S4473 Black Esophagus: A Severely Morbid or Benign Finding?

Introduction: Acute esophageal necrosis (AEN), also known as “black esophagus”, is a rare condition defined by circumferential, black-appearing, esophageal mucosa. The etiology is likely multifactorial secondary to ischemia, impaired mucosal barrier systems, and erosive damage. Upper gastrointestinal bleeding is the most common presentation. Most patients with AEN have significant underlying comorbidities which are then compounded by a triggering event such as shock or severe infection. This case demonstrates a patient with common risk factors and presentation but who had no notable triggering event. Case Description/Methods: An 87-year-old man with atrial fibrillation (on apixaban), BPH, chronic obstructive pulmonary disease, alcohol use of up to ½ bottle of wine per night, and hyperlipidemia presented to the emergency department with 1 day of dark colored emesis and urinary retention and 2 weeks of mild intermittent dyspepsia. The patient was not taking NSAIDs, aspirin, clopidogrel, or other anticoagulants. He had no notable gastrointestinal history and no prior endoscopies. An esophagogastroduodenoscopy performed shortly after admission demonstrated severe grade D erosive esophagitis with necrosis noted from 40 cm (beginning exactly at the Z-line which was regular) to 30 cm with subsequent transition to more normal mucosa at 20 cm and a 5 cm hiatal hernia. The overall findings were consistent with severe grade D, necrotic esophagitis. The patient was treated with IV and then oral proton pump inhibitor, alcohol cessation, and supportive care. He remained hospitalized for congestive heart failure that developed later in his admission. A repeat esophagogastroduodenoscopy 2 months after his initial endoscopic evaluation demonstrated an entirely normal esophagus. Discussion: This case presents an unusual instance of AEN in an elderly patient with no identifiable triggering event. While he had common risk factors (atrial fibrillation, alcohol use), the absence of significant hypotension or sepsis at diagnosis challenges the conventional two-hit hypothesis of AEN pathophysiology and suggests that there might be other, less severe pathways leading to esophageal ischemia and necrosis. This case highlights the need for further research to explore potential benign mechanisms of AEN, especially in patients who do not fit the usual clinical profile.