http://www.medcyclopaedia.com/library/radiology/chapter22/22_2.aspx (pgina donde lo busqu).

Glossary Library / Textbook of Radiology / The gastrointestinal tr / Stomach and duodenum previous in index next in index Printer-friendly version Bookmark This Page

The gastrointestinal tract

Stomach and duodenum

Imaging techniques
Contrast studies The routine contrast examination for gastroduodenal disease is the double-contrast barium meal (DCBM); this has been found consistently superior to single contrast studies. There are many variations in technique for performance of the DCBM, but a frequently used method is a biphasic one that incorporates elements of the single contrast examination. The single contrast barium meal is occasionally justified in very elderly, sick or immobile patients and can be used to answer specific questions, such as determining the presence of gastric outlet obstruction. Water-soluble iodinated contrast media are used where there is suspected perforation or where a recent anastomosis is being tested. The commonest such contrast is 76% sodium methylglucamine diatrizoate ("Gastrografin"). However, this is contra-indicated if there is a risk of airway aspiration or suspicion of an oesophago-tracheal fistula, since its hyperosmolality can precipitate pulmonary oedema. Non-ionic iodinated contrast media are then used (or, alternatively, low-density dilute barium, with caution).

Figure 18. Supine double contrast view of gastric body and antrum showing mosaic-like areae gastricae.

The aim of the DCBM is to see, by appropriate positioning, all parts of the oesophagus, stomach and proximalduodenum in double contrast with good mucosal barium coating, adequate gaseous distension and hypotonia. A measure of good coating is the visualisation of the areae gastricae, which are seen as a mosaic-like pattern in the stomach (Fig. 18). These represent the areas about 1-4 mm in diameter, in the centre of which, the gastric glands open. Their visualisation depends on radiographic technique, barium density and the amount of mucus in the stomach. They are most often seen in the gastric antrum and body. Although controversial there is a suggestion that an increase in size of the areae and their presence in the proximal stomach are associated with increased acid production. Focal abnormalities of the areae are more important; distortion or enlargement may be seen in gastritis around an ulcer or due to superficial infiltration bycarcinoma, and may be the only subtle c1ue to this. Other anatomical features seen in the stomach on DCBM include the rugal folds and the cardia. The folds in the antrum are effaced with distension by gas; if they persist this suggests antral gastitis. The rugae in

the fundus and proximal body should be smooth and relatively straight in the distended stomach. The appearance of the cardia is variable; it may appear en face as a rosette which may be flat or have elevated margins; it may possess a hooded fold - the "burnaus sign"; or it may be seen as a crescentic line. The modem biphasic barium meal should inc1ude double and single contrast oesophagograms, compression views of the gastric antrum and duodenal cap as well as double contrast images of the stomach andduodenum, and an assessment of oesophageal motility. As part of the DCBM it is important to ensure that the second and third parts of the duodenum have been outlined. It is possible to obtain good double-contrast distended views of the descending duodenum. It is rarely necessary nowadays to perform a hypotonicduodenogram using a tube method. If the examination is being performed for suspected gastroduodenal perforation, a water-soluble contrast is used. Profile views of the filled stomach are obtained. The patient is then turned onto the right side to allow duodenal filling and turned through 360. If no obvious extravasation of contrast is seen, the patient should remain on the right side for ten minutes or so and then re-fluoroscoped. If no perforation is seen but is still strongly suspected clinically, delayed films may show contrast excreted through the urinary tract, since Gastrografin is absorbed from the peritoneal cavity. However, this sign is not specific for perforation since inflamed or ischaemic mucosa can allow absorption and thus renal excretion. Computed tomography (CT) CT is useful in gastroduodenal disease for staging of neoplasms and assessment of extramural disease. The patient should be fasted so that solid food in the lumen does not cause confusion with pathological filling defects. Distension of the gut with oral contrast medium is essential. Dilute (3 %) Gastrografin or dilute bariumsulphate suspension is used. As well as positive contrast, a gas- forming agent can be given to distend the stomach and duodenum. Sometimes this can be given in lieu of the final cup of contrast. A hypotonic agent may also be administered if gas is used. This distension allows recognition of wall thickening and intraluminal filling defects. If there is a suspicion of wall thickening the patient can be rescanned in a decubitus or proneposition as appropriate to show the distended non-dependent wall of the viscus, for example right-side up for lesions at the cardia. Normally, a dynamic sequential scan following intravenous bolus administration of contrast is used to show vascular structures and for the identification of liver metastases. Recent CTtechnological advances allow helical (spiral) CT images of the upper abdomen to be obtained with a single breath-hold. CT is also a useful technique in suspected gastroduodenal perforation, being able to detect very small volumes of free intraperitoneal gas or iodinated contrast. Ultrasonography (US) Conventional US has little place in gastroduodenal disease in adults, although wall thickening due to gastriccarcinoma and inflammatory disease in the antrum can often be seen. Real-time US can also be used to study antropyloric emptying and motility non- invasively. Endoscopic ultrasound (EUS) is accurate in the T and N staging of gastric adenocarcioma and the confirmation of linitis plastica. It may also be used to detect and stage gastric lymphoma, and image submucosal tumours such as smooth muscle lesions and distinguish them from extrinsic impressions seen at endoscopy or barium studies. Nuclear medicine scintigraphy Applications of nuclear medicine techniques in the gastroduodenal region include gastric emptying studies and, occasionally, detection of duodenogastric bile reflux. The former is performed with either a solid or liquid phase test meal or both. Serial imaging is performed with computer acquisition and time-activity curves are generated to calculate gastric emptying rate. Bile reflux into the stomach is assessed by injecting intravenously a Technetiumlabelled iminodiacetic acid derivative (e.g. HIDA). This tracer is excreted by the liver into the bile duct and thence the duodenum. If there is significant retrograde passage of tracer into the stomach this can be quantitated.

