ABDOMEN

Question 1

PNEUMOPERITONEUM

GENERAL

Answer 1

• Large volume—usually stomach, duodenum, colonic diverticulum,
post endoscopy or secondary to obstruction.
• Lesser sac—usually gastric or duodenal (rarely oesophagus or
transverse colon).
• Under left lobe of liver—often gastric or duodenal.
• Mesenteric folds—usually small bowel or colon.
• Retroperitoneal—duodenum, ascending/descending colon,
rectum

Question 2

PNEUMOPERITONEUM

Causes

Answer 2

1. Perforation
   (a) Peptic ulcer—gastric or duodenal.
   (b) Inflammation—e.g. diverticulitis, appendicitis, toxic
   megacolon, necrotizing enterocolitis (neonates).
   (c) Obstruction—especially closed loop or large bowel
   obstruction.
   (d) Infarction.
   (e) Malignant neoplasms.
   (f) Trauma—blunt or penetrating.
   (g) Stercoral—due to hard faeces, usually in rectum/sigmoid.
   (h) Foreign body—e.g. fish bone.
   (i) Pneumatosis coli—the cysts may rupture, or gas may
   dissect through the bowel wall without a discrete site of
   perforation.
2. Iatrogenic—e.g. recent surgery or endoscopy, peritoneal dialysis.
   Free gas may be seen on CT up to 18 days after laparotomy
   (though free gas >10 days post-op should be treated with
   suspicion). Resolves faster in the obese, children and following
   laparoscopy (insufflated with CO2—free gas >3 days after
   laparoscopy is suspicious).
3. Pneumomediastinum—see Section 5.36.
4. Introduction per vaginam—e.g. douching.
5. Pneumothorax—via a congenital pleuroperitoneal fistula.
6. Idiopathic

Question 3

GASLESS ABDOMEN

Answer 3

1. Ascites.
2. Fluid-filled bowel—closed-loop obstruction, active pancolitis, early
   mesenteric infarction, bowel washout.
3. Acute pancreatitis—due to excessive vomiting.
4. High obstruction—e.g. gastric outlet obstruction, congenital
   atresia (neonates).
5. Large abdominal mass—pushes bowel laterally.
6. Normal

Question 4

PHARYNGEAL/OESOPHAGEAL POUCHES
AND DIVERTICULA
Upper third

Answer 4

1. Zenker’s diverticulum—posterior, usually on left side, between the
   fibres of inferior constrictor and cricopharyngeus ± an air–fluid
   level.
2. Lateral pharyngeal pouch and diverticulum—through the
   unsupported thyrohyoid membrane in the anterolateral wall of the
   upper hypopharynx. Pouches (transient) are common and usually
   asymptomatic. Diverticula (persistent) are uncommon and seen in
   patients with chronically elevated intrapharyngeal pressure, e.g.
   glass-blowers and trumpeters.
3. Lateral cervical oesophageal pouch and diverticulum—through
   the Killian-Jamieson space, below the level of cricopharyngeus.
   Usually asymptomatic

Question 5

PHARYNGEAL/OESOPHAGEAL POUCHES AND DIVERTICULA
MIDDLE
3

Answer 5

1. Traction—at level of carina, due to tethering of the oesophagus to
   adjacent granulomatous (often calcified) nodes, e.g. due to TB;
   sinus tracts may also be seen.
2. Developmental—failure to completely close a tracheo-oesophageal
   fistula.
3. Intramural pseudodiverticulosis—rare. Multiple tiny flask-shaped
   outpouchings. 90% have associated oesophageal strictures, mainly
   in the upper third

Question 6

PHARYNGEAL/OESOPHAGEAL POUCHES

Lower third

Answer 6

1. Epiphrenic—mimics a hiatus hernia.
2. Ulcer—peptic or related to steroids, immunosuppression or
   radiotherapy.
3. Mucosal tears—Mallory-Weiss syndrome, post oesophagoscopy.
4. After Heller’s operation.
   Mimics
5. Contained oesophageal perforation.
6. Oesophageal anastomosis—may have a small outpouching.
7. Oesophageal duplication cyst communicating with
   oesophagus.

Question 7

OESOPHAGEAL ULCERATION

Answer 7

Inflammatory
1. Reflux oesophagitis—± hiatus hernia. Characteristic signs are:
(a) A gastric fundal fold crossing the gastrooesophageal junction
(GOJ) and ending as a polypoid protuberance in the distal
oesophagus.
(b) Erosions—dots or linear streaks of barium in the distal
oesophagus.
(c) Ulcers—may be linear, serpiginous or round.
2. Barrett’s oesophagus—especially if ulceration is midoesophageal,
though strictures are more common distally. The background
mucosa typically has a reticular pattern. Hiatus hernia in 75%–
90%. Increased risk of adenocarcinoma.
3. Corrosive ingestion—ulceration is most marked at sites of
anatomical hold-up (e.g. aortic arch, GOJ) + diffuse spasm and
oedema. Progresses to a long, smooth stricture.
4. Intramural pseudodiverticulosis—can mimic ulceration.
5. Graft-versus-host disease—rare in the oesophagus.
Infective
1. Candida oesophagitis—mostly in immunosuppressed patients.
Early: small plaque-like filling defects, often orientated in the
long axis of the oesophagus. Advanced: cobblestone or ‘shaggy’
mucosal surface ± luminal narrowing. Ulceration is uncommon.
There may be tiny bubbles on top of the barium column
(‘foamy’ oesophagus). Patients with mucocutaneous candidiasis
or oesophageal stasis due to achalasia, scleroderma, etc. may
develop chronic infection, which is characterized by a lacy or
reticular appearance of the mucosa ± nodular filling defects.
2. Viral—herpes and CMV, mostly in immunocompromised patients,
e.g. HIV (which itself can cause ulcers). May manifest as discrete
ulcers (which may be large) or ulcerated plaques, or mimic
Candida oesophagitis. Discrete ulcers on an otherwise normal
background mucosa are strongly suggestive.
Iatrogenic
1. Oral drug-induced—due to prolonged contact with tetracycline,
quinidine or potassium tablets, at sites of anatomical hold-up.
2. Longstanding nasogastric (NG) tube.
3. Radiotherapy—ulceration is rare. Dysmotility is often the only
abnormality.138 Aids to Radiological Differential Diagnosis
Related to systemic diseases
1. Crohn’s disease—aphthoid ulcers and, in advanced cases,
undermining ulcers, intramural tracking and fistulae.
2. Behçet’s disease—discrete superficial ulcers + history of oral and
genital ulceration.
3. Bullous skin disorders—e.g. epidermolysis bullosa, pemphigus.
Neoplastic
In the presence of a mass or stricture.
1. Carcinoma.
2. Leiomyosarcoma and leiomyoma.
3. Lymphoma.
4. Melanoma

Question 8

OESOPHAGEAL MUCOSAL NODULARITY

Answer 8

1. Reflux oesophagitis and Barrett’s—granular appearance, usually
   mid-distal oesophagus.
2. Glycogenic acanthosis—multiple small well-defined nodules, often
   in upper-mid oesophagus. Seen incidentally in elderly patients, or
   in young patients with Cowden syndrome.
3. Advanced Candida/viral oesophagitis—cobblestone mucosa.
4. Superficial spreading oesophageal carcinoma.
5. Eosinophilic oesophagitis—diffuse narrowing with a corrugated
   or ringed appearance.
6. Oesophageal papillomatosis—due to HPV infection. Laryngeal or
   tracheobronchial papillomatosis may coexist.

Question 9

OESOPHAGEAL STRICTURES—SMOOTH

Answer 9

Inflammatory
1. Peptic—the stricture develops relatively late, ± ulceration. Usually
distal if associated with reflux and hiatus hernia; midoesophageal if
associated with Barrett’s.
2. Corrosives—caustic stricture; typically long and symmetrical; may
take years to develop. More likely with alkalis than acids.
3. Scleroderma—reflux through an open GOJ may produce a
distal stricture. The oesophagus is dilated with poor peristalsis.Abdomen and gastrointestinal tract 139
7
4. Iatrogenic—prolonged use of an NG tube (distal stricture,
probably due to reflux). Also radiotherapy (typically
midoesophageal) and drugs, e.g. bisphosphonates.
5. Crohn’s disease—rare, suggests severe disease.
6. Eosinophilic oesophagitis—strictures may be short (‘ringed’
oesophagus) or long.
Neoplastic submucosal and extrinsic masses
Typically have a smooth contour but focal mucosal ulceration
may be seen.
1. Squamous carcinoma—may infiltrate submucosally. The absence
of a hiatus hernia and the presence of an extrinsic soft-tissue mass
should differentiate it from a peptic stricture, but tumours arising
around the cardia may predispose to reflux.
2. Mediastinal tumours—e.g. lung cancer, lymphadenopathy.
Extrinsic soft-tissue mass ± obstruction.
3. Leiomyoma—focal narrowing due to a smooth, eccentric
submucosal mass. Calcification is highly suggestive if present. Most
common benign oesophageal tumour; most are in the distal third.
May be diffuse (leiomyomatosis), e.g. in Alport syndrome.
4. Rare submucosal tumours—e.g. fibrovascular polyp
(pedunculated, arises from upper oesophagus, can be very large, ±
fat on CT), lipoma (purely fatty on CT), granular cell tumour
(small, usually distal), nerve sheath tumours, haemangioma,
glomus tumour, paraganglioma, solitary fibrous tumour, salivary
gland-type tumours.
5. GIST—the oesophagus is the least common location. Much less
common than leiomyoma (cf. the rest of the GI tract where GIST
is much more common).
6. Metastasis—rare.
Nonneoplastic submucosal and extrinsic masses
1. Oesophageal varices—smooth tubular filling defects; can be distal
(‘uphill’ varices due to portal hypertension) or proximal (‘downhill’
varices due to SVC obstruction).
2. Other vascular impressions—aberrant subclavian or pulmonary
artery; right or double aortic arch; aortic aneurysm or tortuosity.
3. Intramural haematoma—associated with coagulopathy,
protracted vomiting or instrumentation. Acute chest pain,
dysphagia and haematemesis. Focal submucosal mass, high
attenuation on unenhanced CT.
4. Oesophageal duplication cyst—smooth indentation of
oesophagus. Cystic and nonenhancing on CT.140 Aids to Radiological Differential Diagnosis
5. Other rare lesions—e.g. sarcoidosis, fibrosing mediastinitis,
amyloidosis, malakoplakia, actinomycosis.
Others
1. Achalasia—‘rat-tail’ tapering may mimic a stricture; this occurs
below the diaphragm. Marked oesophageal dilatation with food in
the lumen.
2. Oesophageal webs—typically in cervical oesophagus; very short
(shelf-like), arise perpendicularly from the anterior wall. Can be
associated with Plummer-Vinson syndrome. Increased risk of
carcinoma.
3. Bullous skin disorders—epidermolysis bullosa, pemphigus. Short
web-like strictures, may be multiple.
4. Graft-versus-host disease*—rare; short web-like strictures, may be
multiple

Question 10

OESOPHAGEAL STRICTURES—IRREGULAR

Answer 10

Neoplastic
1. Oesophageal carcinoma—increased incidence in achalasia,
Plummer-Vinson syndrome, Barrett’s oesophagus, coeliac disease,
asbestosis, lye ingestion and tylosis. Squamous carcinomas are
most common in the midoesophagus; adenocarcinomas are most
common distally and arise from underlying Barrett’s. Appears as an
irregular filling defect (annular or eccentric) ± shouldering,
ulceration and upstream dilatation. May create a ‘pseudoachalasia’
appearance if very distal. An associated soft-tissue mass or focal
thickening is typically seen on CT.
2. Gastric carcinoma—can directly invade oesophagus.
3. Carcinosarcoma—big polypoid tumour ± stalk arising from the
mid-distal oesophagus, often without obstruction.
4. Leiomyosarcoma—bulky mass, often without obstruction.
5. Lymphoma—usually extension from gastric involvement.
6. Other rare tumours—neuroendocrine tumours, melanoma, Kaposi
sarcoma, other sarcomas.Abdomen and gastrointestinal tract 141
7
Inflammatory
1. Reflux—rarely irregular.
2. Crohn’s disease—rare.
Iatrogenic
Radiotherapy—rare, unless treating an oesophageal carcinoma.
Dysphagia after radiotherapy is usually due to dysmotility. Acute
oesophagitis may occur with a dose of 50–60 Gy (5000–6000 rad)

Question 11

DILATED OESOPHAGUS

Answer 11

1. Obstructing tumour or stricture—see Sections 7.6 and 7.7.
2. Achalasia—patients are often younger than those with carcinoma.
   The oesophagus is often markedly dilated (more so than with
   malignancy) with a smooth ‘beaked’ tapering at the GOJ. Normal
   peristaltic waves should be absent (though some contractility may
   be present)—if not, consider pseudoachalasia due to tumour.
3. Scleroderma*—dilated oesophagus with poor peristalsis and
   contractility. Look for associated lung fibrosis and bowel features.
4. Post oesophagectomy—the gastric pull-up can mimic a dilated
   oesophagus.
5. Iatrogenic—e.g. over-tight gastric band or fundoplication wrap.
6. Chagas disease*—mimics achalasia. Small and large bowel
   (especially sigmoid) may also be dilated. Cardiomegaly is often
   present due to associated cardiomyopathy. Endemic in Central and
   South America.
7. Oesophageal amyloidosis—rare; can mimic achalasia.

