).
Figure 2-1 Good barium coating at UGI series demonstrates a reticular pattern to the gastric antrum (areae gastricae), which is a normal finding.
A contrast (usually barium) examination of the stomach used to be one of the most common imaging examinations before the advent of computed tomography (CT) and endoscopy. It is now rarely performed as a first-line investigation to evaluate for gastric disease. However, knowledge of good upper gastrointestinal (UGI) barium examination technique is still required, particularly because it can detect and characterize most lesions. Small polyps and mucosal lesions are unlikely to be detected by CT, and unless endoscopy is performed, they will be missed.
Barium examination of the stomach usually follows initial examination of the esophagus (see Chapter 1). To promote gastric and duodenal bulb distention, some investigators inject small doses of anticholinergics or glucagon to induce a gastric and duodenal atonic state. Whether or not this is used, the examination of the stomach should not be delayed once the gas granules are swallowed and the initial views of the esophagus with the patient in the upright position have been performed. The patient is immediately placed recumbent to prevent the contrast material from spilling into the duodenum, which usually obscures the stomach, rendering the test inadequate. Once recumbent, the patient is then turned several times to encourage the coating of the mucosa with barium. The sequence of spot radiographs then varies according to institutional preference. Initially, a supine view (to provide an overview of the gastric anatomy) is followed by fundal views, with the patient in the right-side down lateral position (the fundus will be maximally distended with air in this position). After the patient is turned to the supine position (the patient turns to the left), views of the body can be obtained. The patient is then turned to the right anterior oblique position (i.e., the gastric antrum is uppermost) to obtain antral and duodenal bulb views (these regions, being nondependent, will be maximally distended with gas). If there is inadequate coating, the patient is then turned supine again to further coat the antrum and returned to the right anterior oblique position to achieve adequate antral coating and duodenal coating. Further views of the esophagus can now be obtained with low-density (thin) barium with the patient in the prone oblique position, and the patient can be evaluated for hiatal hernia and gastroesophageal reflux disease (GERD). These results may be elicited with the patient in a slight Trendelenburg∗ position, and gravity is used to provoke the GE junction. The patient is finally turned to the prone position for the evaluation of the antrum and duodenum bulb with compression views. The antral and duodenal bulb anatomy is variable, and the patient may need to be rotated in different obliquities or even lateral positions to view them en face.
CT is not a suitable technique for the examination of mucosal disease, unless there is marked gastritis or mucosal lesions are sufficiently large to be visualized. CT is, however, useful when gastric perforation is suspected. The technique is mostly reserved for evaluating primary and secondary gastric tumors and extragastric inflammatory conditions such as pancreatitis. Magnetic resonance imaging (MRI) has little role in the evaluation of gastric disease.
Positron emission tomography (PET) and PET/CT are increasingly used to evaluate gastric malignancy, particularly for local and distant metastases. Although gastritis can cause increased 18F-fluorodeoxyglucose (FDG) uptake, it is not specific and best evaluated with esophagogastroduodenoscopy (EGD). Gastric emptying studies with technetium-99m (99mTc) pertechnetate are commonly used to evaluate the pediatric population (see Chapter 1).
Gastric Disease
Congenital Anomalies
Antral Diaphragm
Antral diaphragm is poorly understood and is likely a result of congenital anomalies in neonates or from fibrotic healing of peptic ulcer disease in adults. There is a mucosal web positioned in the antrum, which, if large enough, can cause gastric outlet obstruction. Antral diaphragm is best recognized by EGD or contrast fluoroscopy, where a thin, well-defined web or diaphragm is seen in the expected location. It may or may not be circumferential.
Pyloric Stenosis
Infantile pyloric stenosis usually presents in males within the first 6 weeks of life, with projectile bilious vomiting due to gastric outlet obstruction from pyloric muscular hypertrophy. Clinically, it may be felt as an olive-shaped mass in the epigastrium. Plain radiograph often demonstrates a distended stomach (Fig. 2-2). Barium examination will confirm gastric distention and outline a bird-beak-like pyloric narrowing (Fig. 2-2). The diagnosis is best made with ultrasound, however, which demonstrates the classic findings of a hypertrophied hypoechoic muscle with measurements that exceed 15 mm longitudinally and 3 mm in diameter of a single wall on transverse images (Fig. 2-3). Treatment is by a pyloromyotomy and is usually curative.
Figure 2-2 Abdominal plain radiograph (A) and UGI series (B) in a 4-week-old boy demonstrating gross gastric dilatation (arrows) and a bird-beak appearance to the gastric outlet.
Figure 2-3 Ultrasound views of the stomach and pylorus in a 5-week-old boy with gastric distention as evidenced by hyperechoic gas in a fluid-filled stomach (A; arrow) and pyloric lengthening (B; arrow) and thickening (C; arrow).
The adult version (hypertrophic pyloric stenosis) is poorly understood and is frequently associated with peptic ulcer disease, which suggests that it is acquired rather than congenital. The findings are similar to those in the neonate with an elongated pyloric channel (up to three times the normal length) and a circumferential mass-like effect within the pylorus, seen by either EGD or contrast studies. Adult pyloric stenosis should be distinguished from prolapsed gastric antral folds that are transient at fluoroscopic evaluation and do not obstruct the gastric outlet.
Gastric Diverticulum
Gastric diverticula can be congenital or acquired, and fundal or antral in location. The fundal diverticulum is usually congenital and the most common of the gastric diverticula. It is positioned posteriorly at the cephalad margin of the lesser curve, close to the inferomedial aspect of the GE junction. It is usually asymptomatic and of no clinical significance, unless it is large whereby stasis and delayed gastric emptying have been recognized. Fundal diverticula can also ulcerate and bleed, and gastric carcinoma has been recognized in the diverticulum.
Gastric diverticula are mostly identified on CT because barium examinations are performed less often. They are readily identifiable, although they are sometimes mistaken for the left adrenal gland on CT, particularly if there is no oral contrast medium within them (Fig. 2-4). Close observation should confirm a connection to the stomach lumen, and a gas/fluid level should clinch the diagnosis (Fig. 2-4). When a UGI series is performed, gas and contrast should outline the diverticulum outside the confines of the normal gastric wall (Fig. 2-5).
Figure 2-4 Axial noncontrast CT in a 51-year-old man with a small gastric fundal diverticulum (arrow).
Figure 2-5 UGI series in a 40-year-old man with a fundal gastric diverticulum (arrow).
Antral diverticula are acquired and are usually small, projecting outward from the antral greater curvature, giving a collar-button appearance; they are sometimes mistaken for a benign gastric ulcer. They may be associated with previous gastric ulcer disease but generally have none of the other features that are usually associated with ulcer disease, including collars and fold thickening. Antral diverticula are also associated with pancreatitis, gastric outlet obstruction, and malignancy.
Hiatal Hernias
Hiatal hernias are classified as either sliding (axial) or rolling (paraesophageal) and are discussed in more detail in Chapter 1. Sliding hernias are far more common and are often visualized on CT (Fig. 2-6). Paraesophageal hernias are uncommon and difficult to identify on CT because they are mostly confused with sliding hernias. Barium studies, however, will identify the gastric fundus within the chest and the GE junction within the abdomen (Fig. 2-7). Even less common are mixed sliding and paraesophageal hernias (Fig. 2-8). Gastroesophageal reflux disease (GERD) is common with sliding hernias, but because the GE junction in paraesophageal hernias lies within the abdomen, reflux is rarely seen. On the other hand, paraesophageal hernias, particularly large ones, are at greater risk for gastric volvulus.
Figure 2-6 Coronal (A) and axial (B) CT in a 47-year-old woman with a sliding hiatal hernia.
Figure 2-7 UGI series in a 72-year-old man with a paraesophageal hernia (arrow). The GE junction lies below the diaphragm.
Figure 2-8 UGI series and axial contrast-enhanced CT in a 44-year-old woman with both a paraesophageal (large arrows) and sliding hiatal hernia (small arrows). The GE junction lies below the diaphragm.
Gastric Volvulus
Gastric volvulus is more common in the elderly, and there are three main types: organoaxial, mesenteroaxial, and mixed organoaxial-mesenteroaxial (Fig. 2-9). Organoaxial occurs when the stomach rotates 180 degrees or more (either anteriorly or posteriorly) around its long axis along a plane from the cardia to the pylorus so that the greater curvature now lies superior to the antrum; it is the so-called upside-down stomach (Fig. 2-10). In organoaxial volvulus, there are two twist points, the esophagogastric junction and the antral-pyloric junction. Contrast medium may not pass through the GE junction, but if it does, it may not then pass through the twisted pylorus. Organoaxial volvulus can be transient and relatively asymptomatic if the twisting is up to, but not more than, 180 degrees. However, when the twisting is complete, it can cause outright obstruction with intense pain, usually little vomiting (because of the obstruction), and difficulty in passing a nasogastric tube. It is usually a surgical emergency that requires the correction of the volvulus to prevent gastric infarction. Organoaxial volvulus is usually a result of large paraesophageal hiatal hernias when a significant proportion or all of the stomach lies in the chest.
Figure 2-9 Schematic representation of organoaxial and mesenteroaxial volvulus.
Figure 2-10 UGI series (A) and coronal CT (B) in a 59-year-old woman with an organoaxial volvulus. The greater curvature (large arrow) is superior (cephalad) and the lesser curvature inferior (small arrow). The GE junction is indicated by the arrowhead.
Mesenteroaxial volvulus is much less common, and the rotation (to the right or left) is around the mesenteric axis (a perpendicular line across the stomach from the lesser to the greater curvature) so that fundus comes to lie caudal to the antrum and pylorus (see Fig. 2-9). It is more common in patients with previous diaphragmatic rupture when large portions of the stomach come to lie in the chest. On plain radiograph of the abdomen, there can be a distended viscus in the left upper quadrant with an air-fluid level and collapsed small bowel if the volvulus has caused obstruction. The diagnosis, however, is readily made with UGI examination, which demonstrates the volvulus (Fig. 2-11). On CT, the precise diagnosis can be more difficult, unless multiplanar reformations are made, which should correspond to the UGI coronal series.
