Erosive gastritis (also known as hemorrhagic gastritis or multiple gastric erosions) is a frequent cause of upper gastrointestinal bleeding, but it is rarely severe. Erosions may be completely asymptomatic. As detected by endoscopy, multiple bleeding erosions are distributed diffusely throughout the gastric mucosa or are localized to the fundus, body, or antrum. The intervening mucosa may appear reddened and friable, or it may appear normal.
Histologically, the mucosal destruction by erosions does not extend below the muscularis mucosae to involve the more vascular submu-cosa; characteristically, the mucosal lesions heal completely. At any one time, different erosions can be observed in various stages of evolution and regression. Erosions may occur in flat mucosa or on the crests of small mucosal mounds which may stud the crests of folds. Between erosions there may be areas of surface epithelium depleted of mucus and focal or diffuse extravasation of blood into the lamina propria. Erosions may develop in mucosa that is histologically normal or that shows changes of any histologic type of gastritis. If the process persists, erosions may extend into the submucosa to form acute ulcers; then bleeding may become severe.
Erosive gastritis can occur for no apparent reason. Many cases, however, are associated with the ingestion of aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs). Because aspirin is not ionized in the acid milieu of the gastric lumen, it is absorbed readily by passive nonionic diffusion. At the neutral intracellular pH within the gastric surface epithelium, aspirin becomes an ionized acid which can destroy the cells and provide an entry point for acid-peptic digestion. When aspirin is given with sodium bicarbonate it does not injure the gastric mucosa because it is ionized and poorly absorbed gastrically. When aspirin is covered with an enteric coating it passes through the stomach and is absorbed in the small bowel. Aspirin and most NSAIDs interfere with prostaglandin synthesis, thus impairing mucosal resistance to injury. NSAIDs such as phenylbutazone or indomethacin are especially associated with erosive gastritis. Acute alcohol ingestion is an important cause of gastric erosions, and portal hypertension is a predisposing factor.
Severe stress secondary to burns, sepsis, trauma, surgery, shock, or respiratory, renal, or liver failure often causes gastric erosions or acute ulcers. Their pathogenesis is poorly understood and probably varies with different predisposing conditions. Alterations in mucosal blood flow may lead to areas of microinfarction with further evolution of the lesion dependent upon acid-peptic digestion. With better intensive care, hyperalimentation, and a strict antacid regimen, erosions in severely stressed patients infrequently progress to ulcers with resultant severe hemorrhage or perforation.
Patients may present with hematemesis and/or melena. Chronic blood loss may occur. Many have no symptoms, but some notice mild epigastric discomfort or nausea. The diagnosis is best made by gastroscopy on the same day as the bleeding episode, because otherwise the lesions may have healed and disappeared. The newer small-caliber screening endoscopes are just slightly bigger than a nasogastric tube and may be passed easily in very sick patients after only pharyngeal anesthesia. Only expert double-contrast x-ray may demonstrate some of these superficial erosions. Presumptive clinical diagnoses of erosive gastritis in patients with upper gastrointestinal bleeding and negative x-rays are often wrong. The source of upper gastrointestinal bleeding is best determined by early esophagogas-troduodenoscopy.
The usual measures for restoring circulating blood volume should be undertaken promptly. Not uncommonly, the bleeding has stopped by the time a tube is passed. If not, lavage of the stomach with iced isotonic saline solution is used, although its efficacy is unproved in all types of upper gastrointestinal bleeding, especially in erosive gastritis. In any event, lavage with noniced saline solution via an Ewald tube may facilitate diagnostic endoscopy by removing some of the obscuring blood. Gravity drainage, not suction, should be used for emptying the saline solution from the stomach, lest suction artifacts be produced which are indistinguishable from acute erosions endoscopically.
If bleeding stops, a regimen of hourly antacids and cimetidine or ranitidine is instituted. If bleeding continues, selective infusion of vasopressin into the left gastric artery or embolization may be warranted. In the rare case in which bleeding continues and is life-threatening, one of the erosions may have progressed to a deeper acute ulcer. If this ulcer can be visualized endoscopically, it may be treatable by electrocoagulation or with a heater probe via the endoscope. If this fails, vagotomy and pyloroplasty with oversewing of the bleeding ulcers is the preferred surgical treatment, but it also may not be successful. Very rarely persistent severe bleeding requires total gastrectomy.