Question 12

TERTIARY CONTRACTIONS IN THE

OESOPHAGUS 4

Answer 12

1. Reflux oesophagitis.
2. Presbyoesophagus—impaired motor function due to muscle atrophy in the elderly. Seen in 25% of people >60 years.
3. GOJ obstruction—from any cause.
4. Neuropathy—e.g. early achalasia (before dilatation occurs), diabetes, alcoholism, malignant infiltration, Chagas disease

Question 13

GASTRIC MASSES AND FILLING DEFECTS
malignant 5
polyps 4
submucosal neoplasms 4
Extrinsic 5
Others 5

Answer 13

Malignant neoplasms
1. Carcinoma—most polypoid carcinomas are 1–4 cm in diameter; any polyp >2 cm is suspicious for malignancy especially if it has a central depression (ulcer). Local adenopathy is common; metastasizes most often to liver and peritoneum.

2. GIST—stomach is the most common location. Variable size and malignant potential. Typically a discrete endophytic or exophytic mass ± central ulcer. Can be large with heterogeneous enhancement on CT/MRI ± cystic, necrotic or haemorrhagic areas. Metastasizes most frequently to liver and peritoneum, but lymphadenopathy is very uncommon and would suggest an
   alternative diagnosis if present. May enlarge with treatment; reduced enhancement suggests response. Can be associated with Carney triad (three types of neoplasms, mainly in young women, including gastric gastrointestinal stromal tumor, pulmonary chondroma, and extra-adrenal paraganglioma) or NF1.
3. Lymphoma*—1–5% of gastric malignancies. Usually NHL. May be ulcerative, infiltrative and/or polypoid; often involves the whole stomach. May mimic carcinoma, but extension across the pylorus (without causing obstruction) and/or marked wall thickening (mean 3–5 cm) suggests lymphoma. Most have adjacent lymphadenopathy. MALT lymphoma is strongly associated with Helicobacter pylori infection.
4. Metastases—frequently ulcerate. Usually melanoma, but lung, breast, lymphoma, carcinoid, Kaposi sarcoma and any adenocarcinoma may metastasize to stomach. Breast metastases are often infiltrative, mimicking linitis plastica.
5. Sarcoma—rare. Many subtypes.

Polyps
1. Hyperplastic—usually multiple, small (<1 cm) and scattered throughout the stomach (predilection for the body/fundus). Associated with chronic gastritis. Can rarely be large (3–10 cm).

2. Fundic gland polyps—usually multiple, small (<5 mm) and found mainly in the fundus. Can be sporadic or associated with FAP.
3. Adenomatous—usually solitary, 1–4 cm, sessile and typically in antrum. High risk of malignant transformation, esp. if >2 cm and if carcinomas are present elsewhere in the stomach (due to dysplastic epithelium). Associated with pernicious anaemia and FAP.
4. Hamartomatous—characteristically multiple, small and relatively sparing of the antrum. Associated with FAP (including Gardner variant), Peutz-Jeghers, Cowden and Cronkhite-Canada syndromes.

Benign submucosal neoplasms-Smooth, well-defined mass with an obtuse angle to the gastric wall.

1. Leiomyoma—much less common than gastric GIST but similar in appearance (including the tendency for central ulceration if large),
   though often more homogeneous in appearance.
2. Lipoma—fat attenuation on CT.
3. Neurofibroma—may be multiple. NB: leiomyomas and lipomas are more common, even in patients with NF1.
4. Other rare neoplasms—e.g. NET (often hypervascular), haemangioma (may be hypervascular ± phleboliths), glomus tumour (hypervascular), plexiform fibromyxoma (myxoid appearance), schwannoma.

Extrinsic indentation

1. Pancreatic tumour/pseudocyst.
2. Splenomegaly/hepatomegaly.
3. Retroperitoneal tumours.
4. Duplication cyst.
5. Splenosis.

Others
1. Gastric fundoplication—may mimic a distorted mass in the fundus. Scarring following gastric band removal can also cause mass-like distortion.

2. Bezoar—mass of undigestible material in the stomach; contains
   mottled gas on CT. Types include tricho- (hair, nearly always young women), phyto- (fruit or vegetable matter), lacto- (milk curds, most common in infants), pharmaco- (medication) and foreign body (e.g. tissue paper) bezoars.
3. Pancreatic ‘rest’—small mass of ectopic pancreatic tissue, usually in the inferior wall of the antrum, resembling a submucosal tumour. Homogeneous enhancement similar to normal pancreas. On MRI, signal characteristics follow normal pancreas; often has a primitive duct remnant which may be visible on MRCP. May become inflamed and undergo necrosis/cystic change. There may be an adjacent stripe of submucosal fat due to recurrent
   inflammation. Can also occur in duodenum, jejunum, Meckel’s diverticulum, liver, gallbladder and spleen.
4. Intramural haematoma—e.g. traumatic, iatrogenic..Hyperattenuating on unenhanced CT.
5. Lymphoid hyperplasia—innumerable 1–3 mm round nodules in
   the antrum and/or body. Associated with H. pylori.

Question 14

GASTRIC FOLD THICKENING

Answer 14

Inflammatory
Characterized by submucosal thickening/oedema, which is near
fluid attenuation on CT, ± mucosal hyperaemia.
1. Gastritis—e.g. due to NSAIDs, alcohol, corrosive ingestion, H.
pylori, CMV, or radiotherapy. Localized or generalized fold
thickening ± ulcers and inflammatory nodules (<1 cm, mostly in
the antrum).
2. Zollinger-Ellison syndrome—due to a gastrinoma causing excess
acid secretion, resulting in multiple and recurrent gastric and
duodenal ulcers. Ulceration in both D1 and D2 is suggestive;
ulceration distal to D2 is virtually diagnostic. Thick hyperaemic
rugal folds ± small bowel dilatation (in response to excess acid).
The underlying gastrinoma is best seen on arterial phase CT.
3. Acute pancreatitis—reactive oedema of gastric wall.
4. Crohn’s disease—mild fold thickening especially in antrum,
aphthoid ulceration ± conical stricture of antrum.
5. Acute eosinophilic gastroenteritis—oedematous folds, most
commonly involves the gastric antrum but rest of the GI tract can
also be involved.
Infiltrative/neoplastic
Fold thickening is of soft-tissue attenuation on CT with
enhancement.
1. Carcinoma—can manifest as focal irregular fold thickening.
2. Lymphoma—usually NHL, may be primary or secondary.
3. Pseudolymphoma—benign reactive lymphoid hyperplasia. Most
have an ulcer near the centre of the area affected.
4. Amyloidosis—wall thickening and dysmotility.
5. Sarcoidosis—focal or diffuse thickening, most common in
antrum. May mimic linitis plastica or Ménétrier disease.
Others
1. Gastric ischaemia—e.g. due to gastric volvulus, arterial
embolization or occlusion, vasculitis or systemic hypotension.
Results in submucosal oedema with reduced or absent mucosal
enhancement ± intramural gas.
2. Ménétrier disease—huge ‘cerebriform’ rugal folds, especially
fundus and body; involvement of antrum is less common. No
rigidity or ulcers. ‘Weeps’ protein sufficient to cause Abdomen and gastrointestinal tract 145
7
hypoproteinaemia (effusions, ascites, oedema e.g. of the small
bowel). Commonly achlorhydric: cf. Zollinger-Ellison syndrome.
3. Portal hypertension—e.g. due to cirrhosis or portal vein
thrombosis. Oedematous stomach ± varices in fundus and
oesophagus if chronic.
4. Emphysematous gastritis—intramural gas due to gas-forming
infections.

Question 15

LINITIS PLASTICA

Answer 15

Neoplastic
1. Gastric carcinoma—signet ring cell adenocarcinoma.
2. Lymphoma—thickening is typically more marked than with
carcinoma.
3. Metastases—especially lobular breast cancer.
4. Local invasion—e.g. from pancreatic carcinoma.
Inflammatory
1. Chronic corrosive ingestion—can cause rigid stricture of body/
antrum extending to the pylorus.
2. Radiotherapy—can cause rigid stricture of antrum with some
deformity. Mucosal folds may be thickened or effaced ± large
antral ulcers.
3. Granulomatous inflammation—Crohn’s disease, TB. Conical
antral stricture.
4. Chronic eosinophilic gastroenteritis—commonly involves gastric
antrum (causing narrowing and nodularity) + small bowel, often
with blood eosinophilia.
5. Sarcoidosis—predilection for antrum, usually in the presence of
disease elsewhere

Question 16

GASTRIC OR DUODENAL OBSTRUCTION

12

Answer 16

1. Benign peptic stricture—most common.
2. Gastric or duodenal tumour—carcinoma, GIST, large polyp
   prolapsing into pylorus. NB: lymphoma does not usually cause
   obstruction.
3. Extrinsic compression/infiltration—e.g. by adjacent pancreatitis,
   pseudocyst, pancreatic cancer, annular pancreas (compressing
   D2) or SMA syndrome (compression of D3 by proximal SMA,
   usually seen in very thin patients especially those who have
   recently lost weight).
4. Gastric volvulus—can be organoaxial (most common in adults,
   typically associated with a large hiatus hernia) or mesenteroaxial
   (most common in children).
5. Other causes of pyloric stricturing—e.g. metastases (especially
   breast) , corrosives, Crohn’s, TB, sarcoidosis, amyloid, syphilis.
6. Obstructing bezoar.
7. Bouveret syndrome—a proximal form of gallstone ileus where
   the calculus obstructs the pylorus or proximal duodenum.
8. Iatrogenic—e.g. slipped gastric band (often obstructs gastric
   body), fundoplication (can restrict burping, resulting in ‘gas
   bloat’ syndrome).
9. Ileus/gastroparesis—e.g. postsurgical, diabetes, opioids.
10. Gastric antral web—very short prepyloric ring or ‘diaphragm’ of
    mucosa; more common in childhood.
11. Midgut malrotation—with either obstructing Ladd’s bands or
    midgut volvulus. Rare in adults, typically presents in infancy.
12. Idiopathic hypertrophic pyloric stenosis—nearly always
    presents in infancy, but has rarely been described in adults.

Question 17

DECREASED/ABSENT DUODENAL FOLDS

Answer 17

1. Scleroderma*—often with dilatation.
2. Coeliac disease*—especially in distal duodenum and jejunum.
3. Crohn’s disease*.
4. Strongyloides.
5. Cystic fibrosis*.
6. Amyloidosis*

Question 18

DUODENAL WALL/FOLD THICKENING OR MASS
Neoplastic 11
Inflammatory  7
Vascular 3
Congenital/developmental 3

Answer 18

Neoplastic
1. Primary adenocarcinoma—most small bowel carcinomas occur in the duodenum or proximal jejunum. Polypoid mass or asymmetric wall thickening on CT ± obstruction. Often metastatic at presentation.
2. Infiltration by adjacent tumour—e.g. pancreatic, gallbladder,
colonic, renal or adrenal carcinoma.
3. Ampullary adenoma/carcinoma—usually obstructs CBD/PD.
4. Lipoma—fat attenuation on CT.
5. Polyps—adenoma (malignant potential, associated with FAP) or
hamartoma (benign, associated with many polyposis syndromes).
6. Brunner’s gland hamartoma—benign polypoid mass of variable
size, usually in D1, often pedunculated. May contain fat or cystic
spaces. Can be multiple.
7. GIST—uncommon in duodenum, usually D2/3. Discrete
endophytic or exophytic mass.
8. Leiomyoma—and other rare mesenchymal tumours, e.g. nerve
sheath tumour.
9. Lymphoma*—usually NHL; nonobstructing mural thickening or
extrinsic mass ± aneurysmal dilatation.
10. Neuroendocrine tumour—avidly enhancing polyp or mass on
CT. Usually nonfunctional; nearly all functional duodenal NETs are
gastrinomas.
11. Metastasis—most commonly melanoma, breast and lung. Can
cause obstruction.

Inflammatory
1. Duodenitis/ulcer—usually D1, related to H. pylori. Focal oedematous wall thickening and avid mucosal enhancement on CT ± large ulcer cavity.
2. Reactive oedema—due to adjacent pancreatitis or cholecystitis.
Mucosal enhancement is less pronounced than in duodenitis.
3. Cystic dystrophy—due to heterotopic pancreatic tissue in the
duodenal wall (D2) which becomes recurrently inflamed, resulting
in intramural cystic change, often with delayed mural
enhancement due to fibrosis ± signs of chronic pancreatitis. See
also Section 7.10 (pancreatic ‘rest’).
4. Paraduodenal (‘groove’) pancreatitis—focal inflammation
between the head of pancreas and duodenum ± cystic change.
Closely related to cystic dystrophy.
5. Crohn’s disease*—mural thickening mainly in D1/2 ± layered
contrast enhancement. Uncommon.
6. Infiltration—e.g. eosinophilic gastroenteritis, mastocytosis
(dense bones), Whipple’s disease (low-density mesenteric nodes),
amyloid.
7. Infections—e.g. Giardia, Strongyloides, worms.