Figure 2-11 UGI swallow in a 68-year-old woman with mesenteroaxial volvulus. The GE junction is inferior (large arrow) and the pylorus, superior (small arrow).
Diffuse Gastric Mucosal Thickening
There are many causes of gastric mucosal abnormalities, both benign and malignant (Table 2-1). The most common cause of benign mucosal disease is gastritis, which remains prevalent throughout the world, primarily because of peptic ulcer disease (Table 2-1).
Table 2-1
Diffuse Gastric Mucosal Thickening
| Benign | Malignant |
| Gastritis (see Table 2-2) Pseudolymphoma Varices |
Carcinoma Lymphoma Metastases |
Gastritis
Gastritis is a generic term that refers to gastric mucosa that has become inflamed and edematous; several causes have been isolated (Table 2-2). Many cases (e.g., erosive, antral, Helicobacter pylori) completely heal once the offending agent is removed, but others (e.g., granulomatous, caustic, radiation) heal with scarring and luminal narrowing. Imaging with a barium UGI series used to be the investigation of choice for the evaluation of gastritis but has now largely been replaced by direct optical endoscopy and because peptic ulcer disease is now readily treated and cured with antibiotics. However, many of the imaging features of gastritis are characteristic, and contrast evaluation of the gastric mucosa remains a valuable diagnostic tool. In general, however, it is not possible to differentiate the specific cause of gastritis by imaging. Most causes will produce either focal or diffuse gastric wall thickening, which should be readily identified with good single- or double-contrast UGI series (Fig. 2-12). However, because a UGI series is performed less frequently, the imaging findings of gastritis are now usually observed on CT as diffusely thickened folds (Fig. 2-13). Similarly, this is a nonspecific finding, which can sometimes be overdiagnosed in the collapsed stomach. Gastritis, which is mainly an inflammatory condition, may also demonstrate increased FDG uptake, whatever the cause (Figure 2-13). Gastritis commonly may be confined to the antrum, with relative sparing of the body and fundus (Fig. 2-14).
Table 2-2
Causes of Gastritis
| Type | Features | Location |
| H. pylori/peptic | Thick lobulated folds, increased areae gastricae | Antrum and body |
| Drugs | Often causes erosions when acute | Antrum, body, fundus |
| Caustic | Thickened folds, ulcers with narrowing when healed | Antrum and body |
| Radiation | Thickened folds and ulcers and antral narrowing when healed | Antrum, body, fundus |
| Eosinophilic | Thickened and nodular folds and antral narrowing | Body and antrum |
| Inflammatory | Aphthous ulcers, thickened folds with larger ulcers in Crohn disease, sarcoid, Behçet syndrome, amyloid | Antrum and body |
| Infectious | Tuberculosis; syphilis can cause linitis plastica | Antrum and body |
| Emphysematous | Thickened folds and gas in wall | Antrum and body |
| Pancreatitis | Thickened folds along greater curvature; gastric narrowing from fluid collections | Body and antrum |
| Hypertrophic | Large lobulated folds | Body and fundus |
| Atrophic | Featureless mucosa with decreased folds and narrowed stomach | Antrum, body, fundus |
Figure 2-12 UGI series in a 41-year-old woman with diffuse gastric fold thickening (arrow) due to profuse gastritis.
Figure 2-13 Axial contrast-enhanced CT (A) and PET (B) in a 71-year-old woman with diffuse gastric mucosal thickening (large arrow) caused by gastritis; some FDG avidity is also apparent (small arrow).
Figure 2-14 Axial (A) and coronal (B) contrast-enhanced CT in a 56-year-old woman with diffuse gastric mucosal thickening (arrows) caused by antral gastritis. The fundus is relatively normal.
Erosive Gastritis
Erosive gastritis evolves from gastritis from several diverse etiologies (Box 2-1). In general, it is not possible to define the precise diagnosis by imaging unless there are other imaging and clinical features that point to the correct disease. They are typified by nodular mucosal thickening (gastritis), predominantly in the antrum, with the hallmark finding at a UGI series of tiny punctate barium pools, sometimes with an edematous radiolucent halo, often along thickened mucosal folds (Fig. 2-15). They must be distinguished from aphthous ulcers and small hematogenous metastases, which can look similar but are usually larger (Figs. 2-16 and 2-17). Good gastric coating is essential because visualization of some gastric erosions can be subtle (Fig. 2-18). Many gastric erosive diseases progress to ulceration, and therefore both are discussed simultaneously.
Figure 2-15 UGI series in a 52-year-old man with gastric mucosal thickening and multiple small gastric erosions, some of which have punctate pools of barium (arrows).
Figure 2-16 UGI series in a 60-year-old woman with multiple aphthous ulcers (arrow).
Figure 2-17 UGI series in a 54-year-old man with multiple bull’s-eye gastric lesions (arrows) due to melanoma metastases.
Figure 2-18 A, UGI in a 54-year-old woman with subtle antral gastric erosions (arrow). B, A magnified view of the erosions (arrow).
Peptic Gastritis and Ulcer Disease
Peptic gastritis used to be far more prevalent and was responsible for tens of millions of deaths worldwide. It was widely assumed for centuries to result primarily from “stress” conditions that were presumed to cause gastric hyperacidity and mucosal inflammation, thickening, erosion, and ulcer disease. Over the centuries, many medications were introduced to alleviate the symptoms until a generation ago, when histamine2 (H2)–receptor antagonists (which block the action of H2, a powerful gastric acid hormonal promoter) and then proton pump inhibitors (which block hydrochloric acid production) were introduced. Both drugs have dramatically improved the morbidity and mortality of the disease, but they do not treat the cause. It was not discovered until the early 1980s that almost all peptic ulcer disease was, in fact, due to an infective agent, H. pylori, a gram∗-negative bacterium present in about 50% of the population. This bacterium causes an excessive production of ammonium, which is toxic to the gastric mucosa. As part of the host’s inflammatory response to the bacteria and ammonia production, excessive gastrin is produced that acts on gastric parietal cells to produce more hydrochloric acid (and more parietal cells), setting up an increasing mucosal inflammatory response, predominantly in the gastric antrum (but also throughout the stomach when the infection is severe). Gastric mucosal thickening, erosions, and eventually ulcer disease ensue. The discovery that the disease is primarily infectious and the fact that it is readily treated by antibiotics have completely transformed the outlook for patients with the disease. In practice, almost all erosions and ulcer disease in the stomach and duodenum are related to infection with H. pylori, though ulcers can be exacerbated or caused by several drugs and alcohol as listed in Box 2-1. Very rarely, diffuse peptic gastritis and ulcer disease can be caused by Zollinger-Ellison† syndrome.
Ulcers are much more frequent in the duodenum than in the stomach, but erosions are often a precursor to frank ulcer disease and are superficial mucosal defects that have not penetrated the submucosa, as ulcers do. The erosions are a frequent cause of UGI hemorrhage. Of note, some patients suffering from major stress disorders (e.g., burns, septic shock) are also susceptible to superficial gastric erosions known as Curling‡ ulcers. A much smaller proportion (approximately 5%) of gastric ulcers are secondary to malignant disease, primary or secondary.
Patients have epigastric pain, symptoms of GERD, nausea, weight loss, hematemesis, and melena. Gastric ulcer symptoms typically occur during eating a meal, whereas duodenal ulcers occur approximately 2 hours later. Complications of gastric ulcers include blood loss, perforation, gastric outlet obstruction (from the fibrotic healing process), and an increased incidence of adenocarcinoma. The diagnosis is usually made by endoscopy or urea breath test studies. Before the widespread use of EGD to evaluate for gastric ulcer disease, the radiologist should have been able to differentiate most gastric ulcers as benign or malignant, particularly with good double-contrast technique. Single-contrast techniques were useful unless the ulcers were large and florid. However, given the widespread use of EGD to evaluate symptomatic gastric disease and the fact that the disease is less common, it is becoming harder for radiologists to gain sufficient experience with the different imaging presentations of gastric ulcer disease. However, the gastrointestinal (GI) radiologist will still likely identify gastric ulcers from time to time on UGI series, and therefore their detection and differentiation into benign or malignant categories are still required. Certain UGI imaging features should be emphasized (Table 2-3).
Table 2-3
Imaging Differentiation of Benign and Malignant Gastric Ulcer Disease
| Features | Benign | Malignant |
| Age | All adult ages | Elderly |
| Sex | Equal between males and females | Males more than females |
| Location | 90% antrum (75% lesser curve) | Antrum, but can occur elsewhere |
| Ulcer position | Central | Eccentric |
| Ulcer shape | Round | Irregular |
| Ulcer collar | Uniform (Hampton line) | Irregular |
| Fold shape | Uniform | Irregular and distorted |
| Fold convergence | To edge of crater | Does not reach ulcer margins |
| Projections beyond gastric wall | Yes | No |
| Multiple | Up to 30% | Uncommon |
| Associated duodenal ulcer | Frequent | Uncommon |
| Carman sign | No | Yes |
| Crescent sign | Yes | No |
| Response to peptic ulcer treatment | Yes | No |
Location: Because almost all benign ulcers occur in the antrum, any ulcer identified in the more proximal stomach should be strongly considered as malignant until proved otherwise.
Ulcer position on mound: The inflammatory reaction surrounding a benign ulcer tends to be uniform, and therefore the ulcer tends to be positioned within the center of the surrounding edematous mass (Fig. 2-19). Malignant masses, on the other hand, are often eccentrically placed within the overall mass, dependent on the underlying vascular supply to that part of the tumor (Fig. 2-20).
Figure 2-19 UGI series in a 44-year-old man with thickened antral folds and a punctate collection of barium at the center (arrow) due to an antral ulcer.
Figure 2-20 UGI series in a 60-year-old man with an eccentric gastric ulcer (large arrow) within a larger gastric cancer (small arrow).
Ulcer shape: Almost all benign ulcers are uniform and round, even if they are large (Fig. 2-21). However, if they are malignant, there are often other imaging features that will steer the radiologist away from benign disease (see Table 2-3). Most malignant ulcers have irregular ulcer margins (Fig. 2-22).
Figure 2-21 UGI series in a 76-year-old woman with a larger benign lesser curve ulcer (arrow).
