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Plain film signs include:
Erect CXR —free gas under diaphragm or liver. Can detect 10 ml of gas. Takes 10 minutes for all gas to rise.
Supine AXR —most sensitive signs are often in the right upper quadrant. Gas outlines both sides of bowel wall, which appears as a white line (Rigler sign). The liver may appear hyperlucent or have an overlying oval gas shadow. The falciform ligament may also be outlined by free gas. In infants, a large volume of gas collects centrally, producing a rounded translucency over the central abdomen (‘football’ sign).
CT is more sensitive for detecting extraluminal gas and can also show focal bowel wall thickening ± mural discontinuity at the site of perforation with adjacent gas bubbles ± extraluminal oral contrast (if given). The distribution of free gas on CT may suggest the site of perforation:
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.
Perforation
Peptic ulcer —gastric or duodenal.
Inflammation —e.g. diverticulitis, appendicitis, toxic megacolon, necrotizing enterocolitis (neonates).
Obstruction —especially closed loop or large bowel obstruction.
Infarction .
Malignant neoplasms .
Trauma —blunt or penetrating.
Stercoral —due to hard faeces, usually in rectum/sigmoid.
Foreign body —e.g. fish bone.
Pneumatosis coli —the cysts may rupture, or gas may dissect through the bowel wall without a discrete site of perforation.
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 CO 2 —free gas >3 days after laparoscopy is suspicious).
Pneumomediastinum —see Section 5.36 .
Introduction per vaginam —e.g. douching.
Pneumothorax —via a congenital pleuroperitoneal fistula.
Idiopathic.
Ascites .
Fluid-filled bowel —closed-loop obstruction, active pancolitis, early mesenteric infarction, bowel washout.
Acute pancreatitis —due to excessive vomiting.
High obstruction —e.g. gastric outlet obstruction, congenital atresia (neonates).
Large abdominal mass —pushes bowel laterally.
Normal.
Zenker's diverticulum —posterior, usually on left side, between the fibres of inferior constrictor and cricopharyngeus ± an air–fluid level.
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.
Lateral cervical oesophageal pouch and diverticulum —through the Killian-Jamieson space, below the level of cricopharyngeus. Usually asymptomatic.
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.
Developmental —failure to completely close a tracheo-oesophageal fistula.
Intramural pseudodiverticulosis —rare. Multiple tiny flask-shaped outpouchings. 90% have associated oesophageal strictures, mainly in the upper third.
Epiphrenic —mimics a hiatus hernia.
Ulcer —peptic or related to steroids, immunosuppression or radiotherapy.
Mucosal tears —Mallory-Weiss syndrome, post oesophagoscopy.
After Heller's operation.
Contained oesophageal perforation.
Oesophageal anastomosis —may have a small outpouching.
Oesophageal duplication cyst communicating with oesophagus.
There may also be nonspecific signs of oesophagitis, e.g. thickening of longitudinal and transverse folds, reduced or absent peristalsis.
Reflux oesophagitis —± hiatus hernia. Characteristic signs are:
A gastric fundal fold crossing the gastrooesophageal junction (GOJ) and ending as a polypoid protuberance in the distal oesophagus.
Erosions—dots or linear streaks of barium in the distal oesophagus.
Ulcers—may be linear, serpiginous or round.
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.
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.
Intramural pseudodiverticulosis —can mimic ulceration.
Graft-versus-host disease* —rare in the oesophagus.
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.
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.
Oral drug-induced —due to prolonged contact with tetracycline, quinidine or potassium tablets, at sites of anatomical hold-up.
Longstanding nasogastric (NG) tube.
Radiotherapy —ulceration is rare. Dysmotility is often the only abnormality.
Crohn's disease *—aphthoid ulcers and, in advanced cases, undermining ulcers, intramural tracking and fistulae.
Behçet's disease* —discrete superficial ulcers + history of oral and genital ulceration.
Bullous skin disorders —e.g. epidermolysis bullosa, pemphigus.
In the presence of a mass or stricture.
Carcinoma .
Leiomyosarcoma and leiomyoma.
Lymphoma*.
Melanoma.
Reflux oesophagitis and Barrett's —granular appearance, usually mid-distal oesophagus.
Glycogenic acanthosis —multiple small well-defined nodules, often in upper-mid oesophagus. Seen incidentally in elderly patients, or in young patients with Cowden syndrome.
Advanced Candida /viral oesophagitis —cobblestone mucosa.
Superficial spreading oesophageal carcinoma.
Eosinophilic oesophagitis —diffuse narrowing with a corrugated or ringed appearance.
Oesophageal papillomatosis —due to HPV infection. Laryngeal or tracheobronchial papillomatosis may coexist.
Peptic —the stricture develops relatively late, ± ulceration. Usually distal if associated with reflux and hiatus hernia; midoesophageal if associated with Barrett's.
Corrosives —caustic stricture; typically long and symmetrical; may take years to develop. More likely with alkalis than acids.
Scleroderma* —reflux through an open GOJ may produce a distal stricture. The oesophagus is dilated with poor peristalsis.
Iatrogenic —prolonged use of an NG tube (distal stricture, probably due to reflux). Also radiotherapy (typically midoesophageal) and drugs, e.g. bisphosphonates.
Crohn's disease *—rare, suggests severe disease.
Eosinophilic oesophagitis —strictures may be short (‘ringed’ oesophagus) or long.
Typically have a smooth contour but focal mucosal ulceration may be seen.