Vascular
1. Varices—due to portal hypertension or thrombosis.
2. Intramural haematoma—e.g. post trauma, coagulopathy.
3. Ischaemia—diffuse submucosal oedema ± poor or absent mucosal
enhancement. Can be widespread in vasculitis secondary to
radiotherapy, collagen diseases and Henoch-Schönlein purpura.

Congenital/developmental
1. Choledochocele—cystic protrusion of distal CBD into ampullary region.
2. Annular pancreas—may mimic annular duodenal thickening; enhancement and MRI signal identical to normal pancreas.
3. Duplication cyst—<5% of intestinal duplications; thin-walled cyst
on CT/MRI often with no luminal communication

Question 19

DILATED SMALL BOWEL
Calibre: proximal jejunum >3.5 cm (4.5 cm if small bowel enema)
mid-small bowel >3.0 cm (4.0 cm if small bowel enema)
ileum >2.5 cm (3.0 cm if small bowel enema).

Answer 19

Normal folds
1. Mechanical obstruction—± dilated large bowel depending on
level of obstruction. Discrete transition point at the site of
obstruction; small bowel faeces sign can help to find this. Always
check for a closed loop as this will require urgent surgery due to
risk of strangulation/ischaemia. Causes of obstruction include:
(a) Extrinsic—e.g. adhesions (most common cause, look for
‘hairpin’ angulations ± small amount of trapped fat within
an adhesive band), hernias (both external and internal),
volvulus, congenital bands (e.g. Ladd’s bands, persistent
omphalomesenteric duct), compression or infiltration by
an adjacent mass or abscess.
(b) Mural—e.g. strictures (Section 7.17), masses (Section 7.18),
intussusception (usually ileocolic), intramural haematoma.
(c) Luminal—e.g. gallstone ileus (look for chronically inflamed
gallbladder adherent to duodenum ± pneumobilia), enterolith
(often related to jejunal diverticulosis), foreign body, bezoar,
mass of parasitic worms (especially ascariasis), distal intestinal
obstruction syndrome (DIOS, due to thick secretions in a
patient with cystic fibrosis).
2. Paralytic ileus—dilated small ± large bowel, no discrete transition
point. Most commonly seen postoperatively but can also be
caused by trauma, sepsis, drugs and metabolic disturbances.
3. Early arterial ischaemia—dilatation is the earliest sign on CT and
reflects an ischaemic ileus. Other signs (e.g. reduced mural
enhancement and pneumatosis) develop as ischaemia progresses.
NB: mural thickening is not a common feature of acute arterial
ischaemia.Abdomen and gastrointestinal tract 149
7
4. Scleroderma—dilated small bowel with crowded valvulae
conniventes (‘hidebound’ appearance) ± antimesenteric
pseudodiverticula (NB: true diverticula are on the mesenteric
border).
5. Coeliac disease and tropical sprue—can produce identical signs.
Dilated fluid-filled small bowel ± effaced jejunal folds and
prominent ileal folds (reversed fold pattern) ± ‘hidebound’
appearance ± mesenteric adenopathy.
6. Chronic intestinal pseudo-obstruction—many causes including
collagen vascular diseases (e.g. SLE), endocrine disorders (e.g.
diabetes), CNS disorders (e.g. Parkinson’s), enteric neuropathies,
myopathies, Ehlers-Danlos syndrome, amyloidosis, drugs (e.g.
opioids) and infections (e.g. Chagas). Resembles paralytic ileus on
imaging; dilatation can be marked.
7. Small bowel diverticulosis (mimic)—especially in the jejunum.
Diverticula can be large and numerous, mimicking small bowel
dilatation, but these do not contain valvulae conniventes.
8. Iatrogenic—vagotomy and gastrectomy may produce dilatation
due to rapid emptying of stomach contents. A side-to-side small
bowel anastomosis may appear as a focally dilated small bowel
segment. Extensive small bowel resection results in compensatory
dilatation of the remaining small bowel ± mild fold thickening.
9. Duplication cyst—can contain gas if it communicates with the
small bowel, mimicking a dilated small bowel segment.
Thick folds
1. Venous ischaemia—especially with closed-loop obstruction.
Dilatation + oedematous thickening is typical (cf. arterial
ischaemia). Reduced mural enhancement suggests progressive
ischaemia.
2. Crohn’s disease—alternating segments of narrowed thick-walled
small bowel (strictures) and dilated thin-walled small bowel (‘skip’
segments).
3. Lymphoma—aneurysmal dilatation of a thickened small bowel
segment.
4. Metastases—especially from melanoma. Can mimic lymphoma.
5. Radiotherapy.
6. Zollinger-Ellison syndrome—ileus ± thickening due to excess
acidity.
7. Amyloidosis*—diffuse thickening + dilatation

Question 20

SMALL BOWEL STRICTURES

Answer 20

1. Crohn’s disease*—either acute inflammatory strictures (longer
   segment, prominent thickening and submucosal oedema, avid
   enhancement, surrounding fat stranding ± inflammatory mass) or
   chronic fibrotic strictures (shorter segment, only mild thickening
   and enhancement, no surrounding inflammation). The presence
   of mesenteric ‘fat wrapping’ around a strictured small bowel
   segment is almost pathognomonic for Crohn’s.
2. NSAID-induced—typically short or very short (diaphragm-like);
   usually multiple in mid-distal small bowel ± ascending colon. Also
   look for papillary necrosis in kidneys.
3. Ischaemic—may be short or long; look for atherosclerotic
   narrowing of the mesenteric arteries. Can also occur in
   microvascular disease and vasculitis (especially Behçet’s).
4. Radiation-induced—typically involves pelvic ileal loops after
   pelvic radiotherapy. Strictures can be long.
5. Anastomotic—especially after resections for Crohn’s.
6. Metastases—usually with metastatic disease elsewhere.
7. Adenocarcinoma—see Section 7.18. The thickening can be
   subtle and mimic a benign stricture, especially in patients with
   Crohn’s (who are at increased risk).
8. Endometriosis*—serosal small bowel deposits can cause
   stricturing. Look for other features of the disease in the pelvis.
9. Mycobacterial infection—TB (terminal ileum) or Mycobacterium
   avium complex (jejunum), often with mesenteric adenopathy.
10. Cryptogenic multifocal ulcerous stenosing enteritis—rare disease
    characterized by multiple idiopathic short strictures typically in the
    ileum, usually without obstruction. No fistulation or abscess.
11. Sarcoidosis*—rare.

Question 21

SMALL BOWEL MASSES

Answer 21

Malignant
1. Metastases—either haematogenous (melanoma, lung, breast) or via
peritoneal spread (ovary, stomach, pancreas, colon, uterus). Usually
multiple + metastases elsewhere ± ascites (if via peritoneal spread).
2. Neuroendocrine tumour (carcinoid)—most common primary
small bowel malignancy beyond the duodenojejunal flexure,
usually in the distal ileum. May be multifocal ± associated with
MEN 1. Avidly enhancing discrete intramural nodule; may cause
obstruction. Mesenteric lymphadenopathy is usually present ±
calcification and desmoplastic reaction. Carcinoid syndrome only
develops with liver metastases.Abdomen and gastrointestinal tract 151
7
3. Adenocarcinoma—most common primary small bowel
malignancy in the duodenum. Ileal lesions are rare (except in
Crohn’s). Short thick-walled annular stricture, usually presenting
with obstruction and commonly with nodal and metastatic disease.
High incidence of second primary tumours.
4. Lymphoma*—secondary > primary. Long segment of small bowel
thickening + aneurysmal dilatation + mesenteric adenopathy;
obstruction is uncommon. Increased risk in coeliac disease.
5. GIST—second most common location after the stomach.
Discrete exophytic heterogeneous soft-tissue mass, often large
at presentation ± central ulceration. Its large size can make it
difficult to ascertain its exact site of origin. No associated
lymphadenopathy. Metastasizes most commonly to the liver
and peritoneum. Associated with Carney triad and NF1.
6. Sarcoma—e.g. leiomyosarcoma (may see tumour thrombus
invading SMV branches), MPNST (in NF1). Similar appearance to
GIST, but much less common

Question 22

SMALL BOWEL MASSES

BENIGN

Answer 22

1. Polyps—these can act as a lead point for intussusception and are
   associated with polyposis syndromes especially if multiple.
   (a) Adenoma—associated with FAP (including Gardner syndrome)
   especially in the duodenum. Has malignant potential.
   (b) Hamartoma—associated with Peutz-Jeghers, Cowden,
   Cronkhite-Canada and juvenile polyposis syndromes. No
   malignant potential in itself, but the syndromes are associated
   with increased risk of various malignancies.
   (c) Inflammatory fibroid polyp—no malignant potential.
2. Crohn’s disease*—an inflammatory mass can mimic a tumour.
3. Intramural haematoma—high attenuation on unenhanced CT.
4. Mesenchymal lesions—e.g. lipoma (fat attenuation), leiomyoma
   (mimics GIST but is less common), haemangioma (avid nodular
   enhancement), neurogenic tumours (e.g. schwannoma,
   neurofibroma and ganglioneuroma, especially in NF1),
   angiomyolipoma, inflammatory myofibroblastic tumour.
5. Amyloidoma—rare manifestation; mimics adenocarcinoma.
6. Mesenteric tumours—e.g. desmoid tumour; can mimic an
   exophytic small bowel GIST if large.
7. Duplication cyst—cystic, on serosal surface of small bowel, most
   commonly distal ileum