Investigation of dyspepsia
Dyspepsia means different things to different individuals. It has been carefully defined as intermittent or continuous pain, discomfort or nausea that is referable to the upper gastrointestinal tract, which is present for at least a month, is not precipitated by exertion and is unrelieved within five minutes by rest. This definition will include patients with organic gastroduodenal disease, GOR disease, various forms of non-ulcer dyspepsia and biliary tract disease. If one considers patients with gastroduodenal dyspepsia of age greater than, say, 45 years or with symptoms that include one or more of constant daily pain, weight loss, vomiting, a past history of gastric ulcer or gastric surgery, then these patients by virtue of their age and/or symptoms, may be expected to have an increased probability of gastric pathology - either benign or malignant compared to younger patients whose symptoms do not have any of the above features. If endoscopic and radiological services are of equal availability it is reasonable for endoscopy to be the primary investigation in the former group (since all of this group require investigation and are likely to need biopsies). Where endoscopicservices are limited, a careful biphasic barium meal should be performed. A barium study may be the initial examination in the latter group. It has been suggested that this latter group may not require initial investigation at all, and that it is acceptable to treat empirically for dyspepsia and to reserve investigation for those with refractory symptoms. In patients with barium-negative dyspepsia consideration should be given to other causes of symptoms such as biliary or pancreatic disease (and US should be performed.) The relationship of non-uIcer dyspepsia to Hehobacter pylori gastric infection remains to be finally clarified. Some patients will respond to eradication of these organisms.

Pathology
Hiatus hernias and gastric rotations Sliding hernias The gastro-oesophageal junction is above the diaphragm (Figs. 11, 19). The size of the herniated proximal stomach is variable. Small sliding hiatus hernias are a very common finding and are often asymptomatic. The major association of sliding hiatus hernias is gastro-oesophageal reflux (see above). Para-oesophagueal hernias These are much less common (about 5%). In this case the gastro-oesophageal junction lies below thediaphragm but all or part of the gastric fundus is above the diaphragm and lies adjacent to the distaloesophagus - usually to the left. Most para-oesophageal hiatus hernias are non-reducible. They may be recognised on a chest radiograph by an air fluid level behind the heart, the nature of which may be confirmed by repeating the radiograph after the patient takes a few mouthfuls of barium. Most patients with paraoesophageal hernias are asymptomatic, but

Figure 19. Sliding hiatus hernia. Area of narrowing is arrowed at level of diaphragmatic hiatus. There is a benign gastric ulcer (small arrow) on the lesser curve, presumed due to recurrent mechanical trauma at the hiatus.

complications are mechanical. Dysphagia may occur when the intrathoracic portion of the stomach fills during a meal and obstructs the distal oesophagus. Obstruction of the herniated portion of the stomach may cause strangulation and perforation. An acute torsion may occur. Mixed hernias In this case the oesophagogastric junction is in the thorax but much of the rest of the stomach also lies in the chest adjacent to the distal oesophagus. A variant of this is the intrathoracic stomach. This is associated with partial twisting of the stomach so that the fundus lies behind the heart, the greater curvature is cranial, and the antrum passes through the diaphragm (Fig. 20). When the fundus lies at a level inferior to the body, distension of the former with food may cause obstruction to the antrum. Similarly obstruction may occur when a herniated fundus returns into the abdomen (Fig. 21). Other viscera, particularly the transverse colon, may also be herniated. Although the intrathoracic stomach is prone to volvulus, chronic volvulus usually only causes mild symptoms. However, acute torsion presents as an emergency. The stomach can undergo two main types of rotation and these are often associated with herniation of the stomach. Organo-axial rotation is a

Figure 20. lntrathoracic stomach. The GOJ is in the thorax (curved arrow), the gastric fundus lies behind the heart, the greater curve is upper-most, due to organo-axial rotatio and the antrum passes through the diaphragm (straight arrow).

Figure 21. Intrathoracic stomach with axial rotation, but fundus ha returned to infradiaphragmatic position with resulting partial obstruction. The nasogastric tube demonstrates the position of the GOJ (arrowed).

twist along the long organic axis of the stomach - that is the line drawn from the fundus to pylorus. The resulting configuration depends on the original orientation of the stomach. If the stomach was horizontally orientated, then the result is a reversal of the normal lesser and greater curves (Fig. 20). When the stomach is more vertically orientated the fundus lies to the right and the antrum points to the left - so called "mirror-image" stomach. Organo-axial rotation is only rarely associated with severe symptoms. Mesentero-axial rotation is less common but much more often

Figure 22. Varioliform erosive gastritis. Multiple punctate erosions are seen in the gastric antrum and body, each surrounded by a halo of oedema.

