserved.

Imaging of bladder transitional cell carcinomas has a number of roles: incidental
discovery of tumor, tumor staging, tumor staging of locally advanced masses and
evaluation of distant metastases and nodal status. Ultrasound has limited role
to play in either diagnosis or staging transitional cell carcinomas of the urinary
tract in general. On CT bladder transitional cell carcinomas appear as either focal
regions of thickening of the bladder wall, or as masses protruding into the bladder
lumen, or in advanced cases, extending into adjacent tissues. Care should be
taken in assessing bladder wall thickness as these changes with the degree of
bladder distension and varies from patient to patient (e.g. patients with bladder
outlet obstruction due to benign prostatic hypertrophy). In general however,
asymmetric mural thickening should be viewed with suspicion. The masses
are of soft tissue attenuation and may be encrusted with small calcifications.
Although unable to distinguish between T1, T2 and T3a (microscopic extravesical
spread), CT is able to distinguish T3b tumours (stranding/nodules in perivesical
fat) and T4 tumours (direct extension into adjacent structures/loss of normal
fat plane). Care should be exercised when interpreting stranding or nodularity
Case 78: Carcinoma Urinary Bladder 239
following transurethral resection or even biopsy, as these changes may be post-

operative. Nodal metastases are common. MRI is superior to other modalities in
locally staging the tumor. Unfortunately FDG is excreted into the urine, and thus
accumulates in the bladder, making it unsuitable for diagnosis of urinary tract
tumors.
Opinion
Carcinoma urinary bladder.
Clinical Discussion
The classical clinical presentation is painless gross hematuria. The risk factors
being smoking, irradiation, exposure to aniline dyes, chemotherapy with
cyclophosphamide. Urothelial (transitional cell carcinomas) are the most
common tumors followed by squamous cell carcinomas and adenocarcinomas.
Bladder cancer typically occurs in men aged 50–70 years and is related to smoking
or occupational exposure to carcinogens. Most urothelial neoplasms are low-
grade papillary tumors, which tend to be multifocal and recur but have a relatively
good prognosis. High-grade invasive tumors are less common and have a much
poorer prognosis. Squamous cell carcinomas and adenocarcinomas occur in the
setting of chronic irritation. Rarer mesenchymal tumors include paraganglioma,
lymphoma, leiomyoma, and solitary fibrous tumor. A tumor located at the
vesicoureteric junction may result in ureteral obstruction and hydronephrosis,
which may present with flank pain. Additionally tumors near the urethral orifice
may result in bladder outlet obstruction and urinary retention. Occasionally
patients only present once systemic symptoms of metastatic disease are present.
Diagnosis and local tumor staging is usually achieved with cystoscopy and full
thickness biopsy.
SECTION
17
Prostate
79. Carcinoma Prostate
CASE
79 Carcinoma Prostate
CASE
A 60-year-old male patient with prostatomegaly and raised prostate specific
antigen (PSA) levels was referred for CT abdomen and pelvis.

Prostate is enlarged with irregular contours (Fig. 1A).The fat plane with posterior
wall of urinary bladder is lost (Fig. 1B). Enhancing metastases is seen in right lobe
of liver (Fig. 1C). Large left pleural effusion with collapse of the underlying lung
(Fig. 1D) is seen.
A B
C D
Figs 1A to D
244 Section 17: Prostate

Prostate cancer usually arises within the peripheral zone near the rectum which
is why a digital rectal exam (DRE) is a useful screening test. Nowadays serum
prostate-specific antigen (PSA) tests and transrectal ultrasound (TRUS)-guided
biopsy are widely used for detecting prostate cancers. Few men now present with
locoregional or metastatic disease identified by standard imaging, i.e. bone scan
or cross-sectional pelvic imaging MRI or CT.
Opinion
Carcinoma prostate with hepatic metastases.
Clinical Discussion
Prostatic carcinoma is the most common malignant tumor in men. Prostatic
adenocarcinoma is the most common histological type. Prostate cancer is
detected by an elevated prostate specific antigen level (normal range is 1–
4 ng/dL). Transrectal ultrasonography (TRUS) is often initially performed in
order to detect abnormalities and to guide biopsy, following an abnormal PSA
level. On ultrasound prostate cancer is usually seen as a hypoechoic lesion in the
peripheral zone of the gland, but can be hyperechoic or isoechoic. USG is used to
direct biopsy of suspicious, hypoechoic regions, usually in the peripheral zone.
Transrectal ultrasound is also the modality of choice for directing brachytherapy
seeds into the prostate gland. USG cannot detect in situ prostate cancer. The
normal prostate gland appears as an elliptical structure on CT scan. Scans of
the abdomen and pelvis are normally obtained prior to the onset of radiation
therapy to identify bony landmarks for planning. In advanced disease CT can
identify enlarged pelvic and retroperitoneal lymph nodes, hydronephrosis and
osteoblastic metastases. The primary indication for MRI of the prostate is in the
evaluation of prostate cancer, after an ultrasound guided prostate biopsy has
confirmed cancer. MRI using endorectal coil, is considered more sensitive than
CT as it can determine extracapsular extension.
.
SECTION
18
Scrotum
80. Hydrocele
81. Testicular Trauma
82. Seminoma
83. Undescended Testis
CASE
80 Hydrocele
CASE
A 35-year-old male with history of scrotal swelling was referred to the department
of radiology for CT abdomen and pelvis.

Axial CT pelvis (Fig. 1) shows accumulation of fluid in tunica vaginalis of both
testes suggestive of bilateral hydrocele.
Fig. 1
248 Section 18: Scrotum

Ultrasonography provides excellent detail of the testicular parenchyma and is the
modality of choice to evaluate hydrocele. It presents as fluid collection surrounding
the testis. It may contain septations. Ultrasound is also useful in identifying
abnormalities in the testis, complex cystic masses, tumors, appendages, or
associated hernia. Plain radiography may be useful for distinguishing an acute
hydrocele from an incarcerated hernia. Gas overlying the groin may indicate
an incarcerated hernia. On CT examination hydrocele appears as hypodense
collection with CT value in HU’s similar to water within the scrotal sac. On MRI
examination hydrocele is of low intensity on T1WI and high intensity on T2WI.
Opinion
Bilateral hydrocele.
Clinical Discussion
Most hydrocele is acquired and the usual presentation is painless enlarged
scrotum. Hydroceles can be secondarily infected. There are two subtypes of
congenital hydrocele.
1. Encysted type with no communication with the peritoneum or tunica vaginalis,
also called spermatic cord cyst. An encysted hydrocele is enclosed between
two constrictions at the deep inguinal ring, just above the testis. It does not
communicate with the peritoneum. It may be located anywhere along the
spermatic cord and can be of any size or shape, but it does not change with
increased peritoneal pressure. On ultrasound, an ovoid or round mass is seen
in the groin along the spermatic cord; internal echogenicity varies depending
on the content.
2. Funicular type which communicates with the peritoneum at the internal ring
and does not surround the testis. This type is also called funiculocele. They are
more frequently encountered in premature infant and children.
CASE
81 Testicular Trauma
CASE
A 40-year-old male with history of road traffic accident came to radiology

Axial CT pelvis (Fig. 1) shows disrupted right testis and fluid collection in right
scrotal sac suggestive of hematocele.
Fig. 1

In trauma there is either a hematocele or testicular hematoma. In the acute
phase the hemorrhage is hyperdense and in the chronic phase it is hypodense.
A hematocele results from scrotal or intra-abdominal hemorrhage. It represents
bleeding between the leaves of the tunica vaginalis and appears as a complex
fluid collection. With time, this collection can develop loculations, which appear
as thick septations. It is important to tell if the testis is intact, because if there is
a rupture, this can sometimes be treated surgically. Testicular rupture is seen as
focal alterations of testicular architecture. A discrete fracture plane is identified
in fewer than 20% of cases, although visible alterations in the testicular contour
are a common finding. The axial CT pelvis demonstrated a large hematocele.
Opinion
Testicular rupture with hematocele.
Clinical Discussion
Blunt injury (e.g. from an athletic accident or motor vehicle collision) is the most
common cause of scrotal trauma, followed by penetrating injury from gunshot
or other assault. Knowledge of the scrotal anatomy and appropriate imaging
techniques are key for accurate evaluation of scrotal injuries. Ultrasonography
(USG) is the first-line imaging modality to help guide therapy for scrotal trauma,
except in degloving injury, which results in scrotal skin avulsion. Trauma often
may result in hematoma, hydrocele, hematocele, testicular fracture, or testicular
rupture. The timely diagnosis of rupture, based on a US finding of discontinuity
of the echogenic tunica albuginea, is critical because emergent surgery results
in salvage of the testis in 80–90% of rupture cases. The radiologist should be
familiar also with other nuances associated with penetrating trauma, iatrogenic
and postoperative complications, and electrical injury. Color flow and duplex
Doppler imaging are highly useful techniques not only for assessing testicular
viability and perfusion but also for evaluating associated vascular injuries such
as pseudoaneurysms. Testicular torsion can occur as a result of minor/incidental
trauma. Testicular torsion occurs when a testicle torts on the spermatic cord
resulting in the cutting off of blood supply. Ultrasound is helpful in confirming
the diagnosis. Testicular torsion implies obstruction of first venous, and later,
arterial flow. The extent of testicular ischemia will depend on the degree of
twisting (180°–720°) and the duration of the torsion. Key findings of a torsed
testis on USG include twisting of the spermatic cord resulting in whirlpool sign
which may be appreciated on Doppler and increase in size of the testis and
epididymis. Homogeneous echotexture is an early finding, prior to necrosis.
Heterogeneous echotexture is a late finding (after 24 hours), implies necrosis.
The key to successful treatment is rapid diagnosis and surgical intervention. If
diagnosed early enough the testis can be detorted with little damage. If the testis
has necrosed, then orchidectomy is required.
CASE
82 Seminoma
CASE
A 28-year-old male with painless progressive swelling in left testis came for CT
abdomen and pelvis.

