Abstract
Stress ulceration, a disease associated with the stress of severe injury, sepsis, and organ failure, has declined in frequency during the last decade. Factors contributing to this decrease include more rapid transport of trauma patients, early resuscitation, avoidance and treatment of complications, and prophylactic maintenance of increased gastric mucosal pH. The pathophysiology of these lesions remains to be elucidated completely; however, both aggressive factors (acid, duodenal reflux, etc.) and a deficiency in defensive mechanisms (gastric mucosal blood flow, gastric mucosal barrier, mucus, bicarbonate, etc.) play a role in their inception. The hemorrhagic complication of stress ulcer, which is usually seen between the fifth and tenth days after admission, remains a sequela associated with a significant rate of mortality.