associated with obstruction and strangulation. The stomach rotates around an axis joining greater and lesser curves and perpendicular to its long organic axis so that the resulting configuration is an "upside-down" stomach. Total volvulus is a rotation greater than 180? with obstruction at GOJ and/or gastric outlet. The patient has sudden epigastric pain, retching without vomitus and collapse. Ischaemia and necrosis of the stomach result. A chest radiograph may show air-fluid levels in the upper abdomen and the mediastinum. A contrast study shows tapering obstruction of the distal oesophagus. Gastritis Radiology is limited in the diagnosis of gastritis and other superficial mucosal disease, but certain patterns are recognisable based on the presence of erosions, thickening or atrophy of folds, hyper -rugosity and wall thickening. Disturbance of the areae gastricae pattern is a further indication of mucosal disease. Erosive gastritis may be acute or chronic and may be asymptomatic or accompanied by dyspeptic symptoms or bleeding. Causes include alcohol, aspirin and other non-steroidal anti-inflammatory drugs, but many are idiopathic. Two patterns of erosive gastritis are seen. The so-called varioliform gastritis comprises multiple aphthous erosions surrounded by a mound of radiolucent oedema, usually orientated along the longitudinal folds and tending to be concentrated in the antrum (Fig. 22). A similar appearance may be seen in Crohn's disease affecting the stomach. The second pattern is of flat erosions without a halo of oedema, but tending to have the same distribution of varioliform gastritis. This variety is more difficult to diagnose on DCBM. Distinction must be made from barium precipitates. Hypertrophic gastropathy is a group of entities characterised radiologically by hyper-rugosity of the stomach. Such conditions include hyperacidity states such as Zollinger-Ellison syndrome and chronic renal failure, Menetrier's disease and hypertrophic gastritis, and are mimicked by infiltration with lymphoma or submucosal spread of carcinoma. Gastric atrophy, such as occurs in pernicious anaemia, is associated with loss of folds on the greater curvature and in the fundus and reduction of the areae gastricae. Eosinophilic gastritis is a condition characterised by peripheral eosinophilia, a history of allergy and protein-losing enteropathy. The stomach only is involved in about half the patients with eosinophilic gastroenteritis. The usual site is the antrum and in the acute stage demonstrates enlarged rugal folds. In the chronic phase there is a contracted nodular antrum. Corrosive gastritis Corrosive damage to the stomach is usually due to acid ingestion, but sometimes alkalis can affect the stomach as well as, more typically, the oesophagus. The radiological findings depend on the stag e of damage. Acutely there is gastric atony, rugal swelling, ulceration, pneumatosis or perforation. These may be visible on plain radiographs. Gradually scarring occurs with resultant deformity and contraction of the stomach (Fig. 23). Gastric ulceration On double-contrast barium meal (DCBM), gastric ulcers are seen as niches or collections of barium. When viewed en face, ulcers on the posterior (dependent) wall are apparent as barium collections when full of contrast, or ring shadows when empty, with or without radiating folds (Fig. 25 a). On the non-dependent (anterior) surface

they are seen en face

Figure 23. Stomach of a young man approximately 3 weeks after Formalin ingestion. The stomach is contracted with sacculation and ulceration and antral narrowing. There is also narrowing and spiculation of the proximal duodenum GOJ and pylorus are arrowed.

Figure 24. Benign gastric ulceration. Two ulcers (arrowed); that on t lesser curve is empty of barium and seen almost in profile a curvilinear outpouching - note that the edges (and those the ulcer in Fig. 19) do not protrude into the lumencompare with Fig. 26. The posterior antral ulcer contains barium.

Figure 25. a) Benign posterior wall gastric ulcer showing radiating folds extending to ulcer crater. b) Malignant antral ulcer with thickened margin and folds amputated short of the ulcer crater.

b
as ring shadows. Anterior wall lesions may not be easily se en without erect and prone compression views. In profile ulcers are seen as barium-filled collections extending beyond the lumen or, if empty, curvilinear lines of barium (Figs. 19, 24). The majority of benign gastric ulcers occur on the lesser curve or in the antrum (usually posterior wall). Greater curve ulcers are more suggestive of malignancy, but even benign ulcers in this site may have amalignant appearance. There appears to be an association between non-steroidal anti-inflammatory drug therapy and benign greater curve ulcers which may progress to gastrocolic fistulae. Pyloric and prepyloric ulcers are usually

Figure 26. Gastric diverticulum just distal to the cardia. Note the gastric folds running into the lesion aiding the distinctio from gastric ulceration.

small and benign. Size is not a good indicator of benign or malignant nature; giant ulcers are often benign. Features on barium meal that help distinguish benign and malignant gastric ulcers are listed in Table 4. As ulcer healing occurs the crater diminishes in size and the oedematous edges disappear. The radiating folds become more apparent as scarring progresses. As re-epithelialisation occurs the crater may end up as a small residual depression (an ulcer scar) or as an area of flat mucosa with radiating folds. Gastric diverticula are not-infrequently misdiagnosed as gastric ulcers. These true (congenital) lesions occur on the posteromedial wall just distal to the cardia (Fig. 26). The typical site and often the demonstration of gastric folds running into them will help distinguish these non-consequential lesions from ulcers.

