Peptic gastritis used to be far more prevalent and was responsible for tens of millions of deaths worldwide. It was widely assumed for cen- turies 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 Figure 2-12. UGI series in a 41-year-old woman with diffuse gastric
fold thickening (arrow) due to profuse gastritis.
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B
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.
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B
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
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introduced. Both drugs have dramatically improved the morbid- ity 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 popula- tion. This bacterium causes an excessive production of ammo- nium, 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 *Hans Christian Joachim Gram (1850-1938), Danish bacteriologist.
Figure 2-15. UGI series in a 52-year-old man with gastric mucosal thickening and multiple small gastric erosions, some of which have punc- tate pools of barium (arrows).
Figure 2-16. UGI series in a 60-year-old woman with multiple aphthous
ulcers (arrow). Fgastric lesions (arrows) due to melanoma metastases.igure 2-17. UGI series in a 54-year-old man with multiple bull’s-eye
B
ox2-1.
Causes of Gastric ErosionsPeptic ulcer disease
Drugs (aspirin, NSAIDs, steroids, KCl, clopidogrel) Alcohol
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.
eventually ulcer disease ensue. The discovery that the disease is primarily infectious and the fact that it is readily treated by anti- biotics 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 sec- ondary 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.
†Robert M. Zollinger (1903-1992), American surgeon; Edwin H. Ellison (1918-1970),
American surgeon.
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 wide- spread 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 differentia- tion into benign or malignant categories are still required. Certain UGI imaging features should be emphasized (Table 2-3).
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).
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).
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 dis- ease, but when they are, they are usually thick and irregular.
Ulcer fold convergence: This is a helpful sign for benign dis-
ease because folds almost always converge right up to the ulcer *Aubrey O. Hampton (1900-1955), American radiologist.
margin, whereas this is uncommon in malignant disease where folds, often irregular, fail to meet the ulcer margin (Fig. 2-24).
Mucosal fold shape: Benign folds simply represent edema-
tous changes and are typically smooth and uniform (Fig. 2-24). Malignant folds often contain the malignancy itself as well as
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B
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).
t
able2-3
Imaging Differentiation of Benign and Malignant Gastric Ulcer DiseaseFeatures 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
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edematous changes and so are more typically irregular, ampu- tated, clubbed, or fused (Fig. 2-25).
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 projec- tion will probably not be appreciated unless visualized tangen- tially, which underlines the importance of obtaining multiple orthogonal views when any abnormality is identified. Malig- nant 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.
Crescent sign: This represents benignity and is seen in ulcers along
the greater curvature of the stomach (usually antrum) where the
†Russell Daniel Carman (1875-1926), Canadian-born American radiologist.
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 poten- tially 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 suf- ficient 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 pre- sentation. 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.