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ROBERT G. MARTINDALE, M.D., PH.D., is Chief, Gastrointestinal Surgery, Department of Surgery, BIW-442, Medical College of Georgia, Augusta, GA 30912 (rmartind{at}mcg.edu).

Purpose. The purpose of this review is to describe the clinical presentation and pathophysiology of stress-related mucosal bleeding and review the strategies to prevent bleeding. Summary. The mortality rate associated with clinically significant stress-related mucosal bleeding is high. Respiratory failure requiring mechanical ventilation for more than 48 hours and coagulopathy are two strong, independent risk factors for bleeding. Splanchnic hypoperfusion is the underlying etiology of stress-related mucosal injury and bleeding. Mucosal damage typically manifests as multiple superficial lesions without perforation, and bleeding often originates in superficial capillaries after the patient is admitted to the intensive care unit. Providing adequate visceral perfusion is vital to preventing bleeding. Gastrointestinal function should be taken into consideration before using enteral nutrition, and enteral nutrition should not be the sole stress ulcer prophylactic therapy. Acid-suppression therapy should be used to raise the intragastric pH above 3.5 because it reduces the incidence of stress-related mucosal bleeding. Proton pump inhibitors are at least as effective, and may be more effective than histamine H2-receptor antagonists in achieving this pH goal and preventing bleeding. Conclusion. The key to reducing mortality from stress-related bleeding in critically ill patients is to prevent mucosal damage. Providing adequate visceral perfusion and acid-suppression therapy can reduce the risk of stress-related mucosal damage and bleeding. Index terms: Critical illness; Gastrointestinal drugs; Gastrointestinal hemorrhage; Mortality; Nutrition; Tolerance

 

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