Editorial
Copyright ©2010 Baishideng. All rights reserved.
World J Gastroenterol. Jul 14, 2010; 16(26): 3219-3225
Published online Jul 14, 2010. doi: 10.3748/wjg.v16.i26.3219
Black esophagus: Acute esophageal necrosis syndrome
Grigoriy E Gurvits
Grigoriy E Gurvits, Department of Gastroenterology, St. Vincent’s Medical Center/New York Medical College, 170 West 12th Street, New York, NY 10011, United States
Author contributions: Gurvits GE is the sole contributor to this work.
Correspondence to: Grigoriy E Gurvits, MD, Department of Gastroenterology, St. Vincent’s Medical Center/New York Medical College, 170 West 12th Street, New York, NY 10011, United States. dr.gurvits@hotmail.com
Telephone: +1-212-6048325 Fax: +1-212-6048446
Received: March 15, 2010
Revised: April 2, 2010
Accepted: April 9, 2010
Published online: July 14, 2010
Abstract

Acute esophageal necrosis (AEN), commonly referred to as “black esophagus”, is a rare clinical entity arising from a combination of ischemic insult seen in hemodynamic compromise and low-flow states, corrosive injury from gastric contents in the setting of esophago-gastroparesis and gastric outlet obstruction, and decreased function of mucosal barrier systems and reparative mechanisms present in malnourished and debilitated physical states. AEN may arise in the setting of multiorgan dysfunction, hypoperfusion, vasculopathy, sepsis, diabetic ketoacidosis, alcohol intoxication, gastric volvulus, traumatic transection of the thoracic aorta, thromboembolic phenomena, and malignancy. Clinical presentation is remarkable for upper gastrointestinal bleeding. Notable symptoms may include epigastric/abdominal pain, vomiting, dysphagia, fever, nausea, and syncope. Associated laboratory findings may reflect anemia and leukocytosis. The hallmark of this syndrome is the development of diffuse circumferential black mucosal discoloration in the distal esophagus that may extend proximally to involve variable length of the organ. Classic “black esophagus” abruptly stops at the gastroesophageal junction. Biopsy is recommended but not required for the diagnosis. Histologically, necrotic debris, absence of viable squamous epithelium, and necrosis of esophageal mucosa, with possible involvement of submucosa and muscularis propria, are present. Classification of the disease spectrum is best described by a staging system. Treatment is directed at correcting coexisting clinical conditions, restoring hemodynamic stability, nil-per-os restriction, supportive red blood cell transfusion, and intravenous acid suppression with proton pump inhibitors. Complications include perforation with mediastinal infection/abscess, esophageal stricture and stenosis, superinfection, and death. A high mortality of 32% seen in the setting of AEN syndrome is usually related to the underlying medical co-morbidities and diseases.

Keywords: Acute esophageal necrosis; Black esophagus; Acute necrotizing esophagitis; Ischemia; Endoscopy; Gastrointestinal hemorrhage