Introduction: A 30-year-old male with a past medical history of HIV on HAART, type 1 diabetes mellitus, end stage renal disease on chronic hemodialysis and blindness presented with two days of epigastric abdominal pain, nausea and non-bloody, non-bilious vomiting. He also endorsed odynophagia to solids. The patient was admitted to the hospital two other times within the last three months for similar complaints of abdominal pain associated with vomiting and anorexia. His symptoms were always thought to be secondary to underlying diabetic ketoacidosis and they would largely resolve with aggressive intravenous fluids and insulin. On this admission, physical examination was significant for mild epigastric tenderness. CT scan of his abdomen revealed circumferential wall thickening of the distal esophagus compatible with esophagitis. The patient underwent an EGD which showed circumferential, blackening of the distal esophagus consistent with acute esophageal necrosis. Biopsies were obtained, which revealed necro-inflammatory mucosa with multiple fungal forms consistent with Candida species. The patient was treated with intravenous esomeprazole and an oral sucralfate suspension, along with fluconazole given the findings of fungal infection on mucosal biopsy. The patient’s symptoms markedly improved. The patient was discharged home with complete resolution of his presenting symptoms to have close endoscopic follow-up at a later date. Acute esophageal necrosis, or the so-called “black esophagus,” is a rare finding first described in 1990 by Goldenberg et al, with an estimated prevalence reported in one autopsy study to be 0.2%. The exact pathogenesis remains unknown but ischemia is believed to be the main inciting event. Low-flow states such as diabetic ketoacidosis, as seen in our patient, result in hypo-perfusion of the distal esophagus, a region that is more “watershed” and less vascularized than the proximal portions of the esophagus. Treatment is largely supportive with correction of the predisposing event and better control of the underlying medical condition. Complications include esophageal perforation, mediastinitis, stricture formation and death.Figure 1: Blackening of the distal esophagus, which classically stops at the GE junction.