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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)


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.
Box 2-1   Causes of Gastric Erosions
Peptic ulcer disease
Drugs (aspirin, NSAIDs, steroids, KCl, clopidogrel)
Crohn disease
Infectious (CMV, HSV)
Behçet syndrome
Major stress conditions (burns, septic shock)
CMV, Cytomegalovirus; HSV, herpes simplex virus; KCl, potassium chloride; NSAIDs, nonsteroidal antiinflammatory drugs.
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.

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.
Carmanmeniscus 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.

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 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 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.


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.


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).
Box 2-2   Benign Gastric Masses
Polyps (hyperplastic, adenomatous, hamartoma, inflammatory fibroid)
Ectopic pancreas
GIST, Gastrointestinal stromal tumor.
Box 2-3   Malignant Gastric Masses
Kaposi sarcoma
GIST, Gastrointestinal stromal tumor.

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

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