Figure 27. Malignant gastric ulcer. Although a typical site (lesser curve, incisural) for abenign ulcer, note the margins protruding into the lumen, characteristic of amalignant lesion (arrowed).

Figure 28. Malignant gastric ulcer seen en face. The ulcer crater is empty of barium and the raised margins typical of malignancy are clearly shown (arrows).

Table 4. Benign versus malignant gastric ulcers (Figs. 19, 24-28)

Feature

Benign

Malignant

Size Site Shape Areae gastricae Edges

Not a good indicator

Not a good indicator

majority lesser curve or antrum variable round, oval, linear irregular extend to crater* +/- ulcer mound/ collar with central and symmetrical niche. Margins of mound form obtuse angle with normal wall. Hampton line smooth, radiate to ulcer* cease away from crater raised edges protruding into lumen

Radiating folds

clubbed, nodular amputated, fused

* but not necessarily when the ulcer is surrounded by significant gastritis If a gastric ulcer is diagnosed on barium meal the question of further investigation prior to treatment will depend on a) the degree of radiological confidence that it is benign, and b) the prevalence of gastric cancer and, particularly, "early" gastric cancer in that community. Laufer introduced the concept of confidence levels in relation to radiological diagnosis of a benign gastric ulcer and found that, if the radiologist is confident of thebenign nature of an ulcer then he/she is rarely wrong. Subsequent studies have confirmed the reliability of a radiological diagnosis of a benign gastric ulcer by DCBM and have suggested that endoscopy and biopsies can be reserved for equivocal or malignant-appearing ulcers or those that do not completely heal on follow-up imaging after ulcer therapy. However, partly due to the oft-quoted ability of malignant ulcers to heal on modem ulcer therapy, many gastroenterologists prefer to perform endoscopy on all radiologically diagnosed gastric ulcers. In communities where "early" gastric cancer is common, it is prudent to follow this policy. It must be remembered that malignant change may be patchy and, therefore, multiple biopsies from all areas of the ulcer rim and crater and, preferably, cytological brushings should be obtained. Where "early" gastric cancer is not prevalent a reasonable costeffective policy for a radiographically benign gastric ulcer is to performendoscopy/biopsy where available prior to therapy and follow-up (if confirmed benign) to complete healing by subsequent DCBM examinations. Gastric carcinoma

Diagnosis The diagnosis of gastric carcinoma is usually made by endoscopy or barium meal. "Early" gastric cancers (EGC), i.e. those limited to mucosa +/- submucosa regardless of the presence of lymph node metastases) are prevalent in some communities, such as Japan, but are relatively uncommon in most Western societies. They can appear as Type I (polypoid), Type II (superficial; Type IIa elevated; Type IIb flat; Type IIc depressed), or Type III (excavated). Mixed types occur. The surface of early polypoid lesions on DCBM is lobular or granular and simulates the areae gastricae. Differentiation is required from adenomas and hyperplastic polyps (see below). Type H lesions are seen as flat mucosal elevations. Where a central depression is present (i.e. superficial erosion) this is irregular in outline with an uneven surface. Folds radiating towards

Figure 29. Diffuse infiltrative gastric carcinoma. causing obstruction at the antrum.

the lesion may show evidence of infiltration such as nodularity, amputation or fusion. Type III lesions demonstrate deeper excavations. Advanced gastric cancers are more common than EGC in Western societies. These involve the muscularis propria or deeper layers. They may be classified on gross radiological appearances as polypoid, ulcerative with raised margins (Figs. 25 b, 27, 28), a larger infiltrative and ulcerating type, and a diffuse infiltrative type (often se en as a constricting tumour in the antrum) (Fig. 29). These correspond to Borrman types 1-4, respectively. Linitis plastica is a diffuse infiltration, predominantly submucosal, which is manifest on contrast studies as a poorly distensible so-called "leather bottle"-stomach. This not infrequently may be overlooked endoscopically and, to a lesser extent, radiographically. Advanced ulcerative or raised cancers are often large and obvious radiologically. All lesions need endoscopic biopsy for confirmation. Staging The need for staging of gastric carcinoma is less obvious than for oesophageal lesions. However, in communities where EGC is prevalent, it is useful to help determine therapy and prognosis, particularly where nonsurgical endoscopic treatment is contemplated. Where advanced lesions are more prevalent it could be argued that surgery, whether for attempted cure or palliation, is the treatment of choice and that pre-operative staging does not influence management. However, surgeons' practices differ; if staging is required then this is best achieved by CT or EUS for local staging, and dynamic enhanced or helical CT (or conventional US) for distant metastases. EUS has been shown consistently superior to CT for local staging, but is of limited availability. CT visualises the thickened gastric wall and its relationship to adjacent structures, but is unable to determine the depth of wall invasion. CT can detect lymph node enlargement but is non-specific, unable to distinguish reactive from malignant nodes. The criterion for enlargement is usually taken as > 10 mm. Since metastases can also be present in non-enlarged nodes, CT is not very sensitive. When performed optimallyCT, using either a dynamic sequential technique with bolus contrast enhancement or the newer spiral (helical) techniques, is relatively accurate (probably in the region of 90%) at showing whether the patient has liver metastases or nor, but is significantly less sensitive at demonstrating all lesions in an individual patient. Moss has suggested a CT staging scheme for gastric carcinoma (Table 5). Table 5.CT Staging of gastric carcinoma (after Moss et al)

Stage I Intraluminal mass without wall thickening (i.e. < 10 mm thick). No metastases. Stage Il Wall thickening > 10 mm without tumour extension or metastases. Stage III Thickened wall with adjacent organ involvement but no distant metastases.