Question 23

SMALL BOWEL WALL THICKENING

Answer 23

Soft-tissue attenuation wall thickening
Submucosal attenuation >25 HU on portal venous phase CT.
1. Neoplasm—see Section 7.18, especially metastases,
adenocarcinoma and lymphoma. Thickening is typically short in
length (except lymphoma and diffuse serosal metastases) and
irregular/eccentric, with obliteration of the normal bowel layers.
2. Active Crohn’s disease—florid transmural inflammation causes
marked segmental thickening, avid mucosal and patchy transmural
enhancement + surrounding fat stranding and vascular
engorgement (comb sign), often with an inflammatory mass or
abscess. Most commonly involves terminal ileum (TI) but can
occur anywhere in the GI tract. Fat wrapping is almost
pathognomonic. Also look for other features, e.g. fibrotic strictures,
relative sparing of the antimesenteric border and fistulation, e.g.
with other bowel loops, skin surface or bladder.
3. Chronic fibrotic strictures—of any cause (see Section 7.17).
Typically short and only mildly thickened + mild homogeneous
enhancement.
4. Intramural haemorrhage—e.g. due to trauma (most common in
duodenum), coagulopathy (most common in jejunum), vasculitis
(e.g. Henoch-Schönlein purpura) or haemolytic uraemic syndrome
(caused by E. coli in children). The thickening is often segmental ±
upstream obstruction. The high mural attenuation is due to
intramural blood rather than enhancement; this can be confirmed
on unenhanced CT (mural attenuation >60 HU). Intraluminal blood
and haemorrhagic ascites may also be present.
Submucosal oedema with avid
mucosal enhancement
Homogeneous submucosal attenuation of <25 HU on CT and T2
hyperintensity on MRI suggests oedema, and avid mucosal
enhancement (relative to normal bowel loops) suggests
inflammation, infection or hyperaemia.
1. Active Crohn’s disease—less florid than the transmural
inflammation above.
2. Focal ulceration or perforation—e.g. peptic ulceration (typically
in duodenum but can occur more distally), small bowel
diverticulitis (jejunal or Meckel’s), fish-bone perforation. Focal
small bowel inflammation + surrounding fat stranding.154 Aids to Radiological Differential Diagnosis
3. Low-grade ischaemia—arterial, venous or vasculitic. The mucosal
hyperenhancement is due to vasodilatation. Often seen at the
border zones of a segment of high-grade ischaemia, but can also
be seen in isolation especially in vasculitis. May be focal,
segmental or diffuse.
4. Shock bowel—due to acute severe hypotension or hypovolaemia
(e.g. major trauma). Diffuse small bowel involvement. Look for
other signs, e.g. IVC collapse, hyperenhancing adrenals.
5. Infectious enteritis—common condition but uncommonly seen
on CT as imaging is usually not indicated. Mild segmental small
bowel thickening + mesenteric adenitis; ileocaecal involvement
suggests Salmonella, Shigella, Yersinia or Campylobacter;
duodenojejunal involvement suggests Giardia or Strongyloides. In
immunocompromised patients with opportunistic infections (e.g.
CMV enterocolitis) the inflammation is often diffuse.
6. Postobstructive oedema—due to recent spontaneous resolution
of SBO, resulting in transient mucosal hyperaemia and
submucosal oedema in a segmental pattern upstream of the
point of obstruction. Check for a recent AXR—if this shows SBO
but the subsequent CT shows normal calibre oedematous small
bowel, this implies the diagnosis.
7. Iatrogenic enteritis
(a) Acute radiation enteritis—usually involves pelvic small
bowel loops; extent depends on number of loops within the
radiation field.
(b) Chemotherapy-induced enteritis—diffuse small bowel
involvement.
(c) Graft-versus-host disease—diffuse small bowel and/or
colonic involvement; occurs after bone marrow transplant.
Mimics opportunistic infection on imaging.
8. Angioedema—due to C1 esterase inhibitor deficiency, may be
hereditary (younger patients) or acquired (older patients, e.g.
due to ACE inhibitors, lymphoma or autoimmune disorders).
Recurrent transient episodes of segmental submucosal oedema,
mucosal hyperenhancement and ascites.
9. Zollinger-Ellison syndrome—duodenal ± proximal jejunal
inflammation due to acid secretions.
10. Eosinophilic enteritis—diffuse thickening of proximal small
bowel + gastric antrum is most common. Peripheral eosinophilia
is usually present.
11. Mastocytosis—diffuse small bowel thickening + splenomegaly,
lymphadenopathy, ascites and sclerotic bones.
Submucosal oedema with normal
mucosal enhancement
Normal mucosal enhancement suggests passive submucosal oedema.
NB: there is some overlap with mucosal hyperenhancement above.Abdomen and gastrointestinal tract 155
7
1. Reactive oedema—focal thickening secondary to adjacent
inflammation, e.g. appendicitis, diverticulitis, pancreatitis,
cholecystitis, abscess.
2. Hypoalbuminaemia—e.g. renal/liver failure, protein-losing
enteropathy. Diffuse submucosal oedema + ascites, pleural
effusions and subcutaneous oedema.
3. Portal venous system congestion
(a) PV/SMV thrombosis—the extent of submucosal oedema is
proportional to the proximity of a thrombus to the bowel;
isolated thrombosis around the portal confluence is less likely
to cause significant oedema, whereas thrombosis extending
into multiple peripheral SMV branches can cause diffuse
oedema.
(b) Portal hypertension—usually due to cirrhosis. Often the right
colon is most affected. Look for varices, splenomegaly, ascites.
(c) Closed loop SBO—dilated cluster of small bowel loops with
two adjacent transition points and variable submucosal
oedema and mucosal enhancement depending on the severity
of venous ischaemia. The mesenteric veins usually appear
focally narrowed adjacent to the point of obstruction—this
reflects extrinsic venous compression by either an adhesive
band (most common cause), neck of an internal hernia or
torted mesentery.
4. Coeliac disease* and tropical sprue—dilated and fluid-filled
jejunum with mild segmental submucosal oedema, reversal of
jejunoileal fold patterns and mesenteric lymphadenopathy.
5. Whipple’s disease—most commonly segmental involvement of
jejunum and distal duodenum + mesenteric lymphadenopathy
with central fat attenuation.
6. Amyloidosis*—diffuse small bowel thickening and dilatation ±
diffuse mesenteric infiltration and adenopathy.
7. Lymphatic obstruction—e.g. by malignancy (including the
desmoplastic reaction associated with carcinoids), sclerosing
mesenteritis, retroperitoneal fibrosis or sarcoidosis. Segmental
or diffuse oedema upstream of the obstruction + chylous ascites.
8. Primary intestinal lymphangiectasia—children and young adults,
due to congenital maldevelopment of lacteals resulting in leakage
of lymph into bowel; presents with protein-losing enteropathy,
peripheral oedema and lymphopenia. Diffuse submucosal oedema,
mesenteric oedema and chylous ascites on imaging.
Submucosal oedema with reduced mucosal
enhancement
Reduced mucosal enhancement (relative to other bowel loops)
suggests acute high-grade ischaemia. Often accompanied by
haemorrhagic ascites (look for dependent layering of dense blood
products, e.g. in pelvis).156 Aids to Radiological Differential Diagnosis
1. Venous ischaemia—e.g. due to closed-loop SBO or acute
extensive SMV thrombosis. Submucosal and mesenteric oedema
occurs earlier and more prominently than in arterial ischaemia.
2. Arterial ischaemia—either thrombotic or embolic SMA occlusion.
Look for splenic/renal infarcts and thrombus in the left atrial
appendage (suggests embolic shower). Reduced mucosal
enhancement occurs earlier than in venous ischaemia.
3. Vasculitis—segmental area or areas of ischaemia, usually in young
patients. Mucosal hyperenhancement is more common than
hypoenhancement. Examples include SLE (± thrombotic bowel
infarction due to antiphospholipid syndrome), polyarteritis nodosa
(look for renal microaneurysms and infarcts), Henoch-Schönlein
purpura (children and young adults, classic skin rash) and Behçet’s
disease (usually TI, can mimic Crohn’s)

Question 24

ILEOCAECAL REGION THICKENING

Inflammatory

Answer 24

1. Acute appendicitis—inflammation can secondarily involve the
   caecal pole and TI, especially in the presence of an abscess,
   potentially mimicking Crohn’s.
2. Crohn’s disease*—the presence of fat wrapping is almost
   pathognomonic and aids differentiation from complicated
   appendicitis. Also, abscesses related to Crohn’s typically have a
   thick rind of enhancing inflammatory tissue around them (cf. the
   thin-walled abscesses in appendicitis). In addition, look for other
   sites of disease distant from the ileocaecal region.
3. Ulcerative colitis*—terminal ileal ‘backwash’ ileitis can be seen
   for up to 25 cm, in the presence of pancolitis.
4. Neutropenic colitis—also known as typhlitis. Inflammation
   typically involves the caecum ± ascending colon and TI. Clinical
   context (neutropenia due to chemotherapy or other cause of
   immunocompromise) clarifies the diagnosis.
5. Right-sided colonic diverticulitis—focal inflammation centred
   on a diverticulum + adjacent fat stranding.
6. Pelvic inflammatory disease—in patients with a low-lying
   caecum, a right-sided tubo-ovarian abscess can involve the
   ileocaecal region, mimicking complicated appendicitis.
7. Radiation enterocolitis—in patients with a low-lying caecum in
   the pelvis.
8. Portal hypertension—most commonly causes oedema of the
   right colon.
9. Behçet’s disease*—most commonly involves TI, mimicking
   Crohn’s.Abdomen and gastrointestinal tract 157
   7
10. Dropped gallstone—post cholecystectomy. Gallstone can
    migrate to the right iliac fossa via the right paracolic gutter and
    cause recurrent abscesses around the ileocaecal region.

Question 25

ILEOCAECAL REGION THICKENING

Infective

Answer 25

1. TB*—can mimic Crohn’s; TI and caecum are predominantly
   involved with stricturing and caecal contraction ± fistulae ±
   necrotic ileocolic nodes. Caecal involvement is more prominent
   than in Crohn’s. <50% have pulmonary TB.
2. Salmonella, Shigella, Yersinia, Campylobacter—typically involve the
   ileocaecal region causing mild inflammation and mesenteric
   adenitis.
3. CMV colitis—right-sided ± TI involvement, may be extensive. Seen
   in the immunocompromised—overlaps with neutropenic colitis.
4. Amoebic colitis—typically involves the caecum and ascending
   colon, with characteristic sparing of the TI. Can cause marked
   colonic thickening and narrowing, mimicking a tumour. Look for
   associated amoebic liver abscess.
5. Actinomycosis—rare; most commonly involves the ileocaecal
   region with an associated strikingly infiltrative soft-tissue mass +
   abscess, often invading abdominal wall ± fistulae. Occasionally
   pelvic bowel is secondarily involved from the gynaecological tract.
6. Histoplasmosis—very rare

Question 26

ILEOCAECAL REGION THICKENING

Neoplastic

Answer 26

1. Adenocarcinoma—caecal and ascending colon tumours can
   invade the TI and can mimic inflammation, especially if
   mucinous—the presence of mucinous ileocolic nodes aids
   differentiation. Caecal tumours can also occlude the appendix
   orifice and cause secondary appendicitis—always have a high
   index of suspicion in an elderly patient presenting with acute
   appendicitis, since the acute inflammation may mask the
   underlying tumour; consider follow-up imaging.
2. Carcinoid—appendix is the most common site (generally benign
   and often too small to see on CT). Most small bowel carcinoids
   originate in the distal ileum and are invariably malignant if >2 cm.
   Discrete hypervascular mural nodule with mesenteric adenopathy ±
   calcification. The desmoplastic reaction may cause lymphatic or
   venous obstruction resulting in segmental ileal oedema, mimicking
   an inflammatory process.
3. Lymphoma*—TI is the most common site.
4. Appendix mucocoele—grossly dilated appendix filled with mucin
   ± mural calcification. Caused by a low-grade mucinous appendiceal
   neoplasm. Results in pseudomyxoma peritonei if it ruptures into
   the peritoneal space.
5. Metastases

Question 27

ILEOCAECAL REGION THICKENING

Ischaemia

Answer 27

1. Isolated caecal necrosis—the caecum is an uncommon but
   recognized site for ischaemic colitis. Focal mural thickening and
   reduced mucosal enhancement ± pneumatosis in the caecal pole,
   usually in an elderly vasculopath without a discrete arterial filling
   defect.
2. Exercise-induced ischaemic colitis—seen in marathon runners.
   Caused by catecholamine-induced splanchnic vasoconstriction and
   dehydration, resulting in watershed ischaemia, which can affect
   the caecum

Question 28

COLITIS ON CROSS-SECTIONAL
IMAGING
Diffuse

Answer 28

1. Ulcerative colitis (UC).
2. Pseudomembranous colitis—Clostridium difficile toxin. Marked colonic wall oedema (mean 15 mm, more than other causes of colitis) with mucosal hyperenhancement + ‘accordion’ sign due to grossly thickened haustra (suggestive but not pathognomonic) ± ascites. Often diffuse but may be right or left sided.
3. CMV—in immunocompromised patients, ± TI involvement.
4. E. coli—diffuse or segmental, nearly always involving transverse colon. Can cause haemolytic uraemic syndrome in children, resulting in intramural haemorrhage and enlarged hyperechoic kidneys.
5. Graft-versus-host disease*—often with diffuse small bowel involvement. Colonic thickening is typically mild—thickness >7 mm strongly suggests an alternative diagnosis, e.g. CMV, C. difficile or neutropenic colitis

Question 29

COLITIS ON CROSS-SECTIONAL
IMAGING
Predominantly right-sided

Answer 29

1. Reactive oedema—e.g. secondary to appendicitis (caecum),
   cholecystitis (hepatic flexure), omental infarction (ascending) or
   postobstructive oedema.
2. Crohn’s disease*—TI involvement usually present and often
   more marked than colonic involvement (cf. TB), but isolated
   Crohn’s colitis can occur. Skip segments and fat wrapping are
   characteristic features.
3. Neutropenic colitis—see Section 7.20. Overlaps with CMV.
4. Salmonella, Yersinia and Campylobacter—usually with TI
   involvement.
5. TB*—see Section 7.20. Necrotic ileocolic nodes are suggestive.
   No fat wrapping (cf. Crohn’s).
6. Amoebiasis—usually right-sided but may be diffuse; TI typically
   spared. May cause toxic megacolon, mass-like amoeboma or liver
   abscess.
7. Portal hypertension—submucosal oedema + other features
   (varices, ascites, splenomegaly).
8. Ischaemic colitis—hypovolaemic states in young patients,
   cocaine users or elderly vasculopaths (isolated caecal necrosis).
9. Angioedema—more common in small bowel.
10. Phlebosclerotic colitis—rare (mostly seen in Japan); involves
    caecum and ascending colon ± extension distally. Caused by
    sclerotic occlusion of mesenteric veins—thread-like calcification
    of small SMV branches close to or within the colonic wall is
    almost pathognomonic. May result in ischaemia/obstruction.

Question 30

COLITIS ON CROSS-SECTIONAL IMAGING
Predominantly left-sided
7

Answer 30

1. Ulcerative colitis*—nearly always involving the rectum and
   extending proximally in a contiguous fashion (cf. skip segments in
   Crohn’s). Proliferation of mesorectal fat is suggestive, but can also
   be seen in Crohn’s and radiation proctitis.
2. Diverticulitis—may be focal thickening around a single inflamed
   diverticulum (look for adjacent fat stranding) or involving a longer
   segment of diverticulosis + surrounding fat stranding ± abscess.
   May occasionally be right-sided.
3. Ischaemic colitis—either involving the inferior mesenteric artery
   territory (distal transverse to rectosigmoid) or watershed areas near
   the rectosigmoid junction and splenic flexure (especially the
   elderly). Rectum usually spared. Submucosal oedema and mucosal
   hyperenhancement in low-grade ischaemia. In high-grade
   ischaemia the mucosa enhances poorly and there may be minimal
   wall thickening; associated pneumatosis suggests infarction.
4. Epiploic appendagitis—usually left-sided but can occur anywhere.
   Well-defined oval or round area of fat with a ‘halo’ of fat stranding
   ± central dense ‘dot’ (thrombosed vessel). Located adjacent to the
   colon ± mild mural oedema.
5. Shigella—can also affect ileocaecal region.
6. Schistosomiasis*—mural calcification is highly suggestive if present.
7. Hermansky-Pudlak syndrome—rare autosomal recessive disorder
   characterized by granulomatous colitis, pulmonary fibrosis,
   bleeding diatheses and oculocutaneous albinism.

