An Under-Appreciated Manifestation of Sepsis and Diabetic Ketoacidosis, the Black Esophagus: A Case Series

Abstract

Incidence of diabetic ketoacidosis (DKA) has been rising within the United States and we are observing increasing rates of complications. We identified three patients in the intensive care unit who presented in DKA with shock and were found to have upper gastroenterologic bleeding (UGIB) from acute esophageal necrosis (AEN). Case 1: A 47-year-old male with a medical history of diabetes and alcoholic cirrhosis presented with delirium and abdominal pain. The patient had hypotension and tachycardia without fever. Serum glucose was 1062 mg/dL and beta-hydoxybutyrate > 9. Exam revealed blood in the oral cavity and rectum, an irregularly irregular heart rate, and encephalopathy. Esophagogastroduodenoscopy (EGD) revealed uniform black mucosa extending from the incisors to the squamocolumnar junction with clear demarcation distal to the squamocolumnar line and circumferential esophagitis in the proximal esophagus. Case 2: A 54-year-old male with a medical history of insulin-dependent diabetes and ischemic cardiomyopathy presented with encephalopathy. The patient had hypotension and tachycardia without fever. Serum glucose was 359 mg/dL and beta-hydroxybutryate > 9. Exam revealed encephalopathy, a regular heart rate, and dried blood in his oral cavity. During DKA treatment he developed melena with a peripheral blood hemoglobin of 9.3 g/dL. EGD revealed black mucosa extending from the mid esophagus to the distal esophagus while sparing the GE junction. Biopsies obtained revealed acute fibrinopurulent exudate with fragments of gray gastric epithelium. Case 3: A 34-year-old male with a medical history of diabetes complicated by neuropathy, gastroparesis, & recurrent esophageal candidiasis presented with encephalopathy and melena. He had hypothermia, hypotension, and tachycardia. Serum glucose was 428 mg/dL and beta-hydroxybutyrate 0.7. EGD revealed sloughing black distal esophagus extending proximally from the GE junction. Biopsy revealed acute inflammatory exudates with necrotic cells and numerous fungal hyphae. The etiology of AEN in DKA is multifactorial. DKA causes transient non-obstructive gastropathy leading to increased reflux into the esophagus and mucosal damage. DKA patients typically have poor nutritional status, which impairs mucosal repair. Diabetics have compromised vasculature and DKA precipitates a prolonged hypotensive state allowing for increased end-organ ischemia. All three cases improved with resuscitation and proton pump inhibitor therapy.FigureFigure