Abstract
Stress ulcers are multiple, superficial erosions of the proximal stomach that develop in the setting of severe physiological stress. Evidence suggests that the mechanism of cytoprotection may be impaired in settings conducive to their development. The two most critical elements in the pathogenesis of the disease are the presence of some luminal acid and some degree of associated mucosal ischemia. The probable endpoint is reduction of intramucosal pH below acceptable physiological limits. In the absence of effective prophylaxis, 30% of patients with stress ulcer disease will develop hemorrhage of life-threatening severity—acute hemorrhagic gastritis—a condition difficult to treat both nonoperatively and operatively. Mortality remains high irrespective of the capacity to control hemorrhage. Prevention is the best treatment. Both H2-receptor antagonists and intragastric titration with antacids have been proposed in prophylaxis. Current evidence suggests that each is equally efficacious for moderately ill patients. However, for the severely ill, antacid titration is superior to cimetidine. A small group of critically ill patients are not effectively treated by either modality. It seems likely that prostaglandins may prove efficacious in this patient population.
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Ritchie, W.P. Prostaglandins. Digest Dis Sci 31 (Suppl 2), 32S–34S (1986). https://doi.org/10.1007/BF01309320
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DOI: https://doi.org/10.1007/BF01309320