Question 31

COLITIS ON CROSS-SECTIONAL IMAGING
Predominantly rectal (proctitis)
8

Answer 31

1. Ulcerative colitis*—proctitis is rare in Crohn’s.
2. Radiation colitis—rectum ± sigmoid.
3. Reactive inflammation—e.g. secondary to perianal sepsis
   (especially in immunocompromised) or prostatic abscess.
4. Sexually transmitted infections—due to receptive anal
   intercourse; e.g. gonorrhoea, HSV, lymphogranuloma venereum
   (LGV), syphilis. Rectum ± sigmoid involvement. LGV also typically
   presents with large necrotic inguinal nodes.
5. Solitary rectal ulcer syndrome—due to recurrent rectal prolapse.
   Diffuse thickening with ulceration of the anterior wall ±
   inflammatory cystic mass (proctitis cystica profunda).
6. Stercoral colitis—due to hard impacted faeces in the rectum.
   Usually in the elderly.
7. Chemical colitis—e.g. hydrogen peroxide enema. Rectosigmoid.
8. Eosinophilic colitis—may be primary or secondary (parasites,
   drugs, autoimmune disorders). The primary form has two peaks
   in infancy and young adults; most commonly involves rectum

Question 32

COLONIC POLYPS ON CT COLONOGRAPHY

6 types of polyps

Answer 32

1. Tubular, tubulovillous and villous adenomas—these form a
   spectrum both in size and degree of dysplasia. Villous adenoma is
   the largest with the most severe dysplasia and highest risk of
   malignancy—these are typically fronded and sessile with a surface
   layer of mucus. Polyps <6 mm have minimal risk of malignancy;
   larger polyps require endoscopic biopsy if clinically appropriate.
   Polyps >2 cm are more likely to be malignant than benign. An
   irregular or ulcerated surface and puckering of the colonic wall at
   the polyp base are also suggestive of malignancy. Polyps may be
   pedunculated, sessile or flat (plaque-like, <3 mm height, most
   difficult to see—a coating of oral contrast can aid identification).
   Adenomas are associated with FAP (including Gardner variant) and
   Turcot syndrome(intestinal polyposis and CNS tumours: most commonly glioblastoma or medulloblastoma).
2. Inflammatory—benign, seen in IBD (UC > Crohn’s). Polyps can be
   seen at all stages of activity of the colitis: acute—pseudopolyps
   (i.e. mucosal hyperplasia); chronic—sessile polyp (resembles villous
   adenoma); quiescent—filiform polyp (worm-like ± branching
   pattern).
3. Hamartomatous—seen in various syndromes (see Part 2).
   Although the polyps themselves are benign, the syndromes are
   associated with an increased risk of various malignancies.
4. Hyperplastic—often multiple and small, typically in younger
   patients. Associated with hyperplastic polyposis syndrome.
5. Nodular lymphoid hyperplasia—in children and adolescents; very
   small, usually in the right colon.
6. Infective—e.g. tuberculoma, amoeboma and schistosomiasis
   (mainly rectosigmoid ± strictures or calcification)

Question 33

Polyp mimics

12

Answer 33

1. Untagged faecal matter—often heterogeneous with tiny gas
   bubbles.
2. Thick folds—especially at the ileocaecal valve (fat attenuation),
   due to spasm (triangular shape on 3D intraluminal view, often
   only seen on one view due to transient nature) or in diverticular
   disease. Typically linear with a smooth surface.
3. Lipoma—fat attenuation may be masked by streak artefact from
   luminal contrast.
4. Other mesenchymal neoplasms—e.g. haemangioma (most
   commonly rectosigmoid ± phleboliths), leiomyoma (usually
   rectosigmoid), fibroma, desmoid tumour, schwannoma,
   neurofibroma, ganglioneuroma, granular cell tumour.
   Submucosal location, smooth overlying mucosa.
5. Metastases—location may be serosal (if via peritoneal spread) or
   submucosal (if haematogenous, e.g. melanoma, lung, breast),
   usually with disease elsewhere ± ascites.
6. Carcinoid tumour—most commonly rectal and small in size.
7. Endometriosis*—serosal deposits especially on rectosigmoid can
   mimic a polyp or mass. Smooth overlying mucosal surface. Look
   for disease elsewhere in the pelvis.
8. Intramural haemorrhage—may mimic a submucosal mass;
   hyperattenuating on unenhanced CT.
9. Internal haemorrhoid or varix—in distal rectum abutting the
   anorectal junction. Varices are typically linear.
10. Inverted diverticulum—may contain a focus of indrawn fat.
11. Inverted appendix stump—following appendectomy.
12. Cystic lymphangioma—rare. Fluid attenuation

Question 34

COLONIC STRICTURES AND MASSES

Neoplastic

Answer 34

1. Carcinoma—irregular mural thickening with ‘shouldering’. May be
   a sessile or semiannular mass or annular stricture. Often <6 cm in
   length. Usually of soft-tissue attenuation except if mucinous (fluid
   attenuation ± calcification). Necrotic or mucinous mesenteric
   nodes are suggestive.
2. Metastasis—via peritoneal or haematogenous spread, usually with
   disease elsewhere ± ascites. Peritoneal metastases most commonly
   deposit on the rectosigmoid. Some primaries (e.g. linitis plastica,
   lobular breast cancer) can cause long smooth thick-walled
   strictures mimicking benign pathology.
3. Direct invasion by adjacent tumours—e.g. transverse colon
   invasion by gastric cancer, rectal invasion by prostate or
   gynaecological tumours.
4. Lymphoma*—long segment irregular thickening, typically without
   obstruction. Usually right colon, may be multifocal.
5. GIST—rare in the colon, most located in the rectum. Large
   endophytic or exophytic mass without lymphadenopathy (cf.
   carcinoma).
6. Sarcoma—e.g. leiomyosarcoma. Rare, often bulky and aggressive,
   indistinguishable from carcinoma. Can occur in the rectum years
   after pelvic radiotherapy

Question 35

COLONIC STRICTURES AND MASSES
Inflammatory and ischaemic
Tend to be symmetrical, smooth and tapered
9

Answer 35

1. Diverticular stricture—differentiation from cancer is not always
   possible. Features suggesting diverticulitis: >10 cm involvement,
   tapered margins, presence of gas-filled diverticula within thickened
   segment, pericolic stranding or fluid, engorged mesenteric vessels.
   Features suggesting cancer: focal shouldered mass, straightening of
   thickened segment, large or necrotic pericolic nodes.
2. Ulcerative colitis*—usually requires extensive involvement for >5
   years; look for associated haustral effacement, submucosal fat
   deposition and mesorectal fat proliferation. Strictures are
   commonest in the sigmoid and may be multiple. Beware of
   malignant complications—these are often irregular annular
   strictures. Risk factors: total colitis, length of history (risk starts at
   10 years and increases with time), epithelial dysplasia especially
   DALM (dysplasia-associated lesion or mass).
3. Crohn’s disease*—single or multiple with skip segments.
4. Ischaemic—infarction heals by stricture formation relatively rapidly.
   Most common at splenic flexure. Tapered margins, may be long.
5. Radiotherapy—occurs several years after treatment, usually in
   rectosigmoid.
6. Anastomotic stricture—especially if there is a history of
   anastomotic leak.
7. Caustic stricture—rectosigmoid.
8. Cathartic colon—due to chronic laxative abuse. Results in narrowcalibre ahaustral colon with long pseudostrictures due to spasm.
   Most commonly involves ascending and transverse colon, spares
   rectum (cf. chronic UC).
9. Sarcoidosis*—rare, usually in the presence of thoracic disease

Question 36

COLONIC STRICTURES AND MASSES

Infective

Answer 36

1. Tuberculosis*—most common in the ileocaecal region with
   contraction of caecum.
2. Amoeboma—rare mass-like form of amoebiasis. Rapid
   improvement after treatment with metronidazole.
3. Actinomycosis—markedly infiltrative mass, most common in
   ileocaecal region.
4. Schistosomiasis*—commonly rectosigmoid. Granulation tissue
   forming after the acute stage (oedema, fold thickening and
   polyps) may cause a stricture.
5. Lymphogranuloma venereum—sexually transmitted Chlamydia.
   Strictures are a late complication, characteristically long and
   tubular, affecting the rectosigmoid ± fistulae

Question 37

COLONIC STRICTURES AND MASSES

Extrinsic masses 8

Answer 37

Pericolic abscess,
endometriosis (usually rectosigmoid), 
desmoid 
tumour, 
solitary fibrous tumour, 
amyloidoma, 
duplication cyst. 
adhesive band may focally distort/narrow the colon mimicking a stricture

Question 38

MEGACOLON IN AN ADULT
Colonic dilatation >6 cm
Nontoxic (without mural abnormalities)
7

Answer 38

1. Distal obstruction—e.g. carcinoma, chronic intermittent sigmoid
   volvulus.
2. Paralytic ileus—many causes . Dilated thin walled colon ± gradual tapering at the splenic flexure without a visible obstructing cause. Small bowel is also often dilated.
3. Chronic pseudoobstruction—symptoms and signs of large bowel
   obstruction but without an obstructing cause on CT. Many causes
   Dilated thin-walled gas-filled colon. High risk of caecal necrosis and perforation despite the lack of mechanical obstruction.
4. Faecal impaction—markedly dilated rectum ± sigmoid due to
   impacted faeces, ± mural thickening due to stercoral colitis.
5. Hirschsprung’s disease and hypoganglionosis—can present in
   adults. Dilated colon with a transition in the sigmoid region.
6. Laxative abuse—dilated ahaustral colon ± spasm.
7. Amyloidosis*—dilatation is the most common manifestation of colonic involvement

Question 39

MEGACOLON IN AN ADULT
Toxic (with severe mural abnormalities.Mural abnormalities include thickening, loss of haustral folds ±pneumatosis or free gas
3

Answer 39

1. IBD*—UC > Crohn’s.
2. Infectious colitis—especially pseudomembranous colitis.
3. Ischaemic colitis

Question 40

PNEUMATOSIS INTESTINALIS
Benign causes (well patient)

Answer 40

1. Idiopathic—also known as pneumatosis cystoides intestinalis;
   usually involves the colon. Appears as clusters of gas-filled
   intramural cysts.
2. Drug-induced—corticosteroids, chemotherapy.
3. Intestinal—pyloric stenosis, intestinal pseudoobstruction, ileus,
   bowel obstruction, IBD.
4. Pulmonary – asthma, emphysema, PEEP, cystic fibrosis.
5. Connective tissue disease—e.g. scleroderma.
6. Iatrogenic—following endoscopy, CT colonography, jejunostomy
   tube, bowel anastomosis.
7. Organ transplants—including small-bowel transplants and
   graft-versus-host disease.

