Research Article: Acute Esophageal Necrosis in a Patient With Prostate Cancer Postchemotherapy

Date Published: April 07, 2020

Publisher: Wolters Kluwer

Author(s): Eric Grisham, Suha Abu Khalaf, Vanessa Kuwajima.


Acute esophageal necrosis (AEN) describes a potentially irreversible injury to esophageal mucosa secondary to vascular hypoperfusion. An 84-year-old man was admitted for the correction of a displaced nephrostomy tube and management of acute kidney injury. During his stay, the patient developed odynophagia and acute gastrointestinal hemorrhage. Despite mild initial symptoms, diffuse circumferential black esophageal mucosa was visualized on endoscopy, and a diagnosis of AEN was made. This unique case highlights the association between AEN and leukopenia, vascular disease, hypercoagulability, and infection. Presentations such as this patient should prompt the physicians’ consideration of this differential earlier.

Partial Text

Acute esophageal necrosis (AEN), also known as black esophagus or Gurvits syndrome, is a rare, multifactorial injury to the esophageal mucosa, which carries a high mortality rate. AEN typically occurs in men and has an estimated prevalence overall of 0.001%–0.28% reported in various studies.1,2 The most well-supported theory explaining the pathophysiology of AEN describes a “two-hit” hypothesis, consisting of a low-flow vascular event that predisposes the esophageal mucosa and possibly the submucosa to caustic injury secondary to exposure to reflux of acid and pepsin.1 We report a case of AEN in an 84-year-old man with prostate carcinoma whose early symptoms were odynophagia and decreased oral intake.

An 84-year-old man was admitted for the correction of a displaced nephrostomy tube and management of acute kidney injury. His medical history was significant for stage IV prostate carcinoma undergoing chemotherapy with docetaxel, bilateral obstructive hydronephrosis, gastroesophageal reflux disease, peptic ulcer disease, hypertension, hyperlipidemia, and ischemic cardiomyopathy. Initial laboratory test result values included white blood cells (WBCs) 11.62 × 109/L, hemoglobin 9.9 g/dL, hematocrit 31.0%, platelets 88 × 109/L, serum glucose 95 mg/dL; creatinine 4.35 mg/dL (baseline 2.92 mg/dL), potassium 5.4 mmol/L, blood urea nitrogen 76 mg/dL, anion gap 24 mmol/L, and alkaline phosphatase 319 U/L. The day after admission, compression doppler ultrasonography revealed a proximal subacute/chronic deep vein thrombosis, and he was found to have a vesicocutaneous fistula infection on suprapubic ultrasound. The patient received coumadin therapy with a heparin bridge, and meropenem which was deescalated to ciprofloxacin.

AEN, also known as black esophagus or Gurvits syndrome, is believed to be the manifestation of microvascular occlusion of the vessels supplying the esophagus and mucosal injury secondary to regurgitated stomach acid and pepsin. Black esophagus was first described in 1914 by Brekke et al in a patient with tuberculosis and sepsis, but the term “AEN” was not coined until 1990.4,5 The definition of AEN is now characterized by “striking circumferential black appearing friable esophageal mucosa extending from the gastroesophageal junction and involving various length of the organ proximally” on EGD or autopsy.4 AEN involves the distal esophagus in 97% of cases but can extend superiorly to include the proximal esophagus, such as in the case of our patient.1

Author contributions: E. Grisham wrote the manuscript, reviewed the literature and is the article guarantor. SA Khalaf edited the manuscript and reviewed the literature. V. Kuwajima edited the manuscript and approved the final manuscript.




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