Stage IV Distant metastases with thickened wall.

The accuracy of EUS in T and N staging of gastric carcinoma is similar to its accuracy in oesophagealcarcinoma and significantly better than dynamic CT, being 80-90% for T and 75% + for N in most series. Once again, there is difficulty in distinguishing benign from malignant nodes although positive and negative predictive values of87.5 % and 82 % have been achieved for nodal metastasis. EUS is highly accurate in distinguishing EGC from advanced cancer. In linitis plastica EUS demonstrates a diffuse thickening of the submucosa and muscularis propria layers.

Figure 30. Submucosal smooth muscle tumour of the gastric body (seen in single contrast) exhibiting central ulceration (arrowed). Note otherwise smooth surface and right angled conjunction with gastric walls.

Other gastric tumours Submucosal tumours Although many cell types can give rise to submucosal tumours in the stomach, the vast majority are smooth muscle lesions - leiomyomas, leiomyoblastomas and the malignant leiomyosarcomas. Radiology essentially cannot distinguish these three lesions. Most smooth muscle tumours are fundal, rounded and often exhibit central ulceration (Fig. 30). The latter accounts for the frequent presentation of bleeding. Size is variable. As for all submucosal lesions they appear on DCBM as smooth surfaced with normal overlying mucosa. In profile the margins are at right angles or obtuse to the line of the gastric wall. Much of the bulk of the tumour may be exophytic to the stomach - an "iceberg" phenomenon. EUS is useful for confirming the origin of the tumourfrom muscularis propria and distinguishing between a submucosal and an extrinsic mass (Fig. 31). For larger lesions where malignancy is suspected, EUS or CT are helpful in assessing infiltration of adjacent structures. Haematogenous metastases from malignant melanoma, breast and lung carcinoma, phaeochromocytoma and, in recent times, Kaposi sarcoma, may give rise to small submucosal tumours. These are usually multiple and have a "bull's eye" or target appearance due to central ulceration. Breast carcinoma may spread submucosally like scirrhous carcinoma.

Figure 31. EUS image of submucosal smooth muscle gastric tumour(leiomyoblastoma), T. Lesion seen to aris from muscularis propria layer of gastric wall (arrow). W=normal wall (see Fig.8); b=water filled balloon covering transducer. (Reproduced with permission of Australasian Radiology

Mucosal polyps These occur in 1-2% of DCBMs. They appear as rounded filling defects in the barium pool on the dependent wall or a ring-shadow on the nondependent wall. They may be pedunculated or sessile. The majority are hyperplastic and possibly result from regeneration following gastritis. The minority are adenomas and are important because of their malignant potential. In addition, there is an increased risk of carcinoma in the same stomach when adenomas are present. Features to help distinguish between hyperplastic and adenomatous gastric polyps are listed in Table 6. However, if there is any doubt, endoscopy and biopsy are recommended. Table 6. Gastric polyps

HYPERPLASTIC

ADENOMATOUS

Frequency Size Number Site

>90% < 1 cm multiple fundus, body

< 10% > 1 cm single or few antrum

Other gastric polyps Although occasionally gastric adenomas occur in Familial Adenomatous Polyposis (F AP), most gastric polyps in this condition are hamartomas. Hamartomas are also seen in Peutz-Jegher syndrome.

Figure 32. Gastric lymphoma. An infiltrative polypoid mass involves the cardia and proximal stomach.

Gastric lymphoma These constitute 1-3 % of all gastric malignancies. Most are of the non-Hodgkin's lymphoma type, and thelesion may be localised to the stomach with or without regional nodes, or part of a generalised involvement.Radiographic appearance on contrast studies is variable. Infiltrative, nodular, ulcerative, polypoid or mixed forms occur (Fig. 32). Sometimes the predominant sign is markedly thickened folds. The site within the stomach is variable. Of ten it is not possible to distinguish lymphoma from carcinoma. Further difficulties arise since mucosal biopsies are frequently negative, as much of the spread is submucosal. Distinction is important since the prognosis is considerably more favourable for lymphoma than for carcinoma. Staging of gastriclymphoma is best performed by a combination of CT and EUS. CT (or transabdominal US) will determine whether there is involvement of regional nodes; CT will define the presence of more generalised disease in other regions and will help assess gastric transmural infiltration. EUS is accurate at mapping out the distribution of disease within the stomach and the depth of intramural and transmural spread. Several EUS patterns of mural spread have been described. The post-operative stomach In the early post-operative period following gastric surgery, contrast studies are required to test for anastomotic leakage (when water soluble contrast agents should be used) and for gastric emptying. In the late post-operative situation, modifications to the standard double contrast technique are required for satisfactory visualisation; if the anatomy is known then this will help determine those modifications. However,endoscopy is superior to radiology in assessing recurrent disease in a gastric remnant or at an anastomosis. Radiology may still be required to determine the anatomy, if this is uncertain, and to assess gastric emptying. Duodenal disease Contrast examination of the duodenum is part of the DCBM. Good distended views are obtainable usinghypotonic agents and it is now rarely necessary to perform hypotonic duodenography using a tube technique. Other modalities, including US, CT, endoscopy and endoscopic retrograde cholangiopancreatography have largely surplanted duodenography in imaging periampullary and pancreatic lesions. The duodenum, extending from the pylorus to the duodenojejunal flexure, is approximately 25-30 cm long and divided into four parts. The first part (the "cap") is about 5 cm in length and extends posteriorly, superiorly and to the right from the pylorus and is triangular in shape on barium studies. The proximal 2-3 cm is intraperitoneal; the rest of the duodenum is retroperitoneal. The second part extends from the superior duodenal flexure, at the end