Question 41

PNEUMATOSIS INTESTINALIS

Life-threatening causes (unwell patient)

Answer 41

1. Intestinal ischaemia—including closed-loop bowel obstruction.
2. Toxic megacolon—due to IBD or severe enterocolitis. Suggests
   imminent perforation.
3. Trauma—suggests significant bowel injury.
4. Stevens-Johnson syndrome—with skin and mucosal involvement

Question 42

BOWEL WALL CALCIFICATION

Answer 42

1. Mucinous adenocarcinoma—calcification can be seen in the
   primary tumour or involved mesenteric nodes.
2. TB*—ileocaecal region.
3. Schistosomiasis*—usually left colon. Also look for hepatic
   calcification.
4. Metastatic calcification—due to renal failure; look for other sites.
5. Calcification within other masses—e.g. GIST, haemangioma.
6. Amyloidosis*.
7. Phlebosclerotic colitis—thread-like calcification of small SMV
   branches close to or within the colonic wall is almost
   pathognomonic

Question 43

BOWEL WALL FAT DEPOSITION

Answer 43

1. Normal variant—especially in the undistended colon of obese
   patients. Tends to disappear when the colon is distended.
2. Chronic IBD—UC (favours rectum and colon) and Crohn’s (favours
   distal ileum). The submucosal fat layer tends to be thicker than in
   normal obese patients and often persists even when the bowel is
   distended; ± mesenteric or mesorectal fatty proliferation.
3. Post chemotherapy or graft-versus-host disease*—may be
   diffuse.
4. Post radiotherapy—in the rectum.
5. Coeliac disease*—in the duodenum and jejunum

Question 44

RECTAL MASS OR THICKENING ON MRI

Malignant neoplasms

Answer 44

1. Adenocarcinoma—intermediate T2 signal mass or irregular
   annular thickening. Loss of underlying mural stratification,
   extramural extension and mesorectal lymphadenopathy suggest
   malignancy. Foci of high T2 signal suggest mucinous histology.
   Signet ring cell tumours can appear like linitis plastica.
2. Squamous cell carcinoma—usually extending from the anus.
3. Rectal invasion by an adjacent tumour—e.g. prostate and
   gynaecological tumours.
4. Carcinoid tumour—discrete nodule, usually <1 cm, with
   homogeneous enhancement. Usually well-differentiated; poorly
   differentiated tumours mimic adenocarcinoma.166 Aids to Radiological Differential Diagnosis
5. GIST—large heterogeneous endophytic or exophytic mass ±
   central ulceration; no lymphadenopathy (cf. adenocarcinoma).
6. Lymphoma*—infiltrative homogeneous nonobstructing mass
   with marked restricted diffusion and lymphadenopathy. The mass
   infiltrates through muscularis without obliterating the muscle
   layers (cf. adenocarcinoma).
7. Metastasis—e.g. from bladder, breast, lung, stomach. May be a
   submucosal mass or may resemble linitis plastica.
8. Sarcoma—e.g. leiomyosarcoma; can occur years after pelvic
   radiotherapy.
9. Melanoma—primary or metastatic. May be T1 bright.
10. Kaposi sarcoma—rare; seen in immunosuppressed patients, e.g.
    AIDS. Diffuse T2 hypointense rectal thickening.

Question 45

RECTAL MASS OR THICKENING ON MRI

Benign neoplasms

Answer 45

1. Adenoma—villous adenomas are often large and appear fronded
   with a cap of T2 bright mucin. A fibrovascular stalk may also be
   visible and is highly suggestive. Underlying rectal wall stratification
   is preserved unless there is malignant transformation.
2. Leiomyoma—discrete T2 hypointense mass, smaller and often
   more homogeneous than GIST but may undergo necrosis or
   calcification. An overlying T2 bright submucosal stripe may be
   seen, confirming origin from muscularis.
3. Lipoma—T1 bright with suppression on fatsat sequences.
4. Nerve sheath tumour—e.g. schwannoma, plexiform neurofibroma
   (in NF1: diffuse lobulated grape-like mass infiltrating rectum and
   surrounding fat).

Inflammatory and infective
See Section 7.21. Usually causes diffuse thickening and oedema,
except proctitis cystica profunda, which appears as a focal
multicystic mass

Question 46

RECTAL MASS OR THICKENING ON MRI

Others

Answer 46

1. Endometriosis*—T2 hypointense fibrosis obliterating the pouch
   of Douglas ± rectosigmoid deposits. Serosal endometriomas
   may be seen, containing T1 hyperintensity (which does not
   suppress on fatsat sequences) + peripheral T2 hypointense
   haemosiderin.
2. Haemangioma—T2 bright ± phleboliths ± feeding vessels. May
   diffusely infiltrate rectum.
3. Extrinsic masses of peritoneal origin—e.g. solitary fibrous
   tumour. See Section 7.33.
4. Infiltrative disorders—e.g. amyloidosis, malakoplakia,
   Rosai-Dorfman disease. Can rarely produce rectal masses.

Question 47

RETRORECTAL/PRESACRAL MASS

Answer 47

1. Abscess—e.g. due to rectal perforation, anastomotic leak or
   supralevator collection related to perianal sepsis.
2. Presacral fibrosis—due to previous radiotherapy or chronic
   sepsis, e.g. previous rectal anastomotic leak. Ill-defined, poorly
   enhancing presacral soft tissue ± tethering of adjacent structures.
3. Local tumour recurrence—of rectal cancer after surgery. Usually
   appears as a discrete soft-tissue nodule with some restricted
   diffusion on MRI.
4. Retrorectal developmental cysts—congenital, associated with
   sacral anomalies. Can be complicated by infection (internal gas),
   haemorrhage or malignant degeneration (nodular mural
   thickening is suspicious).
   (a) Tailgut cyst—multilocular, thin-walled retrorectal cyst
   (‘honeycomb’ appearance), typically sited just above levator
   plate ± a small extension into the intersphinteric plane of the
   anal canal. May contain proteinaceous material
   (hyperattenuating on CT, T1 hyperintense on MRI).
   (b) Duplication cyst—unilocular cyst with its own mucosa,
   submucosa and muscularis. Adherent to rectum ± fistula to
   rectum or anus.
   (c) Epidermoid cyst—unilocular T2 hyperintense cyst ± linear
   hypointensities (keratin strands) + restricted diffusion.
   (d) Dermoid cyst—contains fat and calcification.
   (e) Sacrococcygeal teratoma—typically in neonates, very rare in
   adults.
5. Sacral tumours—especially lymphoma, which may extend into
   the presacral space without causing significant bone destruction.
   Other tumours (e.g. metastases, plasmacytoma, chordoma)
   usually cause bone destruction, making it easier to confirm the
   sacral origin of the mass.
6. Subperitoneal adenomucinosis—well-defined, slow-growing
   septated cystic mass ± calcification. Usually seen after resection of
   a mucinous appendiceal tumour or after proctocolectomy
   performed for UC.
7. Myelolipoma—most common extraadrenal location is presacral.
   Benign, well-defined mass containing fat and soft-tissue elements,
   usually in older patients.168 Aids to Radiological Differential Diagnosis
8. Extramedullary haematopoiesis—presacral mass containing soft
   tissue and often fat; can mimic myelolipoma. Look for signs of
   marrow failure, e.g. bone sclerosis/splenomegaly.
9. Nerve sheath tumours—arising from sacral nerve roots, e.g.
   schwannoma, plexiform neurofibroma in NF1. Extension of a
   mass into an enlarged sacral foramen is characteristic.
10. Anterior sacral meningocoele—a CSF-containing sac protruding
    anteriorly through a defect in the sacrum.
11. Ectopic prostate—rare.
12. Other lesions not specific to the presacral space—e.g.
    sarcomas, solitary fibrous tumour, extraintestinal GIST,
    leiomyoma, lymphangioma, vascular malformations,
    endometrioma

Question 48

ANAL AND PERIANAL MASSES

Answer 48

1. Squamous cell carcinoma—intermediate T2 signal mass, often
   infiltrates internal and external anal sphincters, may spread onto
   perianal skin or extend cranially into rectum.
2. Adenocarcinoma—usually from a distal rectal tumour invading
   the anal canal.
3. Perianal sepsis, fistulae and abscesses.
   (a) Cryptoglandular anal fistula—originates from blockage and
   infection of anal glands located in the intersphincteric plane,
   resulting in a small abscess that drains to the skin surface
   forming a fistula. Classified as intersphincteric, transphincteric
   or suprasphincteric depending on the path of the fistula tract
   relative to the external anal sphincter. Associated perianal
   abscesses are common. Anterior transphincteric fistulae may
   open onto the vagina or posterior scrotum. There is a risk of
   malignant transformation of anal fistula tracts—irregular
   soft-tissue thickening within a tract is suspicious.
   (b) Crohn’s disease*—typically causes multiple complex anal
   fistulae, as well as extrasphincteric fistulae, which originate
   from the distal rectum and course to the skin surface outside
   of the anal sphincter complex.
   (c) Pilonidal sinus—blind-ending sinus tract originating in the
   natal cleft ± subcutaneous abscess. Inflammation may involve
   the coccyx. No communication with anal canal.
   (d) Hidradenitis suppurativa—recurrent infection of sweat
   glands typically in the axillae, groins and perineum. MRI
   shows diffuse subcutaneous oedema with a network of
   multiple sinus tracts and abscesses, which do not
   communicate with the anal canal.
   (e) Neutropenic perianal sepsis—in immunocompromised
   patients; often manifests initially as diffuse perianal
   inflammation without a discrete abscess or fistula tract.
4. Haematoma—e.g. due to pelvic trauma.
5. Condyloma acuminatum—due to HPV infection. Large, irregular,
   superficial, carpet-like perianal mass. Can be invasive and
   transform to SCC.
6. Aggressive angiomyxoma—typically in women of reproductive
   age. Arises from perineal soft tissues, often large and extends
   through the pelvic floor without invading pelvic viscera.
   Heterogeneously T2 hyperintense with a characteristic swirled
   appearance + avid enhancement. Similar but less invasive variants
   can occur, e.g. cellular angiofibroma (in men) and
   angiomyofibroblastoma—these are usually smaller (<5 cm)
   without extending through the pelvic floor and may be more
   homogeneous on MRI.
7. Cyclist’s nodule—seen in keen cyclists and horse riders. Benign
   subcutaneous fibrous mass caused by repetitive perineal
   microtrauma.
8. Metastasis—e.g. from prostate, colon, bladder, lymphoma. Rare.
9. Melanoma—primary or metastatic. May be T1 bright.
10. Sacrococcygeal tumours—metastases, plasmacytoma,
    chordoma.
11. Proximal-type epithelioid sarcoma—rare, usually in young
    adults. Perineum is a common location. Heterogeneous soft-tissue
    mass within subcutaneous fat, often with calcification.
12. Other masses not specific to the perianal region—e.g. lipoma,
    liposarcoma, angiolipoma, solitary fibrous tumour, extramedullary
    plasmacytoma, lymphoma.

Question 49

MESENTERIC AND OMENTAL
FAT STRANDING
Focal

Answer 49

1. Local inflammation—e.g. appendicitis, diverticulitis, cholecystitis,
   mild pancreatitis, gastritis, duodenitis, enteritis (of any cause, e.g.
   Crohn’s), colitis, adjacent to a site of perforation or abscess (e.g.
   tuboovarian, postsurgical). Fat stranding is localized around the
   inflamed organ ± ascites.
2. SMV branch occlusion—e.g. due to thrombosis, closed-loop SBO
   or soft-tissue infiltration (including the desmoplastic reaction seen
   with carcinoid tumours). Fat stranding within the involved
   mesenteric folds due to venous congestion ± bowel wall oedema
   or ischaemia. Ascites is common.
3. Mesenteric panniculitis—idiopathic fibroinflammatory disorder of
   the small bowel mesentery, occasionally associated with
   IgG4-related disease. Characteristic appearance on CT: focal area
   of ‘misty’ mesentery with discrete borders formed by the visceral
   peritoneum, containing prominent lymph nodes which retain their
   elongated shape. The stranding spares a ‘halo’ of fat around the
   mesenteric vessels and nodes. The inflamed mesenteric folds
   appear focally expanded—this is not usually seen in other causes
   of mesenteric stranding. NB: ascites is not a feature of panniculitis
   and suggests an alternative diagnosis.
4. Epiploic appendagitis—small ‘halo’ of inflammation around a
   fatty epiploic appendage ± a central dense ‘dot’ (thrombosed
   vessel). Usually affects the left colon.
5. Omental infarct—discrete area of fat stranding in the greater
   omentum usually involving its free edge (R>L). There may be some
   reactive oedema in the adjacent colon (mimicking colitis), but the
   stranding is centred on the omentum itself. The area of stranding
   is usually >5 cm, larger than in epiploic appendagitis. NB: the
   greater omentum typically lies anterior to all of the bowel loops
   and its blood supply arises from gastroepiploic rather than
   mesenteric vessels. Infarction of the lesser omentum is rare.
6. Mesenteric contusion—post trauma. Look carefully for an
   associated bowel injury.
7. Lymphoma*—can mimic mesenteric panniculitis, but the lymph
   nodes tend to be larger (>1 cm) and more rounded, and the
   stranded mesentery is not usually focally expanded.
8. Whipple’s disease, coeliac disease* and tropical sprue—
   stranding in the jejunal mesentery + low density nodes.
9. Liposarcoma—rare; internal soft-tissue elements may resemble
   fat stranding. Look for mass effect displacing adjacent
   mesenteric vessels (cf. panniculitis where mesenteric vessels are
   undisplaced

