She denied any other abdominal, respiratory or urinary symptoms and the ingestion of non-steroidal anti-inflammatory drugs or MEK inhibitor corticosteroids and recent hospitalization

or surgery. The patient had a chronic history of atrial fibrillation treated with amiodarone (200 mg qd). She also took omeprazole (20 mg qd) on regular basis. She presented normal vital signs, level of consciousness and no fever. Cardio-pulmonary auscultation was normal, except for the presence of arritmic heart sounds. The abdomen was distended and tender especially at the upper quadrants with decreased bowel sounds. Rectal examination excluded melena, but the nasogastric aspiration returned a hematic gastric content. Blood tests showed leukocytosis, Hb 11.9 g/dL, and a CRP of 46 mg/L. Coagulation, platelet count, liver function tests, renal function Dinaciclib and electrolytes were all within normal range. Plain abdominal film excluded perforation. An upper endoscopy revealed an ulcerated hiatal hernia with congestion, ulceration, and areas of apparent necrosis involving the distal esophagus, the gastric fundus (Fig. 1) and the proximal gastric body (Fig. 2), with no active bleeding. These aspects were compatible with acute ischemic gastropathy. A computed tomography scan (CT) showed a normal aorta,

celiac trunk and superior mesenteric artery. The CT also revealed gastric distension and gastric wall thickening with parietal pneumatosis and gas within the portal vein. She was admitted to the Gastrenterology ward and was started on i.v. antibiotics, after organic fluids were collected

for culture. At day one at the ward, she presented with fever and elevated CRP of 155.9 mg/L, without an apparent focus of infection. The remainder days she showed clinical and laboratory improvement. The urine culture identified an Escherichia coli infection. Blood cultures revealed Edoxaban no bacterial growth. She was transfused with a total of 2 units of packed red blood cells. Samples obtained for histological evaluation were consistent with ischemia (Fig. 3). Gastric necrosis is extremely uncommon as the blood supply of the stomach protects it from ischemia. Most frequently, it develops as consequence of acute gastric dilatation1 but can also occur after gastric surgery or therapeutic embolization.2 Mechanical factors can be implied in gastric dilatation and ischemia and infectious causes have been reported, generally involving immunocompromised patients (diabetes, neoplasia)3 and sepsis, as in the case described. Necrosis might be partial (mostly in the lesser curve due to vascular supply) or involving the full organ.3 Emesis, abdominal pain and distension are common and initially mild, but rapid evolution to shock may occur.1 and 3 Plain abdominal films and CT are useful but endoscopy remains the gold tool for prompt diagnosis.2 A delayed diagnosis can be fatal.