The two-hit hypothesis in acute esophageal necrosis: black esophagus in severe atherosclerosis and untreated gastroesophageal reflux disease: a case report.

backgroundAcute esophageal necrosis, also known as "black esophagus," is an uncommon but potentially life-threatening condition marked by diffuse circumferential necrosis of the esophageal mucosa. It typically presents with upper gastrointestinal bleeding, such as hematemesis or melena, in 85-90% of reported cases. Acute esophageal necrosis is often multifactorial in etiology and associated with underlying comorbidities including cardiovascular disease and esophageal mucosal injury. Owing to its rarity, atypical presentations of acute esophageal necrosis can delay diagnosis and appropriate management. This case is noteworthy for its nonclassical presentation and its support of the "two-hit" hypothesis for acute esophageal necrosis pathogenesis. CASE PRESENTATION: A 71-year-old African American male with a medical history of coronary artery disease and untreated gastroesophageal reflux disease presented with odynophagia, epigastric discomfort, and nonradiating chest pain. He notably denied hematemesis or melena. Esophagogastroduodenoscopy revealed extensive circumferential black discoloration of the distal esophageal mucosa consistent with necrosis, along with duodenal ulcers. Biopsy findings confirmed the diagnosis of acute esophageal necrosis along with evidence of Candida infection. The patient was treated conservatively with intravenous proton pump inhibitors (esomeprazole), oral fluconazole, and sucralfate. A repeat esophagogastroduodenoscopy performed after several weeks demonstrated complete mucosal healing and resolution of necrosis.

conclusionThis case highlights an atypical, nonbleeding presentation of acute esophageal necrosis and reinforces the importance of maintaining clinical suspicion even in the absence of classic symptoms. It underscores the relevance of the "two-hit" hypothesis, where ischemic insult and impaired mucosal defense act synergistically to cause esophageal necrosis. Timely endoscopic evaluation and early initiation of appropriate therapy led to favorable outcomes in this high-risk patient. Increased awareness of such presentations can aid in earlier diagnosis and reduce the high morbidity and mortality associated with acute esophageal necrosis.