Question 50

MESENTERIC AND OMENTAL
FAT STRANDING
Diffuse

Answer 50

1. Oedema—e.g. cardiac, hepatic or renal failure,
   hypoalbuminaemia, angioedema.
2. Severe acute pancreatitis—can cause widespread fat necrosis
   throughout mesenteric and retroperitoneal fat, which initially
   appears as diffuse fat stranding, later consolidating into nodular
   fat necrosis, which can mimic malignancy, but resolves over time.
3. Diffuse peritonitis—e.g. due to perforated peptic ulcer, faecal
   peritonitis, TB.
4. Main SMV/PV occlusion—e.g. due to thrombosis, soft-tissue
   infiltration (especially pancreatic cancer) or midgut volvulus.
5. Portal hypertension—due to cirrhosis. Look for varices,
   splenomegaly and ascites.
6. Disseminated peritoneal malignancy—can appear as diffuse fat
   stranding or ill-defined nodularity, especially in omentum.
7. Diffuse enteritis—e.g. due to chemotherapy, graft-versus-host
   disease, CMV, eosinophilic enteritis, mastocytosis. See Section
   7.19.
8. Lymphatic obstruction or lymphangiectasia—see Section 7.19.
9. Amyloidosis*—can cause diffuse infiltration and stranding
   throughout intraabdominal fat. Calcification is suggestive if
   present. Ascites is often absent (cf. the other causes in this list).
10. Familial Mediterranean fever*—see Section 7.34.
11. Sarcoidosis*—rare; usually with lymphadenopathy and disease
    elsewhere.
12. Erdheim-Chester disease*—very rare; typically with periaortic
    and perinephric soft-tissue thickening.
13. Post small bowel transplantation—a normal postsurgical
    finding, but if severe or persistent can suggest lymphoedema,
    venous thrombosis, transplant rejection, graft-versus-host disease
    or opportunistic infection (CMV

Question 51

MESENTERIC LYMPHADENOPATHY

15

Answer 51

1. Reactive lymphadenopathy—due to mesenteric adenitis, infectious mononucleosis (+ splenomegaly) or any cause of bowel inflammation. Nodes are usually only mildly enlarged and retain their elongated shape. Can also be seen in systemic autoimmune disorders (e.g. SLE, RA, vasculitis) as part of generalized lymphadenopathy.
2. Lymphoma*—enlarged rounded homogeneous mesenteric nodes with a tendency to form confluent masses, which encase but do not occlude mesenteric vessels. The nodes may cause lymphatic obstruction resulting in mesenteric stranding, which can mimic panniculitis, but usually the nodal enlargement is a more prominent feature than the stranding.
3. Metastatic lymphadenopathy—most commonly from large or small bowel, e.g. adenocarcinoma (nodes are typically close to the primary tumour, ± central mucin) or carcinoid (+ calcification and desmoplastic reaction). Advanced gastric, pancreatic and hepatobiliary malignancies can also spread to mesenteric nodes, as well as more distant primaries such as melanoma, lung, breast and Kaposi sarcoma (often hypervascular). Note that GISTs do not typically spread to lymph nodes.
4. Mesenteric panniculitis—lymph nodes tend to retain their elongated shape and are a less prominent feature than the degree of mesenteric stranding.
5. Mycobacterial infection—e.g. TB (typically necrotic, most commonly ileocolic) and Mycobacterim avium complex (solid or necrotic, most commonly jejunal).
6. HIV—due to the infection itself, or opportunistic infection (especially mycobacterial) or as part of immune reconstitution inflammatory syndrome (IRIS, typically seen <3 months after initiation of highly active antiretroviral therapy).
7. Sarcoidosis*—usually in the presence of thoracic disease ± liver
   and spleen involvement.
8. Coeliac disease* and tropical sprue—low density (fatty) nodes that may be markedly enlarged ± fat-fluid levels (cavitating mesenteric lymph node syndrome). Look for jejunoileal fold reversal and mild jejunal thickening and dilatation. There is also an increased risk of lymphoma with coeliac disease.
9. Whipple’s disease—low density (fatty) nodes ± mild jejunal thickening.
10. Aseptic abscesses—rare extraintestinal manifestation of IBD (especially Crohn’s). More commonly involves the spleen, but can present with necrotic mesenteric lymphadenopathy.
11. Familial Mediterranean fever*
12. Castleman disease—enlarged hypervascular lymph nodes.
13. Amyloidosis*—with mesenteric stranding ± calcification.
14. Mastocytosis*—with bowel wall thickening, splenomegaly and
    sclerotic bones.
15. Neurofibromatosis*—multiple mesenteric neurofibromas can mimic lymphadenopathy, though neurofibromas tend to be of lower attenuation on CT

Question 52

PERITONEAL, OMENTAL OR 
MESENTERIC MASS
Solid
neoplasms 9
Fibro/inflammatory processes 5
Miscellaneous 8

Answer 52

Neoplasms
1. Metastasis—either via peritoneal spread (e.g. ovary, stomach,
pancreas, colon, uterus, bladder; often with ascites) or
haematogenous (e.g. melanoma, lung, breast). Metastases from
GISTs or sarcomas are not usually associated with ascites.
2. GIST—can be large and very exophytic, making it difficult to
identify the site of bowel origin. Can rarely be extraintestinal.
Large heterogeneous mass ± peritoneal or liver metastases.
3. Solitary fibrous tumour—usually benign and slow-growing, more
common in pleura than peritoneum. Well-defined, hyperenhancing
mass ± internal necrosis, haemorrhage, calcification or cystic
change. Often has internal vessels (flow voids on MRI). Tends to
displace rather than invade adjacent structures.
4. Desmoplastic small round cell tumour—rare, highly aggressive
malignant peritoneal tumour usually seen in males aged 15–25
years. Single or multiple peritoneal masses usually arising from
pelvis + internal necrosis, haemorrhage or calcification. Often
metastatic at presentation. Adenopathy is common (cf. GIST).
5. Malignant mesothelioma—see Section 7.34; can rarely present as
a focal mass.
6. Sarcomas—rare, many types; nonspecific heterogeneous mass,
often invading adjacent structures. Leiomyosarcoma may invade
mesenteric veins, creating tumour thrombus.
7. Benign mesenchymal tumours—rare, typically well-defined, e.g.
neurofibroma, schwannoma, leiomyoma, fibroma, haemangioma
(often contains phleboliths).
8. Ectopic gastrinoma—most arise from the pancreas or duodenum,
but rarely gastrinomas can be ectopic, usually arising within the
‘gastrinoma triangle’ close to the pancreas, duodenum, pylorus or
common bile duct. Typically well-defined and hypervascular +
gastric fold thickening (Zollinger-Ellison syndrome).
9. Extramedullary plasmacytoma—rarely occurs in the mesentery.

Fibroinflammatory and infiltrative processes
1. Desmoid tumour—well- or ill-defined mesenteric mass, variable
enhancement; often related to previous surgery, trauma or
Gardner syndrome. Local recurrence is common after resection.
2. Retractile mesenteritis—end-stage of mesenteric panniculitis.
Spiculated fibrotic mesenteric mass ± calcification, usually
occluding vessels and lymphatics ± ascites. Mimics carcinoid
lymphadenopathy + desmoplastic reaction.
3. Inflammatory pseudotumour—nonspecific well- or ill-defined
mass. Associated with IgG4-related disease.
4. Actinomycosis—markedly infiltrative mass, usually originating from
the uterus (associated with an IUD) or ileocaecal region.
5. Amyloidoma—rare mass-like form of amyloidosis. Usually contains
calcification.

Others
1. Haematoma—due to trauma, surgery, coagulopathy, aneurysm or
bleeding neoplasm. High attenuation on unenhanced CT; no
enhancement—look for pseudoaneurysm or active contrast
extravasation to suggest site of bleeding. Haemorrhagic ascites is
often present. Blood-fluid levels within the haematoma suggest
coagulopathy (‘haematocrit’ sign).
2. Splenosis/wandering splenunculus—the former is seen post
splenic trauma or surgery, due to discrete peritoneal implants of
splenic tissue (no vascular pedicle). The latter is a congenital
splenunculus which has a long vascular pedicle and can be located
anywhere in the peritoneal cavity (or even herniate into the chest
via diaphragmatic foramina). Both enhance similarly to the spleen
with identical signal characteristics on MRI. Diagnosis can be
confirmed on sulphur colloid scan or heat-damaged red blood cell
scan.
3. Endometriosis—most common in the pelvis, but deposits can be
seen anywhere in the peritoneal cavity. Low T2 signal (± foci of
high T1 signal) on MRI with susceptibility artefact on T2.
4. Dropped gallstones—post cholecystectomy, often located close to
liver. Variable attenuation on CT, may be calcified. Often small and
multiple. Usually T1 and T2 hypointense on MRI (except pigment
stones that may be T1 hyperintense). No enhancement. Can act as
a nidus for recurrent abscess formation.
5. Peritoneal loose body—due to a torted and detached epiploic
appendage, which develops concentric outer layers of
homogeneous fibrous tissue. Round or oval mass with a smooth
surface; typically contains a central focus of calcification, giving a
‘boiled egg’ appearance. Usually mobile, can be large.
6. Parasitic leiomyoma—due to a detached uterine fibroid which
adheres to the peritoneum, most often in the pelvis. Well-defined,
typically T2 hypointense on MRI.
7. Foreign body granuloma—usually due to retained surgical
materials. May be calcified.
8. Osseous metaplasia—secondary to trauma or recurrent abdominal
surgery. Multiple linear or branching ossified masses.

Question 53

PERITONEAL, OMENTAL OR
MESENTERIC MASS
Cystic

Answer 53

1. Loculated fluid collection/abscess—e.g. due to perforation,
   peritonitis, pancreatitis, foreign bodies (e.g. fish or chicken bones
   that have penetrated the bowel) or postsurgical collections
   (including those related to dropped gallstones or gossypibomas—
   retained surgical materials). Internal gas bubbles suggest infection
   or perforation, except in the case of gossypibomas which often
   contain gas; these also contain a curvilinear radiopaque marker
   which aids diagnosis. Beware of haemostatic packing materials;
   these are deliberately left inside the abdomen post-op to stop
   bleeding and can mimic an abscess.
2. Pseudocyst—most commonly due to subacute pancreatitis
   (>4 weeks old, most commonly in lesser sac), but can also be
   seen post trauma due to incomplete resolution of a haematoma.
   Smooth fibrotic wall, which may be thick; no internal
   enhancement.
3. Cystic metastasis—from a mucinous primary, e.g. ovary,
   stomach.
4. Pseudomyxoma peritonei—most commonly due to a low grade
   mucinous tumour of the appendix which perforates into the
   peritoneal cavity. Large volume of multiloculated mucinous fluid,
   which may mimic ascites on CT—look for surface scalloping of
   the liver or spleen suggesting mass effect (not seen in simple
   ascites). Curvilinear septal calcification may be seen.
5. Lymphangioma—congenital lymphatic anomaly, most common
   true cyst. Multicystic mass that tends to be elongated, insinuating
   between organs without much mass effect. Thin septa ± mild
   enhancement or calcification. The fluid may be of low
   attenuation (chylous).
6. Enteric duplication cyst—unilocular, usually attached to bowel.
   Thin wall containing normal bowel wall layers, which may be
   appreciable on US or MRI.
7. Enteric/mesothelial cyst—indistinguishable on imaging. Both
   present as a simple unilocular cyst.
8. Benign multicystic mesothelioma—benign cystic neoplasm
   arising from the peritoneum, typically in young women. Usually a
   multilocular cyst on imaging with thin walls ± mild septal
   enhancement.
9. Peritoneal inclusion cyst—typically located in the pelvis in
   premenopausal women who have adhesions related to surgery,
   trauma, pelvic inflammatory disease or endometriosis. Caused by 176 Aids to Radiological Differential Diagnosis
   the accumulation of fluid released during ovulation which is not
   reabsorbed due to the adhesions, resulting in cysts which often
   have unusual shapes, conforming to adjacent structures without
   mass effect. No discrete wall.
10. Omphalomesenteric duct cyst—congenital, due to a persistent
    omphalomesenteric duct with focal cyst formation. The persistent
    duct may be seen connecting the cyst to the umbilicus and/or
    distal ileum.
11. Hydatid cyst—unilocular or multilocular depending on stage.
    Usually caused by rupture of a hepatic hydatid. May be multiple.
    No internal septal enhancement.
12. Cystic change in a solid lesion—e.g. necrotic mesenteric nodes,
    GIST, schwannoma

Question 54

PERITONEAL, OMENTAL OR
MESENTERIC MASS
Fat-containing

Answer 54

1. Fat necrosis.
   (a) Omental infarct—see Section 7.31; can appear mass-like.
   Involutes over time. Can become infected.
   (b) Epiploic appendagitis—see Section 7.31; typically <5 cm.
   Infarcted appendages may detach, becoming peritoneal
   loose bodies, which are often rim-calcified with central fat.
   (c) Acute pancreatitis—can cause widespread nodular fat
   necrosis mimicking peritoneal carcinomatosis; resolves over
   time.
   (d) Encapsulated fat necrosis—can occur anywhere, often due
   to trauma or surgery. Fatty mass with a smooth fibrous
   capsule ± internal stranding and calcification; can mimic
   liposarcoma, but will involute over time.
   (e) Idiopathic nodular panniculitis—typically causes multifocal
   nodular necrosis of subcutaneous fat, but can rarely also
   involve the mesentery.
2. Mesenteric panniculitis—see Section 7.31; the discrete margins
   and focal mesenteric expansion can mimic a mass lesion, but the
   undisplaced centrally located mesenteric vessels within the lesion
   aid diagnosis.
3. Postsurgical omental flaps—e.g. following liver surgery or
   duodenal repair, or for pelvic floor reconstruction following
   abdominoperineal resection. These flaps can undergo infarction
   especially in the pelvis, thereby developing internal soft-tissue
   elements which may mimic local tumour recurrence.
4. Pseudolipoma of Glisson’s capsule—small fatty lesion attached
   to the liver capsule; represents a detached epiploic appendage.
5. Liposarcoma—rare; more common in the retroperitoneum, but
   these are often large and it can be difficult to categorize their
   origin. Fatty mass containing soft-tissue components.
6. Lipoma—purely fatty, usually very difficult to see as it blends
   in with the surrounding mesenteric fat. Sometimes the local Abdomen and gastrointestinal tract 177
   7
   mass effect can be appreciated, and if there is generalized
   mesenteric oedema this usually spares the lipoma, making it
   easier to see.
7. Hibernoma—benign tumour of brown fat, rare in the abdominal
   cavity. See Section 7.35.
8. Fat-containing metastases—e.g. from teratoma or recurrent
   liposarcoma.
9. Fatty mesenteric lymph nodes—in coeliac disease, tropical
   sprue and Whipple’s disease (see Section 7.32).
10. Extramedullary haematopoiesis—can rarely involve the
    mesentery, creating soft-tissue masses containing a variable
    amount of soft tissue and fat.
11. Haemangioma/lymphangioma—can rarely contain foci of fat.
12. Hydatid cyst—can rarely contain foci of fat if chronic.
13. Failed renal transplant—thinned poorly enhancing cortex +
    hypertrophy of renal sinus fat can mimic a fat-containing mass.
    Iliac fossa location.

