MON-LB123 Diagnosis and Management of Euglycemic DKA in the Setting of SGLT2 Inhibitor Use and Prostate Abscess

Introduction: SGLT2i has been associated with euglycemic DKA by increasing lipid oxidation and glucagon synthesis. In the event of an underlying infection, increased ketogenesis could lead to the presentation of DKA. Clinical case: A 35 year old male patient who was recently diagnosed with type 2 Diabetes mellitus after he presented to his primary care physician with increased urinary frequency, frothy urine. He was found to have a hemoglobin A1c of 12.5% and blood glucose 408 mg/dl. Urinalysis was negative for nitrites and leukocyte esterase. Patient endorsed to have one sexual partner and safe sexual practices. Urinary gonorrhea and chlamydia antigens were negative. He was diagnosed with diabetes mellitus and was started on ertugliflozin, exenatide and bactrim for possible UTI. Three days later, the patient presented to the ED with dysuria, polyuria, rectal pain, nausea and fatigue. Patient appeared to be in distress with tachypnea and tachycardia. Physical exam showed signs of dehydration. Laboratory evaluation revealed blood glucose at 185 mg/dL. Given the history of recent diagnosis of diabetes mellitus and SGLT2 inhibitor use, euglycemic DKA was suspected. ABG revealed metabolic acidosis (arterial blood gas pH 7.32, pCo2 20, pO2 130) with elevated anion gap of 24, HCO3 level of 10 mmol/L (reference range 22 - 28 mmol/L) and beta-hydroxybutyrate of 5.7 mmol/L (reference range 0 - 0.3 mmol/L). The lactate levels were normal. Wbc count 20,100. Urinalysis showed glucose 4+, ketones 4+, WBC 4, negative for infection. Computed tomography scan of his abdomen and pelvis with contrast showed 3.7 x 2.7 cm prostate abscess and acute cystitis. Patient was treated for euglycemic DKA with infusion of insulin and dextrose 10% with 0.45% NS. Careful monitoring of his blood sugar was required as it dropped with slight increase in infusion rate. He was started on ciprofloxacin for prostate abscess. Patient’s metabolic acidosis resolved and he showed clinical improvement. Endocrinologist was on consult. Patient was switched to insulin regimen for glycemic control. Conclusion: SGLT2i class of drugs has been increasingly used in the treatment of diabetes due to improved cardiovascular outcomes and renal protective effects. However, diagnosing DKA can be a concern while treating patients with this drug. While the SGLT2i is responsible for his euglycemic presentation, DKA was likely triggered by his prostate abscess. They can be used safely with extensive education to the physicians about euglycemic DKA presentation. Management requires starting D10 infusion along with insulin drip to avoid the risk of hypoglycemia.