Figure 2-22 A, UGI in a 71-year-old woman with a large greater curvature malignant ulcer (large arrow) with a surrounding irregular mound (small arrows) due to infiltrated adenocarcinoma. B, Axial contrast-enhanced CT demonstrating a malignant gastric ulcer (small arrow), which projects into the gastric lumen surrounded by the malignant mass (large arrow).
Ulcer collar: This represents the area of edema around the ulcer and is typically uniform in benign disease; it is also known as a Hampton∗ line, representing the radiolucent line across the neck of an ulcer (i.e., it separates barium in ulcer from gastric lumen) (Fig. 2-23). Ulcer collars may not be present with malignant disease, but when they are, they are usually thick and irregular.
Figure 2-23 UGI series in a 61-year-old woman with a benign lesser curve gastric ulcer with a Hampton line (arrow) consistent with a benign ulcer.
Ulcer fold convergence: This is a helpful sign for benign disease because folds almost always converge right up to the ulcer margin, whereas this is uncommon in malignant disease where folds, often irregular, fail to meet the ulcer margin (Fig. 2-24).
Figure 2-24 UGI series in a 69-year-old man with a large benign lesser curve ulcer (large arrow) with uniform fold convergence on the ulcer (small arrow).
Mucosal fold shape: Benign folds simply represent edematous changes and are typically smooth and uniform (Fig. 2-24). Malignant folds often contain the malignancy itself as well as edematous changes and so are more typically irregular, amputated, clubbed, or fused (Fig. 2-25).
Figure 2-25 UGI series of the stomach demonstrating a malignant gastric ulcer. There is a central pooling of barium in the gastric ulcer surrounded by fused and clubbed mucosal folds (arrow).
Visualization of an ulcer within or outside gastric wall: Benign, particularly acute, ulcers often project outside the gastric wall as they erode through the mucosa (see Fig. 2-21). This projection will probably not be appreciated unless visualized tangentially, which underlines the importance of obtaining multiple orthogonal views when any abnormality is identified. Malignant ulcers tend to erode less outside of the stomach wall, but rather, into the gastric lumen as an intraluminal mass (see Fig. 2-22). Occasionally, the position of a chronic benign ulcer can also appear confined within the stomach wall because of the chronic fibrosis, contraction, and distortion of the surrounding gastric wall.
Concurrent duodenal ulcer disease: This is unusual with malignant gastric disease, and its presence strongly suggests benign gastric ulceration.
Carman†meniscus sign: This is the radiological representation of a large, flat ulcer with heaped-up edges (Figs. 2-22 and 2-26). There is a radiolucent halo on compression views, which represents the heaped-up edges, with a convex outer shape to the trapped barium in the ulcer crater.
Figure 2-26 UGI series in a 70-year-old woman with a radiolucent halo (large arrow) due to a Carman meniscus sign that surrounds a central maliginant ulcer crater (small arrow).
Crescent sign: This represents benignity and is seen in ulcers along the greater curvature of the stomach (usually antrum) where the barium pool protruding outside the mucosa has a concavity away from the gastric lumen and gives the appearance of a crescent.
The complications of benign gastric ulcer disease are potentially fatal. These include hemorrhage after the ulcer erodes into adjacent arterial or venous structures and perforation into either the retroperitoneum or, more commonly, the peritoneum. In most patients, however, the ulcers will heal by fibrosis if left untreated with antibiotics (Fig. 2-27). The fibrosis can be sufficient to cause gastric antral scarring and narrowing, which may be severe enough to cause gastric outlet obstruction (Figs. 2-28 and 2-29). Patients usually have had chronic symptoms of peptic ulcer disease and so generally do not have the short history of symptoms—vomiting, abdominal fullness/mass, and pain—that is associated with gastric outlet obstruction. Should they have such symptoms, however, then other, more sinister causes (e.g., malignancy) should be considered. The obstruction is usually caused by chronic fibrosis and scarring compounded by acute inflammation from recurrent and active ulceration from pyloric channel or duodenal bulb disease. Usually the stomach distends gradually over months and years as luminal distention steadily progresses, and it can be massively distended at the time of presentation. The stomach is usually filled with a mixture of fluid and food residue. Complete obstruction is unusual, and some food, fluid, and gas will pass into the duodenum. The food and fluid are readily identified on plain radiographs (possibly with a fluid level). The site of obstruction can be confirmed with barium studies (presuming no perforation) rather than with water-soluble contrast media because the latter will often be too diluted to yield diagnostic information.
Figure 2-27 UGI series in a 72-year-old man with a healing gastric ulcer. Radiating folds (arrow) converge on the previous ulcer.
Figure 2-28 UGI series in a 59-year-old man with antral deformity (arrow) due to chronic scarring from peptic ulcer disease.
Figure 2-29 UGI series in a 48-year-old woman with Zollinger-Ellison syndrome and repetitive antral ulceration with chronic stricture and residual ulcers (arrow).
Drug-Induced Gastritis
Alcohol, aspirin, and other nonsteroidal antiinflammatory drugs (NSAIDs) frequently cause focal gastric irritation, particularly with chronic or high-dose use. Erosions and peptic ulcer disease can follow simple gastric mucosal hypertrophy and are the second most-common causes of peptic ulceration, after H. pylori–induced peptic disease.
Corrosive Gastritis
Acute ingestion of alkali or acid will predominantly affect the esophagus, but if enough of the toxin is ingested, it can pass into the stomach (predominantly the antrum if ingested in the upright position) and lead to marked antral mucosal edema and ulceration (Fig. 2-30). A large ingestion of toxin is associated with a poor prognosis because the stomach (or esophagus) can readily perforate in the acute phase (as evidenced at imaging by peritoneal fluid and pneumoperitoneum). If the patient survives, healing usually occurs with antral stricture formation (Fig. 2-31). The appearance can mimic antral narrowing and linitis plastica, common to several other diseases.
Figure 2-30 UGI series in a 39-year-old man with marked gastric wall mucosal thickening and ulceration (arrow) after caustic ingestion.
Figure 2-31 UGI series and axial contrast-enhanced CT in a 35-year-old man with antral and duodenal fixed strictures (arrows) due to prior caustic ingestion.
Radiation Gastritis
Radiation gastritis is less commonly observed because of the more refined radiation therapy techniques and portals. When observed, it is usually due to the acute radiation effects of nonspecific mucosal thickening, which may ulcerate if the radiation doses were too severe. The healing process occurs by fibrosis with the narrowing of the affected segment.
Eosinophilic Gastroenteritis
This rare disease is characterized by diffuse eosinophilic infiltration of the gut, primarily the stomach, but also the esophagus and small and large bowel. It is associated with peripheral eosinophilia, elevated immunoglobulin E (IgE) levels, and food allergies. Patients have nonspecific symptoms of abdominal pain, nausea, vomiting, diarrhea, and weight loss. Findings include gastric erosions, ulceration, and diffuse infiltration with mucosal thickening and nodularity, particularly of the distal stomach and proximal small bowel. The latter findings can be difficult to distinguish from other causes of gastric and small bowel thickening, including Crohn disease, Zollinger-Ellison syndrome, and lymphoma. Chronic disease can present with a constricted antral and gastric body, secondary to fibrosis, which is difficult to distinguish from other causes of linitis plastica.
Crohn Disease (see Chapters 4 and 5)
Crohn disease is usually associated with Crohn disease elsewhere in the small bowel and colon and typically demonstrates aphthous ulceration when involving the stomach (see Fig. 2-16). Crohn disease represents a transmural process with submucosal lymphoid follicular proliferation with the ulceration of the overlying mucosa (seen also in the esophagus and small and large bowel). Noncaseating granulomas are characteristic of the disease. On UGI series, there is a small ulcer crater surrounded by an edematous halo or ring (see Fig. 2-16). Healing occurs by fibrosis, which may produce a narrowed antrum with the more proximal stomach mucosa preserved. Occasionally, Crohn disease involves the whole stomach, preventing it from dilatation and giving it a linitis plastica appearance.
Sarcoidosis
Sarcoidosis is rare, although the stomach is the most commonly affected GI organ. Patients have abdominal pain, sometimes diarrhea, and symptoms of GI reflux. Acute disease results in gastritis with mucosal thickening, which can ulcerate. Gastric granulomas can be identified at biopsy. Healing is by fibrosis, which can produce a linitis plastica appearance.
Infectious Gastritis
Phlegmonous gastritis is now rarely observed and results from bacterial infection of the gastric wall (gram-positive streptococci and staphylococci and gram-negative coliforms). It is typically seen in alcoholics who have had repeated episodes of gastritis.
Emphysematous gastritis, which is most commonly seen in elderly patients with poorly controlled diabetes, is similar to patients with emphysematous cholecystitis. It is due to overwhelming mural infection with gas-forming organisms and is fatal if left untreated, so aggressive antibiotic therapy, surgery, or both may be required. The imaging diagnosis is recognized on CT as diffuse gas within the stomach wall and portal venous system, usually in a diabetic patient (Fig. 2-32).
Figure 2-32 Coronal CT with soft tissue windows (A) and lung window settings (B) in a 67-year-old diabetic woman with mural gastric gas (arrow) due to emphysematous gastritis.
Tuberculosis and syphilis are rare manifestations of gastritis, although tuberculosis is endemic in the developing world, where tuberculous gastritis is more common and may be associated with tuberculosis elsewhere in the body. Acutely, there is nonspecific gastric mucosal thickening, which may progress to ulceration (Fig. 2-33). The chronic fibrosing reaction that both diseases then produce can cause an antral constrictive process, not unlike a linitis plastica finding (Fig. 2-34). Syphilis can produce similar findings (Fig. 2-35).
Figure 2-33 Axial contrast-enhanced CT in a 35-year-old woman with gastric wall thickening (large arrow) and hyperenhancement of the gastric mucosa (small arrow) due to tuberculosis.
Figure 2-34 UGI series in a 70-year-old man with antral narrowing (arrow) and a linitis plastica type appearance due to chronic tuberculosis.
Figure 2-35 UGI series in a 39-year-old woman with diffuse gastritis (arrow) and ulceration due to syphilis infection.