of the first part, inferiorly to the inferior flexure. At the apex of the superior flexure there is often a redundant mucosal fold which may be mistaken for a lesion on contrast studies. On the posteromedial wall of the descending duodenum is the major papilla which appears on hypotonicduodenography as a rounded or oval filling defect. The appearance is variable but there are usually mucosal folds which serve as landmarks, the most constant of which is a vertical fold extending distally from the papilla and a hooded fold covering the papilla itself (Fig. 33). The minor papilla is much less frequently seen radiologically. The third part of the duodenum extends from the inferior flexure almost

Figure 33. Normal hypotonic duodenogram showing area of major papilla. Hooded fold (h) covering papilla (p), oblique fo (f), proximal longitudinal fold (pl), distal longitudinal fo (dl) and probable site of minor papilla (a). The pattern o mucosal folds is quite variable.

horizontally and to the left across the midline. The fourth part begins where the duodenum becomes more vertical and directed superiorly towards the duodenojejunal flexure. The duodenum terminates at the suspensory ligament of Treitz. The normal mucosal pattern of the duodenal bulb on DCBM is smooth and relatively featureless. A minority of patients exhibit a fine recticular pattern or small punctate collections ofbarium which are evenly spaced and appear as triangular spiculations in profile. The latter must be distinguished from erosions (which are irregularly spaced, less numerous and associated with oedema and other signs of duodenitis) and barium precipitates (which are more dense and wash off during the procedure).

Figure 34. Brunner's gland hyperplasia/nodular erosive duodenitis. Note multiple nodules in duodenal cap, several with central erosion. p=pylorus.

Table 7. Duodenal "tumour-like" filling defects

BLH

Brunner's glands

Heterotopic gastric mucosa

Crohn's disease

Nodular duodenitis

Site Size Number

DI &D2 1-2 mm uniform size

D1 +/- D2 up to 1 cm occ. central depression

juxtapyloric small angular

variable variable

D1 +/- D

variable

thick folds thick fo ulceration strictureserosions

Duodenal nodular filling defects A guide to differential diagnosis of nodular defects is given in Table 7. Benign lymphoid hyperplasia (BLH) may be a normal finding in a small number of individuals or associated with immunoglobulin deficiency and BLH elsewhere in the bowel. Brunner's gland hyperplasia is most prominent in the duodenal bulb, decreasing below the papilla. Several patterns have been described: focal hyperplasia consisting of solitary lesions or small clusters; diffuse with innumerable small uniform nodules; multifocal; hyperplasia with evidence ofduodenitis; hyperplasia with erosive duodenitis (Fig. 34). There is also an association with hyperacidity states and chronic renal failure. Crohn's disease of the duodenum is usually associated with other signs besides nodularity, including ulceration, thick folds and stricturing. There is of ten antral involvement, as well as disease elsewhere in the GI tract. Heterotopic gastric mucosa is seen in about 5 % of barium meals and is of doubtful pathological significance, although there is same evidence that there is an

Figure 35. Duodenal ulceration. One moderate sized ulcer (arrowe and other possible small erosions are seen. There are oedematous folds with linear collections ofbarium amon them, some radiating towards a central erosion. Note th tenting of the base of the duodenal cap due to fibrotic scarring (open arrow).

Figure 36. Multiple duodenal erosions with radiating and oedemato folds and duodenal cap deformity. Consistent with duodenal ulceration and duodenitis. Note the coarse are gastricae in the stomach antrum suggesting gastritis.

association with H. pyloris infection. Non-specific duodenitis Although there is controversy regarding the true nature of non-specific duodenitis, and the natural history is somewhat different than duodenal ulceration, it is probably part of the spectrum of peptic ulcer disease.Barium studies are not especially accurate, but criteria for diagnosis include nodularity, thickened folds (> 4 mm thick), bulbar deformity and punctate collections of barium with halos of oedema, representing erosions. There is a significant false negative rate and false positive rate for DCBM. False positives occur particularly when the diagnosis is made on the presence of only one radiological sign. The pattern of duodenitis may sometimes be predominantly nodular (Fig. 34). There is considerable overlap with Brunner's gland hyperplasia; indeed the two often coexist and it is not clear whether the nodules of duodenitis represent inflammatory infiltrate or Brunner's glands. Duodenal ulceration Duodenal ulcers are linear, rounded or irregular in shape on barium studies. About 10% are multiple and about half occur on the anterior wall, and as such are more difficult to diagnose; compression and profile views, including prone-oblique views are needed. When acute there may be little or no associated wall deformity. Radiating folds and cap deformity are more commonly seen when the ulcer is more longstanding (Figs. 35, 36). The healing process causes fibrosis, deformity and pseudodiverticula (Fig. 37). The base of the pseudodiverticulum, when present, points to the ulcer crater. Deformity of the cap is assumed to be related to a past history of duodenal ulcer. When distortion is severe it is often difficult to be definite as to whether an ulcer is currently present. It is usually satisfactory in these circumstances, if the patient has appropriate symptoms, to assume the presence of an ulcer and treat accordingly. In particular, the presence of a pseudodiverticulum usually means that there is an ulcer. Approximately 5% of duodenal ulcers occur distal to the cap: most of these occur on the medial wall proximal to the papilla of Vater. They are often difficult to demonstrate radiologically due to accompanying spasm and oedema. In these circumstances healing often leads to stricturing. Ulcers distal to the papilla should suggest Zollinger-Ellison syndrome.