Axial CT abdomen and pelvis shows a solid enhancing left testicular mass
(Fig. 1A) and intra-abdominal lymphadenopathy (Fig. 1B).

Abdominal and pelvic CT is important in visualizing metastases both as a part
of primary staging of seminoma testes and also in primary diagnosis when a
testicular mass is of unknown etiology. Metastases to the para-aortic lymph nodes
at the level of the renal vessels are the typical first site of spread owing to the
lymphatic drainage of the testicles relating to embryological testicular descent.
The nodal metastases are often bulky, of homogeneous density and tend to encase
surrounding vessels. Inguinal or iliac lymph node metastases suggest lymphatic
spread via the scrotum and therefore local tumor extension beyond the tunica
vaginalis. Visceral metastases are seen in around 5% of patients at presentation
(lung, liver, bone, brain). Staging CT of the chest is only indicated when there
is an abnormal chest X-ray. Fluoro-2-deoxy-D-glucose (FDG) positron emission
tomography (PET) has been evaluated for its utility in staging and restaging of
seminomatous and nonseminomatous tumors.
Opinion
Left testicular seminoma.
B
Figs 1A and B
Clinical Discussion
Germ cell tumors are the most common malignancy in men aged 15–35 years,
with seminoma accounting for one third of such cases. Risk factors for seminoma
are (1) Undescended testis is the major risk factor for testicular germ cell tumors;
(2) Increased risk in the contralateral normally descended testis; (3) Previous
tumor in contra lateral testis; (4) Family history of testicular germ cell tumor;
(5) Testicular microlithiasis; (6) Other risk factors include infections such as HIV,
mumps, orchitis and history of trauma or organ transplant immunosuppression.
The most common presentation is with a painless testicular mass. Bilateral
tumors are rare. Diagnosis following trauma is common as it draws the patient’s
attention to the lump. Back pain, abdominal discomfort or abdominal mass may
be a presenting feature in the patients who have retroperitoneal nodal metastases.
Presentation with distant and extra nodal metastases is rare.
CASE
83 Undescended Testis
CASE
A 6-year-old male child with empty scrotal sac was subjected to ultrasound and
CT abdomen.

Ultrasound (Figs 1A and B) and CT abdomen and pelvis (Figs 1C and D) show right
and left testis in respective inguinal regions suggestive of bilateral undescended
testes.
A B
C D
Figs 1A to D

An absence of testes in the scrotal sac is called cryptorchidism and may be termed
as undescended testes, ectopic testes, atrophic or absent testes. Ultrasound
shows a homogeneously hypoechoic ovoid structure, similar to contralateral
testes, with an echogenic mediastinum testes. Sonography is excellent in
location of testes, high up in scrotum or within inguinal canal. However, its use is
limited in intra-abdominal, pelvic or retroperitoneal/ectopic testes. Ultrasound
is also inconclusive in atrophic small testes, where it is difficult to differentiate
from lymph nodes. MRI is the best cross-sectional modality to assess crypto-
orchidism. Coronal T1W images can show gubernaculum testes and spermatic
cord, which can be followed to locate the undescended testes. Also, ectopic
pelvic or retroperitoneal location of testes can be identified. Diffusion-weighted
MRI shows restriction and hyperintense testes.
Opinion
Undescended testes.
Clinical Discussion
Testes remain in the intra-abdominal location till 7 months of gestation,
when it descends into the inguinal canal through the deep inguinal ring.
The gubernaculum is the ligament, which connects the testes to the scrotum.
Under hormonal influence gubernaculum testes contracts, and testes descends
into the scrotum. Undescended testes are associated with premature birth,
smoking and alcohol intake during pregnancy, androgen, Prader-Willi syndrome,
Noonan syndrome, cloacal exstrophy, Prune-Belly syndrome and gestational
diabetes.
Orchidopexy is the preferred procedure in case of viable testes high-up in
scrotum or within inguinal canal. However, it is done after 1 year of age because
testes may descend during first year of life under testosterone influence. Any
nonviable, atrophic or ectopic testis is however not left, and orchidectomy is the
only option as there is high risk of malignant transformation.
SECTION
19
Penis
84. Penile Carcinoma
CASE
84 Penile Carcinoma
CASE
A 56-year-old male with history of foul smelling discharge from penis with sore
came to department of radiology for CT abdomen and pelvis.

CT pelvis is showing enhancing mass and architectural distortion of glans and
extending to the shaft of penis (Figs 1A and B).

Squamous cell carcinoma of the penis is most commonly located in the glans
penis in 40% of cases. In decreasing order of frequency, other locations include
the prepuce, coronal sulcus, and shaft. The spread of penile cancer usually
A B
Figs 1A and B
258 Section 19: Penis
occurs via lymphatic vessels, with the Buck fascia acting as a barrier to corporal
invasion and hematogenous spread. The lymphatic spread of cancer from the
penis differs with the location of the primary lesion. The lymphatic vessels of the
skin of the penis and prepuce drain primarily into the superficial inguinal nodes.
The lymphatic vessels of the glans penis drain into the deep inguinal and external
iliac nodes, and those of the erectile tissue and penile urethra drain into the
internal iliac nodes. Because there is communication between lymphatic vessels,
bilateral lymphadenopathy may be seen with a unilateral tumor. Invariably, the
lymphatic vessels of the penis first drain into the inguinal nodes before reaching
the pelvic nodes.
Opinion
Penile carcinoma.
Clinical Discussion
Patients with penile carcinoma presents with complaints of redness, rash and
foul smelling discharge from the penis, pain, growth or sore on the penis of more
than four weeks duration, generally occurs above 55 years of age, bleeding from
the penis or from under the fore skin, change in color of the penis or phimosis.
Risk factors for penile carcinoma include HIV, human papillomavirus (HPV),
genital warts, poor hygiene, smegma, balanitis, phimosis, and paraphimosis. The
treatment of penile cancer varies depending on the site and extent of the primary
cancer and the presence of metastatic inguinal lymphadenopathy. Circumcision
alone may cure patients with small tumors of the distal prepuce, whereas
tumors of the glans penis and distal shaft require partial penectomy, including
a 2-cm tumor-free margin. Bulky tumors of the proximal penis are treated with
total penectomy and perineal urethrostomy. Inguinal lymphadenectomy can
be performed at the time of the penile surgery or later. The current approach
for dealing with palpable inguinal lymph nodes includes re-evaluation after
4–6 weeks of antibiotic therapy. This approach is based on the principle that
reactive lymphadenopathy will resolve following antibiotic treatment, whereas
neoplastic lymphadenopathy will persist. The continued presence of lymph
nodes in the inguinal region is treated with bilateral inguinal lymphadenectomy.
Radiation therapy with external beam irradiation and brachytherapy has yielded
local control rates similar to those for surgical resection. Radiation therapy and
laser therapy are the best conservative therapeutic options for localized disease.
Treatment for metastases is generally palliative.
SECTION
20
Uterus
85. Broad Ligament Fibroid
86. Hydrometrocolpos
87. Pyometra
88. Endometrial Carcinoma
89. Carcinoma Cervix
90. Vaginal Carcinoma
91. Ureterovaginal Fistula
92. Vulval Carcinoma
CASE
85 Broad Ligament Fibroid
CASE
A 35-year-old female with history of pain in lower abdomen was referred to
radiology department for CT scan abdomen including pelvis.

CT shows a homogeneous moderately enhancing well defined soft tissue density
mass in left adnexa (F) attached to superolateral aspect of uterus (U). Left ovary
is seen separately from the mass (O). It has same imaging characteristics as the
uterine myometrium (Figs 1A to D). Findings are suggestive of broad ligament
fibroid.

A broad ligament fibroid occurs in relation to the broad ligament and is considered
as variation of uterine leiomyoma. Usually seen as hypoechoic, solid, well-
circumscribed adnexal mass, larger lesions show heterogeneous appearance.
There is no interface between tumor and uterus and no relation to the ipsilateral
ovary. CT imaging characteristics are similar to uterine fibroid. They are usually of
soft tissue density but may exhibit coarse peripheral or central calcification with
variable enhancement pattern. On MRI signal characteristics in uncomplicated
cases are essentially similar to a uterine leiomyoma. Fibroids appear as sharply
marginated areas of low to intermediate signal intensity on T1- and T2-weighted
MRI scans. Most lesions enhance on post contrast images similarly to the
myometrium, while larger leiomyomas tend to enhance heterogeneously.
Opinion
Broad ligament fibroid.
262 Section 20: Uterus
A B
C D
Figs 1A to D
Clinical Discussion
It is an extra-uterine leiomyoma arising from the broad ligament usually from
a stalk. Torsion of the leiomyoma can occur if it is pedunculated. Differential
diagnosis include unusual leiomyomas like pedunculated sub-serosal leiomyoma
projecting towards the broad ligament, solid ovarian neoplasms particularly
those with dominant fibrous components like ovarian fibroma, fibrothecoma
and Brenner tumor which are inseparable from the ovary.
CASE
86 Hydrometrocolpos
CASE
A 11-year-old patient came with history of pain in abdomen since 5 days and was
referred to radiology department for CT scan abdomen.

