Acute esophageal necrosis complicating diabetic ketoacidosis in a patient with type II diabetes mellitus and excessive cola consumption: a case report

Acute esophageal necrosis (AEN) implicates poor tissue perfusion, functionally defective mucosal barrier, and corrosive injury of the esophageal mucosa, typically characterized by diffuse, circumferential greyish or black discoloration of the esophagus in esophagogastroduodenoscopy. Low-volume states, as diabetic ketoacidosis (DKA), predispose to AEN. Cola drinks diminish the esophageal pH by decreasing the lower esophageal sphincter pressure. We report a 47-year-old male shepherd with chest pain, nausea, odynophagia and gradual decline in level of consciousness, who reported consumption of 6–7 L of cola beverages per day, and was diagnosed with DKA. The patient had a record of type 2 diabetes mellitus and coronary heart disease, and he was administered empagliflozin 25 mg q24 hours, vildagliptin 50 mg bid, metformin 1000 mg bid, and insulin glargine 24 IU q 24. Esophagogastroduodenoscopy was indicative of a diffuse, edematous, and eroded mucosa of grey colour from the upper to the lower esophageal sphincter. CT scan supported the diagnosis, revealing diffuse thickening and edematous imaging of the esophageal wall with an abnormal edge of the mucosa in the lower half of the esophagus. Seven days after rigorous treatment with fluid resuscitation, insulin restoration, esomeprazole, fluconazole, cefoxitine, and metronidazole, the patient was ameliorated. A second endoscopy revealed obvious improvement. Pathophysiology, diagnosis, and treatment of DKA/AEN intertwining are thoroughly discussed. In conclusion, clinicians should not disregard AEN in the differential diagnosis of patients with DKA and clinical symptoms of esophagitis.