Candidiasis of the stomach is recognized in the immune-compromised population but is observed less commonly because gastric acid usually neutralizes the yeast organisms. The appearances are similar to those in the esophagus, with multiple small plaque-like filling defects of the gastric lining. They, as with yeast organisms in the esophagus, can bleed if ulceration is severe.
Amyloidosis
Amyloidosis of the stomach, in either its primary or secondary systemic form, is rare and can cause a range of findings, from focal (which may be mass-like) to diffuse mucosal thickening and ulceration. In primary amyloidosis, there is no known underlying predisposing condition, and GI involvement is more common than with the secondary form. One variant of the primary type is focal rather than systemic and can involve only the GI system. In secondary amyloidosis, chronic underlying disease is present, including rheumatoid arthritis, chronic lung disease (tuberculosis/bronchiectasis), and multiple myeloma.
Pancreatitis
Severe pancreatitis can cause such diffuse peripancreatic inflammatory change that it can produce gastric wall and mucosal inflammation (Fig. 2-36). The stomach may be narrowed, due to both the inflammatory process and the associated mass effect from peripancreatic acute fluid collections (Fig. 2-37). Once the acute pancreatitis has subsided, the outlet obstruction should subside, although chronic peripancreatic fluid collections (pseudocyst formation) may develop, which can exacerbate any gastric narrowing and cause gastric outlet obstruction (Fig. 2-38).
Figure 2-36 UGI in a 47-year-old woman with greater curvature inflammation (arrow) due to underlying acute pancreatitis.
Figure 2-37 Axial contrast-enhanced CT in a 64-year-old woman with acute pancreatitis and antral narrowing (arrow) due to the acute inflammatory process.
Figure 2-38 Axial contrast-enhanced CT in a 47-year-old woman with compression of the stomach (arrow) due to a lesser sac pseudocyst from recent pancreatitis (there is the tip of nasogastric tube in the stomach).
Ménétrier Disease (Hypertrophic Gastritis)
Ménétrier∗ disease has an uncertain etiology, is more common in males, and usually follows a viral illness or infection with H. pylori. It is characterized by profusely thickened gastric folds throughout the stomach (although it can be focal), with or without ulceration. It is not always associated with hyperacidity, and many patients have reduced gastric acid production (hypochlorhydria) because of parietal cell destruction. There is also secretion of large volumes of mucus, sometimes sufficient to cause hypoalbuminemia. Patients have postprandial epigastric pain, weight loss, and signs of hypoalbuminemia. The diagnosis is one of exclusion (i.e., no history of aspirin or excessive alcohol use, negative H. pylori test result), although at biopsy, there is characteristic crypt hyperplasia, which is thought to predispose the patient to the development of gastric adenocarcinoma. At imaging, the disease should be suspected if the mucosal folds are grossly thickened, particularly if there are concomitant clinical symptoms (Fig. 2-39). These are usually severe enough to be recognized on CT (Fig. 2-40).
Figure 2-39 UGI series in a 55-year-old man with hypertrophic gastritis (arrow).
Figure 2-40 Axial contrast-enhanced CT in a 52-year-old man with marked gastric mucosal thickening (arrow) due to hypertrophic gastritis. There is also marked hepatic steatosis.
Pseudolymphoma
This uncommon benign disease is due to a lymphoreticular hyperplasia with infiltration of the gastric mucosa. It causes fold thickening that often can ulcerate. The findings can be confused with carcinoma or lymphoma radiologically, especially because anemia is common to both diseases. Pseudolymphoma can also present as a more infiltrative process, again causing confusion between this and other, malignant conditions.
Zollinger-Ellison Syndrome
Zollinger-Ellison∗ syndrome is the result of a triad of gastric hyperacidity, ulcers, and a gastrin-producing tumor of the pancreas or duodenum. The primary neuroendocrine tumor secretes excessive gastrin, causing parietal cell stimulation and overproduction of gastric acid. This hyperacidity can be profound, leading to massive ulceration of the stomach, particularly the antrum, and proximal small bowel (Figs. 2-29 and 2-41). The hyperacidity in the small bowel also results in excessive small bowel hypersecretion, causing diarrhea and malabsorption. Chronic ulceration can heal with a fibrotic narrowed gastric antrum (Fig. 2-29) and may be sufficiently severe to give a linitis plastica appearance to the stomach.
Figure 2-41 A, Axial contrast-enhanced CT in a 70-year-old man with diffuse gastric mucosal thickening due to Zollinger-Ellison syndrome (arrow). B, A 4-cm pancreatic tail gastrinoma is present (arrow).
The primary tumor is hypervascular, but because it is often small, it can be missed, even with a dedicated arterial-phase CT scan through the pancreas and duodenum. It is most commonly found in the duodenal wall (50% to 70%) and pancreas (20% to 40%). A strong clinical suspicion may require the patient to undergo laparotomy and preoperative endoscopic ultrasound or palpation to detect the tumor. Very careful analysis of the pancreas and duodenum is required to identify any arterially enhancing lesions, which may represent the tumor. They are often not identified in the portal venous phase. Liver metastases, when present, are also hypervascular and therefore are best detected with a dedicated arterial-phase CT scan, particularly if they are small.
Atrophic Gastritis
In contrast to other forms of gastritis, which are characterized by gastric mucosal thickening, atrophic gastritis results in loss of normal mucosa (Fig. 2-42). It is much less common than other forms of gastritis and is acquired either from a prolonged H. pylori infection or from autoimmune causes. The former usually affects the antrum, whereas the latter typically affects the body and fundus. The autoimmune disease is responsible for pernicious anemia. There is antibody destruction of gastric parietal cells, leading to hypochlorhydria and elevated gastrin levels. The ensuing parietal cell loss leads to the loss of protein intrinsic factor (IF) production, which is necessary for normal vitamin B12 absorption. Normally, the combined IF-B12 molecule is recognized by terminal ileal receptors and transported into the portal circulation. Lack of IF results in vitamin B12 malabsorption (as does loss of the normal terminal ileum, e.g., from Crohn disease or surgery). This loss of vitamin B12 then results in a megaloblastic-type anemia.
Figure 2-42 UGI series in a 60-year-old woman with a featureless stomach due to atrophic gastritis. There is also a small antral polyp (arrow).
The hypochlorhydria or achlorhydria from parietal cell destruction results in mucosal atrophy, gastritis, and intestinal metaplasia with absent or reduced gastric folds and almost complete loss of the gastric fundus. The stomach demonstrates reduced, but not absent, peristalsis and may demonstrate antral fold thickening and erosions resulting from a more severe compounding gastritis. Patients with pernicious anemia are at risk of developing carcinoma from the gastric metaplasia.
Solitary Gastric Masses
There are several benign and malignant focal gastric masses, most of which are common to other regions in the GI tract and can be solitary or multiple (Boxes 2-2 and 2-3).
Gastric Polyps
Gastric polyps are mucosal in origin and classified into hyperplastic, adenomatous, and hamartomatous polyps; there is also the rarer inflammatory fibroid polyp.
Hyperplastic Polyps
Hyperplastic polyps are also known as regenerative or inflammatory polyps because they are thought to result from chronic inflammation. They are the most common benign epithelial tumor in the stomach. They are usually multiple and small (<1 cm), usually in the body or fundus, and are sessile with no stalk (Fig. 2-43). They are difficult to differentiate from other forms of polyps, so their diagnosis is usually made after biopsy. They are not precursors of malignant disease, although there is an increased incidence of gastric carcinoma elsewhere in the stomach.
Figure 2-43 UGI series in a 47-year-old woman with multiple gastric mucosal lesions (arrows) due to hyperplastic polyps.
Adenomatous Polyps
Adenomatous polyps occur more commonly in the distal stomach and are similar to the colonic variety and therefore are predisposed to adenocarcinoma, particularly as they enlarge and therefore require removal. However, unlike the colon, most are sessile, and villous or tubulovillous adenomas are less commonly recognized. They are usually single, but when they are multiple, other polyposis syndromes (familial polyposis coli and Gardner∗ syndrome) should be considered (Figs. 2-44 and 2-45).
Figure 2-44 UGI in a 54-year-old man with a lesser curve smooth mucosal filling defect (arrow) due to a gastric adenomatous polyp.
Figure 2-45 UGI in a 44-year-old man with Gardner syndrome and multiple gastric adenomatous polyps.
They are best visualized by UGI or EGD as irregular, lobulated surfaces, sometimes cauliflower-like. When larger tubulovillous antral polyps do occur, they often prolapse into the pyloric canal because of peristaltic action and cause gastric outlet obstruction.
Hamartomatous Polyps
Hamartomatous polyps are usually associated with Peutz-Jeghers† or Cronkhite-Canada‡ syndromes (see Chapter 5) and therefore are associated with small bowel (and sometimes large bowel) polyps and mucocutaneous pigmentation. Although there is a slight preponderance for small bowel carcinoma, they only have a very slight association with gastric cancer. They are identified as multiple, small, usually sessile polyps and are diagnosed with the accompanying clinical features (Fig. 2-46). The even rarer Cowden’s∗ disease (multiple hamartoma syndrome) results in widespread GI hamartomas with thyroid and breast masses.
Figure 2-46 UGI series in a 38-year-old man with several small hamartomatous polyps (arrow).
Inflammatory Fibroid Polyps
Inflammatory fibroid polyps are also known as eosinophilic granulomas because of their histological concentration of eosinophilic cells (not to be confused with eosinophilic gastritis). On imaging they appear as a smooth-walled mucosal mass with or without ulceration, usually in the distal stomach. They are usually asymptomatic.
Benign Intramural Gastric Tumors
Benign intramural gastric tumors include gastrointestinal stromal tumors (GISTs), lipomas, lymphangiomas, hemangiomas, schwannomas, and neurofibromas. A GIST is a nonepithelial sarcoma and the most common submucosal mesenchymal tumor throughout the GI tract, with 70% occurring in the stomach, 20% in the small bowel, and approximately 10% in the esophagus. They usually grow slowly and are mostly benign, but when they are large, they can become malignant and metastasize to distant organs. They are thought to arise from the interstitial cells of Cajal∗ (responsible for peristaltic regulatory function) and express the c-kit (CD117) receptors, which can be detected by immunohistochemistry. GISTs are part of the Carney† triad of gastric GIST, functioning extraadrenal paraganglioma, and a pulmonary chondroma.