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.
Mediastinal tumours —e.g. lung cancer, lymphadenopathy. Extrinsic soft-tissue mass ± obstruction.
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.
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.
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).
Metastasis —rare.
Oesophageal varices —smooth tubular filling defects; can be distal (‘uphill’ varices due to portal hypertension) or proximal (‘downhill’ varices due to SVC obstruction).
Other vascular impressions —aberrant subclavian or pulmonary artery; right or double aortic arch; aortic aneurysm or tortuosity.
Intramural haematoma —associated with coagulopathy, protracted vomiting or instrumentation. Acute chest pain, dysphagia and haematemesis. Focal submucosal mass, high attenuation on unenhanced CT.
Oesophageal duplication cyst —smooth indentation of oesophagus. Cystic and nonenhancing on CT.
Other rare lesions —e.g. sarcoidosis, fibrosing mediastinitis, amyloidosis, malakoplakia, actinomycosis.
Achalasia —‘rat-tail’ tapering may mimic a stricture; this occurs below the diaphragm. Marked oesophageal dilatation with food in the lumen.
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.
Bullous skin disorders —epidermolysis bullosa, pemphigus. Short web-like strictures, may be multiple.
Graft-versus-host disease* —rare; short web-like strictures, may be multiple.
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.
Gastric carcinoma —can directly invade oesophagus.
Carcinosarcoma —big polypoid tumour ± stalk arising from the mid-distal oesophagus, often without obstruction.
Leiomyosarcoma —bulky mass, often without obstruction.
Lymphoma* —usually extension from gastric involvement.
Other rare tumours —neuroendocrine tumours, melanoma, Kaposi sarcoma, other sarcomas.
Reflux —rarely irregular.
Crohn's disease *—rare.
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).
Obstructing tumour or stricture —see Sections 7.6 and 7.7 .
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.
Scleroderma* —dilated oesophagus with poor peristalsis and contractility. Look for associated lung fibrosis and bowel features.
Post oesophagectomy —the gastric pull-up can mimic a dilated oesophagus.
Iatrogenic —e.g. over-tight gastric band or fundoplication wrap.
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.
Oesophageal amyloidosis —rare; can mimic achalasia.
Uncoordinated, nonpropulsive contractions.
Reflux oesophagitis .
Presbyoesophagus —impaired motor function due to muscle atrophy in the elderly. Seen in 25% of people >60 years.
GOJ obstruction —from any cause.
Neuropathy —e.g. early achalasia (before dilatation occurs), diabetes, alcoholism, malignant infiltration, Chagas disease.
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.
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 or NF1.
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.
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.
Sarcoma —rare. Many subtypes.
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).
Fundic gland polyps —usually multiple, small (<5 mm) and found mainly in the fundus. Can be sporadic or associated with FAP.
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.
Hamartomatous —characteristically multiple, small and relatively sparing of the antrum. Associated with FAP (including Gardner variant), Peutz-Jeghers, Cowden and Cronkhite-Canada syndromes.
Smooth, well-defined mass with an obtuse angle to the gastric wall.
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.
Lipoma —fat attenuation on CT.
Neurofibroma —may be multiple. NB: leiomyomas and lipomas are more common, even in patients with NF1.
Other rare neoplasms —e.g. NET (often hypervascular), haemangioma (may be hypervascular ± phleboliths), glomus tumour (hypervascular), plexiform fibromyxoma (myxoid appearance), schwannoma.
Pancreatic tumour/pseudocyst .
Splenomegaly/hepatomegaly.
Retroperitoneal tumours.
Duplication cyst.
Splenosis.
Gastric fundoplication —may mimic a distorted mass in the fundus. Scarring following gastric band removal can also cause mass-like distortion.
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.
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.
Intramural haematoma —e.g. traumatic, iatrogenic. Hyperattenuating on unenhanced CT.
Lymphoid hyperplasia —innumerable 1–3 mm round nodules in the antrum and/or body. Associated with H. pylori .
Increased prominence of gastric folds. CT assessment is aided by gas or water distension.
Characterized by submucosal thickening/oedema, which is near fluid attenuation on CT, ± mucosal hyperaemia.
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).
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.
Acute pancreatitis —reactive oedema of gastric wall.
Crohn's disease *—mild fold thickening especially in antrum, aphthoid ulceration ± conical stricture of antrum.
Acute eosinophilic gastroenteritis —oedematous folds, most commonly involves the gastric antrum but rest of the GI tract can also be involved.
Fold thickening is of soft-tissue attenuation on CT with enhancement.
Carcinoma —can manifest as focal irregular fold thickening.
Lymphoma* —usually NHL, may be primary or secondary.
Pseudolymphoma —benign reactive lymphoid hyperplasia. Most have an ulcer near the centre of the area affected.
Amyloidosis* —wall thickening and dysmotility.
Sarcoidosis* —focal or diffuse thickening, most common in antrum. May mimic linitis plastica or Ménétrier disease.
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.
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 hypoproteinaemia (effusions, ascites, oedema e.g. of the small bowel). Commonly achlorhydric: cf. Zollinger-Ellison syndrome.
Portal hypertension —e.g. due to cirrhosis or portal vein thrombosis. Oedematous stomach ± varices in fundus and oesophagus if chronic.
Emphysematous gastritis —intramural gas due to gas-forming infections.
Diffuse gastric wall thickening and rigidity with effacement of rugal folds.
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