Abstract

INTRODUCTION: Acute Esophageal Necrosis (AEN), also known as Black Esophagus or Gurvit’s syndrome, is a rare disorder that can present as an acute gastrointestinal (GI) bleed. Given the high risk of perforation and mortality, a GI bleed in the correct clinical context should put AEN on the differential. We discuss clinical, endoscopic and management of AEN. CASE DESCRIPTION/METHODS: 57-year-old female with hypertension and gastroesophageal reflux disease presented after a pre-syncopal event. She was admitted for septic shock secondary to urinary tract infection. She was hypothermic with a blood pressure of 76/48 mm Hg on arrival to the ICU. She was started on broad spectrum antimicrobials, in addition to, norepinephrine and vasopressin to maintain mean atrial pressures above 60 mmHg. On ICU day two, she had multiple episodes of coffee-ground emesis and was intubated for airway protection. Her hemoglobin acutely dropped from 8 g/dl to 6.8 g/dl over 12 hours. EGD revealed circumferential ulceration of the lower esophagus with areas of necrosis. Patient was started on high-dose intravenous proton pump inhibitor and supportive therapy with treatment of septic shock. Three days later an endoscopic nasojejunal tube was placed for enteral feeding which revealed increasing amounts of viable mucosa with a decrease in the area of necrosis. There were no further GI bleed and patient was discharged 30 days later. DISCUSSION: AEN is multifactorial with a combination of an ischemic insult, corrosive injury to the mucosa from gastric contents and impaired reparative mechanism in setting of acute illness. Risk factors include male sex, older age and multiple chronic medical conditions. Men are four times more commonly affected than women. Diagnosis is made via direct visualization with findings of circumferential black discoloration of the distal esophagus that abruptly ends at the gastroesophageal junction. With comparatively less dense vasculature, the distal esophagus is the water-shed area of the esophagus. Treatment of AEN focuses on aggressive treatment of underlying disease, supportive therapy, and acid suppression. Complications of AEN include esophageal perforation, mediastinitis, and abscess formation. Long term complications include stricture formation and stenosis. Insertion of nasogastric tube should be avoided given the high risk of perforation secondary to the friability of the esophageal mucosa. In our patient, endoscopically placed nasojejunal tube was a safer alternative to restoring enteral feeding.

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