Submucosal intramural gastric tumors, including GISTs, all have similar imaging findings at upper GI (Fig. 2-47). They appear with a well-defined border en face, but with a smooth intraluminal projection in profile (side-on), with the characteristic obtuse borders (although this finding is variable depending on the size of the tumor), with similar CT appearances (Figs. 2-27 and 2-48). Some may ulcerate, particularly if larger, which can be seen as a bull’s-eye or target lesion (barium pooling in the ulcer crater surrounded by a halo) (Fig. 2-49). If they are larger than 2 cm, they are best evaluated by contrast-enhanced CT, where they demonstrate the features of an intramural mass, which usually extends beyond the confines of the stomach wall. Sometimes, they appear as a predominantly extragastric mass and demonstrate heterogeneous enhancement, with areas of necrosis and ulceration if larger (Fig. 2-50). Calcification is recognized in up to 25% of cases.
Figure 2-47 UGI in a 38-year-old woman demonstrating a smooth, rounded submucosal mass (arrow) that proved to be a benign GIST.
Figure 2-48 Axial (A) and coronal (B) CT in a 44-year-old man with a smooth intraluminal submucosal filling defect at the gastric fundus (arrows) due to a GIST.
Figure 2-49 Axial (A) and coronal (B) CT in a 55-year-old woman with a transmural gastric mass with ulceration (arrows) due to a benign GIST.
Figure 2-50 Axial CT in a 60-year-old woman with a 6-cm predominantly exophytic gastric mass (arrow) due to a benign GIST.
Lipomas and lymphangiomas can change shape on compression because of their soft nature (Fig. 2-51). Lipomas typically occur in the gastric antrum and can prolapse into the duodenum. They can be diagnosed by their fatty density on CT (Fig. 2-52). Hemangiomas of the stomach are rare, are usually multiple, and are recognized with associated venous vascular calcification. They are associated with Bean∗ syndrome (or blue rubber bleb nevus syndrome) and autosomal dominant disease. Patients often have multiple GI hemangiomas, usually in the stomach, that often bleed. Other mesenchymal tumors cannot be differentiated by CT or UGI series and generally require removal for final diagnosis (Fig. 2-53).
Figure 2-51 UGI in a 44-year-old woman with a smooth submucosal mass (arrow) due to a lipoma.
Figure 2-52 Axial CT in a 50-year-old woman with a fatty submucosal antral mass (arrow) due to an antral gastric lipoma.
Figure 2-53 Axial contrast-enhanced CT in a 33-year-old man with a small submucosal gastric mass (arrow) that was proved to be a fibromyxoma at histological examination. This cannot be differentiated from most submucosal masses on CT.
Duplication Cysts
Duplication cysts occur anywhere along the GI tract and are rare in the stomach. They are smooth-walled submucosal filling defects, usually along the greater curvature. They may communicate with the stomach and therefore fill with contrast media at fluoroscopy, giving a large diverticulum-like appearance.
Ectopic Pancreas
Ectopic pancreas is usually asymptomatic, although it can bleed occasionally. Some reports state it occurs in up to 10% of patients, but the incidence in clinical practice is likely to be much lower. The submucosa of the gastric antrum or proximal duodenum is the most common site, but its presence in the esophagus to the ileum has been described. Classically, the ectopic pancreas contains small, smooth-filling defects, with a central umbilication that represents a rudimentary pancreatic duct (Fig. 2-54).
Figure 2-54 UGI series in a 40-year-old woman with a small mucosal antral lesion due to ectopic pancreas (arrow).
Carcinoid
Carcinoids are rare in the stomach and are usually benign. Most probably go undetected, but when they are larger, they may ulcerate and bleed and may therefore be sometimes confused with gastric carcinoma. They are not commonly detected by CT, but they may appear as generally smooth, rounded hypervascular masses after the administration of intravenous (IV) contrast material (Fig. 2-55).
Figure 2-55 Axial contrast-enhanced CT in a 49-year-old woman with a 1.5-cm hypervascular intragastric mass (arrow) due to gastric carcinoid.
Gastric Varices
The dilated submucosal gastric vein, like its esophageal equivalent, can cause life-threatening hemorrhage. It can be secondary to portal venous hypertension but is more commonly associated with splenic vein thrombosis (i.e., pancreatic malignancy, pancreatitis, thrombotic disorders).
Diagnosis is usually made by EGD, but on UGI series, there is fold-thickening typically in the fundus because of the dilated submucosal vessels (Fig. 2-56). The diagnosis is usually associated with esophageal varices and may only be visualized with the patient in the prone or supine position that creates enough venous distention to be visible on UGI series. The varices are usually far better visualized by CT than UGI (Fig. 2-57).
Figure 2-56 UGI series in a 64-year-old man with multiple nodular filling defects at the gastric cardia (arrow) due to gastric varices.
Figure 2-57 Axial (A) and coronal (B) contrast-enhanced CT in a 54-year-old man with chronic pancreatitis and multiple gastric varices (arrows).
Gastric Carcinoma
Gastric carcinoma is the third most common GI malignancy after colonic and pancreatic carcinoma. It arises from the gastric mucosa (it is slightly more common in the gastric fundus), and most gastric carcinomas are adenocarcinomas (95%). It is more common in men, and risk factors include H. pylori infection, alcohol, smoking, pernicious anemia, chronic atrophic gastritis, adenomatous polyps, Ménétrier disease, prior gastric surgery (Billroth II), salted and smoked food (especially fish), and foods with high nitrite or nitrate content. Gastric atrophy and carcinoma are associated, but because mild gastric atrophy is common in the elderly, it is not certain whether there is any cause and effect. Therefore it is not unusual for antral and body carcinomas to be associated with gastric atrophy, probably as a simple result of aging. Patients with severe atrophic changes (i.e., those with pernicious anemia), however, are definitely at risk for the development of gastric carcinoma and should be serially monitored (usually by EGD). The staging of gastric cancer follows international TNM staging criteria (Table 2-4).
Table 2-4
Staging of Gastric Carcinoma
| Stage | Findings |
| 0 | Carcinoma in situ; limited to mucosa |
| 1A | Transmucosal (5-year survival 85%) |
| 1B | Transmucosal and up to 6 regional lymph nodes involved or muscularis invaded |
| II | Transmucosal with 7-15 regional lymph nodes involved or muscularis involvement with 6 regional lymph nodes or serosal involvement without regional lymph nodes |
| IIIA | Muscularis involvement with 7-15 adjacent nodes; serosal invasion with up to 6 local nodes (5-year survival 50%); local organ invasion but no nodes |
| IIIB | Serosal involvement with 7-15 regional nodes |
| IV | Adjacent organs and at least 1 regional lymph node; more than 15 regional nodes; distant metastases |
Patients usually have symptoms of heartburn and a loss of appetite. As the disease progresses, there may be nausea and vomiting from partial gastric outlet obstruction, and many ulcerate and produce hematemesis or melena. Early imaging features on UGI series can vary. These may demonstrate either a small irregular intraluminal polypoid lesion or a raised plaque-like nodular lesion, which may ulcerate. It may also appear like a flat ulcer with edematous walls and radiating irregular or amputated folds that end abruptly (unlike benign ulcers, which demonstrate smooth radiating folds) (Figs. 2-20, 2-22, 2-25, 2-58, and 2-59). As the disease progresses, there is a progressively enlarging irregular polyp or a nodular polyp, often with ulceration as evidenced by an intraluminal filling defect or patches of barium trapped between the polypoid folds (see Fig. 2-59). The tumor margins are shelf-like (acute angled), and the folds converging toward a tumor with or without an ulcer are enlarged, irregular, fused, or nodular (see Fig. 2-25). A classic malignant ulcer feature at UGI series is the Carman meniscus sign (used to differentiate it from benign ulcer disease), whereby an elevated, flattened lesion with a central ulcer crater demonstrates a radiolucent margin or halo on prone compression views because of the raised tumor margins (see Figs. 2-20, 2-22, and 2-25).
Figure 2-58 UGI in a 66-year-old woman with thickened antral folds and a small filling defect (arrow) on the distal lesser curve that was proved to be early gastric adenocarcinoma.
Figure 2-59 Barium UGI series in a 44-year-old man with fundal polypoid mass (arrow) due to gastric adenocarcinoma.
Most gastric carcinomas will not be evaluated by UGI series, however, because the diagnosis and initial assessment will be made mostly by EGD. Patients are then referred for a staging CT. The primary tumor, particularly when it is small, can be hard to identify by imaging, and without prior knowledge of an underlying gastric cancer, the radiologist could easily miss it (Fig. 2-60). This problem with identification is compounded by the difficulty of evaluating the nondistended stomach, where gastric wall thickening is often contemplated, but simply represents a normal collapsed stomach. As the tumor increases, however, a discrete mass should be identified, and most tumors will be visualized once they become transmural and stage III and IV cancers develop (Fig. 2-61). Regional lymph nodes may be small and difficult to detect on CT, but their location in relation to the stomach should alert the radiologist to the diagnosis. PET imaging is sometimes used, not as a first-line investigation but rather as a tool for the evaluation of regional and remote metastases, particularly smaller lymphadenopathy (Figs. 2-61 and 2-62). Some tumors appear as if they are lower esophageal tumors, but they represent cardial tumors that invade into the lower esophagus (Fig. 2-62). Others present with the appearance of a leather-bottle stomach (also known as linitis plastica; see later in this chapter), which typically arises in the antrum and infiltrates along the gastric wall, producing a concentric narrow antrum (Figs. 2-63 and 2-64).
Figure 2-60 Axial noncontrast-enhanced CT in a 57-year-old man with a subtle 2-cm gastric mass (arrows) that was found to be gastric adenocarcinoma.
Figure 2-61 Axial contrast-enhanced CT (A and B) and PET (C) in a 62-year-old man with mural thickening of the gastric body (large arrows) due to adenocarcinoma, which demonstrates marked FDG uptake (small arrow).
Figure 2-62 Barium swallow, axial contrast-enhanced CT, and PET in a 66-year-old woman with a cardial tumor extending into the lower esophagus (A; arrowhead) and metastatic lymph nodes (B; arrows) with uptake on PET (C; arrows).
