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8. Other Gastric Diseases

Partial (antral) or total gastric volvulus is a rare cause of acute upper abdominal pain and vomiting. These obstructions can arise by themselves, or as torsion within a hiatus hernia. Volvulus within a hernia is not uncommon in the elderly, when there may be no symptoms. The belief that twisting obstruction poses an important risk to the blood supply is probably unjustified. Gastric aspiration is followed by surgical relief of the volvulus in those who present with obstruction.

Sudden gross gastric distention and acute dilatation of the stomach can arise after any form of upper abdominal surgery, including cholecystectomy, and especially after vagotomy, after childbirth and in diabetic coma. The causes are uncertain. Vomiting of relatively clear gastric contents is succeeded by the production of dirty brown or feculent material and the development of abdominal distention. Prompt decompression with a large-bore stomach tube and intravenous fluid replacement are required. After a variable interval the condition should then resolve spontaneously.

8.1.1 GASTRIC RUPTURE

Acute, nontraumatic, spontaneous rupture of the stomach is a rare, catastrophic and poorly understood event. The majority of ruptures occur on the lesser curvature. They have also been reported to occur during upper gastrointestinal radiography using barium, sodium bicarbonate ingestion, nasal oxygen therapy, cardiopulmonary resuscitation and labor, and during the postpartum period.

Hypertrophic pyloric stenosis is an idiopathic condition that may occur in infants or adults. The muscle of the pyloric canal is unduly hypertrophied. Infantile hypertrophic pyloric stenosis is more common in boys than in girls (the sex ratio is approximately 10:1), is a frequent anomaly (its incidence is about 3 per 1,000 live births) and is thought to be due to a combination of genetic predisposition and some abnormality of fetal or early postnatal development. Symptoms usually develop in the first few weeks after birth and characteristically consist of copious projectile vomiting of the gastric contents after feeding. On examination there is usually visible gastric peristalsis; a lump can be felt abdominally in the region of the pylorus. Barium-meal examination is not usually necessary but will confirm the presence of a narrow segment, 1-2 cm long, at the pylorus. The condition must be distinguished clinically from esophageal atresia (which involves onset at birth of difficulties with swallowing) and duodenal obstruction/atresia (which involves bile-stained vomitus). A minor proportion of all cases settle in the first two to three months with conservative management with anticholinergic drugs, but most patients will require early surgery with Ramstedt's procedure (pyloromyotomy).

Occasionally, adult patients present with obstructive symptoms resulting from pyloric stenosis associated with muscular hypertrophy. This is rarely if ever caused by recurrence of infantile pyloric stenosis; it is usually associated with juxtapyloric peptic ulceration, but sometimes the problem seems to be due to primary hypertrophic stenosis arising in adult life. The differential also includes pyloric mucosal diaphragm and annular pancreas. Pyloric obstruction requires pyloroplasty together with a procedure such as vagotomy if there is an associated ulcer.

8.2.1 GASTRIC DIVERTICULA

Gastric diverticula occur most commonly near the cardia on the lesser curve, but occasionally are found in the prepyloric region. They seldom cause symptoms. Their principal importance lies in the likelihood of confusion with gastric ulceration.

8.2.2 PSEUDOLYMPHOMA

Localized lymphoid hyperplasia of the stomach is also known as pseudolymphoma. The lesions are raised, flat or nodular folds, and are often associated with gastric ulceration. The etiology of this condition remains unclear, but Helicobacter pylori infection has been implicated. It is difficult to exclude lymphoma using radiology or endoscopic biopsy; thus, a resected specimen is required for diagnosis.

8.2.3 GASTRIC INFECTIONS AND INFESTATIONS

Gastric acid provides a bactericidal barrier against infection. Acid-suppressive pharmacotherapy, hypochlorhydria or gastric surgery may increase the risk of bacterial infection. Recent attention has been turned to Helicobacter pylori, a spiral bacillus found in the upper gastrointestinal tract, particularly the gastric antrum. H. pylori has been associated with chronic gastritis in addition to peptic ulcer disease.

Helicobacter pylori infection is now recognized to be a major causative factor associated with a spectrum of gastroduodenal disease. It is found in about 95% of patient with gastritis and 100% with chronic active gastritis. It is found in 90-95% of patients with duodenal ulcer and 60-80% of patients with gastric ulcer. It is also highly associated with gastric carcinoma and gastric lymphoma. The association of H. pylori infection with nonulcer dyspepsia is more controversial and as yet not convincingly substantiated.

Viral infections such as cytomegalovirus (CMV) and herpes simplex virus are very often found in immunocompromised hosts. They are associated with gastric erosions, although CMV has been found in intact mucosa. Cultures or endoscopic biopsies and smears demonstrating intranuclear inclusions are helpful in establishing a diagnosis. Candida albicans is commonly found in the gastric ulcers or erosions of immunocompromised hosts. Candidal infection should be a consideration in an ulcer that fails to heal. In the immunocompromised host, parasites such as Strongyloides stercoralis may become overwhelmingly disseminated. Histoplasmosis and mucormycosis involving the stomach are rare causes of gastric ulceration and bleeding.

