title: Pathogenesis, diagnosis and treatment of acute gastric mucosal lesions.
abstract: Stress ulcers are multiple superficial mucosal lesions which occur mainly in the fundus of stomachs of seriously ill patients and should be differentiated from reactivation of a pre-existent ulcer diathesis, Cushing's ulcer following head injury, or drug-induced gastritis. It is generally agreed that luminal acid and pepsin are required for ulceration to develop. Experimental evidence suggests that backdiffusion of acid is closely related to the formation of ulcers. In the absence of overt disruption of the gastric mucosal barrier, ischaemia appears to compromise the ability of the gastric mucosa to dispose of backdiffusing acid, which then results in a decrease in intramural pH and ulceration. Reflux of duodenal contents and diffusion of urea from the blood may contribute to the formation of ulcers. Although endoscopic studies have demonstrated gross mucosal injury within hours of the stressful event in nearly 100 per cent of patients examined, most stress ulcers heal when normal gastric defence mechanisms are restored. However, in a small percentage of patients, stress ulceration may lead to frank gastrointestinal haemorrhage requiring medical and/or surgical intervention. Endoscopic findings in conjunction with the history usually differentiates stress ulcer from other bleeding lesions. Angiography may be used if endoscopy fails to identify the bleeding site. Most episodes of bleeding from stress ulceration resolve on medical management consisting of saline lavage, antacids, and adequate supportive measures. Pharmacoangiography with selective infusion of vasopressin or embolization may be of benefit in selected patients with continued bleeding. Surgery is a last resort and has a predictably high mortality. The operation of choice is controversial, but vagotomy, pyloroplasty and oversewing the ulcers may be a good initial operation. Continued bleeding subsequent to vagotomy and pyloroplasty would require near total gastrectomy. Since results of surgical therapy in established stress ulcer disease are poor, the prevention of bleeding is the most rational approach to the management of this disease. The key to prophylaxis is the maintenance of normal intragastric pH. Antacids appear to be superior to cimetidine in preventing bleeding from stress ulcers, so long as the gastric content is buffered to a pH of 3.5 or greater. In seriously ill patients found in respiratory-surgical intensive care units, hourly titration with antacids is the standard against which other forms of prophylaxis must be rigidly compared.
mesh_terms: D000863:Antacids / Q000627:therapeutic use; D002927:Cimetidine / Q000627:therapeutic use; D004724:Endoscopy; D005743:Gastrectomy; D005744:Gastric Acid / Q000378:metabolism; D005753:Gastric Mucosa / Q000098:blood supply / Q000378:metabolism; D006801:Humans; D006863:Hydrogen-Ion Concentration; D010434:Pepsin A / Q000378:metabolism; D010438:Peptic Ulcer Hemorrhage / Q000188:drug therapy / Q000601:surgery; D012039:Regional Blood Flow; D013276:Stomach Ulcer / Q000175:diagnosis / Q000209:etiology* / Q000628:therapy; D013315:Stress, Psychological / Q000150:complications*; D014667:Vasopressins / Q000627:therapeutic use
chemical_list: D000863:Antacids; D014667:Vasopressins; D002927:Cimetidine; D010434:Pepsin A