Figure 2-63 UGI series (A) and axial (B) and coronal (C) contrast-enhanced CT in a 67-year-old woman with marked antral narrowing (arrows) due to antral linitis plastica from gastric adenocarcinoma.
Figure 2-64 UGI series (A) and axial contrast-enhanced CT (B) in a 72-year-old woman with fixed narrowing of the gastric body and antrum (linitis plastica appearance) (arrows) due to gastric adenocarcinoma.
A rarer gastric carcinoma, known as scirrhous carcinoma, also typically arises in the antrum and produces a linitis plastica or leather-bottle appearance (Fig. 2-63). This may also extend more proximally to involve the gastric body (Fig. 2-65). Polypoid carcinoma is less common and frequently ulcerates. Such tumors appear as large polypoid and irregular filling defects, usually in the distal stomach, but they can occur elsewhere (see Fig. 2-59).
Figure 2-65 UGI series in a 66-year-old woman with a linitis plastica– appearing stomach due to scirrhous gastric carcinoma.
Gastric carcinoma metastasizes early, to regional lymph nodes, by direct extension, or to a remote area (Figs. 2-62 and 2-66). It has a tendency to metastasize to the ovaries, which is known as Krukenberg∗ tumor (Fig. 2-67). It can frequently cause peritoneal spread with mesenteric nodular metastases, so-called omental caking (Fig. 2-68).
Figure 2-66 Axial contrast-enhanced CT in a 70-year-old man with infiltrative mass of the gastric body (large arrow) that has spread beyond the confines of the gastric wall (small arrow).
Figure 2-67 Coronal and axial-contrast enhanced CT in a 51-year-old woman with an antral gastric carcinoma (A; large arrow) and bilateral adnexal masses (B; small arrows) due to Krukenberg metastases.
Figure 2-68 Axial contrast-enhanced CT in a 50-year-old woman with gastric cancer and peritoneal metastatic disease with ascites and omental cake (arrow).
Malignant Gastrointestinal Stromal Tumors
Malignant GISTs are generally larger than benign GISTs and tend to extend exophytically to the stomach rather than into it (Figs. 2-69 and 2-70). They also infiltrate the gastric wall as a polypoid nodular mass with frequent ulceration (Fig. 2-71). The c-kit (CD117) receptors are effectively targeted by c-kit tyrosine kinase inhibitors (imatinib), which have proved to be highly effective chemotherapeutic agents for malignant GISTs, particularly smaller (< 5 cm) tumors.
Figure 2-69 UGI series in a 47-year-old woman with a large gastric mass with central ulceration (arrow) due to a gastric GIST.
Figure 2-70 A, Axial and coronal contrast-enhanced CT in a 30-year-old woman with a malignant gastric GIST (large arrow). B, A large part of the mass (small arrow) is exophytic to the stomach. There are perigastric metastatic lymph nodes (arrowhead).
Lymphoma
The GI tract is the most common site for extranodal lymphoma (up to 30% of abdominal lymphomas). The stomach is the most common site, followed by the small bowel, and finally the colon. Esophageal involvement is very rare. Although there are many types of lymphoma (the World Health Organization currently lists 43 varieties), the most common lymphomatous GI tract disorders are non-Hodgkin† lymphomas and include those listed in Table 2-5, with diffuse large B cell the most common. The stage is determined by the Ann Arbor classification (Table 2-6).
Table 2-5
Lymphomas Usually Associated with Gastrointestinal Malignancy
| B-cell Lymphoma | Grade | Features |
| Diffuse large B-cell | High grade | Low-grade MALT that has transformed diffuse large B-cell; most common type—anywhere along GI tract |
| MALT-type | Low grade | H. pylori gastritis causative; usually in the stomach, less commonly in the small bowel; low grade in indolent type |
| Mantle cell | Higher grade | Any area of GI tract; typically polypoid lesions; poorer prognosis |
| AIDS-related lymphoma | High grade | Second most common malignancy in AIDS patients after Kaposi sarcoma; mainly in the stomach and small bowel; EBV related; aggressive |
| PTLD | Lower grade | EBV related; GI tract is the most common site |
| Burkitt lymphoma | High grade | EBV related; 50% curable |
| T-cell lymphomas | High grade | Subtypes peripheral, anaplastic large cell, angioimmunoblastic and cutaneous |
| EATL | High grade | Associated with celiac disease; jejunum is mostly involved |
| Mediterranean | High grade | Spectrum of alpha heavy chain disease and immunoproliferative small intestinal disease |
∗Denis Burkitt (1911-1993), Irish physician.
AIDS, Acquired immune deficiency syndrome; EATL, enteropathy-associated T-cell lymphoma; EBV, Epstein-Barr virus; GI, gastrointestinal; MALT, mucosa-associated lymphoid tissue; PTLD, posttransplant lymphoproliferative disorder.
Table 2-6
Ann Arbor Staging of Lymphoma
| Stage I | Single lymph node region (I); involvement of single extralymphatic organ/site (IA) |
| Stage II | Two or more lymph node sites on one side of diaphragm (II); involvement of single organ (IIE) |
| Stage III | Lymph nodes both sides of diaphragm (III); involvement of extralymphatic organ (IIIE); splenic disease (IIIS); both spleen and extralymphatic organ (IIISE) |
| Stage IV | Diffuse or disseminated involvement of one or more sites; extralymphatic organs |
Primary gastric lymphoma is uncommon (about 2% of all lymphomas), but metastatic lymphoma is much more common, and the stomach is the most common GI site for lymphoma. Most are B-cell, non-Hodgkin lymphomas, ranging from well-differentiated mucosa-associated lymphoid tissue (MALT) type to high-grade large-cell disease. Mantle cell and T-cell lymphomas are rarer recognized types. The latter can be difficult to distinguish from the more common adenocarcinoma. MALT lymphoma most commonly affects the stomach and represents a low-grade B-cell lymphoma. Because of its low grade, it can be difficult to detect with either CT or PET. It is heavily associated with H. pylori, which is thought to be causative as a result of the chronic inflammatory reaction induced in the infected stomach. Treatment and eradication of gastric H. pylori are often curative.
At imaging, there are various presentations of gastric lymphoma, including a large ulcerating lesion, multiple polypoid lesions (with or without ulceration), or an infiltrating mass that can result in a linitis plastica appearance (Figs. 2-72, 2-73, and 2-74). These features can usually be observed on CT, but differentiation from other malignant diagnoses is sometimes difficult because of similar appearance on imaging. CT will readily demonstrate extragastric extension or remote adenopathy and hepatosplenomegaly.
Figure 2-72 Axial (A) and coronal (B) CT and PET (C) in a 68-year-old man with a large lobular and polypoid gastric mass (arrows) due to gastric lymphoma, which is PET avid.
Figure 2-73 Axial contrast-enhanced CT in a 56-year-old man with gastric dilatation due to diffuse antral wall circumferential thickening (arrows) caused by primary gastric B-cell lymphoma.
Figure 2-74 UGI series (A) and axial contrast-enhanced CT (B) in a 53-year-old man with fixed diffuse gastric narrowing, mucosal irregularity (arrow), and a linitis plastica appearance of the stomach due to gastric lymphoma.
Posttransplant lymphoproliferative disorder (PTLD) occurs as a complication after prolonged immunosuppression, mostly among transplant recipients. It is due to an uncontrolled proliferation of B cells infected with Epstein-Barr virus (EBV) and the disease; therefore it has similarities with Burkitt lymphoma. The disease can respond to the cessation of the immunosuppressive therapy, although some patients progress to typical non-Hodgkin B-cell lymphoma. Extranodal involvement is much more common than nodal involvement and affects the GI tract most commonly, typically the small bowel, then the colon, stomach, duodenum, and esophagus in descending frequency. Most other abdominal organs can also be involved, including the lung and central nervous system. Implanted allografts can also succumb to disease (e.g., liver, renal, heart/lung).
Imaging features in the bowel are similar to other GI lymphoma, including circumferential wall thickening (sometimes marked) and aneurysmal luminal dilatation. Characteristically, the disease ulcerates and then perforates far more frequently than other types of lymphoma.
Burkitt Lymphoma
This is a B-cell lymphoma first described as an EBV-mediated lymphoma endemic to central Africa. This virally induced tumor (Epstein-Barr∗) most often involves the maxilla in younger adults and children, but colonic involvement, particularly of the ascending colon, is well recognized. Other forms of Burkitt lymphoma include the sporadic type, again mediated by EBV, and more commonly produce ileocecal lymphoma. A third variant, termed immunodeficiency-associated Burkitt lymphoma (a variant of posttransplant lymphoproliferative disease), occurs in immunosuppressed patients, particularly those with human immunodeficiency virus (HIV) and acquired immune deficiency syndrome (AIDS) but also those taking immunosuppressive drugs.
Metastases
Metastatic disease to the stomach is usually focal and small but can occasionally be larger, particularly with melanoma. These classically result in a bull’s-eye mucosal lesion (although simple mucosal masses are also recognized) that appears as a circular metastatic mucosal deposit with a central ulcerated depression (see Fig. 2-17). On UGI examination, contrast will collect in the ulcer crater in the supine position if the lesion is on the posterior wall or conversely on the anterior wall if the patient is in the prone position. These are often multiple and most commonly seen in melanoma, breast cancer, and lung cancer.
Breast cancer and lymphoma can also cause a linitis plastica appearance, infiltrating along the gastric wall rather than producing discrete mucosal masses (Fig. 2-75). Other primary malignancies (e.g., ovarian and pseudomyxoma peritonei) can envelop the stomach with metastatic deposits and give the appearance of linitis plastica (Fig. 2-76). Direct invasion of the stomach from adjacent malignancies (e.g., the pancreas) will produce irregular nodular folds and an intraluminal mass if lesions are large (Fig. 2-77). Esophageal cancer can invade the gastric cardia, producing appearances similar to the lower esophageal tumors, with nodular irregular folds and an associated mass.
Figure 2-75 UGI swallow in a 69-year-old woman with a linitis plastica appearance of the stomach due to breast cancer metastasis. There is incidental sliding hiatal hernia.
