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).