Korean J Leg Med.  2014 Feb;38(1):30-33. 10.7580/kjlm.2014.38.1.30.

Acute Necrotizing Esophagitis: An Autopsy Case Report and Literature Review

• Choi M
• Jung GU
• Shim YT
• Koo HN
• Choi BH
• Chung NE
• Choi YS
• Kim YS

• KMID: 2305462
• DOI: http://doi.org/10.7580/kjlm.2014.38.1.30

Abstract

Acute necrotizing esophagitis (AEN), also called "black esophagus," is a rare disorder with an unknown pathogenesis. Endoscopic findings generally show black pigmentation throughout the esophagus. This case also offered rare views of the gross anatomy of this disorder. Histological examination revealed that the mucosal and submucosal layers of the esophagus were involved in the severe necrotizing inflammation. The chief manifestation of this disease is hematemesis from hemorrhage of the upper gastrointestinal tract with a typically multifactorial etiology. AEN is also characterized by a clear boundary at the gastroesophageal junction where the necrosis stops. In this study, we report an autopsy case of a 61-year-old man with necrotizing inflammation throughout the esophagus and esophageal necrosis from the laryngopharynx to the gastroesophageal junction. The patient was a disabled person with a history of alcohol abuse who was also diagnosed with mild coronary arteriosclerosis and fatty liver on the basis of the underlying diseases. In this case, the main etiology for poor perfusion from the distal esophageal area was likely underlying illness, history of alcoholism, and malnutrition.

Keyword

Acute esophageal necrosis; Black esophagus; Hematemesis; Autopsy

MeSH Terms

Alcoholism
Autopsy*
Coronary Artery Disease
Disabled Persons
Esophagitis*
Esophagogastric Junction
Esophagus
Fatty Liver
Hematemesis
Hemorrhage
Humans
Hypopharynx
Inflammation
Malnutrition
Middle Aged
Necrosis
Perfusion
Pigmentation
Upper Gastrointestinal Tract

Figure

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  Fig. 1. The scene investigation showing that the floor around the deceased was soaked with coagulated blood and various writhing traces were made on it.

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  Fig. 2. Gross view of necrotizing inflammation of lower esophagus. The black esophagus was terminated at the esophagogastric junction, abruptly. The suspected erosive lesion on decomposed gastric mucosa is also observed.

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  Fig. 3. Gross view of necrotizing inflammation of upper esophagus shows a clear demarcating line of black esophagus emerging under the laryngopharynx.

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  Fig. 4. Microscopic finding of the esophagus reveals transmural acute and chronic inflammatory cell infiltrates with extensive denudation, necrosis and necrotic debris of the mucosa (H&E, × 100).

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