CT scan pelvis shows a large well defined elliptical collection seen in the uterine
endometrial cavity and also in vagina (Figs 1A to D). The contents of this collection
are clear.
A B
C D
Figs 1A to D

Hydro/hematometrocolpos is accumulation of sterile fluid (hydro)/blood
(hemato)/or pus (pyo) within the uterus (metra) and vagina (colpos). The
condition is caused by an obstruction due to an imperforate hymen, a transverse
vaginal septum, or stenosis-atresia of the vagina. Presents either in infancy (due
to influence of maternal hormones) or puberty. Vagina usually dilates more than
uterus (due to elastic walls) and are associated with Müllerian duct anomalies
(especially didelphys uterus). Sonographically, there is a cystic midline mass that
may contain mildly echogenic areas in the fluid collection representing mucous
secretions or blood. CT can also show distended fluid filled uterine cavity and
vagina. MR is sometimes helpful for further evaluation, especially if Müllerian
duct anomaly is present. Associated abnormalities are uterine didelphys,
bicornuate uterus, renal agenesis, intestinal aganglionosis, imperforate anus,
urogenital sinus and also vertebral and cardiac anomalies.
Opinion
Hydrometrocolpos.
Clinical Discussion
Hydrometrocolpos is characterized by an expanded fluid filled vaginal cavity with
associated distention of the uterine cavity. It may present in infancy with a lower
abdominal mass, or be delayed till menarche. Hydrocolpos and hydrometrocolpos
are due to vaginal or cervical obstruction and can present in either the newborn
period or around puberty. In newborn girls, hydrometrocolpos accounts for
15% of abdominal masses. Obstructions caused by an imperforate hymen
are generally not associated with other congenital abnormalities. Frequently,
imperforate anus, cloacal exstrophy, and persistent urogenital sinus will have
associated hydrometrocolpos. McKusick-Kaufman syndrome is an autosomal
recessive multiple malformation syndrome characterized by hydrometrocolpos
and postaxial polydactyly. Mayer-Rokitansky-Küster-Hauser syndrome com
bines a variety of uterine anomalies, vaginal atresia with normal Fallopian tubes
and ovaries, and is the second most common cause of primary amenorrhea.
Complications of hydrometrocolpos include reflux of the endometrial tissue via
the Fallopian tubes (i.e. hematosalpinx) may result in secondary endometriosis,
endo-/myo-/parametritis, hydronephrosis, pelvic abscess and urinary tract
infection.
CASE
87 Pyometra
CASE
A 55-year-old female with history of carcinoma cervix and post chemotherapy
came with a history of pain abdomen, fever and distension.

Contrast-enhanced computed tomography (CECT) scan of pelvis (Figs 1A to D)
shows enhancing large fluid collections in the uterus in a patient who had earlier
A B
C D
Figs 1A to D
undergone chemotherapy for carcinoma cervix. No mass is seen in the cervix

however it is stenosed.

Pyometra is an infection of endometrial cavity and a collection of pus distending
the uterine cavity. It occurs principally when there is a stenosed cervical os, usually
due to uterine or cervical malignancy. In order for pyometra to develop, there
must be both an infection and blockage of cervix. Signs and symptoms include
lower abdominal pain, fever with rigors, and discharge of pus from uterus.
Opinion
Pyometra.
Clinical Discussion
Causes of pyometra are endometritis/pelvic inflammatory disease, uterine
malignancies, pelvic irradiation, cervical stenosis, retained products of
conception, imperforate hymen. It is more common in postmenopausal women
than women of child bearing age in whom hematometra is more common. CT
shows enhancing collection in the uterine cavity. In case of ruptured pyometra CT
shows evidence of ascites with features of inflammation. Exploratory laparotomy
is diagnostic.
CASE
88 Endometrial Carcinoma
CASE
A 59-year-old female with history of post menopausal bleeding was referred to
radiology department for CT scan abdomen and pelvis.

CT shows collection in the uterine cavity lined on all sides by a thick irregular
endometrial wall (Figs 1A to D). Biopsy proved this to be a high grade carcinoma
of endometrium.

The diagnosis of endometrial carcinoma is usually made by endometrial biopsy
or by dilatation and curettage. Transvaginal ultrasound is the preferred method
of screening for endometrial abnormalities in high-risk patients such as those
on estrogen replacement therapy and tamoxifen treatment for breast carcinoma.
The appearance of endometrial carcinoma on ultrasound is variable, ranging
from a completely normal-appearing uterus; to echogenic thickening of the
endometrium (greater than 15 mm in premenopausal and greater than 5 mm
in postmenopausal women); to an irregular, heterogeneous, hyperechoic
endometrium with ill-defined hypoechoic or isoechoic areas. CT has a role in
assessing for distant metastases. Although not generally used for initial diagnosis
or local staging, endometrial carcinoma may be encountered on CT. Oral, rectal,
and IV administration of contrast material is necessary for optimal CT evaluation.
Following IV contrast administration, nonuniform contrast enhancement of
the tumor may occur but to a much lesser degree than the usually intense and
uniform enhancement of the normal myometrium. Thus, the endometrial tumor
may become apparent on postcontrast images as a lesion with relatively low
attenuation. On post contrast CT it may show diffuse thickening or mass within
endometrial cavity. Endometrial carcinoma spreads by local infiltration from the
endometrium to the myometrium and along the lower uterine segment to the
cervix. Other routes of spread follow lymphatic channels.
A B
C D
Figs 1A to D
Opinion
Endometrial carcinoma.
Clinical Discussion
Endometrial carcinoma is the most common gynecologic cancer. Risk
factors include obesity, nulliparity, estrogen replacement, estrogen-secreting
ovarian tumors, late-onset menopause, diabetes mellitus, anovulatory cycles,
polycystic ovaries, and adenomatous hyperplasia. Most endometrial cancers
Case 88: Endometrial Carcinoma 269
are adenocarcinomas. Presentation peaks at around the 6th decade. Patients

commonly present at an early stage, with post menopausal bleeding as the initial
symptom. CT is the imaging modality used most commonly in clinical practice
to determine the extent of spread of endometrial cancer. It can also present as
polypoid mass surrounded by endometrial fluid or as a heterogeneous soft tissue
mass and fluid expanding the endometrial cavity.
CT staging of endometrial cancer is based on the surgical/pathologic FIGO
classification, as shown below:
Stage I: Tumor confined to the uterine corpus
Stage II: Tumor invades cervical stroma, but does not extend beyond the uterus
Stage III: Local and/or regional spread of the tumor
Stage IV: Tumor invades bladder and/or bowel mucosa and/or distant metastases.
CASE
89 Carcinoma Cervix
CASE
A 43-year-old female came with history of vaginal bleeding and discharge and
was referred to radiology department for CT scan.

Figures 1A to E (A) Plain CT pelvis (Fig. 1A) shows a hyperdense cervical mass
with loss of fat plane anteriorly with urinary bladder and posteriorly with rectum;
(B) Immediate postcontrast CT shows normal contrast uptake by left kidney.
Right kidney shows gross hydronephrosis; (C to E) show invasion of the uterus,
urinary bladder, rectum and right lower ureter.

In locally confined disease, a cervical mass may be seen by ultrasound. In locally
advanced disease, the cervix may become diffusely enlarged, inhomogeneous,
and irregularly marginated.
Cervical cancer and the normal cervical stroma usually have similar
attenuations on CT images that are obtained without intravenous contrast
enhancement. Therefore, the tumor and the normal cervical parenchyma cannot
be reliably distinguished on nonenhanced CT scans. After the intravenous
administration of contrast material CT shows an enlarged cervix with normal
contrast enhancement or an enlarged cervix with inhomogeneous areas of
hypoattenuation but without a discrete mass that is clearly delineated or an
enlarged cervix with a circumscribed solid mass that has an enhancement
which is less than that of the normal cervical stroma and shows a homogeneous
or heterogeneous hypoattenuation. Cervical cancer frequently obstructs the
endocervical canal, resulting in accumulation of serous, hemorrhagic, or
purulent fluid in the uterine cavity. The presence of hydrometras should raise the
suspicion of cervical or endometrial carcinoma. Cervical cancer spreads by either
local infiltration into parametrium, pelvic sidewall, and adjacent organs (vagina,
ureters, bladder, and rectum) or by lymphatic spread to the pelvic (obturator and
Case 89: Carcinoma Cervix 271
A B C
D E
Figs 1A to E
external, internal, and common iliac) and para-aortic lymph node. In advanced
cases hematogenous metastases to the lungs, liver, brain, and bones can occur.
Opinion
Carcinoma of cervix.
Clinical Discussion
Carcinoma of the cervix is a malignancy arising from the cervix. It typically
presents in younger women with the average age of onset at around 45 years.
Risk factors include human papilloma virus infection, multiple sexual partners
and early age of first sexual intercourse. Cervical carcinoma arises from the
squamo-columnar junction. In order to be radiographically visible, tumors must
be at least stage Ib or above. MRI is the imaging modality of choice to depict the
primary tumor and assess local extent due to its improved contrast resolution
and multiplanar capability. Distant metastatic disease is best assessed with CT
or PET where available. CT in general is not very useful in assessment of the
primary tumor but can be useful in assessing advanced disease. It is performed
primarily to assess adenopathy but also has roles in defining advanced disease,
monitoring distant metastasis, planning the placement of radiation ports, and
guiding percutaneous biopsy. The treatment and prognosis of invasive cervical
carcinoma depends on tumor volume, extent of disease, histological grade,
vascular and lymphatic spread.
CASE
90 Vaginal Carcinoma
CASE
A 55-year-old female with complaints of pain in pelvis and vaginal bleeding was
referred for CT abdomen and pelvis.

