LBSUN289 Ketonuria — A Possible Early Indicator Of Impending Euglycemic DKA In Setting Of Recent SGLT-2 Inhibitor Use And Acute Stress

Abstract

Introduction - Euglycemic DKA is a notorious entity; previously thought to be primarily afflicting type 1 diabetics and rarely type 2 diabetics in a state of relative insulin deficiency, it has now become a major cause of concern and lead to the issuance of FDA warning in 2015 with regards to its link with SGLT-2 inhibitors. Although DKA is characterized by hyperglycemia, metabolic acidosis and ketogenesis, euglycemic DKA poses a diagnostic challenge as it remains disguised under the cover of euglycemia. Moreover, in the setting of recent SGLT-2 inhibitor use, this definition becomes even more of a paradox as SGLT-2 inhibitors, by the virtue of their action, promote ketogenesis thereby further adding to this enigma. Case presentation - A 67 year old male with hypertension and diabetes mellitus type 2 (on Metformin and Empagliflozin) presented to the emergency room with dizziness. He woke up to go to the bathroom that day and felt weak, dizzy and like he was going to fall. He endorsed nausea and vomiting but denied headache, fever, chills, chest pain, shortness of breath, abdominal pain, and problems with urination/bowel movements. He was afebrile and hemodynamically stable. On examination, left sided dysmetria, loss of coordination, and axial imbalance were noted. No motor/sensory deficits. Labs were significant for WBC count 10 k/mm cu (4 - 11), Creatinine 0.78 mg/dL (0.7 - 1.3), Glucose 279 mg/dL (70 - 99), Bicarbonate 21 mmol/L (21 -31), Anion gap 19 mmol/L (6 - 14), and Lactate 3.2 mmol/L (0.7 - 2). Urinalysis showed glucosuria (glucose >500 mg/dL) and ketonuria (ketones 20 mg/dl). CT head was negative but MRI brain showed left inferior cerebellar peduncle acute ischemic infarct. Stroke protocol was initiated and he transferred to telemetry. The next day, labs showed Glucose 166, Bicarbonate 13, Anion gap 21, and Ketones 5.6 mmol/L (<0.6). Since blood glucose levels remained less than 250 mg/dl with concurrent anion gap metabolic acidosis in the setting of recent Empagliflozin use, he was transferred to ICU for insulin infusion for management of euglycemic diabetic ketoacidosis. Subsequently, he was transitioned to a basal-bolus insulin regimen and transferred to the floors. Discussion - SGLT-2 inhibitors reduce renal tubular glucose reabsorption, causing glycosuria, and promote ketonemia directly by enhancing ketogenesis via glucagon secretion from the pancreatic alpha cells and indirectly by decreasing the renal clearance of ketone bodies. In the setting of acute stress, such as stroke in our patient, and recent SGLT-2 inhibitor use, the presence of ketonuria should be recognized as an early ominous warning sign for euglycemic DKA. A targeted approach detailing diagnostic and therapeutic interventions should be designed to halt its progression in its track before it transforms into the dreaded euglycemic DKA. Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.