Acute oesophageal necrosis (black oesophagus)

Necrosis esofágica aguda (esófago negro)

Ignasi Galtés^1,2, María Ángeles Gallego¹, Raquel Esgueva³ and Carles Martin-Fumadó¹

¹Institut de Medicina Legal de Catalunya. Ciutat de la Justícia. Barcelona, Spain.
²Unitat de Medicina Legal i Forense. Departament de Psiquiatria i de Medicina Legal. Facultat de Medicina. Universitat Autònoma. Barcelona, Spain. ]]> ³Instituto Nacional de Toxicología y Ciencias Forenses Barcelona. Departamento de Anatomía Patológica. Barcelona, Spain

Background

Acute oesophageal necrosis (AEN) is a rare entity characterized by a black aspect in oesophageal mucosa, mainly distal and with a variable extension at the proximal level, terminating abruptly at the gastro-oesophageal junction (1).

Case report

A 54-year-old man was admitted to hospital after being found unconscious in his home. He had a history of alcoholism, multiple drug addictions, and type I diabetes mellitus. At admission, he had hyperglycaemia (550 mg/dL) with glucosuria and ketone bodies in the urine, along with septic shock refractory to bilateral alveolar infiltrates and severe respiratory failure. The patient died 24 hours post admission due to multiple organ failure, with diabetic ketoacidosis decompensated by possible respiratory infection in a patient with polytoxicomania. The autopsy confirmed the presence of acute bilateral bronchopneumonia, chronic pancreatitis, severe hepatic steatosis, and generalized congestive changes. At the oesophagus, AEN was evident (Figs. 1 and 2).

Discussion

The incidence of AEN in endoscopic studies is less than 0.3% and contrasts with the 10.3% described in autopsies. The transitory nature of the causal stimulus and the tendency for rapid healing could explain this discrepancy (2,3). The aetiology is multifactorial, with predisposing factors including male sex, advanced age, malnutrition, alcoholism, cardiovascular diseases, and chronic kidney disease. Hypoperfusion, decreased mucosal defensive barrier, and the presence of gastro-oesophageal reflux have been proposed as physiopathologic mechanisms (4). Diabetic decompensation could be an important factor, particularly ketoacidosis, suggesting a relationship between the degree of proximal damage and of hyperglycaemia (5). The differential diagnosis is made with melanosis, pseudomelanosis, malignant melanoma, acantosis nigricans, charcoal deposits, and caustic poisoning (1). Our case is unusual for the diagnosis and for its extension, despite showing no signs of bleeding. The latter is especially relevant, given the exceptional anatomopathology report on this patient.

Acknowledgements

The authors are grateful to Elaine M. Lilly, PhD, for English language revision of the manuscript.

References

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3. Augusto F, Fernandes V, Cremers MI, et al. Acute necrotizing esophagitis: A large retrospective case series. Endoscopy 2004;36:411-5. DOI: 10.1055/s-2004-814318.         [ Links ]

4. Gurvits GE, Cherian K, Shami MN, et al. Black esophagus: New insights and multicenter international experience in 2014. Dig Dis Sci 2015;60:444-53. DOI: 10.1007/s10620-014-3382-1.         [ Links ]

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