Figure 37. Gross deformity of the duodenal cap due to chronic duodenal ulceration. Note pseudodiverticula (arrows). u=ulcer.

Complications Acute bleeding presents as haematemesis and/or melaena. Radiology plays little part in the initial diagnosis; occasionally angiography is required for diagnosis when endoscopy is unsuccessful or equivocal, or for therapeutic intervention when endoscopic treatment fails or surgery is contraindicated. Labelled redcellnuclear medicine scanning may also sometimes be indicated prior to angiography to localise a source of blood loss. However, its accuracy in the upper GI tract has been questioned. Ulcer perforation presents as an "acute abdomen"; usually free intraperitoneal gas is seen under the diaphragms on plain abdominalradiographs. A water-soluble contrast meal may be required for confirmation. An ulcer may penetrate into adjacent structures: involvement of the pancreas may present as an acute pancreatitis; penetration into the bile duet will also present acutely with gas seen in the biliary system on plain films. In the chronic stage the healing process may give rise to duodenal or gastric outlet obstruction, seen on plain films as a distended stomach, easily confirmed on a contrast study. In some eases obstruction may be at least in part due to oedema in the acute phase and may resolve with conservative management. Zollinger-Ellison syndrome This syndrome is due to the hypersecretion of gastric acid in response to a gastrin-secreting tumour. The tumours are usually in the pancreas, but a significant proportion are extrapancreatic. Occasionally there isdiffuse islet-cell hyperplasia. Between 40 and 70% of tumours are malignant, but slow growing. Metastases are of ten evident at the time of diagnosis. Although 75% of associated peptic ulcers are gastric or in the duodenal bulb, distal duodenal ulcers and/or multiple ulcers should suggest the diagnosis. Other signs on GI contrast studies include excess fluid residue and hyperrugosity in the stomach, duodenitis with erosions and Brunner's gland hyperplasia, a dilated descending duodenum with thickened folds, and jejunal fold thickening with increased small bowel fluid and rapid transit. Reflux oesophagitis is also commonly present. Coeliac disease Duodenal abnormalities seen on DCBM may be the first clues to the diagnosis, particularly in those patients presenting atypically. The characteristic finding is the so-called "bubbly bulb", due to multiple small defects in a mosaic-like pattern. The appearance is similar to heterotopic gastric mucosa (see above), but is more diffuse. Thickened folds in the descending and distal duodenum may also be seen. Duodenal changes in pancreatic disease Duodenography in pancreatic pathology has become much less important since the advent of more specific imaging modalities for pancreatic disease. However, abnormalities of the descending duodenum are apparent in both inflammatory and neoplastic disease of the pancreatic head. Signs of pancreatic disease include those of pancreatic enlargement, such as widening of the duodenal loop, stricturing, and a mass impression on the second or third parts of the duodenum; these are non-specific and seen in both inflammatory and neoplastic disease. Other signs are nodularity and mass indentation of the wall of the duodenum; these are suggestive but not diagnostic of neoplastic pancreatic disease as are spiculation and tethering of folds. Inflammatory masses tend to lead to more smooth impressions and thickened folds but these signs, too, are by no means specific. Similarly, non-specific, is the "inverted 3 sign", due to a mass impression on the medial wall of the descending duodenum which is tethered at the site of the major papilla. Blunt duodenal trauma Duodenal laceration/perforation Bowel or mesenteric injury occurs in about 5 % of cases of significant blunt abdominal trauma. Duodenal injury (perforation or haematoma) is usually the result of a deceleration force when the body is restrained by a seat belt. Fixation of the second and third parts of the duodenum retroperitoneally to the posterior abdominalwall leads to a propensity to shearing injury. In addition, compression of the third part of the duodenum can occur where it overlies the spine. Early diagnosis of duodenal perforation is essential since delay is associated with increased mortality. CT is the investigation of choice in blunt upper abdominal trauma when hepatic, splenic, pancreatic, renal, duodenal or mesenteric injury is suspected and the patient is haemodynamically stable. In patients who are unstable diagnostic peritoneal lavage (DPL) or urgent surgery is indicated. DPL has largely been replaced by CT in stable patients, but in some centres this is still performed, although the sensitivity is less in retroperitoneal trauma to the duodenum than in intraperitoneal injury. When lavage is undertaken this should preferably be after CT to avoid errors in interpretation of fluid or gas in the peritoneum. CT is performed using oral contrast (3 % Gastrografin), administered by a nasogastric tube if necessary which allows aspiration of the stomach at the end of the procedure. Approximately 250 ml are given 30-40 minutes before the scan, and a further similar volume immediately prior to it. Scans are performed using an intravenous contrast bolusenhanced dynamic incremental technique. Contiguous slices are obtained from the diaphragm to the pelvis and then at intervals in the pelvis. Images are viewed at appropriate soft tissue windows; in addition, lung windows are recorded for the upper slices to help exclude basal lung pathology, haemothorax or pneumothorax. The findings in duodenal trauma include haemoperitoneum and/or retroperitoneal fluid (both of which are nonspecific), extraluminal gas (a sign formerly regarded as reasonably specific for hollow viscus perforation but recently there have been doubts raised as to itsspecificity), extravasation of contrast medium (specific but infrequent), a "sentinel clot" (a high-attenuation blood clot seen adjacent to the involved bowel), thickened bowel wall, or mesenteric infiltration (a non-specific sign). The reported sensitivity of CT in duodenal injury is variable indifferent series, but it should be noted that the signs may be subtle. In addition, distinction of duodenal from adjacent pancreatic contusion may be impossible on CT.