Contrast-enhanced computed tomography (CECT) scan abdomen and pelvis
(Figs 1A and B) shows abnormal enhancing soft tissue seen in the region of the
vault and entire vagina with few nonenhancing necrotic areas. The lesion is seen
abutting the rectum with loss of fat planes and is also seen involving the anal
canal. Bilateral iliac and right inguinal lymphadenopathy are also seen.

Squamous cell carcinoma makes up about 85% of primary vaginal malignancies.
This tumor arises from the posterior wall of the upper third of the vagina. The main
patterns of disease are an ulcerating or fungating mass or an annular constricting
lesion. CT is recommended for assessment of groin, pelvis, and extra pelvic lymph
A B
Figs 1A and B
Case 90: Vaginal Carcinoma 273
node metastasis. CT criteria for lymph node metastases are based on short-axis
diameter of ≥ 1 cm, thus, CT cannot detect metastases in lymph nodes < 1 cm.
Because the treatment and prognosis change with the presence of pelvic lymph
node metastases, it is imperative to find the metastases. CT is not helpful in local
staging of the tumor because of its low soft-tissue contrast resolution; however,
CT can assess the involvement of bladder or the rectum, detect metastases to the
lungs and the bone, and help plan radiation treatment. At magnetic resonance
(MR) imaging, squamous cell carcinoma has intermediate signal intensity on T2-
weighted images and low signal intensity on T1-weighted images.
Opinion
Vaginal carcinoma with lymph node metastasis.
Clinical Discussion
Carcinoma in situ is often treated with surgery. However, the standard therapeutic
intervention for patients with carcinoma of the vagina is radiation therapy.
Advanced stages are often treated with radiotherapy and chemotherapy.
CASE
91 Ureterovaginal Fistula
CASE
A 50-year-old female with history of hysterectomy 7 months back complaining
of urinary incontinence through vagina was referred to radiology department for
CT scan abdomen and pelvis.

Early post contrast CT image of pelvis shows fluid in vagina (Fig. 1A). The vagina
is completely opacified with contrast on delayed image (Fig. 1B). Hydronephrosis
and hydroureter is seen on left side. The left distal ureter is communicating with
the vagina (Fig. 1C) as a result of ureterovaginal fistula.

Uretero-vaginal fistula refers to a fistulous communication between ureter and
vagina. The diagnosis may be made by direct visualization on vaginoscopy and
cystourethroscopy. Excretory urography can help in diagnosing ureterovaginal
fistula. In this a vaginal swab is kept during the procedure, which gets soaked with
contrast. Although, differentiation with vesicovaginal fistula is difficult, oblique
images may demonstrate ureterovaginal fistula. Delayed contrast enhanced CT
helps in direct visualization of the fistulous tract. Vesicovaginal fistula may be a
co-existing finding.
Opinion
Ureterovaginal fistula.
Clinical Discussion
Patients of ureterovaginal fistula come with complaints of incontinence of
urine, fever with chills due to secondary urinary tract infections. Ureterovaginal
fistula predominantly occurs as a result of ureteral injury during gynecological/
Case 91: Ureterovaginal Fistula 275
B C
Figs 1A to C
obstetric surgery like abdominal/vaginal/radical hysterectomy, cesarean section

and other pelvic surgical procedures like vascular and urological surgery. This
fistula can also result from locally advanced malignant disease, radiation therapy
and pelvic trauma. The main aim of the treatment of ureterovaginal fistula is
the resolution of the urinary leakage, prevention of urosepsis and preservation
of renal function. Treatment of choice is nephrostomy and ureteral stent
placement. Complications associated with ureterovaginal fistula repair, are
urinary extravasation and ureteral stricture formation.
CASE
92 Vulval Carcinoma
CASE
A 75-year-old female came with history of vaginal growth and bleeding. CT
abdomen and pelvis was done.

Figure 1 shows asymmetric soft tissue density lesion seen in vulva on right
side. No local or distant intra-abdominal metastases were seen on contrast CT
abdomen. Biopsy showed it to be a squamous cell carcinoma of vulva.
Comments and explanation

Primary vulvar cancer is a rare gynecological malignancy that originates from the
vulva. The most common histological type by far is squamous cell carcinoma.
Fig. 1
Case 92: Vulval Carcinoma 277
The tumor commonly involves the labia majora and minora. The labia majora
are the most common site followed by the labia minora. The clitoris may rarely be
involved. CT scan gives information about the size, shape, and position of tumors
and can be helpful to see if the cancer has spread to other organs. It can also
help find enlarged lymph nodes. MRI is useful in accurately assessing the size
of vulval lesion and assessing groin lymph node metastasis. Overall, MRI may
be best suited for determining the extent of local disease and invasion, although
it is also helpful in identifying groin nodal metastases and assessing the depth
of these nodes from the skin, which assist radiation planning. CT and PET/CT
can help detect and determine the extent of distant disease, however, PET/CT is
best used to identify lymph node metastases, where clinical assessment fails and
detect distant spread, which ultimately supports optimal treatment planning.
Opinion
Vulval carcinoma.
Clinical Discussion
The cause of vulvar cancer is unclear; however, some conditions such as
lichen sclerosus, squamous dysplasia or chronic vulvar itching may precede
cancer. In younger women affected with vulval cancer, risk factors include low
socioeconomic status, human papillomavirus (HPV) infection, multiple sexual
partners, cigarette use and cervical cancer. Patients that are infected with HIV
tend to be more susceptible to vulvar cancer as well. Typically, a lesion presents
in the form of a lump or ulcer and may be associated with itching, irritation, local
bleeding or discharge or pain during sexual intercourse. Adenocarcinoma can
arise from the bartholin gland and present with a painful lump. MRI may play
a role in evaluation of the local extent of disease in advanced cases, especially if
urethral invasion is suspected, as well as in the evaluation of lymphadenopathy.
Vulval cancer appears on US as a soft-tissue mass with internal vascularity. On CT,
vulval cancer appears as a nonspecific soft-tissue mass. On MRI, it demonstrates
intermediate signal intensity on T1W sequences and high signal intensity on T2W
sequences. MRI may also be used to differentiate recurrence from post-therapy
changes.
SECTION
21
Ovary
93. Ovarian Vein Thrombosis
94. Ovarian Tumor
CASE
93 Ovarian Vein Thrombosis
CASE
A 26-year-old postpartum female came with history of lower abdominal pain and
fever not responding to antibiotics and was referred to department of radiology
for CT abdomen and pelvis.

CECT pelvis (Fig. 1) shows intravascular filling defects in both ovarian veins
diagnosed as bilateral ovarian vein thrombosis.
Fig. 1
282 Section 21: Ovary

Ovarian vein thrombosis (OVT) occurs most commonly in postpartum patients,
and can result in pulmonary emboli. Presentation is usually with acute pelvic
pain in the post partum period, where it is termed puerperal ovarian vein
thrombosis (POVT) or post-partum ovarian vein thrombosis. On sonography, the
thrombosed ovarian vein appears as an anechoic to hypoechoic tubular structure
extending superiorly from the adnexa, lateral to the IVC or aorta retroperitoneally.
Doppler ultrasound can provide a quick and inexpensive initial examination with
findings of absence of color-flow filling and spectral waveform. CT angiography
is the investigation of choice. On CECT the thrombosed ovarian vein is visualized
as an enlarged tubular retroperitoneal structure, originating in the region of
the adnexa and extending cephalad in the retroperitoneal region to the level of
the renal veins, representing thrombus with peripheral rim-enhancement of the
vein. Secondary signs on CT scans are perivascular inflammatory stranding, an
enlarged uterus that contains fluid, and inhomogeneously enhancing parauterine
mass believed to be secondary to accompanying pelvic thrombophlebitis.
Multiplanar reconstructed coronal images would improve visualization of the
IVC thrombus in its entire length, therefore are helpful in evaluating the extent
of a thrombus.
Opinion
Bilateral ovarian vein thrombosis.
Clinical Discussion
Postpartum ovarian vein thrombosis is an uncommon complication of the
postpartum period. OVT can be accurately diagnosed by appropriate noninvasive
radiologic modalities to start early therapy with anticoagulants and intravenous
antibiotics. OVT can cause serious complications such as sepsis, IVC thrombosis,
pulmonary thromboembolism, and renal vein thrombosis and they may cause
death. OVT occurs 80–90% on the right side; this could be caused by compression
of the right ovarian vein against the sacral promontory due to an enlarged
retroverted uterus and presence of retrograde flow in the left ovarian vein. Most
commonly the right ovarian vein is involved, possibly due to retrograde flow in
the left vein preventing stasis and ascending infection. The CT findings consist
of a tubular structure with an enhancing wall and low-attenuation thrombus in
the ovarian veins. In patients in whom ultrasound examination is suboptimal,
due to overlying bowel gas, MRI should be preferred over CT because it does not
require intravenous administration of iodinated contrast material and has no risk
of radiation, and allows optimal evaluation of the inferior vena cava.
CASE
94 Ovarian Tumor
CASE
A 65-year-old female came with history of pain and lump in abdomen and was
referred to radiology department for CT scan abdomen and pelvis.

