ABDOMEN Flashcards Preview

Radiology differential diagnosis > ABDOMEN > Flashcards

Flashcards in ABDOMEN Deck (63)
Loading flashcards...
1
Q

PNEUMOPERITONEUM

GENERAL

A

• 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

2
Q

PNEUMOPERITONEUM

Causes

A
  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
3
Q

GASLESS ABDOMEN

A
  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
4
Q

PHARYNGEAL/OESOPHAGEAL POUCHES
AND DIVERTICULA
Upper third

A
  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
5
Q

PHARYNGEAL/OESOPHAGEAL POUCHES AND DIVERTICULA
MIDDLE
3

A
  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
6
Q

PHARYNGEAL/OESOPHAGEAL POUCHES

Lower third

A
  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.
7
Q

OESOPHAGEAL ULCERATION

A

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

8
Q

OESOPHAGEAL MUCOSAL NODULARITY

A
  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.
9
Q

OESOPHAGEAL STRICTURES—SMOOTH

A

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

10
Q

OESOPHAGEAL STRICTURES—IRREGULAR

A

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)

11
Q

DILATED OESOPHAGUS

A
  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.
12
Q

TERTIARY CONTRACTIONS IN THE

OESOPHAGUS 4

A
  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
13
Q
GASTRIC MASSES AND FILLING DEFECTS
malignant 5
polyps 4
submucosal neoplasms 4
Extrinsic 5
Others 5
A

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.

  1. 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.
  2. 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.
  3. 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.
  4. 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).

  1. Fundic gland polyps—usually multiple, small (<5 mm) and found mainly in the fundus. Can be sporadic or associated with FAP.
  2. 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.
  3. 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.

  1. 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.
  2. 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.
  3. Intramural haematoma—e.g. traumatic, iatrogenic..Hyperattenuating on unenhanced CT.
  4. Lymphoid hyperplasia—innumerable 1–3 mm round nodules in
    the antrum and/or body. Associated with H. pylori.
14
Q

GASTRIC FOLD THICKENING

A

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.

15
Q

LINITIS PLASTICA

A

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

16
Q

GASTRIC OR DUODENAL OBSTRUCTION

12

A
  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.
17
Q

DECREASED/ABSENT DUODENAL FOLDS

A
  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*
18
Q
DUODENAL WALL/FOLD THICKENING OR MASS
Neoplastic 11
Inflammatory  7
Vascular 3
Congenital/developmental 3
A

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

19
Q

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).

A

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

20
Q

SMALL BOWEL STRICTURES

A
  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.
21
Q

SMALL BOWEL MASSES

A

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

22
Q

SMALL BOWEL MASSES

BENIGN

A
  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
23
Q

SMALL BOWEL WALL THICKENING

A

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)

24
Q

ILEOCAECAL REGION THICKENING

Inflammatory

A
  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.
25
Q

ILEOCAECAL REGION THICKENING

Infective

A
  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
26
Q

ILEOCAECAL REGION THICKENING

Neoplastic

A
  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
27
Q

ILEOCAECAL REGION THICKENING

Ischaemia

A
  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
28
Q

COLITIS ON CROSS-SECTIONAL
IMAGING
Diffuse

A
  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
29
Q

COLITIS ON CROSS-SECTIONAL
IMAGING
Predominantly right-sided

A
  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.
30
Q

COLITIS ON CROSS-SECTIONAL IMAGING
Predominantly left-sided
7

A
  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.
31
Q

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

A
  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
32
Q

COLONIC POLYPS ON CT COLONOGRAPHY

6 types of polyps

A
  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)
33
Q

Polyp mimics

12

A
  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
34
Q

COLONIC STRICTURES AND MASSES

Neoplastic

A
  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
35
Q

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

A
  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
36
Q

COLONIC STRICTURES AND MASSES

Infective

A
  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
37
Q

COLONIC STRICTURES AND MASSES

Extrinsic masses 8

A
Pericolic abscess,
endometriosis (usually rectosigmoid), 
desmoid 
tumour, 
solitary fibrous tumour, 
amyloidoma, 
duplication cyst. 
adhesive band may focally distort/narrow the colon mimicking a stricture
38
Q

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

A
  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
39
Q

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

A
  1. IBD*—UC > Crohn’s.
  2. Infectious colitis—especially pseudomembranous colitis.
  3. Ischaemic colitis
40
Q
PNEUMATOSIS INTESTINALIS
Benign causes (well patient)
A
  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.
41
Q

PNEUMATOSIS INTESTINALIS

Life-threatening causes (unwell patient)

A
  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
42
Q

BOWEL WALL CALCIFICATION

A
  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
43
Q

BOWEL WALL FAT DEPOSITION

A
  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
44
Q

RECTAL MASS OR THICKENING ON MRI

Malignant neoplasms

A
  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.
45
Q

RECTAL MASS OR THICKENING ON MRI

Benign neoplasms

A
  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

46
Q

RECTAL MASS OR THICKENING ON MRI

Others

A
  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.
47
Q

RETRORECTAL/PRESACRAL MASS

A
  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
48
Q

ANAL AND PERIANAL MASSES

A
  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.
49
Q

MESENTERIC AND OMENTAL
FAT STRANDING
Focal

A
  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
50
Q

MESENTERIC AND OMENTAL
FAT STRANDING
Diffuse

A
  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
51
Q

MESENTERIC LYMPHADENOPATHY

15

A
  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
52
Q
PERITONEAL, OMENTAL OR 
MESENTERIC MASS
Solid
neoplasms 9
Fibro/inflammatory processes 5
Miscellaneous 8
A

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.

53
Q

PERITONEAL, OMENTAL OR
MESENTERIC MASS
Cystic

A
  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
54
Q

PERITONEAL, OMENTAL OR
MESENTERIC MASS
Fat-containing

A
  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.
55
Q

PERITONEAL THICKENING

Nodular or irregular

A
  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 ,.
56
Q

PERITONEAL THICKENING

Smooth

A
  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
57
Q

ABDOMINAL WALL MASS

Lesions arising from the skin

A
  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
58
Q

ABDOMINAL WALL MASS

Lesions containing fat

A
  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
59
Q

ABDOMINAL WALL MASS

Iatrogenic or traumatic lesions

A
  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.
60
Q

ABDOMINAL WALL MASS

Cystic lesions

A
  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.
61
Q

ABDOMINAL WALL MASS

Malignant neoplasms

A
  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
62
Q

ABDOMINAL WALL MASS

Benign neoplasms

A
  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
63
Q

ABDOMINAL WALL MASS

Other lesions

A
  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