Beaujon O. Davidson, MD; Amy R. Esposito, MD; Andrew S. Korman, MD; Joseph Kim, MD; Mark I. Siegel, MD; Rebecca K. Calabrese, MD; Gabriel S. Levi, MD; David L. Carr-Locke, MD

Disclosures

February 14, 2013

In This Article

"Black Esophagus"

Acute esophageal necrosis, otherwise known as "black esophagus," is a rare condition associated with significant morbidity.[1] The overall mortality of acute esophageal necrosis approaches 32%.[2] Men are 4 times more commonly affected than women, usually in the sixth decade of life.[2]

Esophagogastroduodenoscopy often demonstrates diffuse, circumferential dark-colored or black pigmentation of the distal esophagus, ending sharply at the Z-line of the gastroesophageal junction.[2] Histologic findings may show necrosis of the mucosa, submucosa, deranged muscle fibers, and thrombosed vessels.[3]

Common causes of acute esophageal necrosis include gastric outlet obstruction, malnutrition, cancer, infection, caustic ingestion, ischemia, and any condition causing hypoperfusion and vascular volume depletion.[4,5]Other causes of black esophagus include melanosis or pseudomelanosis, malignant melanoma, coal dust deposition, and acanthosis nigricans.[6,7,8,9,10]

Patients with acute esophageal necrosis classically present with upper gastrointestinal bleeding. The distal one third of the esophagus is typically affected first, given its watershed vascular supply.[11] However, proximal progression of disease is not uncommon.[12]

Treatment is focused on the underlying cause and involves fluid resuscitation when necessary, gastric acid suppression with intravenous proton pump inhibitors, and parenteral nutritional supplementation. The potential complications of acute esophageal necrosis include esophageal stricture or stenosis, perforation, and death.[2]

We present a case of acute esophageal necrosis in a young woman with diabetic ketoacidosis whose early symptoms were only otalgia and sore throat.

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