Figure 2-76 UGI series in a 54-year-old man with a linitis plastica– appearing stomach due to diffuse pseudomyxoma peritonei. There is an additional submucosal impression on the greater curvature (arrow) due to an additional metastatic deposit.
Figure 2-77 Axial contrast-enhanced CT in an 83-year-old woman with pancreatic carcinoma that invades the stomach (arrow).
Kaposi Sarcoma
Kaposi∗ sarcoma has become more common since the onset of the AIDS epidemic. However, because AIDS can now be effectively treated, this complication is seen less often in developed countries. It is a herpes virus–induced neoplasm that promotes a vascular endothelial tumor, usually of the skin, although involvement of any aspect of the GI tract is relatively common, particularly the esophagus and stomach. Although the lesions are usually asymptomatic, they can ulcerate (particularly when they are large) and cause GI hemorrhage. They are usually multiple and discrete, but they can also be diffuse in nature. They present as large submucosal masses, with or without central ulceration (Fig. 2-78).
Figure 2-78 UGI in a 43-year-old man with a multiple gastric masses (arrows) due to Kaposi sarcoma.
Linitis Plastica Stomach
Linitis plastica stomach refers to a constricted, rigid, partial or whole noncontractile stomach thought to resemble the appearance of a leather bottle once used by hikers and travelers. The antrum and body are preferentially affected rather than the gastric fundus. The most common cause is gastric carcinoma, infiltrating diffusely along the gastric wall, rather than causing its more common intraluminal mass. Linitis plastica stomach is more often seen in anaplastic or undifferentiated gastric carcinoma and hence has a very poor prognosis. There are other causes of a linitis plastica stomach, both benign and malignant (Table 2-7).
Table 2-7
Causes of Linitis Plastica (Leather-Bottle) Stomach
| Malignant | Benign |
| Gastric carcinoma Lymphoma Metastases (breast, lung) |
Eosinophilic gastroenteritis Crohn disease Tuberculosis, syphilis Caustic ingestion Sarcoidosis Zollinger-Ellison syndrome (multiple ulcers) |
The diagnosis is readily made by EGD or barium fluoroscopy but should also be recognized at CT. Typically, there is a rigid noncontractile stomach without recognizable mucosal folds, usually starting at the antrum and progressing proximally (see Figs. 2-34, 2-35, 2-64, 2-65, 2-74, and 2-76). In general, it does not extend distally to cross the pylorus. At CT, the stomach lumen is narrowed (particularly in the antrum), with thickened infiltrated tumor in the gastric wall (see Figs. 2-64, 2-73, and 2-74). Associated regional lymphadenopathy and distant metastases are readily observed with the appropriate CT technique.
Gastric Outlet Obstruction
There are both benign and malignant causes of gastric outlet obstruction (Table 2-8). Most of the benign gastric causes result in outlet obstruction through fibrosis as a consequence of the healing phases. The most common benign cause is a result of chronic peptic ulcer disease, but as described earlier, this is less prevalent and responds well to antibiotics, so it is now relatively rare.
Table 2-8
Causes of Gastric Outlet Obstruction
| Congenital | Pyloric stenosis |
| Mechanical | Bezoar Diaphragmatic hernia Volvulus |
| Inflammatory | Peptic ulcer disease Pancreatitis Crohn disease |
| Infection | Tuberculosis Syphilis |
| Corrosives | Linitis plastica |
| Malignancy | Carcinoma Lymphoma |
| Radiation therapy | Radiation stricture |
More common are malignant causes, the most prevalent being gastric cancer (Fig. 2-79) (often scirrhous type) and pancreatic adenocarcinoma (see Fig. 2-63). Both can infiltrate along the gastric wall, causing antral constriction and outlet obstruction. Lymphoma, like that elsewhere in the GI tract or pancreaticobiliary system, tends not to be obstructive but rather mass-like without mechanically constrictive effects. However, if very large, it may ultimately cause outlet obstruction.
Figure 2-79 Plain abdominal radiography (A) and axial contrast-enhanced CT (B) in a 69-year-old man with gastric outlet obstruction and a distended stomach (small arrows) due to an antral gastric cancer (large arrow).
Gastric Bezoar
Gastric bezoars are composed of plant and vegetable matter (phytobezoar) or hair (trichobezoar), the first being more common and more likely to cause associated ulcer disease from local abrasion. In general, bezoars do not obstruct unless they are large and act with a ball-valve effect. They are more common after gastric reconstructive surgery when there is a smaller stomach lumen. Trichobezoars tend to be much larger than phytobezoars at presentation, when they are filled with hair and food residue and are typically black in color (Figs. 2-80 and 2-81). Patients often have an underlying psychiatric diagnosis.
Figure 2-80 Axial (A) and coronal (B) CT in a 16-year-old girl with a large heterogeneous gastric filling defect (arrows) due to trichobezoar.
Figure 2-81 Abdominal plain radiograph (A) and coronal contrast-enhanced CT (B) in a 23-year-old woman with gross gastric dilatation and multiple luminal filling defects due to a phytobezoar (overingestion of macaroni).
The persimmon bezoar is a unique bezoar noted in Native Americans after unripened fruit from the persimmon tree has been eaten. After ingestion, it coagulates with gastric acid into a gelatinous mass, sometimes leading to gastric outlet obstruction.
Other bezoars include lactobezoars, which consist of solidified undigested milk, and pharmacobezoars, which consist of undigested and accumulated multiple medications. Other foreign object bezoars include swallowed drug-filled condoms, typically seen in smugglers, that get lodged in the gastric antrum and pylorus. Rarely, other nondescript foreign objects are swallowed by children or by institutionalized and psychiatric patients.
At imaging, there may be a soft tissue mass noted on plain radiography, but a UGI will readily identify a mottled complex mass with barium interspersed within the bezoar. This tissue can also be identified on CT, which demonstrates a mottled appearance of gas within the bezoar that does not enhance after the administration of IV contrast material.
Functional Obstruction
True atonic conditions that cause gastric distention should be distinguished from chronic air swallowing or ingestions of large quantities of carbonated drinks that simply distend the stomach with gas. The term gastroparesis refers to delayed gastric emptying, usually due to atonic conditions rather than to mechanical obstruction. As such, it may be due to autonomic neuropathic causes, most commonly diabetes. As elsewhere in the gut, dehydration and electrolyte disturbance or recent surgery resulting in an ileus can result in temporary loss of gastric contractions. Some acutely ill and terminally ill patients can have agonal atony with an acutely distended, atonic stomach. Many drugs are also responsible for gastroparesis, particularly those with anticholinergic effects; narcotics and antidepressants can cause gastric stasis. At imaging, the dilated stomach is often visualized on plain radiograph, but CT will more likely confirm the nonspecific stomach dilatation (Fig. 2-82).
Figure 2-82 Coronal conrast-enhanced CT in a 71-year-old woman with gastric atonic dilatation.
Scleroderma can cause neuromuscular destruction and subsequent atonic stomach, similar to its manifestations elsewhere in the GI tract. Chronic intestinal pseudoobstruction, a very rare entity affecting the neuromuscular plexuses throughout the bowel, can cause an atonic stomach and gastric dilatation. Other neurogenic conditions of central or peripheral neuropathies (syphilis, poliomyelitis, diabetes) can also result in chronic gastric atony.
Postsurgical Stomach
A Billroth∗ I, or B1, is simply the removal of the pylorus and end-to-end anastomosis of the stomach to the duodenum. A Billroth II, or B2, operation involves antrectomy and a side-to-side anastomosis of the jejunum to the greater curvature of the stomach. The afferent limb consists of the duodenum, which is now a blind ending (with preservation of the normal bile duct anatomy) and a variable length of jejunum. The efferent loop, into which gastric contents should preferentially empty, is the distal component of the side-to-side anastomosis (Fig. 2-83). If stomach contents preferentially empty into the afferent limb, then afferent loop syndrome can develop (see later in chapter).
Figure 2-83 UGI series in a 56-year-old woman who underwent a normal Roux-en-Y gastric bypass opereation. There is a choledochojejunostomy with the afferent limb (large arrow) and normal reflux of contrast into the bile ducts. The efferent limb (small arrow) is of normal caliber.
For the prevention of bile reflux into the stomach, which can cause severe gastritis, a modification of the Billroth II technique involves creation of a Roux†-en-Y anastomosis. In this instance, the afferent duodenal limb is still a blind ending with a normal insertion of the bile duct, but it is inserted into the efferent jejunal limb distal to the gastrojejunal anastomosis. This loop may be brought to the gastric remnant anterior to the transverse mesocolon (antecolic) or posteriorly (retrocolic), with the latter having a shorter loop, which is thought to more closely match normal physiological conditions. The Roux-en-Y anastomosis is also used for hepaticojejunostomy and choledochojejunostomy and is increasingly commonly with gastric bypass surgery.
Complications of Gastric Surgical Procedures
There are numerous complications to gastric surgery, and they can be divided into early and late (Table 2-9). Some complications (infection and hemorrhage) are common to most surgical procedures.
Table 2-9
Complications of Gastric Surgical Procedures
Leakage
Leakage usually occurs at the anastomotic sites shortly after surgery. Patients are usually imaged with water-soluble contrast media 24 hours after surgery to document any leaks before liquid diets begin. The study is often performed via a nasogastric tube. Leaks will be recognized as collections of contrast, often linear at or near an anastomosis, often in a direction away from or perpendicular to the axis of the organ. It is important to obtain orthogonal views to clearly identify the site, size, and direction of the leak. If no leak is identified, then barium may be administered to better define the anatomy and to determine whether there is any evidence of slow transit time through the stomach or small intestine (both of which are relatively common postsurgically because of ileus and perianastomotic edema). Barium may also identify a small leak missed by water-soluble contrast media. This will likely be of little significance, and the extravasation of barium will likely be minimal, local, and contained. Alternatively, larger leaks will likely be identified on CT, with extraluminal gas, fluid, or contrast material (Fig. 2-84).
Figure 2-84 Axial contrast-enhanced CT in a 67-year-old man who underwent a recent Roux-en-Y procedure and an afferent limb leak with extraluminal gas and fluid (arrow).
