Peptic Ulcers - Clinical Tree

Gastric or duodenal ulcers (peptic ulcers) are thought to occur in about 10% of adults in the West. Peptic ulcers are important not only because of the frequent occurrence of pain or other symptoms but also because of the morbidity and mortality associated with complications such as bleeding and perforation.

Epidemiology and Pathogenesis

Duodenal ulcers are more common than gastric ulcers, occurring in adults of all ages, whereas gastric ulcers develop mainly in people over age 40. ^, Peptic ulcers are equally common in men and women.

Almost all duodenal ulcers are caused by Helicobacter pylori , whereas the vast majority of gastric ulcers are caused by H. pylori or nonsteroidal anti-inflammatory drugs (NSAIDs). Other possible causes of gastric ulcers include tobacco, alcohol, coffee, stress, duodenogastric reflux of bile, delayed gastric emptying, and hereditary factors.

HELICOBACTER PYLORI GASTRITIS

H. pylori is a gram-negative spiral bacillus first isolated on endoscopic biopsy specimens from the stomach by Warren and Marshall in 1983. Since then, this organism has been recognized as the major cause of gastric and duodenal ulcers. The prevalence of H. pylori gastritis is 60% to 80% in patients with gastric ulcers and 95% to 100% in patients with duodenal ulcers.

Although the pathogenesis of ulcers in patients with H. pylori gastritis is uncertain, these individuals have increased gastrin secretion with high basal and peak acid outputs. Most people infected with H. pylori never develop ulcers, but a virulent cagA -positive strain of the organism is more likely to be associated with duodenal ulcers and, to a lesser degree, gastric ulcers.

NONSTEROIDAL ANTI-INFLAMMATORY DRUGS

The prevalence of gastric ulcers in patients on aspirin or other NSAIDs is 15% to 30%. ^, NSAIDs have been shown to inhibit prostaglandin production by blocking the formation of cyclooxygenase 1 (COX-1). ^, Because prostaglandins have cytoprotective properties, inhibition of prostaglandin synthesis may cause gastric mucosal injury and ulceration. Aspirin has also been shown to disrupt the mucus gel layer in the stomach, allowing acid to damage the gastric mucosa, even in the absence of increased acid secretion. ^, Altered mucosal resistance is therefore thought to be a major factor in ulcer pathogenesis. Nevertheless, gastric ulcers have been induced in cats by intravenous infusion of aspirin. The development of these ulcers therefore appears to be mediated by both topical and systemic effects of NSAIDs.

Chronic NSAID use is associated with an increased frequency not only of gastric ulcers but also of ulcer complications such as perforation, obstruction, and bleeding. ^, ^, A careful NSAID history should therefore be obtained in all patients with H. pylori– negative gastric ulcers because of the likelihood that these ulcers are NSAID-related.

TOBACCO, ALCOHOL, AND COFFEE

Some investigators have found that cigarette smokers are more likely to develop ulcers than nonsmokers, ^, whereas others have found no association between smoking and ulcers. Alcohol and coffee may stimulate acid secretion, but their role in ulcer pathogenesis remains uncertain.

STRESS

The role of stress in the development of peptic ulcers is controversial. Some investigators have found that emotional stress contributes to the development of gastric ulcers by increasing peptic acid secretion, ^, but others have found no association between stressful life events and ulcers.

GASTRODUODENAL REFLUX OF BILE AND DELAYED GASTRIC EMPTYING

Some patients with gastric ulcers have high concentrations of bile acids in the stomach, implicating duodenogastric reflux of bile in ulcer pathogenesis. Gastric outlet obstruction or gastroparesis may also predispose to the development of gastric ulcers by prolonging exposure of the stomach to its own peptic secretions. Such ulcers have been called Dragstedt ulcers based on the name of the investigator who described them.

HEREDITARY FACTORS

A small percentage of patients with peptic ulcers have a family history of ulcers, most likely related to hereditary rather than environmental factors. ^, Peptic ulcers are also more common in patients with genetic syndromes such as multiple endocrine neoplasia type 1, systemic mastocytosis, and tremor-nystagmus-ulcer syndrome.

