Acute esophageal necrosis (AEN), or “black esophagus,” is a rare phenomenon with increasing interest due to its unclear mechanism and multifactorial associated etiologies. It is an endoscopic diagnosis demonstrating proximal mucosal extension of circumferential black friable mucosa from the distal esophagus that spares the gastroesophageal junction. We present the case of a 47-year-old Caucasian male with a medical history of type 2 diabetes mellitus & compensated alcoholic cirrhosis presenting to the emergency department with abdominal pain and intractable nausea with vomiting. The patient was afebrile, hypotensive, and tachycardic, with initial blood tests demonstrating a serum glucose 1062 mg/dL, creatinine 3.12 mg/dL, and a blood gas consistent with a high anion gap acidosis with a venous pH of 7.167. The patient was treated appropriately for diabetic ketoacidosis with normalization of blood sugars, and further examination revealed a small amount of blood in the oropharynx and rectum. He was started on intravenous (IV) octreotide and an IV proton pump inhibitor (PPI). An esophagogastroduodenoscopy (EGD) was performed, which demonstrated moderate to severe circumferential esophagitis noted in the proximal esophagus with uniformly black ulcerations extending to the squamocolumnar junction with clear demarcation of this finding distal to the squamocolumnar line (Figure 1), in addition to multiple duodenal ulcers. The patient was subsequently treated with oral high dose PPI twice daily and discharged in good condition. This case illustrates the importance of including AEN in the vast differential diagnosis of gastrointestinal (GI) bleeding. The prevalence of AEN is around 0.2% and has an associated mortality as high as 36% in studies when patients have a comorbidity. AEN typically affects elderly men who commonly suffer from diabetes mellitus (specifically diabetic ketoacidosis), duodenal ulcers, malignancy, alcohol abuse, and acute renal insufficiency among other comorbidities. In addition, malnutrition can predispose patients to developing AEN due to decreased GI mucosal barrier system repair. Our report aims to explore the natural progression of AEN, potential therapeutic measures, and complications of the disease process.Figure 1