Blood Brothers: Concurrent Duodenal Ulcer and Acute Esophageal Necrosis Illuminates the Pathogenesis of Black Esophagus

Abstract

Introduction: Acute esophageal necrosis (AEN), also known as black esophagus, is a rare condition that tends to afflict older men with multiple comorbidities. Hypoperfusion is thought to be a key trigger in disease pathogenesis, with resultant heightened susceptibility to mucosal injury. Methods: We present a case of AEN with concurrent duodenal ulcer, which highlights the hypothesized vascular pathogenesis. Results: An 84 year-old man presented with nausea and severe sepsis from Klebsiella bacteremia. Medical history included insulin-dependent diabetes, hypertension, cerebrovascular disease, splenectomy, bladder cancer, and recurrent urinary infections. He developed hematemesis and painless hematochezia with 7-gram hemoglobin drop and 60 mmHg systolic blood pressure decrement. Risk factors for bleeding included occasional ibuprofen use and acute kidney injury. Esophagogastroduodenoscopy revealed circumferential black esophageal mucosa with white exudates extending continuously from 20 cm beyond the incisors to the gastroesophageal junction (Image 1). There was an abrupt transition to normal mucosa entering the stomach (Image 2). A 1.5 cm ulcer with adherent clot resistant to vigorous irrigation was found in the posterior duodenal bulb (Image 3). Esophageal biopsy revealed necrotic tissue with acute inflammation and no fungal organisms. Bleeding persisted despite gastroduodenal artery embolization, requiring 15 units of packed red cells. Bleeding ceased following duodenotomy with ulcer imbrication. The patient had no antecedent esophageal symptoms and did not develop dysphagia or odynophagia in the convalescent period. Following a normal upper GI barium series, he tolerated dietary advancement and was discharged on proton pump inhibitor therapy. Discussion: Duodenal bulb pathology often co-occurs with AEN owing to a common blood supply arising from branches off the celiac axis. As a relative watershed area, the distal esophagus is susceptible to ischemic injury in patients with underlying vasculopathy. We hypothesize that a flow-limiting celiac axis lesion may contribute to this concurrent pathology, and could predispose to recurrence with hypotensive events. In this case, the bleeding duodenal ulcer may have either caused the hypoperfusion or resulted from it. Sepsis preceded the bleeding and is a known co-factor in the development of AEN. Gastric outlet obstruction from bulb edema may promote further esophageal injury, but was not observed in this case.Figure 1Figure 2Figure 3