Muhammad Sajeel Anwar, MD1, Umer Farooq, MD2, Anaba Ali Jajja, MBBS3, Ans Ahmad Jajja, MBBS4; 1United Health Services Hospitals, Binghamton, NY; 2Loyola Medicine/MacNeal Hospital, Berwyn, IL; 3University of Health Sciences, Vestal, NY; 4University of Health Sciences, Bahawalpur, Punjab, Pakistan
Introduction: Black discoloration of esophageal mucosa is termed as acute esophageal necrosis (AEN) and has a mortality as high as 35%. Predisposing factors are caustic ingestion, aortic dissection, prolonged vomiting following binge drinking, diabetic ketoacidosis (DKA), infections, and gastric outlet obstruction. AEN in the absence of caustic ingestion is a rare entity with a prevalence of 0.2%. We describe a case of AEN postulated to be due to multifactorial etiologies.
Methods: A 47-year-old woman with a past medical history of poorly controlled type 2 diabetes mellitus presented with nausea, vomiting, diarrhea, and altered mental status. She was afebrile and had sinus tachycardia (118 bpm). Initial evaluation revealed a WBC count of 17 K/UL, blood glucose 1001 mg/dL, and an anion gap metabolic acidosis with elevated beta-hydroxybutyrate. She was treated with insulin drip, fluids, and electrolyte replacement for diabetic ketoacidosis (DKA). During hospitalization, she reported chest discomfort on swallowing and melanotic stools resulting in hemoglobin (HGB) drop to 7.5 mg/dL. She received a unit of RBCs, and endoscopy revealed circumferential dark brownish to gray discoloration of the entire esophagus with hemorrhagic spots (Figure 1). Biopsy of the esophageal segment revealed no intact mucosa, abundant necroinflammatory debris, and scant denuded stromal tissue (Figure 2). Viral or cytopathological changes were absent. Her dysphagia, tachycardia, and leukocytosis resolved with a rise in HGB to 8.5 mg/dL upon supportive management, including PPIs, esophageal cytoprotection with sucralfate, and bowel rest with Nil Per Os. Later, the diet was advanced as tolerated, and she was discharged on PPIs and sucralfate with instructions to undergo a follow-up endoscopy in 8 weeks. Discussion: Pathogenesis of AEN involve ischemia and chemical injury, and low flow states render patients at high risk. Our patient remained hemodynamically stable during the entire hospital stay, and the AEN was attributed to DKA, binge drinking, and protracted emesis. Commonly it presents with upper gastrointestinal bleeding, which prompts upper endoscopy leading to the diagnosis. The diagnosis can become challenging if symptoms are nonspecific (swallowing discomfort), or the blood loss through the GI tract is more subtle, signifying that AEN should not be overlooked in patients at risk. A high index of suspicion and early endoscopy, as in our case, helps prevent morbidity and high mortality from this disease process.
Upper endoscopic image of acute esophageal necrosis.
Biopsy results of acute esophageal necrosis.
Disclosures: Muhammad Sajeel Anwar indicated no relevant financial relationships. Umer Farooq indicated no relevant financial relationships. Anaba Ali Jajja indicated no relevant financial relationships. Ans Ahmad Jajja indicated no relevant financial relationships.