CT abdomen and pelvis shows a moderately enhancing soft tissue density lesion
in right adnexa. Right ovary is not seen separately from the mass. This turned out
to be an undifferentiated epithelial ovarian malignancy (Figs 1A and B).
In another case contrast CT abdomen shows a large cystic lesion with
enhancing thick septae and enhancing mural nodules arising from right ovary
confirmed as adenocarcinoma (Figs 2A to D).
A B
Figs 1A and B
284 Section 21: Ovary
A B
C D
Figs 2A to D

The imaging appearance of ovarian tumors ranges from cystic to solid masses.
Epithelial ovarian tumors represent 60% of all ovarian neoplasms and 85% of
malignant ovarian neoplasms. Subtypes of epithelial tumors include serous,
mucinous, endometrioid, clear cell, and Brenner tumors. Serous cystadenoma
is a thin-walled, unilocular or multilocular tumor filled with serous fluid. This
tumor is very common and may mimic a physiologic cyst or, occasionally, an
atypical mature cystic teratoma that lacks the characteristic eccentric mural
nodule. Mucinous cystadenoma is less common, is almost always multilocular,
and may be large. In many of these tumors, the MR imaging and CT appearance of
the individual locules may vary as a result of differences in degree of hemorrhage
or protein content. Although there is considerable overlap in morphologic
characteristics and corresponding imaging features that in many cases prevents
definitive preoperative characterization as benign or malignant. Features that
are suggestive of malignant epithelial tumors include a thick, irregular wall; thick
septae; papillary projections; and a large soft-tissue component with necrosis.
Case 94: Ovarian Tumor 285
Opinion
Ovarian tumor.
Clinical Discussion
Ovarian tumors are classified as epithelial tumors, germ cell tumors, sex
cord–stromal cell tumors, and metastatic tumors on the basis of tumor
origin. Characterization of an ovarian mass is of the utmost importance in
the preoperative evaluation of an ovarian neoplasm. It helps in deciding the
management. Epithelial ovarian tumors can be classified as benign, malignant
or borderline. The two most common types of epithelial neoplasms are serous
and mucinous tumors. A benign serous cystadenoma manifests as a unilocular or
multilocular cystic mass with homogeneous CT attenuation, a thin regular wall
or septum, and no endocystic or exocystic vegetation. A tumor that manifests
as a multilocular cystic mass that has a thin regular wall and septa or which
has liquids of different attenuation but has no endocystic or exocystic vegetation
is considered to be a benign mucinous cystadenoma. Mucinous cystadenomas
tend to be larger than serous cystadenomas at presentation. Bilaterality
and peritoneal carcinomatosis are seen more frequently in serous than in
mucinous cystadenocarcinomas. Mucinous adenocarcinoma can rupture and
is associated with pseudomyxoma peritonei. Features that are more suggestive
of benign epithelial tumors include a diameter less than 4 cm, entirely cystic
components, a wall thickness less than 3 mm, lack of internal structure, and the
absence of both ascites and invasive characteristics such as peritoneal disease or
adenopathy. Imaging findings that are suggestive of malignant tumors include
a thick, irregular wall; thick septa; papillary projections; and a large soft-tissue
component with necrosis. Ancillary findings include pelvic organ invasion, and
implants (peritoneal, omental, mesenteric), ascites, and adenopathy increase
diagnostic confidence for malignancy. Features such as wall thickening, septa,
and multilocularity are less reliable indicators of malignancy because they are
frequently seen in benign neoplasms, particularly cystadenofibromas, mucinous
cystadenomas, and endometriomas. Mature teratoma is the most common
benign ovarian tumor in women less than 45 years old. At CT, fat attenuation
within a cyst, with or without calcification in the wall, is diagnostic for mature
cystic teratoma. Benign ovarian enlargement includes mature cystic teratomas,
cystadenomas and fibrothecomas. Mature cystic teratoma may be associated
with complications from torsion, rupture, or malignant degeneration. Bilateral
solid ovarian enlargement may be benign or malignant.
SECTION
22
Abdominal Wall
95. Abdominal Wall Sarcoma
96. Abdominal Wall Hernia
CASE
95 Abdominal Wall Sarcoma
CASE
A 70-year-old male with history of abdominal distension and loss of weight was

Axial post contrast CT image of abdomen (Fig. 1) shows a large heterogeneous
soft tissue mass seen to arise from the anterior abdominal wall. The lesion is
Fig. 1
290 Section 22: Abdominal Wall
having central hypodense areas and peripheral enhancement. The bowel loops
are displaced posteriorly and laterally. There is no evidence of calcification within
the lesion. On histopathological examination it turned out to be abdominal
sarcoma.

Sarcoma is malignant tumor of mesenchymal origin, that originates from the
soft tissues rather than bone. They are classified on the basis of tissue seen on
histology. Soft-tissue sarcomas are rare tumors that can affect any age, gender,
and anatomic subsite. They have unique growth features, tending to extend
within compartments and along fascial planes on a path of least resistance. On CT
sarcomas are predominantly large, poorly demarcated, heterogeneous masses of
muscle density with hemorrhage or necrosis. Computed tomography is useful
for detection, defining extent, and predicting resectability of the primary tumor,
evaluation of response to treatment, and detecting recurrence and metastasis.
Opinion
Abdominal wall sarcoma.
Clinical Discussion
A mass is the most common sign of a soft tissue tumor. It usually is painless.
It grows through the lines of least resistence so symptoms might appear late.
Malignant soft tissue tumors occur twice as often as primary bone sarcomas.
Approximately 45% of sarcomas occur in the lower extremities, 15% in the upper
extremities, 10% in the head-and-neck region, 15% in the retroperitoneum, and
the remaining 15% in the abdominal and chest wall. The soft tissue sarcoma can
be treated with surgery and if the tumor is unresectable then radiotherapy or
chemotherapy can be used.
CASE
96 Abdominal Wall Hernia
CASE
A 55-year-old male with history of painless swelling over left lateral aspect of
abdomen in lumbar region since 20 years was referred to the Department of
Radiology for CT scan abdomen and pelvis. Six month back he suffered injury from
bull’s horn on the site of swelling. After that incident the swelling has gradually
increased and attained the present size. No history of surgical intervention at the
local site.

Patient’s photograph and X-ray abdomen show swelling in left lateral aspect
of abdomen (Figs 1A and B). CT images (Figs 1C and D) show a defect in
anterolateral aspect of abdominal wall in left lumbar region with elevation of the
external oblique muscle. Omental fat is seen herniating through this defect. No
bowel loops or organs are seen to be herniating.

Abdominal wall hernia is protrusion of abdominal structures through the
abdominal wall containing (1) an opening in the abdominal wall, and (2) a hernia
sac consisting of abdominal contents enclosed by peritoneum. Abdominal wall
hernias are a frequent imaging finding in the abdomen. Lumbar hernias occur
through defects in the lumbar muscles or the posterior fascia, below the 12th rib
and above the iliac crest. They usually occur after surgery or trauma. Diffuse lumbar
hernias may also occur, usually after flank incisions in kidney surgery, and may
contain bowel loops, retroperitoneal fat, kidneys, or other viscera. Although most
abdominal wall hernias are asymptomatic, they may develop acute complications
that necessitate emergent surgery. Most cases of bowel obstruction secondary to
abdominal wall hernia occur after incarceration and strangulation. CT findings
include dilated bowel proximal to the hernia and normal or reduced caliber, or
collapsed bowel distal to the obstruction. Strangulation refers to ischemia caused
by a compromised blood supply. Findings in ischemia include wall thickening,
292 Section 22: Abdominal Wall
A B
C D
Figs 1A to D
abnormal mural enhancement, mesenteric vessel engorgement, fat obliteration

and mesenteric haziness.
Opinion
Abdominal wall hernia.
Clinical Discussion
Types of abdominal wall hernias include inguinal hernia, femoral hernia, ventral
hernia, lumbar hernia and incisional hernia. Most common complications
of abdominal wall hernias are bowel obstruction secondary to the hernia,
Case 96: Abdominal Wall Hernia 293
incarceration, and strangulation. These complications can often be detected at

clinical evaluation. Presenting symptoms may include abdominal pain, vomiting,
and distention. Physical examination may reveal a firm, tender abdominal wall
mass. Several different surgical procedures are used to repair abdominal wall
hernias, ranging from open or laparoscopic suture repair to the use of mesh.
To date, tension-free mesh repair has been accepted as the standard surgical
technique for the majority of abdominal wall hernias, regardless of defect size
and is most commonly used.
SECTION
23
Miscellaneous
97. Inguinal Hernia
98. Omental Infarction
99. Primitive Neuroectodermal Tumor
100. Fetus-in-Fetu
101. Lymphangioma
CASE
97 Inguinal Hernia
CASE
A 50-year-old male with inguinal swelling was subjected to CT abdomen and
pelvis.

