Introduction: Acute esophageal necrosis, or “black esophagus,” is an extremely rare clinical entity, occurring in 0.01-0.28% of endoscopic cases. It can be caused by several medical conditions, and it is thought to arise from a combination of impaired mucosal barrier and chemical and ischemic insults to the esophagus. Acute esophageal necrosis usually presents with severe complications due to delayed diagnosis. We present a case of acute esophageal necrosis triggered by severe metabolic ketoacidosis in a diabetic patient. Description: A 60-year-old male patient with benign prostatic hyperplasia, diabetes, hypertension, hyperlipidemia, presented to emergency department due to altered mental status, malaise, shortness of breath and multiple episodes of vomiting. Laboratory tests revealed severe high anion gap metabolic acidosis (pH 6.9, bicarbonate 36), elevated lactate, positive ketones in the blood and hyperglycemia > 500.Diabetic ketoacidosis was diagnosed and treated per guidelines with significant improvement. Initial CT abdomen revealed air-distended, thickened thoracic esophagus; patient was started on IV proton pump inhibitors for possible esophagitis. Seven days after admission, he had hematemesis with retrosternal chest pain, hypotension, tachycardia, and a hemoglobin drop from 7.4 to 6.7 g/dL, requiring a blood transfusion. Gastroenterology was consulted, and the patient was placed on nothing per oral and intravenous fluids. Esophagogastroduodenoscopy was done and noted diffuse mucosal changes characterized by discoloration, sloughing and ulceration in the middle and lower third of the esophagus suggestive of acute esophageal necrosis. Patient treated with IV pantoprazole, sucralfate, lidocaine swish/swallow, metoclopramide and after 24 hours NPO, a clear liquid diet was started, leading to significant improvement in symptoms. Discussion: Acute esophageal necrosis (AEN) associated with diabetic ketoacidosis (DKA) remains an exceedingly rare clinical entity. It is critical to recognize AEN as it is associated with a mortality of 32%. Because AEN shares many symptoms with DKA, maintaining a high clinical suspicion and carefully evaluating patients in the appropriate context can help prevent serious complications and reduce mortality.
QINAMI et al. (Sun,) studied this question.