S2277 Black Esophagus! A Devastating Sequela of Complete Heart Block

Abstract

Introduction: Acute esophageal necrosis (AEN) or black esophagus is a rare condition arising due to ischemic injury of the esophagus. Usually, it involves the distal portion given its relative hypovascular nature compared to other esophageal segments. Here we highlight a patient found to have hemorrhagic shock secondary to black esophagus after initial presentation for complete heart block. Case Description/Methods: A 75-year-old female presented after a syncopal episode. She was hypotensive on arrival with EKG showing complete heart block. An emergent transvenous pacer was placed given cardiogenic shock with eventual upgrade to permanent pacer. Unfortunately, she decompensated shortly after placement of permanent pacer with new altered mentation. EKG showed an appropriately paced rhythm. Labs revealed sudden anemia with hemoglobin 6.9 g/dL down from 10.1 g/dL. Echocardiogram was negative for pericardial effusion. Pacer site was clean, dry, and intact. Initially, the etiology of her anemia was unclear given lack of overt blood loss. However, the patient began having several bouts of melenic stools with hemodynamic instability requiring vasopressor support. Medication review revealed that the patient had been started on aspirin and clopidogrel the day prior given concerns for acute coronary syndrome. An emergent bedside EGD showed diffuse circumferential panesophageal black mucosa and severely ulcerated stomach and duodenum consistent with ischemic injury. No visible vessel or active bleeding was identified. Unfortunately, the patient continued having melenic stools requiring blood transfusions. However, nuclear medicine bleeding scan could not localize the source of bleed. A goals of care discussion was held with the family who ultimately opted for hospice care. Discussion: Commonly seen as an incidental finding, black esophagus is an exceedingly rare entity with a prevalence of 0.2%. Its pathophysiology is not well understood, but thought to involve a 2-hit sequence where the initial insult predisposes to injury caused by a second insult. In our patient, her initial insult was clearly cardiogenic shock secondary to complete heart block followed by the second insult likely due to the introduction of antiplatelet agents. Unfortunately, treatment is largely supportive and prognosis is poor with mortality rates ranging from 13-35%. As such, clinicians should consider AEN as part of their differential for GI bleed given the potential for devastating consequences.