Abdomen and gastrointestinal tract

Published on 12/06/2015 by admin

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Last modified 12/06/2015

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6

Abdomen and gastrointestinal tract

6.1

Pneumoperitoneum

Radiological signs

1. Plain film (sensitivity 50–70%)

2. CT (greater sensitivity than plain film) – suspected perforation

6.3

Pharyngeal/oesophageal pouches and diverticula

Upper third

6.4

Oesophageal ulceration

In addition to ulceration there may be non-specific signs of oesophagitis:

Inflammatory

1. Reflux oesophagitis± hiatus hernia. Signs characteristic of reflux oesophagitis are:

2. Barrett’s oesophagus – to be considered in any patient with oesophageal ulceration or stricture but especially if the abnormality is in the body of the oesophagus (although strictures are more common in the lower oesophagus). Hiatus hernia in 75–90%. Usually endoscopic diagnosis.

3. Candida oesophagitis – predominantly in immunosuppressed patients. Early: small, plaque-like filling defects, often orientated in the long axis of the oesophagus. Advanced: cobblestone mucosal surface ± luminal narrowing. Ulceration is uncommon. Tiny bubbles along the top of the column of barium – the ‘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.

4. Viral – herpes and CMV occurring mostly in immunocompromised patients. May manifest as discrete ulcers or ulcerated plaques, or mimic Candida oesophagitis. Discrete ulcers on an otherwise normal background mucosa are strongly suggestive of a viral aetiology.

5. Caustic ingestion – ulceration is most marked at the sites of anatomical hold-up and progresses to a long, smooth stricture.

6. Radiotherapy – ulceration is rare. Altered oesophageal motility is frequently the only abnormality.

7. Crohn’s disease* – aphthoid ulcers and, in advanced cases, undermining ulcers, intramural tracking and fistulae.

8. Drug-induced – due to prolonged contact with tetracycline, quinidine and potassium supplements.

9. Behçet’s disease.

10. Intramural diverticulosis.

6.5

Oesophageal strictures – smooth

Inflammatory

1. Peptic – the stricture develops relatively late. Most frequently at the oesophagogastric junction and associated with reflux and a hiatus hernia. Less commonly, more proximal in the oesophagus and associated with heterotopic gastric mucosa (Barrett’s oesophagus). ± Ulceration.

2. Scleroderma* – reflux through a wide open cardia may produce stricture. Oesophagus is the commonest internal organ to be affected. Peristalsis is poor, cardia wide open and the oesophagus dilated (contains air in the resting state).

3. Corrosives – acute: oedema, spasm, ulceration and loss of mucosal pattern at ‘hold-up’ points (aortic arch and oesophagogastric junction). Strictures are typically long and symmetrical, may take several years to develop and are more likely to be produced by alkalis than acid.

4. Iatrogenic – prolonged use of a nasogastric tube. Stricture in distal oesophagus probably secondary to reflux. Also drugs e.g. bisphosphonates.

6.6

Oesophageal strictures – irregular

6.8

Stomach masses and filling defects

Primary malignant neoplasms

1. Carcinoma – most polypoidal carcinomas are 1–4 cm in diameter. (Any polyp > 2 cm in diameter must be considered to be malignant). Endoscopic US accurate in local staging for early disease. CT superior for more advanced disease.

2. Lymphoma* – 1–5% of gastric malignancy. Usually non-Hodgkin’s. May be ulcerative, infiltrative and/or polypoid. Often cannot be distinguished from carcinoma, but extension across the pylorus is suggestive of a lymphoma. MALT lymphoma is strongly associated with Helicobacter pylori infection. CT – marked hyopattenuating wall thickening; mean 3–5 cm. Whole stomach involved in 50%. Most (not all) have adjacent lymphadenopathy.

3. GIST – commonest in stomach but also small bowel, colon and mesentery. Variable size and malignant potential. Cell-surface marker (c-KIT) detectable by immunohistochemistry. Large tumours hyperenhancing and often heterogeneous on CT/MRI. Ulceration and fistulation common. 50% have metastasis at presentation (liver, peritoneum). May enlarge with treatment: reduced enhancement suggests response.

6.9

Thick stomach folds/wall

Thickness greater than 1 cm. CT assessment of non-distended stomach remains limited, but CT after gas or water distension is often useful.

6.13

Duodenal mural/fold thickening or mass

Neoplastic

1. Adenocarcinoma – 50–70% of small bowel carcinoma occurs in duodenum or proximal jejunum. Polypoidal mass or asymmetric wall thickening on CT. 50% have metastasis at presentation.

2. Lipoma.

3. Brunner gland hamartoma – 10% of benign duodenal tumours. Usually D1. No malignant potential. 1–12 cm sessile or pedunculated filling defect.

4. Adenoma – malignant potential; associated with familial adenomatous polyposis.

5. GIST – unusual in duodenum; usually D2, D3; large size, heterogeneous rim enhancement and local invasion suggest malignant transformation.

6. Leiomyoma.

7. Lymphoma – usually non-Hodgkin’s, T cell; CT-segmental non-obstructing mural thickening or extrinsic mass with or without aneurysmal dilatation.

8. Neuroendocrine tumour – 2–3% occur in duodenum; polypoidal or mass with rapid contrast enhancement and washout on CT.

9. Metastasis – most common melanoma, breast and lung.

Inflammatory/infiltrative

1. Duodenitis/ulcer – usually D1 related to H. pylori. Focal wall thickening and avid enhancement on CT. May see large ulcer cavity.

2. Crohn’s disease – mural thickening on CT/MRI ± layered contrast enhancement. Mild signs occur in duodenum in up to 40%, but severe involvement only occurs in 2%. D1 and D2 predominantly affected.

3. Cystic dystrophy – possible secondary to heterotopic pancreatic tissue in duodenal wall – D2. Presents with weight loss, pain and obstruction. Well-defined duodenal wall cysts on CT/MRI/US scan often with delayed mural enhancement due to fibrosis ± signs of chronic pancreatitis. Inflammatory changes in acute episode.

4. Groove pancreatitis – segmental inflammation between the head of pancreas and duodenum.

5. Varices.

6. Diverticulum – up to 23%; may be large.

7. Duplication – less than 5% of intestinal duplications; thin-walled cyst on CT/MRI often with no luminal communication.

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