Gastroparesis
Delayed gastric emptying with no discernible obstruction is either an early transient (due to an ileus-type picture) or a late and chronic complication of gastric surgery. Either may be due to surgical damage to the vagus nerve. The stomach remains markedly distended with gastric fluid and food, and the patient is often nauseated and vomiting. Bezoars may develop secondary to the gastric stasis.
Marginal Ulcers
Marginal ulcers usually occur in the efferent limb, rather than afferent limb, because of peptic ulceration of the jejunal mucosa, although ischemia secondary to surgical manipulation of the surrounding vasculature can compound the problem (Fig. 2-85). Any predisposing factors (e.g., aspirin, steroid, or alcohol) will also exacerbate the development of an ulcer. These are usually identified by EGD or UGI because they are unlikely to be identified by on CT, unless they are large.
Figure 2-85 UGI series in a 67-year-old man after a partial gastrectomy and a Roux-en-Y procedure now with an anastomotic gastrojejunal ulcer (arrow).
Obstruction
Obstruction may occur early at the gastrojejunal anastomosis because of transitory, self-limiting edema or because of longer-term complications from fibrotic stricture resulting from the surgical procedure or resulting from an anastomotic or marginal ulcer. A more sinister cause results from a gastric carcinoma at the gastrojejunal anastomotic site.
Internal hernias that develop after gastric surgery occur when a loop of small bowel, usually jejunum, herniates through mesenteric hiatal orifices created at the time of the original operation. Although they are uncommon, the two most common hernias that are associated with gastric surgery involve small bowel herniation through a transmesenteric or transmesocolic peritoneal defect (Figs. 2-86 and 2-87). As the loops become more obstructed because of stricture formation from the narrow hiatal orifice, the patient has increasing abdominal pain, nausea, and vomiting. The loops of small bowel can become strangulated and may undergo volvulus (more commonly identified with transmesenteric hernias).
Figure 2-86 UGI in a 55-year-old man with prior bariatric surgery now with small bowel obstruction due to a jejunal transmesenteric herniation and volvulus (arrow).
Figure 2-87 Axial (A) and coronal (B) contrast-enhanced CT in a 38-year-old woman after bariatric surgery with jejunal obstruction (arrows) due to a closed-loop obstruction.
Obstruction can also occur with intussusception of the jejunum through the gastrojejunal anastomosis. This uncommonly occurs with a jejunojejunal intussusception that progresses retrograde toward the gastrojejunal anastomosis and finally into the anastomosis itself, giving the appearance of an intragastric mass. The mass may have a “coiled-spring” appearance on barium studies, similar to that seen with intussuscepta elsewhere in the small bowel, and if the mass is large enough, it may obstruct the stomach.
Dumping Syndrome
Dumping syndrome is common to all gastric surgical procedures, whereby the rapid delivery of sugars into the small bowel through the gastrojejunal anastomosis creates an osmotic fluid overload in the bowel with diarrhea, palpitations, pallor, sweating, and postural hypotension.
Afferent Loop Syndrome
Afferent loop syndrome is relatively uncommon and is due to the obstruction of the afferent limb (duodenum or jejunum) proximal to the gastrojejunal anastomosis. It results from distention and bacterial overgrowth of the afferent limb. Patients often experience epigastric fullness after eating, and bilious vomiting, sometimes projectile, is a characteristic symptom as the distended loop decompresses abruptly. Bacterial overgrowth from the prolonged stasis of the afferent limb can result in malabsorption. CT is the imaging method of choice and demonstrates a dilated and obstructed loop in the right upper quadrant (Fig. 2-88).
Figure 2-88 Axial (A) and coronal (B) contrast-enhanced CT in a 47-year-old woman after a Whipple procedure and an obstructed afferent loop (large arrow) with secondary biliary dilatation (small arrow).
Gastric Bypass (Bariatric) Surgery
There are a variety of surgical procedures designed to promote weight loss in patients with morbid obesity, either for patient preference or for treatment of obesity-associated type II diabetes. The essential surgical goal is to markedly reduce stomach volume to create early satiety after food ingestion, thereby reducing longer-term caloric intake. There two common procedures are Roux-en-Y gastric bypass surgery and laparoscopic adjustable gastric banding (lap band). The former procedure (of which there are several versions) is more common with the creation of a smaller upper gastric remnant (15 to 30 mL) that is directly connected to a loop of jejunum so that food “bypasses” the main larger lower gastric (approximately 400 mL), or excluded, remnant. Because it is still producing gastric secretions, the excluded remnant is still connected to the small bowel with the retained duodenum and proximal jejunum, which is connected to the efferent loop (directly connected to the small upper pouch) via a Roux-en-Y limb (Fig. 2-89).
Figure 2-89 Schematic representation of a Roux-en-Y bariatric operation. There is a small proximal gastric pouch and larger extruded gastric remnant.
Increasingly, however, the surgery is being performed laparoscopically, and the separation of the two smaller and larger pouches is often achieved with staples (termed a sleeve gastrectomy). This procedure usually results in complete separation (to minimize fistulization into the larger remnant or the connection of the two pouches) (Fig. 2-90).
Figure 2-90 Schematic representation of a sleeve gastrectomy.
Complications of the bariatric surgical procedures include infection, hemorrhage, adhesions, intussuscepta, internal hernia formation, anastomotic leakage and fistulization, stricture, and ulceration (Figs. 2-91, 2-92, and 2-93). Nutritional deficiencies can occur, particularly with distal anastomotic procedures. Small leaks are best demonstrated by water-soluble contrast swallow examinations and are seen as contrast material spilling into the peritoneal cavity. This study is routinely performed 24 hours after surgery to check for leaks before more formal liquid feeds start. If no initial leak is seen, barium may be administered to give better depiction of the anatomy and to confirm there is no tiny leak. Larger leaks, which may evolve into abscesses, are best visualized by CT. Internal herniation can be transmesenteric through either the transverse mesocolon or the small bowel mesentery (see Fig. 2-86 and Chapter 4).
Figure 2-91 Axial contrast-enhanced CT in a 33-year-old woman with a leak after bariatric surgery with extraluminal gas (large arrow) and fluid (small arrow).
Figure 2-92 A and B, UGI swallow in a 36-year-old woman after bariatric surgery with a gastro gastric fistula (large arrows). There is contrast in the extruded segment (small arrows).
Figure 2-93 Axial (A) and coronal (B) CT in a 58-year-old woman with a post-bariatric gastrogastric fistula with contrast present in both the efferent limb (large arrows) and extruded stomach (small arrows).
An alternative approach to creating the small upper gastric pouch is the laparoscopic adjustable gastric band or lap band. This is an inflatable silicone device, placed approximately 3 cm distal to the GE junction, that effectively mimics the stapling procedure but is less invasive and thought to lead to less morbidity (Figs. 2-94 and 2-95). Unlike the stapling procedure, the larger gastric pouch is not excluded from the digestion process; rather, the band creates a small upper pouch and delays emptying into the larger lower gastric pouch. As the upper pouch fills with food, it also creates early satiety. The ingestion of food therefore stops, and that which was ingested slowly passes into the larger gastric pouch for normal digestion. The band’s tightness can be tailored to the patient’s weight-loss regimen and can be tightened or loosened accordingly through a small access port under the skin (see Fig. 2-94).
Figure 2-94 Abdominal plain radiograph demonstrating a normal lap-band prosthesis (arrows).
Figure 2-95 UGI series in a 33-year-old woman with a normal-appearing lap-band procedure with a small gastric remnant and positioning of the band (arrows).
The main complication is that the lap band can “slip” so that the lower larger pouch herniates or prolapses above the band, leaving a larger upper pouch and causing constriction of the stomach at its widest part. This can lead to obstruction or strangulation and would require urgent surgery (Fig. 2-96). Alternatively, the band can be too “loose” so that the stomach is not constricted and early satiety does not occur. This can be adjusted by tightening the band, assuming it has not slipped distal to its intended position.
Figure 2-96 UGI series in a 39-year-old woman with slipped gastric band. The lap-band has “slipped” cephalad (arrow) so there is a very small gastric volume above the ring and the stomach fills normally with barium.
Nissen Fundoplication
Nissen∗ fundoplication is an open or laparoscopic surgical procedure, used to treat GERD, that involves creating a gastric fundal wrap (usually 360 degrees) around the lower esophagus to strengthen the lower esophageal sphincter (see Chapter 1). The procedure is generally effective, although complications of dysphagia, dumping syndrome, achalasia, and a difficulty with belching are recognized. The major complication is loosening of the wrap, with patients having recurrent symptoms of GERD (Fig. 2-97).
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∗ Friedrich Trendelenburg (1844-1924), German surgeon.
∗ Hans Christian Joachim Gram (1850-1938), Danish bacteriologist.
† Robert M. Zollinger (1903-1992), American surgeon; Edwin H. Ellison (1918-1970), American surgeon.
‡ Thomas Blizard Curling (1811-1888), British surgeon.
∗ Aubrey O. Hampton (1900-1955), American radiologist.
† Russell Daniel Carman (1875-1926), Canadian-born American radiologist.
∗ Pierre E. Ménétrier (1859-1935), French pathologist.
∗ Robert M. Zollinger (1903-1992), American surgeon; Edwin H. Ellison (1918-1970), American surgeon.
∗ Eldon J. Gardner (1909-1989), American geneticist.
† Johannes Peutz (1864-1940), Dutch physician; Harold Jeghers (1904-1990), American physician.
‡ Leonard W. Cronkhite, Jr., American pediatrician; Wilma J. Canada, American radiologist.
∗ Cowden’s disease. Named after the first described patient.
∗ Santiago Ramón y Cajal (1852-1934), Spanish pathologist.
† J Aidan Carney, American pathologist.
∗ William B. Bean (1909-1989), American physician.
∗ Friedrich Ernst Krukenberg (1871-1946), German physician.
† Thomas Hodgkin (1798-1866), British physician and pathologist.
∗ Michael A. Epstein (1921-2006), British pathologist and virologist; Yvonne Barr (1932- ), British virologist.
∗ Moritz Kaposi (1837-1902), Hungarian physician and dermatologist.
∗ Theodor Billroth (1829-1894), German surgeon.
† César Roux (1857-1934), Swiss surgeon.
∗ Rudolph Nissen (1896-1981), Swiss surgeon.