Clinical Findings

Patients with peptic ulcers often present with epigastric pain, but others experience right upper quadrant, back, or chest pain or other symptoms such as bloating, belching, nausea, vomiting, anorexia, and weight loss. Depending on the clinical findings, the differential diagnosis may include reflux esophagitis, gastritis, duodenitis, cholecystitis, irritable bowel syndrome, ischemic bowel disease, Crohn’s disease, pancreatitis, and gastric or pancreatic carcinoma.

The diagnosis of peptic ulcers is complicated by the fact that some patients with classic ulcer symptoms are not found to have ulcers, whereas other patients with peptic ulcers are asymptomatic. ^, When gastric or duodenal ulcers penetrate posteriorly into the pancreas, the normally rhythmic epigastric pain associated with ulcers is replaced by a more constant pain radiating to the back. In contrast, free perforation of a peptic ulcer causes peritonitis. A delay of more than 24 hours from the time of diagnosis to surgery is a major contributing factor for the high mortality rates in patients with perforated peptic ulcers.

Patients with antral, pyloric channel, or duodenal ulcers sometimes present with recurrent nausea and vomiting secondary to varying degrees of gastric outlet obstruction. Other patients with pyloric channel ulcers may develop the so-called pyloric channel syndrome with severe postprandial epigastric pain relieved by vomiting.

Peptic ulcers are the most common cause of upper gastrointestinal (GI) bleeding, accounting for about 50% of cases. Some patients have one or more episodes of massive hemorrhage manifested by hematemesis, melena, or rectal bleeding, whereas others have chronic, low-grade GI bleeding manifested by guaiac-positive stool or iron-deficiency anemia. Gastric ulcers are more likely to bleed than duodenal ulcers, probably because of the greater ulcer size and older age of the patient.

Treatment

The treatment for peptic ulcers depends on the underlying cause. In patients with documented H. pylori gastritis, there is strong evidence that eradication of H. pylori leads to more rapid healing of gastric and duodenal ulcers and a much lower rate of ulcer recurrence. ^, As a result, it is widely believed that all patients with H. pylori –related gastric or duodenal ulcers should undergo combination therapy with antibiotics and antisecretory agents (proton pump inhibitors) to accelerate ulcer healing and decrease the rate of ulcer recurrence. ^, Because this therapy is highly effective in eradicating H. pylori , ^, affected individuals can be cured of their ulcer disease unless they become infected by another strain of the organism.

In the absence of H. pylori, H2 receptor antagonists and proton pump inhibitors have proved to be highly effective in accelerating healing of peptic ulcers by suppressing acid secretion. Because NSAID-related gastric ulcers are associated with decreased synthesis of prostaglandins, misoprostol (a synthetic prostaglandin E analogue) has been used to accelerate ulcer healing in these patients.

Surgery may be required for recurrent or intractable ulcers that fail to heal on medical therapy, for ulcer complications such as bleeding, obstruction, and perforation, and for ulcers that have equivocal or suspicious findings on barium studies or endoscopy. The most common operations include partial gastrectomy, vagotomy and pyloroplasty, and hyperselective vagotomy (see Chapter 23 ). Because of improved medical treatment of peptic ulcers, the need for surgery has decreased considerably in these patients.

Radiographic Findings

GASTRIC ULCERS

Shape

Gastric ulcers typically appear on double-contrast studies as round or ovoid collections of barium ( Figs. 17.1 and 17.2 ), but some have a linear, rod-shaped, rectangular, serpiginous, or flame-shaped configuration ( Fig. 17.3 ). Linear ulcers constitute about 5% of all gastric ulcers and most likely represent a stage in the evolution of ulcer healing. ^,

Fig. 17.1, Lesser curvature gastric ulcers.

Fig. 17.2, Posterior wall gastric ulcer.

Fig. 17.3, Gastric ulcers of different shapes.

Size

Most gastric ulcers detected on single-contrast barium studies are larger than 5 mm in size. In contrast, double-contrast studies are better able to distend the stomach and efface normal folds, enabling visualization of smaller ulcers ( Fig. 17.4 ). Regardless of technique, larger ulcers tend to be located more proximally in the stomach. Although giant gastric ulcers (ulcers greater than 3 cm in size) are associated with a higher risk of complications such as bleeding and perforation, the size of the ulcer crater has no relationship to the presence of carcinoma ( Fig. 17.5 ).