8.2.3.1 Helicobacter pylori gastritis

Helicobacter pylori (H. pylori) is a small (3 x 0.5 µm) gram-negative, micro-aerophilic urease-producing rod-shaped bacillus, which has been closely linked to both acute and chronic active type B gastritis, especially of the antrum (Figure 8). H. pylori is an important pathogenic factor in peptic ulcer disease.

H. pylori is present in almost all cases of chronic active gastritis, which most commonly involves antral inflammation but may spread to the whole stomach over time. H. pylori does not colonize areas of intestinal metaplasia, but has been seen in the distal esophagus of some patients with Barrett's esophagus.

The source of H. pylori is unknown, although person-to-person spread is probably demonstrated by intrafamilial clustering and a high prevalence of seropositivity in institutionalized persons, those of low economic status, and populations in less developed countries. The prevalence of H. pylori infection increases with age; in Western countries it is uncommon before the third decade but thereafter increases with seropositivity at the rate of approximately 1% per year of age.

Most people with H. pylori-associated gastritis are asymptomatic and have normal-appearing gastric mucosa at endoscopy. The histologic spectrum of H. pylori-associated gastritis ranges from minimal to severe inflammation, but the organisms noted in the mucous layer are associated with severe depletion of mucus and an intense inflammation, which most often is chronic, although neutrophils can be noted in some instances. Eradication of H. pylori with antibiotics has resulted in a marked lessening in the severity of the gastritis.

8.2.3.1.1 Diagnosis

  The organism can be identified on histology with conventional hematoxylin- and eosin-stained sections at high-power magnification, but is more easily seen with the Warthin-Starry or the modified Giemsa stains. The enzyme-linked immunosorbent assay (ELISA) is the most widely employed serologic method; its sensitivity and specificity are greater than 90%. Rapid urease tests can be performed on tissue biopsies in the endoscopy unit since H. pylori produces large amounts of urease, which can convert urea into ammonia and carbon dioxide. Rapid urease tests involve urease and pH indicator gel, into which the biopsy is placed. The presence of H. pylori results in an alkaline pH of the medium and a color change when the pH rises. Approximately 75% of the positive tests occur between 20 minutes and 1 hour, and 90% are positive between 6 and 24 hours. Carbon-urea breath tests using carbon ¹³C and ¹⁴C employ carbon-labeled urea that is fed to the patient and is subsequently hydolyzed by the H. pylori urease, resulting in the formation of ammonia and carbon dioxide. This labeled carbon dioxide in the breath is then measured.

8.2.3.1.2 H. pylori association with peptic ulcer disease

  Numerous studies have established the close association of antral H. pylori and peptic ulcer disease. Over 90% of patients with duodenal ulcer have H. pylori identified in gastric antral biopsies. The association for gastric ulcer and H. pylori is up to 85%. Although ulcers can be healed with a variety of agents that do not eradicate H. pylori, in these cases relapse is common. However, when the H. pylori organism is eradicated the impact on the subsequent course of duodenal ulcer is dramatic. The recurrence rate in patients in whom H. pylori is eradicated ranges from 0-4% per year. This is in marked contrast to those who remain H. pylori-positive, whose recurrence rates vary from 40-80% per year.

H. pylori infection is associated with doudenal ulcer by way of an antral-predominant gastritis that is accompanied by a decrease in somatostatin and an increase in gastrin. This may augment gastric acid secretion, which may already be high as a result of genetic factors. Increased gastric acid secrection leads to gastric metaplasia in the duodenum, which can be colonized by H. pylroi leading to duodenal bulb inflammation, duodenitis and duodenal ulcer. The ulcer diathesis may reflect more damaging strains of the organisms, greater density of the infecting organisms or an exaggerated host inflammatory response (Figure 9).

The therapy for the eradication of H. pylori has evolved over the past decade (Table 10). The early regimen of bismuth triple therapy included a bismuth compound (PeptoBismol^®) plus metronidazole and tetracycline or bismuth plus metronidazole and amoxicillin. The therapy is effective in patients with metronidazole-sensitive H. pylori infection but not very effective in those with metronidazole-resistant strains. This regimen has limited compliance because of dosing frequency and adverse effects.

Therapy later evolved to combinations of a proton pump inhibitor (PPI) and one antibiotic, usually clarithromycin. Eradication rates with a PPI plus clarithromycin are usually between 70 and 85%. The addition of a second antibiotic to the regimen, usually metronidazole, has led to much higher eradication rates, such as 88-94% for a PPI plus metronidazole and clarithromycin. With amoxicillin and clarithromycin the eradication rates are between 75 and 96%; the rates decrease about 10% with amoxicillin and metronidazole compared to the previous two combinations.

8.2.3.1.3 Nonulcer dyspepsia and H. pylori

  The role of H. pylori infection in nonulcer dyspepsia remains an important question. There may be a subset of patients with nonulcer dyspepsia whose symptoms are due to H. pylori infection. However, many patients harboring H. pylori are symptom-free. Acute infection with H. pylori is associated with belching, pyrosis and malaise, and may be associated with decreased gastric acid secretion. At present, there is no evidence to suggest that the presence of H. pylori is associated with any particular symptom cluster related to functional dyspepsia.