INTRODUCTION: Acute esophageal necrosis, a very rare cause of upper GI bleeding, is seen mainly in elderly men. We report a new case in an elderly woman. CASE DESCRIPTION/METHODS: A 90-year-old woman with a history of DM, HTN, and CHF presented with SOB and abdominal pain of 2-day duration. She didn’t vomit. Confusion, pallor, and large melanotic bowel movement were noted. Temperature was 36.1°C, BP 86/68 mmHg, HR 104 bpm, and RR 22 br/min. She had bilateral shallow coarse breath sounds and otherwise unremarkable abdominal and neurological exams. Urine ketones was negative, plasma glucose 98 mg/dL, WBC 40.8 K/mcL, hemoglobin 9.3 g/dL, platelet 437 K/mcL, GFR 18 mL/min/1.73 m2, lactate 15.5 mmol/L, and procalcitonin 1.49 ng/mL. Blood culture was negative. Chest CT showed small bilateral pleural effusions and ground glass opacities. Abdominal CT showed fecal impaction. Working diagnoses included septic/hypovolemic shock, pneumonia, encephalopathy, acute upper GI bleed, and acute hypoxic respiratory failure. Volume resuscitation, vasopressors (norepinephrine, phenylephrine, and vasopressin), mechanical ventilation, broad spectrum antibiotics (vancomycin, cefepime, and azithromycin), total parenteral nutrition, and proton pump inhibitor were started. EGD revealed friable, black, circumferential esophageal mucosal changes starting 25-30 cm from incisors and extending to GE junction without gastric outlet obstruction (Figure 1). Follow up EGD one week later showed slow healing with black and thin tissue, starting 4 cm proximal to GE junction without stricture (Figure 2). She continued to be encephalopathic, requiring mechanical ventilation and vasopressor support. She died upon intensive care withdrawal at family request. DISCUSSION: Our patient had endoscopic diagnosis of acute ischemic esophagitis, which was likely due to compromised esophageal perfusion secondary to septic/hypovolemic shock in the setting of chronic vascular compromise. Biopsy to differentiate ischemic esophageal necrosis from other etiologies, such as infection and malignancy, carries a high risk for perforation and was not performed. As seen in our patient, acute esophageal necrosis typically affects the relatively hypovascular distal esophagus down to GE junction and quickly resolves when blood flow is restored. Nevertheless, mortality remains high due to the underlying conditions. Unlike our case, acute esophageal necrosis affects mainly men, with a men/women ratio of 4/1.