Gastric Ischemia: An Under-Recognized Cause of Upper GI Bleeding?

Abstract

A 73-year-old male with coronary artery disease was admitted with progressive dyspnea and multiple episodes of exertional syncope and found to have decompensated heart failure with elevated right heart pressures and moderate pulmonary hypertension by right heart catheterization. Diuresis was initiated. Clinical course was complicated by a persistent hypotension, hemothorax, and bacteremia. Repeat right heart catheterization on hospital day 16 demonstrated normal right heart pressures and mildly elevated pulmonary artery pressures. Sildenafil was started on hospital day 20 to treat pulmonary hypertension. Several hours later, the patient experienced transient syncope with orthostatic hypotension which was attributed to sildenafil. Within 12 hours, the patient had 2 black stools with a decrease in hemoglobin from 11 to 8.8gm/dL, and he was taken for urgent upper endoscopy. This showed a large, confluent area of ulceration with adherent clot and exudate concentrated in the fundus and proximal body with sparing of the antrum. The clinical and endoscopic presentation was consistent with ischemic injury. Repeat upper endoscopy 6 days later re-demonstrated partially healed, confluent ulcerations. Sildenafil was not resumed, and the patient had no further hypotension or gastrointestinal bleeding prior to discharge. Histology revealed no evidence of Helicobacter pylori or malignancy. Gastric ischemia is thought to be uncommon due to the extensive collateral blood supply to the stomach; however, there is reason to think that it is clinically under-recognized. Evaluation of gastric reactance as a measure of tissue ischemia in 100 critically ill adults demonstrated changes consistent with gastric ischemia in 80% of patients irrespective of underlying illness. The clinical syndrome of “stress gastritis” is classically found in the proximal stomach. Several mechanisms have been proposed to explain the greater susceptibility of the fundus and body to ischemic injury. Models of hemorrhagic shock demonstrate increased energy deficits in the fundus and body correlated with increased mucosal ischemic injury; this was potentiated by fasting prior to hemorrhagic insult. Acid exposure and ischemia have an additive effect on the risk of ulcer formation; in the bed bound patient, the fundus will have greater acid exposure due to pooling. Particularly in vasculopaths, gastric ischemia should be considered as a potential cause of upper gastrointestinal bleeding.Figure: Ulcerations in proximal stomach.Figure: Sparing of distal gastric body and antrum.