1 INTRODUCTION
Acute esophageal necrosis (AEN), commonly referred to as “black esophagus” or “acute necrotizing esophagitis”, is a rare cause of upper gastrointestinal bleeding. It was first described in the medical literature in 1990 by Goldenberg et al., and was brought into the spotlight in 2007 by Gurvits et al. (1,2). In endoscopic examinations, the prevalence of AEN is rare and reported to be up to 0.28% (3,4). The precise etiology of the disease remains unknown, but is presumed to be multifactorial with mucosal ischemia, injury by the reflux of gastric chemical contents, and an impaired mucosal barrier associated with debilitated physical states (3,4). It has been reported that patients usually present multiple comorbidities, the most common being diabetes mellitus, followed by hypertension, alcohol abuse, chronic kidney disease, coronary heart disease, dyslipidemia, peripheral artery disease, malignancy, liver cirrhosis, gastroesophageal reflux disease, congestive heart failure, and chronic obstructive pulmonary disease (5). Diabetes mellitus leads to marked microvascular disease that can be an important contributor to the development of esophageal necrosis (3,6-8).
Clinical presentation is remarkable for upper gastrointestinal bleeding, with most patients presenting with hematemesis or melena (3,4). Serious acute complications include perforation and mediastinitis (9). The most common long-term complication is stricture formation, which may occur in up to 10% of cases (3,9). A mortality rate as high as 32% has been reported, likely related to comorbidities (3,4). The mortality rate specific to AEN is approximately 6%, largely due to esophageal perforation (2-4,9). A standard treatment for AEN is not yet established, but most reports have recommended the treatment of coexisting clinical conditions, systemic resuscitation with intravenous fluid therapy, glycemic control, use of aggressive intravenous proton pump inhibitors, and parenteral nutrition (3,4,9).
Here, we report a case of “black esophagus” induced by diabetic ketoacidosis (DKA).