Location

Most benign gastric ulcers are located on the lesser curvature or posterior wall of the gastric antrum or body. ^, ^, ^, In contrast, only a small percentage are located on the anterior wall or greater curvature. ^, ^, ^, Older people are more likely to develop ulcers high on the lesser curvature of the stomach, also known as geriatric ulcers .

Benign greater curvature ulcers are almost always located in the distal half of the stomach, and the vast majority are caused by aspirin or other NSAIDs. ^, Because benign ulcers rarely occur high on the greater curvature, any ulcers in this location should be considered worrisome for malignant tumor. Except for these high greater curvature ulcers, the location of the ulcer has no relationship to the presence of carcinoma.

Gastric ulcers are occasionally found within hiatal hernias. Such ulcers usually occur on the lesser curvature aspect of the hernia (where it is compressed by the adjacent diaphragm) and are known as riding ulcers . Hiatal hernias are inaccessible to manual palpation, so double-contrast studies are essential for showing these ulcers.

Morphologic Features

Ulcers on the lesser or greater curvature of the stomach are readily visualized in profile on barium studies, permitting analysis of the size, shape, and depth of the ulcer crater as well as associated findings. In contrast, ulcers on the anterior or posterior wall may be difficult or impossible to visualize in profile, so these ulcers must be evaluated based on their en face appearance.

Lesser Curvature Ulcers

Ulcers on the lesser curvature typically appear as smooth, round or ovoid craters that project beyond the contour of the adjacent gastric wall (see Figs. 17.1 and 17.4 ). ^, Upright compression views sometimes reveal a thin radiolucent rim of edema separating barium in the ulcer from barium in the adjacent lumen, also known as a Hampton’s line . ^, In other patients, the rim of undermined mucosa may become more edematous, producing a wide radiolucent band, or ulcer collar (see Fig. 17.1B ). Occasionally, edema and inflammation surrounding the ulcer produces an ulcer mound , seen in profile as a smooth, bilobed, hemispheric protrusion into the lumen on both sides of the ulcer. The outer borders of these ulcer mounds usually form obtuse, gently sloping angles with the adjacent gastric wall. Hampton’s lines and ulcer mounds or collars are considered to be classic features of benign gastric ulcers, but these findings are present in only a small percentage of all patients with lesser curvature ulcers.

Retraction of the gastric wall adjacent to lesser curvature ulcers sometimes leads to the development of smooth, symmetric folds that radiate directly to the edge of the ulcer crater (see Fig. 17.1A ). Lesser curvature ulcers may also be associated with focally enlarged areae gastricae because of edema and inflammation in the adjoining mucosa (see Fig. 17.1A ). Occasionally, lesser curvature ulcers cause retraction of the opposite wall, producing an incisura on the greater curvature.

Greater Curvature Ulcers

At one time, almost all ulcers on the greater curvature of the stomach were thought to be malignant. It is now recognized, however, that benign ulcers do occur on the distal half of the greater curvature in patients on aspirin or other NSAIDs ( Figs. 17.6 and 17.7 ). ^, The location of these ulcers on the greater curvature is presumably related to the effect of gravity as the dissolving pills collect in the most dependent portion of the stomach, causing localized mucosal injury on the greater curvature. Such ulcers have been called sump ulcers because of their dependent location. These greater curvature ulcers occasionally penetrate inferiorly into the gastrocolic ligament, producing a gastrocolic fistula (see later, “Fistulas”).

Fig. 17.6, Greater curvature gastric ulcers caused by aspirin and indomethacin.

Fig. 17.7, Giant greater curvature gastric ulcers caused by aspirin.

In contrast to ulcers on the lesser curvature, greater curvature ulcers may appear to have an intraluminal location because of circular muscle spasm and retraction of the adjacent gastric wall (see Fig. 17.7A ). Greater curvature ulcers may also be associated with thickened, irregular folds and considerable mass effect secondary to marked edema and inflammation accompanying the ulcers (see Fig. 17.7 ). ^, Because of these morphologic features, benign greater curvature ulcers often have a suspicious radiographic appearance, so the usual radiographic criteria for differentiating benign and malignant ulcers elsewhere in the stomach are unreliable for ulcers in this location. ^,

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