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Management of stress ulcers

David W Mercer, MD
Matthew R Goede, MD
Section Editor
David I Soybel, MD
Deputy Editor
Wenliang Chen, MD, PhD


Stress ulcers were once a major cause of morbidity and mortality in critically ill patients. However, with the advent of ulcer prophylaxis and improved critical care, surgical intervention is only necessary for a small number of patients with life threatening hemorrhage or perforation from stress ulcers [1].

The nonsurgical management, indications for surgery, and surgical management of patients with stress ulcers are reviewed here. The epidemiology, pathogenesis, clinical manifestations, and prophylaxis of stress ulcers, as well as the nonsurgical treatments of upper gastrointestinal bleeding are discussed elsewhere. (See "Stress ulcer prophylaxis in the intensive care unit" and "Approach to acute upper gastrointestinal bleeding in adults".)

The surgical treatment of peptic ulcer disease (not stress ulcer disease) is presented separately. (See "Surgical management of peptic ulcer disease".)


Stress gastritis may be referred to as diffuse mucosal injury, stress-related mucosal disease, stress ulceration, hemorrhagic gastritis, erosive gastritis, Curling’s ulcer, and Cushing’s ulcer. Stress-related erosive syndrome was first described in 1971 [2]. A commonality to all is the presence of multiple superficial erosions of the gastric mucosa, beginning in the proximal acid-secreting portion of the stomach and progressing distally. Cushing’s ulcers develop following central nervous system injury. Morphologically, Cushing’s ulcers tend to be single and deep and may involve the esophagus, stomach, or duodenum [3]. Curling’s ulcers occur following burns involving greater than 30 percent total body surface area. Curling’s ulcers can occur in the stomach or duodenum [4]. Stress gastritis erosions occur after physical trauma, shock, hemorrhage, and sepsis. Thus, stress gastritis represents end-organ failure of the stomach in critical illness.

Stress gastritis erosions can be identified within hours following injury and occur nearly universally (in the absence of prophylaxis) following severe shock [5]. These erosions appear as wedge-shaped mucosal hemorrhages with necrosis of the superficial mucosal cells. If these erosions continue to progress and extend into the submucosa, significant and life-threatening bleeding may arise. The pathogenesis of stress gastritis is presented elsewhere. (See "Stress ulcer prophylaxis in the intensive care unit", section on 'Pathophysiology'.)


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Literature review current through: Sep 2016. | This topic last updated: Sep 1, 2015.
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