Acute Esophageal Necrosis Leading to Esophageal Stricture: A Rare Complication of Diabetic Ketoacidosis in a 12-Year-Old Girl
Presentation Number: SAT-762
Date of Presentation: June 15th, 2013
Brenden E Hursh*, Alice J Foster, Angelica Oviedo, Collin Barker and Laura Stewart
British Columbia Children's Hospital, Vancouver, BC, Canada
Background: Acute esophageal necrosis may occur in the setting of an acute illness associated with hypoperfusion. Possible complications include esophageal stricture. We are aware of 10 previous case reports of acute esophageal necrosis associated with diabetic ketoacidosis (DKA), and no cases have been previously reported in children with DKA.
Clinical Case: A 12-year-old girl presented in severe DKA with pH 6.81 (7.35-7.45), blood glucose 36.2 mmol/L (3.3-7), and large urine ketones (normal = no ketones). At presentation, she had altered mental status with concern for cerebral edema, her blood pressure was initially unobtainable, and she was “toxic-appearing”. Additionally, in her initial course she had coffee-ground emesis. Her acute presentation was complicated by influenza A illness with pleural effusion and pneumonia, and she required chest tube placement. After hospital discharge she subsequently went on to develop progressive dysphagia. Her oral intake decreased over the next month, and she had an 8.7 kg weight loss. Evaluation by endoscopy revealed esophageal stricture, and her endoscopic and histologic findings were consistent with recent necrosis. Despite multiple esophageal dilation procedures she continues to have a severe stricture of her distal esophagus. She has ongoing difficulty tolerating oral intake of solids and liquids, and she has suffered significant morbidity as a result of this rare complication of DKA.
Clinical Lessons: This is the first reported case of esophageal stricture developing in a child with DKA. The initial endoscopic appearance is a circumferentially black-appearing and friable esophageal mucosa, and this gives way to thick white exudate with underlying friable pink mucosa. Suggested etiologies include the relative watershed area of the distal esophagus, the low pH of gastroesophageal reflux further decreasing mucosal blood flow, and the decreased function of mucosal barrier systems that is seen in malnourished states. Severe complications can include stricture formation or perforation. We will present a literature review of acute esophageal necrosis, describing the management and prognosis of this rare condition. We will also discuss this patient's difficult course, and her ongoing management with regards to esophageal stricture, nutrition, and insulin management. Endocrinologists should be aware of this possible complication of DKA because early recognition could improve the clinical course.
Nothing to Disclose: BEH, AJF, AO, CB, LS