Alcohol Induced Ischemic Gastric Necrosis

Purpose: Ischemic gastric necrosis (IGN) is a rare clinical entity with an unknown incidence. Etiologies include atherosclerosis, embolism, infection, corrosive burns, and idiopathic. Most reported cases have had advanced necrosis and required surgical treatment. Methods: We report a case of epigastric pain and upper GI bleeding caused by IGN due to alcohol ingestion which was managed conservatively. Results: A 43 year old male with a past medical history of AIDS, hypertension, and chronic alcohol abuse presents to the emergency department with epigastric pain and hematemesis for 1 day. The patient admitted to drinking 10 beers and a 1/3 pint of vodka the previous day. He denied use of any illicit substances or medications for 3 weeks. He had a heart rate of 122, however his blood pressure remained stable. Abdominal examination revealed epigastric tenderness to light and deep palpation, however no rebound or guarding. Laboratory evaluation noted normal basic chemistry, amylase, lipase, coagulation and hepatic panels. The hemoglobin was 9.0 g/dL, platelet count was 53,000 and white blood cell count was 1,900. The patient was started on pantoprazole and octreotide intravenous drips and emergent upper esophagogastroduodenoscopy (EGD) was done. EGD found candida esophagitis and a small Mallory-Weiss tear. Biopsies were obtained from the stomach as the mucosa was noted to be diffusely edematous, erythematous, and friable. Post procedure the patient was placed on IV fluconazole and continued on the pantoprazole drip. Serial blood counts showed a drop in the hemoglobin. Four units of packed red blood cells were transfused with an appropriate response in hemoglobin and vital signs. The patient was started on a clear liquid diet the following day. There were no further episodes of hematemesis and no further transfusions were required. Repeat EGD was done 72 hours after admission noted decreased gastric edema and friability. Pantoprazole drip was changed to twice a day oral dosing and the diet was advanced. Pathology showed ischemic mucosal necrosis of the stomach. There were no viral inclusion bodies, H. pylori or vasculitis noted. The patient was subsequently discharged with planned follow up. Conclusion: IGN has been scarcely reported in the literature. To our knowledge, this is the first reported case of alcohol induced IGN. EGD and biopsy confirmation are important to help guide therapy. Treatment should include acid suppression with proton pump inhibitor, aggressive hydration and blood transfusion to prevent further ischemia and necrosis. Repeat EGD is warranted to evaluate the severity and response to conservative treatment, and to determine the need for surgical intervention.