CT scan abdomen shows a large inguinal hernia on right side. Bowel is seen
herniating in right scrotal sac (Figs 1A to C). Small inguinal hernia seen on left
side (Fig. 1B).
B C
Figs 1A to C
298 Section 23: Miscellaneous

Inguinal hernia is the most common type of hernia and most often acquired.
Most commonly occur in males. There are two types of inguinal hernia, direct and
indirect. Plain X-ray abdomen shows bowel loop below inguinal ligament. On
Sonography and CT examination bowel loops and omentum are seen in inguinal
canal. Direct inguinal hernias exit medial and anterior to the course of the inferior
epigastric vessels, then are directed inferior to the inferior epigastric vessels as
the hernia sac protrudes. They represent a bulge in the anterior abdominal wall
lateral to the rectus muscle. The lateral crescent sign on CT represents the laterally
displaced and compressed inguinal canal, including its fat and contents. This
sign may be less useful in cases of extremely large hernias, which may compress
the inguinal canal to such an extent that it may not be readily detectable at CT.
Spermatic cord lipomas should not be confused with fat-containing hernias or
the lateral crescent sign, as lipomas are typically located lateral or inferior to
the spermatic cord and cause no compression of its contents, whereas inguinal
hernias protrude anteromedial to the cord. Indirect inguinal hernias are the most
common and are caused by the protrusion of peritoneal content through a patent
internal inguinal ring, lateral to the inferior epigastric vessels. In men, the hernia
can extend along the spermatic cord into the scrotum while in women; the hernia
may follow the course of the round ligament into the labia majora. The peritoneal
sac containing bowel loops protrudes through the inguinal canal and emerges at
the external inguinal ring. Retroperitoneal organs such as the urinary bladder,
distal ureters or colon may be incorporated into the hernia.
Opinion
Bilateral inguinal hernia.
Clinical Discussion
Indirect inguinal hernia is commoner and herniates lateral to the inferior
epigastric artery, anterior to the spermatic cord in males and follows the round
ligament in females. Direct inguinal hernia is less common and herniates medial
to the inferior epigastric artery, through a defect in the Hesselbech’s triangle.
The first sign of an inguinal hernia is a small bulge on one or both sides of the
groin, the area just above the groin crease between the lower abdomen and the
thigh. The bulge may increase in size over time and usually disappears when
lying down. Other signs and symptoms are discomfort or pain in the groin when
straining, lifting, coughing, or exercising and improves with rest. Indirect and
direct inguinal hernias may slide in and out of the abdomen into the inguinal
canal. An incarcerated hernia happens when part of the fat or small intestine
from inside the abdomen becomes stuck in the groin or scrotum and cannot go
back into the abdomen. When an incarcerated hernia is not treated, the blood
supply to the small intestine may become obstructed, causing “strangulation”
of the small intestine. This lack of blood supply is an emergency situation and
can cause the section of the intestine to die. Open surgery and laparoscopy are
treatment options. Inguinal hernias may contain any organ or tissue found in
Case 97: Inguinal Hernia 299
the lower abdomen. These may include but are not limited to fat, small or large
bowel, a portion of the bowel wall (Richter hernia), omentum, incarcerated
appendix (Amyand hernia), bladder, Meckel’s diverticulum (Littré hernia), and
gonads. Complications of hernia include intestinal obstruction, incarceration,
volvulus, perforation, appendicitis or diverticulitis, and tumors that may be
found incidentally in the hernia.
CASE
98 Omental Infarction
CASE
A 60-year-old female with history of pain in abdomen, nausea and vomiting was

Plain and contrast CT abdomen and pelvis shows non enhancing oval essentially
fat density omental lesion in the paraumblical region lying posterior to left rectus
abdominis muscle measuring 5.6 × 3 cm. There is fat stranding in adjacent
surrounding (Figs 1A to D).
A B
C D
Figs 1A to D
Case 98: Omental Infarction 301

Omental infarction is a rare cause of acute abdomen. Abdominal ultrasound
shows focal area of increased echogenicity with fat stranding. CT findings are
a solitary large nonenhancing omental mass with heterogeneous attenuation,
which is most often located in the right lower quadrant, deep to the rectus
abdominis muscle and either anterior to the transverse colon or anteromedial
to the ascending colon. Although omental infarction may have a CT appearance
that resembles that of acute epiploic appendagitis (Epiploic appendagitis is an
uncommon cause of abdominal pain, it is benign, nonsurgical, self-limiting
inflammatory process of the epiploic appendices), it lacks the hyperattenuating
ring that is seen in epiploic appendagitis. In addition, whereas the central focal
lesion in acute epiploic appendagitis is most often less than 5 cm long and is
located adjacent to the sigmoid colon, the lesion in omental infarction is larger
and most commonly is located next to the cecum or the ascending colon.
Opinion
Omental infarction.
Clinical Discussion
Clinical features are often nonspecific, and the presumptive diagnosis in
children is most often appendicitis. Torsion of the omentum, may be primary or
secondary. In primary torsion, a mobile segment of omentum rotates around a
proximal fixed point in the absence of any associated intra-abdominal pathology.
Factors that predispose a patient to torsion include anatomical variations of
the omentum itself, e.g. accessory omentum, and narrowed omentum pedicle.
Precipitating factors are those causing displacement of the omentum, including
trauma, violent exercise, and hyperperistalsis with resultant increased passive
movement of the omentum. The omentum twists around a pivotal point, usually
in a clockwise direction, venous return is compromised, and the distal omentum
becomes congested and edematous. As the torsion progresses arterial occlusion
leads to acute hemorragic infarction and eventually necrosis of omentum occurs.
CASE
99 Primitive
Neuroectodermal Tumor
CASE
A 32-year-old female presented to the department of radiology with palpable
mass in abdomen and pain.

CT pelvis (Figs 1A and B) reveal a large heterogeneously enhancing soft tissue
density lesion involving the right iliopsoas muscle. A round calcified focus is seen
within it. No evidence of fat density within this lesion. The diagnosis of primitive
neuroectodermal tumor (PNET) was confirmed on histopathology.

Primitive neuroectodermal tumor (PNET) is rare, highly malignant small-cell
neoplasm that most often arises from the chest wall or paravertebral region.
Retroperitoneal PNETs tend to be large and aggressive. The imaging characteristic
of peripheral PNETs is nonspecific. However, they should be considered in the
differential diagnosis for a large, aggressive retroperitoneal mass. Most of them
show heterogeneous enhancement with areas of necrosis.
A B
Figs 1A and B
Case 99: Primitive Neuroectodermal Tumor 303
Opinion
Primitive neuroectodermal tumor (PNET).
Clinical Discussion
PNET is a malignant neural crest tumor. It usually occurs in children and young
adults under 25 years of age. The Askin tumor, a PNET of the chest wall, is seen
mostly among children and adolescents. It is closely related to Ewing's sarcoma
of the same location, both tumors showing the same chromosomal translocation.
Pain and deformity of the chest wall are the cardinal clinical signs of the tumor.
Askin tumors show a female predilection, with typical presentation being in the
second decade.
PNET gets its name because the majority of the cells in the tumor are derived
from neuroectoderm; it is classified into two types, based on location in the
body: peripheral PNET and CNS PNET. The peripheral PNET is now thought
to be virtually identical to Ewing sarcoma. PNETs of the CNS generally refer to
supratentorial PNETs.
CASE
100 Fetus-in-Fetu
CASE
A 5-year-old male presented with palpable mass in abdomen and was referred to
the department of radiology for CT scan abdomen and pelvis.

X-ray abdomen reveal a large well demarcated mass occupying a large central
part of upper abdomen with few dense linear structures (Fig. 1A) CT abdomen
reveal a large heterogeneous density mass lesion in the peritoneal cavity
displacing the normal structures. The mass has solid, cystic, fatty and osseous
components. Few well formed tubular bones and joints are seen (Figs 1B and
C), the fat plane between the lesion and adjacent abdominal structures is well
maintained. Complete surgical excision of the lesion (Fig. 1D) was performed
and the diagnosis was confirmed on histopathology.

Fetus-in-fetu is an extremely rare abnormality that occurs secondary to abnormal
embryogenesis in a monochorionic diamniotic pregnancy where a nonviable
fetus becomes enclosed within a normally developing fetus. Most occur in the
abdomen/retroperitoneal cavity, CT typically shows an abdominal mass with
some components favoring fetal parts within the abdomen of another neonate.
Opinion
Fetus-in-fetu.
Clinical Discussion
Imaging plays an important role to correctly diagnose evaluates the case in a
prospective manner. The diagnosis of fetus in fetu can be made with abdominal
conventional radiographs, by identifying a vertebral column and/or specific bony
Case 100: Fetus-in-Fetu 305
A B
C D
Figs 1A to D
structures. The CT findings are those of a mass that consisted of a round or tubular
collection of fat that surrounded a central bony structure. The identification of
vertebrae or long bones is essential for establishing this diagnosis prospectively.
This entity is distinguished from an intrabdominal teratoma by its embryological
origin, its unusual location in the retroperitoneal space, its invariable benignity,
and by the presence of vertebral organization with limb buds and well-developed
organ systems. The most important feature that has been used to distinguish
between fetus-in-fetu and teratoma is the presence of a vertebral column.
Identification of the vertebral column indicates that fetal development of the
included twin must have advanced at least to the primitive streak stage to develop
a notochord, which is the precursor of the vertebral column.
CASE
101 Lymphangioma
CASE
A young 18-year-old male patient complaining of pain in left iliac region since
one year was referred to radiology department for CT scan abdomen.