Duodenal haematoma In distinction to duodenal perforation, intramural haematoma may present late - up to one or two weeks following the injury. Haematoma is commoner in children than in adults, in whom duodenal and small bowel perforations are more likely. The signs on contrast studies (and on CT) include partial or total obstruction from the mass effect of the haematoma and a "stacked coin" or "picket-fence" appearance of thickened transversefolds. Symptoms usually subside on conservative management. Spontaneous intramural duodenal haematomaoccurs in patients on anticoagulants and in those with bleeding diatheses. Signs are essentially the same as for the traumatic variety. Superior mesenteric artery syndrome This is a controversial condition manifest by partial obstruction in the third part of the duodenum where it passes between the aorta and the superior mesenteric artery. It is reported to occur following marked weight loss from a variety of causes and also in patients in body casts. Vomiting is a prominent feature. Bariumstudies show partial obstruction with proximal dilatation of the second part of the duodenum. There is often "to-and-fro" peristalsis within the dilated segment. The diagnosis is apparent when the obstruction is seen fluoroscopically to be relieved when the patient is turned prone. However, CT or US may be needed to exc1ude a mass lesion at the root of the mesentery causing obstruction. Duodenal diverticula These are frequent findings on upper GI barium studies. They are regarded as acquired pulsion-type diverticula, and may be single or multiple. The commonest site is the medial wall of the descending duodenum. Their nature is usually obvious; differentiation from ulcers is made by the appearance of mucosal folds extending into the mouth of the lesion and variability of shape during the examination. Pseudodiverticula are associated with duodenal ulceration and most commonly occur in the bulb. Duodenal diverticula are nearly always asymptomatic, but occasionally give rise to complications: diverticulitis may occur and duodenocolic fistula has been reported to follow this; this may be more common with laterally placed diverticula. Obstructionis rarely seen when inspissated food impacts inside the lesion. There is evidence that periampullary diverticula are associated with an increase in the incidence of common duct calculi and a recurrence ofcalculi following cholecystectomy. Congenital abnormalities Occasionally congenital abnormalities may present in adulthood. Annular pancreas causes narrowing of thelumen of the descending duodenum due to a ring of pancreatic tissue. There is usually a defect on the lateral wall of the duodenum associated with an "hour-glass" type stricture. Patients may present with duodenalobstruction, pancreatitis or peptic ulceration. An intraluminal diverticulum, due to an incomplete congenitalweb, may cause obstruction to the second or third parts of the duodenum and is seen as a "wind-sock" filling defect within the lumen. Duplication cysts manifest as submucosal or extramural masses. Duodenal neoplasms Tumour-like filling defects in the duodenum are dealt with above. True primary neoplasms of the duodenumare rare. Usually endoscopy and biopsy are necessary for diagnosis. Adenomas tend to occur in the first or second parts and may be sessile or pedunculated, appearing as filling defects or ring shadows on bariumstudies. In polyposis syndromes they may be multiple. They have significant malignant potential. Similarly villous adenomas are of high malignant potential and should be removed; these appear as cauliflower-shaped filling defects, usually near the papilla. Other benign neoplasms include smooth muscle tumours and lipomas. Primary malignant neoplasms are most commonly adenocarcinomas, but lymphomas, smooth muscle tumours and carcinoids are also seen. Adenocarcinomas are polypoid, ulcerating or stricturing. There is a propensity for the peri-ampullary region. Peri-ampullary carcinomas may arise from duodenal mucosa, the Ampulla of Vater itself, from pancreatic tissue or from the bile duct. There is an association of peri-ampullary duodenalcarcinoma with familial polyposis, particularly Gardner's syndrome. Duodenal lymphomas have similar characteristics to small bowel lesions (see below). Duodenal carcinoid tumours have variable malignantpotential. Ectopic islet-cell tumours occur in the duodenal wall and are associated with ulcers. Secondarymalignant tumours affecting the duodenum usually result from direct spread from neighbouring organs such as colon, gallbladder, pancreas and right kidney.

Figure 38.Normal enteroclysis demonstrating catheter i first jejunal loop and well distended jejunum and proximal ileum with normal pattern of valvulae conniventes.

Richard M. Mendelson