S4244 The Dark Side of Upper Gastrointestinal Bleeding: Acute Esophageal Necrosis in a Patient With Cirrhosis

Introduction: Acute esophageal necrosis is a rare condition characterized by circumferential black discoloration of the distal esophageal mucosa. Diagnosis is made via esophagogastroduodenoscopy (EGD) and treatment involves supportive care. This case highlights acute esophageal necrosis (AEN) in a patient with decompensated cirrhosis. Case Description/Methods: A 64-year-old man with cirrhosis due to alcohol use, esophageal varices, and chronic portal vein thrombosis presented with hematemesis. Physical exam was unremarkable. Lab results showed hemoglobin 11.9 g/dL and platelets 130 K/uL. Computed tomography abdomen/pelvis with intravenous (IV) contrast showed mild ascites and stable varices. EGD showed circumferential black, ulcerated distal esophageal mucosa suggestive of AEN, and 2 non-bleeding duodenal ulcers (Forrest Class III). No specimen were collected. Management included nil-per-os (NPO) status with IV fluids for 4 days followed by clear liquid diet. Patient was also started on sucralfate and ceftriaxone. EGD on day 7 showed significant improvement and the patient was discharged on sucralfate with a follow-up EGD in 2 weeks. Discussion: AEN is rare (0.2% incidence) and typically presents with hematemesis, melena, and anemia. EGD findings show patchy or circumferential pigmentation of the distal esophageal mucosa with a distinct demarcation from the normal mucosa at the gastroesophageal junction. The distal esophagus is prone to ischemic injury due to its watershed blood supply. Biopsy was avoided due to a 5% perforation risk. AEN has a mortality rate of 32% and risk factors include male sex, age >65, cirrhosis, diabetes, hypertension, chronic kidney disease, gastroesophageal reflux disease, gastric/duodenal ulcers, hemodynamic compromise, alcohol intoxication. Cirrhosis contributes to AEN through variceal bleeding, malnutrition, impaired mucosal integrity and ability to heal. Our patient’s risk factors included male sex, duodenal ulcers, cirrhosis, and decreased esophageal blood flow due to chronic portal vein thrombosis. Management is supportive, starting with NPO for 24 hours and transitioning to oral feeds. If not tolerated, total parenteral nutrition is preferred over nasogastric feeding due to perforation risk. IV proton pump inhibitors should be initiated promptly and with clinical improvement patients can be transitioned to sucralfate to aid in mucosal healing. Early diagnosis and treatment improve outcomes, emphasizing the need for a broad differential in cirrhotic patients with upper gastrointestinal bleeding.