1. The term stress ulcer refers to mucosal damage in the upper gastrointestinal (GI) tract that occurs with extreme physiologic stress.

2. When associated with clinical bleeding or perforation, the condition is called stress ulcer syndrome (SUS).

1. Stress ulcers occur predominantly in the fundus and body of the stomach.

2. Duodenal ulcers are uncommon in SUS, but when seen, are usually in conjunction with proximal gastric lesions.

3. Bleeding from SUS typically occurs within 2 weeks of intensive care unit (ICU) admission and usually presents as hematemesis, gross blood from a nasogastric tube, or melena.

1. As many as 52% to 100% of patients admitted to ICUs have endoscopic evidence of gastric mucosal damage within the first day of ICU admission, but most are asymptomatic.

2. Overt GI bleeding is estimated to occur in 1.5% to 8% of ICU patients.

1. Mortality rates can be as high as 50% to 80% in patients who bleed, although death is usually attributed to the underlying disease.

2. Stress ulcer bleeding may serve as a marker for severely ill patients.

A. Patients in ICU with coagulopathy or requiring mechanical ventilation for >48 hours are statistically more likely to develop SUS.

B. Shock, hypotension, sepsis, and major burns (>35% body surface area) are more common in patients with SUS.

C. Patients with acute intracranial head trauma and coma (Curling and Cushing ulcers, respectively) are also at increased risk of having stress ulcers.

1. Although gastric acid is essential for stress ulceration, the following impairments of mucosal defense mechanisms are also required:

a. Disruption of the bicarbonate-rich mucus layer lining the stomach by refluxed upper intestinal contents including bile salts.

b. Failure of mucosal cell reorganization, which normally helps to cover denuded mucosa.

2. Stress results in splanchnic vasoconstriction leading to gastric mucosal ischemia, which ultimately leads to both a decrease in synthesis of mucus, and a drop in intramucosal pH from a deficit of systemic bicarbonate that normally buffers back diffusion of hydrogen ions.

3. Subsequent reperfusion contributes to injury from hyperemia and an enhanced inflammatory response while decreasing the synthesis of cytoprotective prostaglandins.

1. Stress ulcers come to clinical attention when they bleed.

2. Significant stress ulcer bleeding occurs in 2% to 6% of critically ill patients and presents within 14 days of the onset of physiologic stress or ICU admission as hematemesis, gross blood from the nasogastric tube, or melena.

3. Patients with thermal injury from burns or with an acute intracranial disease, including head trauma and coma, appear to be at increased risk (Curling ulcers and Cushing ulcers).

4. Abdominal pain is unusual except in the infrequent setting of perforation.

1. The earliest mucosal changes are found in the most proximal part of the stomach and include pallor, mottling, and submucosal petechiae.

2. Superficial linear erosions and ulcers are formed when these lesions coalesce.

3. Eventually, diffuse mucosal damage may result, with bleeding and rarely, perforation.

1. The risk of bleeding and overall prognosis are related to the severity of the underlying illness, aggressive management of which should always take precedence. Maintaining adequate hemodynamic support is key in prevention of SUS.

1. Antisecretory drugs.

a. Histamine-2-receptor antagonists.

i. Administered by intermittent intravenous (IV) bolus or, preferably, continuous infusion, which is better at maintaining the desired gastric pH levels.

ii. Patients with a creatinine clearance of <30 mL/minute should receive half the recommended dose, and caution should be exercised in patients with thrombocytopenia.

iii. Reduces the incidence of clinically important bleeding without increasing the risk for ventilator-associated pneumonia.

iv.

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