Question 55

PERITONEAL THICKENING

Nodular or irregular

Answer 55

1. Metastatic peritoneal carcinomatosis—e.g. from ovary, stomach,
   pancreas, colon, appendix, uterus, bladder. Peritoneal thickening
   may be subtle and is often best seen in the pelvis, paracolic gutters
   and subphrenic spaces. Usually associated with ascites, omental
   nodularity or caking ± obstruction of bowel, bile ducts or ureters.
2. Primary peritoneal carcinoma—identical appearance to peritoneal
   carcinomatosis, but without a visible primary tumour. Almost
   exclusively in women, usually postmenopausal. Psammomatous
   calcification is common.
3. Lymphomatosis—secondary peritoneal involvement is more
   common and typically associated with widespread 178 Aids to Radiological Differential Diagnosis
   lymphadenopathy (more than with peritoneal carcinomatosis).
   Primary peritoneal lymphoma occurs in immunocompromised
   patients and is not usually associated with lymphadenopathy or
   disease elsewhere. Leukaemia can produce a similar appearance.
4. Malignant mesothelioma—of the peritoneum. Most commonly
   causes diffuse ‘sheet-like’ thickening throughout the peritoneum +
   ascites ± omental caking, usually with pleural plaques suggesting
   prior asbestos exposure. M>F. Lymphadenopathy is uncommon
   and would suggest an alternative diagnosis.
5. Tuberculous peritonitis—nodular peritoneal thickening ± ascites
   (in the ‘wet’ form), often with necrotic mesenteric nodes,
   calcification and ileocaecal involvement. Also look for thoracic
   disease.
6. Leiomyomatosis peritonealis disseminata—peritoneal
   dissemination of benign leiomyomas, typically in premenopausal
   women with uterine fibroids. On imaging the masses are well
   defined, of low T2 signal and often heterogeneously enhancing,
   similar to fibroids. Omental caking is absent, and ascites is minimal
   (cf. malignant peritoneal disease).
7. Gliomatosis peritonei—benign peritoneal implants of mature glial
   tissue, nearly always in the presence of an ovarian teratoma.
   Indistinguishable from peritoneal metastases on imaging ,.

Question 56

PERITONEAL THICKENING

Smooth

Answer 56

1. Acute peritonitis—e.g. due to bowel inflammation, perforation,
   postsurgical sepsis (e.g. anastomotic leak, collections), pancreatitis,
   bile leak, spontaneous bacterial peritonitis. Peritoneal thickening is
   usually mild, and ascites is typically present.
2. Diffuse peritoneal malignancy—e.g. carcinomatosis, lymphomatosis,
   mesothelioma. Thickening can sometimes appear smooth on imaging.
3. Portal hypertension—can cause mild peritoneal thickening (partly
   due to serpiginous subperitoneal shunts) with ascites and diffuse
   fat stranding.
4. Tuberculous peritonitis—thickening may be smooth, though
   usually thicker than in acute peritonitis. Ascites may be present
   (‘wet’ form) or absent (‘dry’ form). Look for other features of TB.
5. Sclerosing encapsulating peritonitis—usually in patients on
   long-term peritoneal dialysis. Smooth peritoneal thickening (often
   thicker than in acute peritonitis) encasing loops of bowel ± linear
   calcification.
6. SLE peritonitis—diffuse mild peritoneal thickening and ascites ±
   bowel wall oedema or vasculitis.Abdomen and gastrointestinal tract 179
   7
7. Familial Mediterranean fever*—rare inherited disorder prevalent
   in the Mediterranean, characterized by recurrent self-limiting
   attacks of peritonitis ± pleurisy, synovitis and pericarditis. CT
   findings are nonspecific and may include peritoneal thickening,
   ascites and diffuse mesenteric or omental fat stranding.
8. Sarcoidosis*—rare, usually in the presence of disease elsewhere

Question 57

ABDOMINAL WALL MASS

Lesions arising from the skin

Answer 57

1. Epidermal inclusion cyst—also known as a sebaceous cyst.
   Smooth and rounded contour, typically attached to skin surface.
   Usually of fluid attenuation on CT ± rim calcification, no internal
   enhancement. Variable signal on MRI. Can rupture or become
   infected.
2. Dermatofibrosarcoma protuberans (DFSP)—lobulated mass
   extending from the skin into subcutaneous fat.
3. Melanoma—arises from skin ± subcutaneous extension.
4. Sweat gland tumours—well-defined, solid-cystic mass extending
   from the skin into subcutaneous fat.
5. Keloid scar—focal cutaneous thickening at site of previous surgery
   or trauma

Question 58

ABDOMINAL WALL MASS

Lesions containing fat

Answer 58

1. Hernias—e.g. inguinal, femoral, paraumbilical, epigastric,
   hypogastric, Spigelian, lumbar, incisional. Contain fat ± bowel or
   other abdominal organs. May mimic a lipoma if the hernial neck is
   very small and difficult to see.
2. Lipoma—encapsulated purely fatty mass ± thin septa. May be
   subcutaneous or intramuscular. May be multiple in familial multiple
   lipomatosis. Features concerning for liposarcoma include rapid
   growth, size >5 cm, location deep to subcutaneous fascia and
   internal soft-tissue elements.
3. Liposarcoma—fatty mass containing soft-tissue elements <1 cm
   (well-differentiated) or >1 cm (dedifferentiated). NB: myxoid and
   pleomorphic variants contain minimal or no fat.
4. Fat necrosis—ill-defined subcutaneous soft-tissue nodules with
   internal fat and without significant mass effect. Usually
   posttraumatic; occasionally secondary to warfarin. If widespread,
   consider idiopathic nodular panniculitis.180 Aids to Radiological Differential Diagnosis
5. Haemangioma—lobulated mass, may extend through fascial
   planes. Often contains phleboliths and foci of fat. T2 hyperintense
   on MRI, variable enhancement.
6. Hibernoma—rare benign tumour of brown fat. Well-defined,
   slightly higher attenuation than normal fat on CT + internal septa
   ± enhancement. A prominent feeding vessel is almost
   pathognomonic. Typically shows high FDG uptake on PET.
7. Other rare lipomatous tumours—e.g. angiolipoma, chondroid
   lipoma, osteolipoma, lipoleiomyoma

Question 59

ABDOMINAL WALL MASS

Iatrogenic or traumatic lesions

Answer 59

1. Haematoma—most common in rectus abdominis muscle. May be
   related to trauma, surgery, protracted coughing/vomiting or
   coagulopathy (internal blood-fluid levels suggest the latter).
   Hyperattenuating on unenhanced CT, no internal enhancement.
   Look for an associated pseudoaneurysm or active contrast
   extravasation.
2. Postsurgical seroma—encapsulated unilocular homogeneous fluid
   collection, often large. May become infected.
3. Injection site—e.g. insulin, heparin. Small subcutaneous focus of
   fluid/nodularity ± gas bubbles, most common in lower abdominal
   wall or buttocks. Can form a discrete injection granuloma over
   time (often calcified). Recurrent insulin injections can cause
   ill-defined subcutaneous soft-tissue thickening (lipohypertrophy).
4. Foreign body granuloma—e.g. related to sutures (stitch
   granuloma, typically located at one end of a surgical scar),
   wood splinters (very low attenuation on CT), shotgun pellets,
   dropped gallstones within the abdominal wall. Calcification is
   common.
5. Heterotopic ossification—at sites of prior surgery (most common
   along linea alba) or trauma.
6. Skull bone flap—stored in the abdominal wall after craniectomy
   to keep the bone viable.

Question 60

ABDOMINAL WALL MASS

Cystic lesions

Answer 60

1. Abscess—e.g. postsurgical collection (± wound dehiscence),
   extension of intraabdominal sepsis into abdominal wall,
   penetrating Crohn’s disease, infected haematoma, infected
   umbilical sinus, disseminated septic emboli, necrotizing fasciitis
   (look for gas dissecting along fascial planes), pyomyositis, TB,
   actinomycosis (ill-defined, often solid).
2. Lymphangioma—macrocystic or microcystic. Often extends
   through tissue planes.
3. Cysticercosis*—multiple subcutaneous and intramuscular cysts or
   calcifications depending on stage of disease.

Question 61

ABDOMINAL WALL MASS

Malignant neoplasms

Answer 61

1. Soft-tissue metastasis—e.g. from lung, breast, ovary, uterus,
   colon, melanoma; usually in the presence of widespread disease.
   May be seen in isolation at surgical incisions or port/needle tracts.
   Irregular soft-tissue nodule ± central necrosis. Intramuscular
   metastases are often subtle on CT.
2. Malignant invasion of abdominal wall—by an intraabdominal
   tumour.
3. Soft-tissue sarcomas—many types. Often large, heterogeneous
   and invasive.
4. Lymphoma*/leukaemia—can present as a discrete homogeneous
   mass or ill-defined thickening

Question 62

ABDOMINAL WALL MASS

Benign neoplasms

Answer 62

1. Neurofibroma—multiple in NF1; may be cutaneous and
   pedunculated, subcutaneous or intramuscular. Well-defined round,
   tubular or plexiform mass oriented along a nerve. Low attenuation
   on CT, T2 hyperintense with ‘target’ sign on MRI.
2. Schwannoma—well-defined rounded mass arising from a nerve.
   T2 hyperintense on MRI ± cystic change. May be densely calcified
   (‘ancient’ schwannoma).
3. Solitary fibrous tumour—well-defined avidly enhancing mass,
   often with internal vessels (flow voids on MRI). Tends to displace
   rather than invade other structures.
4. Leiomyoma—rare, usually seen in young patients or those with
   HIV. Well-defined subcutaneous soft-tissue mass. May also occur in
   the inguinal canal in premenopausal women (round ligament
   leiomyoma).
5. Inflammatory pseudotumour—rare. Nonspecific well- or
   ill-defined mass, may be invasive

Question 63

ABDOMINAL WALL MASS

Other lesions

Answer 63

1. Desmoid tumour—most commonly in rectus abdominis, related
   to previous surgical incision, trauma or Gardner syndrome. Can
   also be seen postpartum (± caesarean section), where the main
   differential is endometriosis. Well- or ill-defined mass. Early tumours
   are cellular, T2 hyperintense and avidly enhancing; longstanding
   tumours become collagenous, T2 hypointense and mildly
   enhancing. Internal T2 hypointense bands and a ‘fascial tail’ along
   the muscle fascia are highly suggestive features.
2. Endometriosis*—typically seen at a caesarean-section or
   hysterectomy scar, usually without evidence of pelvic disease. Small 182 Aids to Radiological Differential Diagnosis
   spiculated mass, homogeneous on CT, slightly T2 hyperintense to
   muscle on MRI ± foci of T1 hyperintensity, mild enhancement.
3. Abdominal wall varices—due to portal hypertension. May be seen
   around stoma sites. Round ligament varicosities may be seen in the
   inguinal canal in pregnant women.
4. Undescended testis—in the inguinal canal. Increased risk of
   malignancy.
5. Accessory breast tissue—seen anywhere along the line of the
   embryologic mammary streak. ‘Feathery’ subcutaneous breast
   tissue that may be attached to skin surface ± accessory nipple.
6. Muscle swelling/oedema—e.g. due to myositis, rhabdomyolysis
   or angioedema.
7. Rosai-Dorfman disease*—rare; can present with nonspecific
   subcutaneous soft-tissue nodules or thickening