A Case of Euglycemic DKA With SGLT 2 Inhibitor Use- A Diagnostic and Therapeutic Dilemma

Abstract

Background: The increasing use of SGLT-2 inhibitors driven by the apparent renal and cardiovascular benefits has been associated with increased incidence of euglycemic diabetic ketoacidosis (DKA), we present a case of euglycemic DKA following bariatric surgery in a patient on SGLT-2 inhibitors. Case: 32 year old female with history of diabetes mellitus, obesity, hypertension, and triglyceride induced pancreatitis was admitted for an elective gastric sleeve procedure. She was diagnosed with type 2 diabetes after birth of her first child. Prior to the surgery she was treated with metformin 1000 mg twice daily, Empagliflozin 25 mg once daily, Tresiba 46 units and Humalog 12–15 units with each meal. She was placed on a strict calorie restricted diet leading up to the surgery. Empagliflozin and metformin were held 1 day prior to the surgery, insulin was decreased. Patient’s laparoscopic surgery was complicated by bleeding and hypotension and had to be converted to open surgery. Post operatively labs showed metabolic acidosis with bicarbonate level of 13 mmol/l (22–33), anion gap of 22 (7–17) and arterial pH of 7.29. Serum glucose of 223 mg/dl (65- 99), AST 541 u/l (10–50) ALT 580 u/l (10–50), beta hydroxy butyrate 5.89 mmol/l (< 0.28), serum osmolality 305. Urinalysis showed a glucose of 500 mg /dl with the presence of large ketones. She was started on an insulin infusion and transferred to the ICU for close monitoring and management of euglycemic DKA. She was eventually transitioned to a basal bolus regimen of insulin at discharge with discontinuation of SGLT - 2 inhibitor therapy. Later, it was revealed that the patient had history of EDKA while on SGLT2 inhibitors, which was not reported to her new endocrinologist and hence she was re-initiated on them a year ago. Discussion: Euglycemic DKA [EDKA] in the setting of SGLT- 2 inhibitor use has been associated with Type I diabetes with an incidence of 9.4 % whereas in type II at a rate of 0.2 %. In type 2 diabetics, it is more common in patients with beta cell insufficiency and may predict risk of developing type 1 diabetics which is likely the case in our patient. SGLT2 inhibitors act by promoting glucosuria, which in turn promotes sodium and ketone body reabsorption and increased ketone body production because of increased glucagon to insulin ratio. (1) Most patients with DKA while on SGLT 2 inhibitor have a precipitating event like dehydration, infection, surgery or change in insulin dose. We propose that strict carbohydrate diet and continuation of SGLT2 inhibitors before bariatric surgery resulted in EDKA. It led to complications peri-operatively. In conclusion, despite the increasing benefits of SGLT2 inhibitors in type 2 diabetics, one must be cognizant of its limitations and in particular association with EDKA. This especially holds true for patients suspected to have beta cell dysfunction or ketosis prone diabetes and patients on strict/low carbohydrate diets.