CT abdomen and pelvis (Figs 1A to D) show ill defined fluid density lesion with
imperceptible wall in the retroperitoneum surrounding the aorta and IVC.
A B
C D
Figs 1A to D
Case 101: Lymphangioma 307
It extends along the left iliac vessels into the left half of pelvis. No evidence of
enhancement is seen in this lesion. Surrounding fat planes are preserved. This
lesion represents lymphangioma.

Lymphangiomas are benign lesions of vascular origin that show lymphatic
differentiation. They occur in many anatomic locations and may have a pediatric
or adult clinical presentation. After birth, they can become markedly dilated as
a result of both the collection of fluid and the budding of pre-existing spaces.
They may form unilocular or multilocular cystic masses and can encroach on
vital structures. Sonographically, lymphangiomas are most often multilocular
cystic masses that are anechoic or contain echogenic debris. At CT, cystic
lymphangioma typically appears as a large, thin-walled, multiseptate cystic mass.
Its attenuation values varies from that of fluid to that of fat. If hemorrhage occurs,
the intracystic attenuation values may simulate a solid tumor mass or abscess.
An elongated shape and crossing from one retroperitoneal compartment to an
adjacent one are characteristic of the mass. Rarely, cystic lymphangiomas may
have wall calcification. Signal pattern of lymphangiomas on MRI resembles that
of fluid: low signal intensity on T1W images and high signal intensity on T2W
images. The presence of hemorrhage or infection in the lesion may alter the MRI
signal pattern to give a more solid appearance.
Opinion
Lymphangioma.
Clinical Discussion
Lymphangiomas are benign congenital abnormalities of the lymphatic system.
They are thought to arise from sequestrations of embryonic lymph sacs; these sacs
are found in the neck and retroperitoneum. 75% of lymphangiomas occur in the
neck. Lymphangiomatosis is a rare disease with multifocal lymphatic proliferation
that typically presents during childhood and involves multiple parenchyma
organs including the lung, liver, spleen, bone, and skin. Because lymphangiomas
present across a wide age range of patient ages and occur in many sites, they
are associated with a broad spectrum of clinical and radiologic manifestations.
The acute presentation of lymphangiomas can cause abdominal pain, tenderness,
distension, fever, leukocytosis, peritonitis, dysuria, and guarding. The abnormal
ducts vary in size from microscopic to several centimeters and there is a variable
component of fibrous adventitia. The large cystic lesions are also known as cystic
hygromas. Surgical excision is the treatment of choice. The long-term prognosis
is excellent if complete excision has been achieved.
Index
A Appendix 13, 57
Apple core sign 54
Abdomen 11, 100, 103, 178, 199 Arteries
acute 301 abdominal 177
pain in 27, 29, 173 mesenteric 177
distension of 70 renal 14
severe pain in 45 stenosis, renal 176
Abdominal wall hernias, types of 292 Ascaris lumbricoides 139
Abscess 167 Askin tumors 303
appendicular 63, 64 Aspergillosis 93
formation 63 Autoimmune disease 132
hepatic 97, 98 Autoimmune disorders 56
pyogenic 97 Autosomal dominant polycystic kidney
splenic 166, 167 disease 204
Acalculous cholecystitis 131, 132, 134
Adenocarcinoma 35, 41, 54, 81, 283
duodenal 42 B
ileal 54 Balthazar score 148
mucinous 285 Beckwith-Wiedemann syndrome 119
Adenoma 54 Behçet’s disease 93
adrenal 189 Berry’s aneurysm, cerebral 204
hepatic 108, 109 Bicornuate uterus 264
Adenopathy, peripheral 48 Biliary cirrhosis 130, 139
Adrenocorticotropic hormone 190 Biliary injury 96
Adult polycystic kidney disease 204 Black pigment stones 139
Aganglionosis, intestinal 264 Bladder 299
Agenesis, renal 200, 264 diverticulum 233
Alcohol abuse 148 Blunt abdominal trauma 219
American Association for Surgery of Blunt injury 250
Trauma 95, 219, 220 Bowel injuries 163
American Joint Committee on Cancer 228 Broad ligament 15
Ampulla of Vater 155 fibroid 261
Androgen 254 Brood capsules 101
Anemia 75 Budd-Chiari syndrome 91, 92, 126
Angiodysplasia 52
Angiomyolipoma 110, 111
hepatic 110, 111 C
renal 221, 222 Calculus cholecystitis 133, 134
Antiphospholipid syndrome 93 Cancer
Aorta 171 cervical 270, 277
abdominal 174, 177-179, 182, 183 colorectal 78
Aortic aneurysm, abdominal 179 esophageal 22
Aortic dissection 204 rectal 82
Aortic thrombus 182 Carcinoma
infrarenal 183 cervix 270, 271
Aplasia colorectal 78
renal 199 duodenum 41
uterovaginal 200 endometrial 267, 268
Appendicitis 61, 62 esophageal 21, 22
gallbladder 142, 143 Cystitis 235, 236

gastric 36 acute 236
hepatocellular 110, 112, 113, 117, 126 cystica 236
ileal 53 glandularis 236
penile 257, 258 Cysto-biliary fistulas 102
periampullary 155 Cystolithiasis 130
prostate 243, 244 Cystourethrogram, micturating 234
rectal 82
rectum 81 D
sigmoid 77
colon 78 Daughter vesicles 101
stomach 35, 36 Diabetes
urinary bladder 237, 239 gestational 254
vulval 276, 277 mellitus 132
Cardiovascular disorders 132 Diaphragm 25
Caroli disease 121 eventration of 28, 29
Cecum 57 Diarrhea 68
Celiac trunk 177 Distension, abdominal 41
Cell carcinoma, renal 181, 226, 227 Diverticulitis 73
Cholangiocarcinoma 120, 121, 123, 124 sigmoid 72, 73
extrahepatic 123, 124 Diverticulosis, colonic 204
intrahepatic 120, 121 Dolichoectasia, intracranial 204
Cholangitis 122, 130, 139 Doughnut sign 68
primary sclerosing 121, 139 Duodenum 57
Cholecystitis 134, 141 Dysphagia 21, 23
acute 134
calcifying 141 E
emphysematous 136, 137, 141
Cholecystocholedochal fistula 141 Emphysema, surgical 163
Cholecystopathia chronica calcarea 141 End stage renal failure 204
Choledochal cyst 129, 130 Endometrium, high grade carcinoma of
Choledocholithiasis 130, 138, 139 267
Cholelithiasis 130, 140, 141 Escherichia coli 215, 236
Cloacal exstrophy 254 Esophageal carcinoma, staging of 22
Clonorchis sinensis 139 Esophagus, leiomyomatosis of 23
Cluster sign 98 Ewing’s sarcoma 303
Colon 65 Extracorporeal shock wave lithotripsy 209
Common iliac artery, bilateral 183
Computed tomography scan 33, 92, 100, F
112
abdomen 1, 23, 27, 33, 35, 47, 51, 55, 57, Fallopian tubes 15
61, 63, 67, 74, 77, 81, 89, 97, 91, Familial adenomatous polyposis 42, 119
106, 110, 115, 118, 129, 147, 149, Fatigue 48
201, 205, 263 Fecal occult blood test 82
chest 27 Fetal alcohol syndrome 119
pelvis 1, 61, 63, 74, 97, 106, 115, 118 Fever 75
renal angiography 176 Fistula
thorax 23 pancreatic 155
Constipation, chronic 53 ureterovaginal 274
Contrast enhanced computed tomography Flank pain, severe 209
scan 70, 94, 201, 265 Fluoro-2-deoxy-D-glucose 251
abdomen 51, 67, 91, 142, 149, 272 Focal fatty liver 87
pelvis 272 Foramen of Winslow 14
Couinaud classification of liver 1
Crescent sign 179, 183 G
Crohn’s disease 42, 46, 75
Cyst 204 Galactosemia syndrome 92
multiple 203 Gallbladder 5
rupture 204 carcinoma 139, 143, 144
simple hepatic 89, 90 phrygian cap 5
Index 311
polyp 139 Inguinal lymphadenectomy 258

