Stress-related mucosal damage (SRMD) of the upper gastrointestinal tract is being increasingly recognized in critically ill patients. Its precise pathogenesis is unknown. Acid is a prerequisite for the development of mucosal injury. However, mucosal defense factors that maintain the integrity of the gastric mucosal barrier are equally important. Therapy is directed toward reducing the intraluminal acid concentration. Since histamine H2-receptor antagonists became available in 1977, they have been used for the prevention and treatment of SRMD. They offer the potential for use as an effective parenteral as well as oral agent that could obviate the need for frequent antacid administration and eliminate some of the troublesome side effects that accompany an intensive antacid regimen. Although the beneficial effects of H2 blockers are probably related to their ability to inhibit acid secretion, recent evidence suggests that they may also act by mechanisms independent of their antisecretory effect. Numerous controlled studies have confirmed that cimetidine, being superior to placebo and equivalent to antacids, is effective therapy for SRMD. Sucralfate, a basic aluminum salt of sucrose octasulfate, has been shown to protect animal and human gastric mucosa from a variety of injurious agents. However, few clinical trials have evaluated the efficacy of sucralfate in SRMD. Exogenous prostaglandins also have been shown to protect gastric mucosa from a variety of insults. Although exogenous prostaglandins may work by augmenting mucosal defense mechanisms, most clinical studies have used antisecretory doses of prostaglandin drugs, making it difficult to discount the antisecretory component as being responsible for efficacy.