porcelain 139-141, 144 Intussusception, colocolic 68
wall, calcification of 141 Ischemia 61
Gallstone 148
ileus 141 J
Gardner’s syndrome 42, 54, 119
Gastroesophageal junction 20, 21 Jejunum 57
Gastrointestinal stromal tumor 33, 34, 49, angiodysplasia of 51, 52
50
Gastrointestinal system 9 K
Gastrointestinal tract 33
Genitourinary malformations 119 Kidney
Germ cell tumor 252 dysplastic 201
Gerota’s fascia 147, 228 failure 119
Glycogen storage disease 119 ureters, and bladder 212, 232
Klebsiella pneumoniae 215
Krukenberg tumor 35
H
Hayfork sign 68 L
Helicobacter pylori infection 35
Hemangioma 103, 104, 126 Labia majora 277
hepatic 103 Labia minora 277
Hematemesis, complaints of 35 Laceration
Hematoma 94-96 renal 219, 220
parenchymal 163 splenic 163
subcapsular hepatic 163 Leukemia 116
Hematosalpinx 264 Ligament of Treitz 9
Hematuria 220 Littré hernia 299
Hemoglobinuria, paroxysmal nocturnal 93 Liver 1
Hemoperitoneum 94, 163, 164 biopsy 92
Hemorrhage 118, 156, 204 focal fatty infiltration of 87, 88
Hepatectomy, partial 114 function tests 117
Hepatic cyst, benign developmental 90 laceration 94
Hepatitis B 114 parenchyma, adjacent 143
Hepatitis C 114 segments, anatomy of 1
Hepatoblastoma 118, 119 Lump, abdominal 63
Hiatus hernia 19, 20 Lung carcinoma, primary 194
Hounsfield units 190 Lymph node
Human papillomavirus infection 277 metastasis 273
Hutch diverticulum 233 prepyloric 35
Hydatid cyst 100, 101 Lymphadenopathy
hepatic 100, 101 mediastinal 48
Hydatid disease, hepatic 101 regional 48
Hydrocele 247 Lymphangioma 306, 307
bilateral 247, 248 Lymphoid tissue 76
Hydrometrocolpos 263, 264 Lymphoma 35, 47
Hydronephrosis 274 ileocecal 47
proximal 206 small bowel 47
Hyperplasia
fibronodular 112 M
focal nodular 106, 107, 115, 126 Mackenrodt’s ligament 15
lymphoid 62 Mayer-Rokitansky-Küster-Hauser
Hypertension, portal 130, 186 syndrome 264
McBurney’s point 62
I McKusick-Kaufman syndrome 264
Meckel’s diverticulum 299
Inguinal hernia 297, 298 Mesenteric artery thrombosis, acute 175
bilateral 298 Metastases
indirect 298 adrenal 194
hepatic 41, 115, 116, 244 female 13

nodal 239 male 15
Midgut volvulus 57 Pelviureteric junction 206, 207
Mirizzi syndrome 141 obstruction 205, 207
Müllerian duct anomalies 200, 264 Peutz-Jhegers syndrome 54
Multicystic dysplastic kidney 202 Peyer’s patches 76
Multiple endocrine neoplasia 193 Pheochromocytoma 192, 193
Murphy’s sign 134 adrenal 193
Myometrium 14 Pneumatosis intestinalis 55, 56
Myxedemic ileus, acute 71 Pneumoperitoneum 73
Polycystic kidney 203
N bilateral 203
disease 204
Necrosis 61 Portal vein thrombosis 184-186
pancreatic 154 Positron emission tomography 120, 251
Neoplastic polyps 78 Post-Whipple’s surgery 155
Nephroblastoma 224 Potter syndrome 200
Neurofibromatosis 193 Pouch of Douglas 15
Non-Hodgkin’s lymphoma 47 Prader-Willi syndrome 254
ileocecal 47 Prostate 243
Non-steroidal anti-inflammatory drugs cancer 244
209 specific antigen tests 244
Noonan syndrome 254 Prune-Belly syndrome 254
North American National Wilms’ Tumor Pseudoaneurysm 96, 148
Study Group 224 Pseudocyst 148-150, 152
pancreatic 149, 151
O Pyelography, intravenous 232
Pyelonephritis, emphysematous 215, 218
Obstruction, small bowel 45, 46 Pyometra 265, 266
Ogilive’s syndrome 71 causes of 266
Omental infarction 300, 301
Organ of Zuckerkandl 193
Organs
R
abdominal 94 Renal pelvic calculus 209
injury, abdominal 163 Reye’s syndrome 92
Ovarian neoplasms 284 Rib fracture 163
Ovarian tumor 283, 285 Richter hernia 299
epithelial 284 Roux-en-Y hepaticojejunostomy 130
Ovarian vein thrombosis 281, 282
bilateral 282
S
P Sarcoma 35
abdominal 290
Pain Scleroderma 56
abdominal 41, 82, 189 Scoliosis 171
acute 204 Seminoma 251
hypochondriac 136 Shock, hemorrhagic 222
intermittent abdominal 202 Small bowel wall, multiple segments of 55
Pancreas 8, 145 Small intestine, primary neoplasms of 54
enlargement of 148 Sphincter of Oddi 8, 130
Pancreatitis 139, 148, 156 Spleen 8, 164
acute 147, 148, 154 abscess of 167
necrotizing 153, 154 Splenic vein, thrombosis of 184
severe acute 154 Squamous cell carcinoma 22, 239, 257,
Papillary mucinous tumors, intraductal 272, 276
151 Staghorn calculi 210, 211
Parasites 62 bilateral 210
Pelvic calculus, renal 208 Stomach 21, 31
Pelvis 178 Sturge-Weber syndrome 193
Index 313
Superior mesenteric artery 57, 58, 171 Urogenital sinus 264

syndrome 171, 173, 175 Urogram, intravenous 206
Superior mesenteric vein 57 Uropathy, obstructive 208
thrombosis of 184 Uterine didelphys 264
Uterosacral ligament 15
T Uterovesicle pouch 15
Testes, undescended 253, 254

Testicular seminoma 251 V
Thrombosis 174 Vaginal bleeding 270
Todani classification system 130 Vaginal carcinoma 272, 273
Trauma Vaginal discharge 270
hepatic 94 Vein thrombosis, renal 217, 218
renal 219 Vena cava
splenic 163 inferior 180
testicular 249 superior 180
Tuberculosis Vesical calculus 231, 232
abdominal 75 Vesicoureteric reflux 234
gastrointestinal 75 Vesicoureteric junction calculi, bilateral
pulmonary 75 213
Tuberous sclerosis 193 Vomiting 29
Tumors 62 von Hippel-Lindau disease 193
adrenal 193 von Meyenburg complex 90
periampullary 157 Vulvar cancer, primary 276
small bowel 54
U W
Ulcerative colitis 121 Whipple’s surgery 155
Ultrasonography, transrectal 244 Whirlpool’ appearance 57
Upper gastrointestinal system 9 Wilms’ tumor 116, 119, 181, 223, 224, 225
Ureteric calculus 212
Urinary bladder diverticulum 233 Z
Urinary tract infection, recurrent 202, 204,
234 Zoonosis, parasitic 101

101 CT Abdomen Solutions

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101 CT Abdomen Solutions

101 CT Abdomen Solutions

Hariqbal Singh MD DMRD

Yasmeen Khan DMRE

The Health Sciences Publisher

Jaypee Medical Inc. Jaypee Brothers Medical Publishers (P) Ltd.

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101 CT Abdomen Solutions

We thank Professor MN Navale, Founder President, Sinhgad Technical Educa­

CT Anatomy: Abdomen and Pelvis1

SECTION 5 Small Bowel

20. Sigmoid Diverticulitis 72

SECTION 16 Urinary Bladder

SECTION 22 Abdominal Wall

PHYSICAL PRINCIPLE OF CT SCAN IMAGING

Electron Beam CT (EBCT)

Table 2: Attenuation value of various tissues on CT scan

Window Level (WL) and Window Width (WW)

Fig. 4 Volume rendered image—posterior coronal plane

Fig. 5 Volume rendered image—posterior oblique coronal plane

Fig. 1 Anatomy of liver segments

Normal cystic duct is 2 cm long and 2 mm wide. Maximum diameter of normal

– Bare area of liver

Fig. 4 Axial CT section showing appendix

When two folds of peritoneum connect a portion of bowel to the retro­

Radiological Findings on CT Examination

esophagus. This is suggestive of upward displacement of the stomach through

Comments and Explanation

Radiological Findings on CT Scan Examination

Comments and Explanation

in neuromotor functional disorders. In addition it must be distinguished from

Radiological Findings on CT Examination

Comments and Explanation

Radiological Findings on CT Examination

Comments and Explanation

Radiological Findings on CT Scan

Comments and Explanation

Radiological Findings on CT Scan

Other Cases of Carcinoma Stomach

Comments and Explanation

of gastric carcinoma is improved by using thin-section sequences and helical or

obstruct the gastrointestinal lumen or infiltrative lesions that impair stomach

Radiological Findings on CT Examination

Comments and Explanation

intestinal obstruction and jaundice, hematemesis, melaena, and occult blood in

9 Small Bowel Obstruction

Radiological Findings on CT Examination

Comments and Explanation

Radiological Findings on CT Examination

Comments and Explanation

translocations, infections, environmental factors, immunodeficiency states, and

Radiological Findings on CT Examination

Comments and Explanation

Radiological Findings on CT Examination

Comments and Explanation

Radiological Findings on CT Examination

Comments and Explanation

Radiological Findings on CT Scan

Comments and Explanation

We thank Professor MN Navale, Founder President, Sinhgad Technical Educa

CT Anatomy: Abdomen and Pelvis1

20. Sigmoid Diverticulitis 72

When two folds of peritoneum connect a portion of bowel to the retro