THU359 A Classical Case Of SGLT-2 Inhibitor Euglycemic Ketoacidosis In A Patient With Glucotoxicity

Disclosure: S. Amankwah: None. O.B. Olajide: None. Background: SGLT-2 inhibitors have been demonstrated to be beneficial in protecting comorbid cardiovascular or kidney disease while providing modest improvement in glycemia. However, they are not ideal for initial therapy for patients with very poorly controlled type 2 diabetes. This is a case where SGLT-2 inhibitor monotherapy led to diabetic ketoacidosis. Clinical Case: A 68-year-old woman with type 2 diabetes for 30 years, hypertension, hyperlipidemia, and depression presented to the hospital with complaints of headache, nausea, vomiting, dizziness, fatigue for the past three days. She had no fever, cough, shortness of breath or dysuria. She had not been taking any oral hypoglycemic agents for many months as she was trying to control her diabetes with lifestyle modifications. However, after the passing of her husband three months prior, she became less motivated in managing her health. Ten days prior to her hospitalization, the patient was newly prescribed empagliflozin 10 mg daily by her primary care provider due to uncontrolled hyperglycemia. She refused to resume metformin due to her history of gastrointestinal intolerance. She was previously on glipizide, but this was not restarted as she previously had poor glycemic control on it. On arrival at the ER, her temperature was 97.9 F, heart rate 112 bpm, respiratory rate 22 bpm, blood pressure 105/63 mmHg, and pulse oximetry on room air was 97%. Physical exam was unremarkable. Her serum glucose was 228 mg/dL, anion gap 15, pH 7.1, serum bicarbonate 15 mEq/L, serum acetone 3+, urine ketones greater than 150 mg/dL, serum creatinine 1.26 mg/dL and hemoglobin A1c was 13.2%. Her chest X-ray was unremarkable and COVID 19 test was negative. Euglycemic diabetic ketoacidosis (EDKA) was suspected secondary to the use of empagliflozin. This was discontinued and the patient was treated with intravenous insulin and fluids. Her serial blood tests showed resolution of ketoacidosis within 12 hours, and she was then transitioned to subcutaneous insulin. She was discharged home after 2 days of hospitalization on insulin therapy. Discussion: This case demonstrates the potential for SGLT-2 inhibitors to cause EDKA. It is important to acknowledge this complication can happen in cases where SGLT-2 inhibitors are used as monotherapy in diabetic patients with glucotoxicity. The mechanism of action of SGLT2 inhibitors is to enhance excretion and block reabsorption of filtered glucose from the proximal convoluted tubule. The resultant glycosuria creates a state of carbohydrate starvation and volume depletion, increasing the glucagon/insulin ratio, resulting in a state of severe dehydration and ketosis. Patients with glucotoxicity are at a higher risk to develop ketoacidosis as they have marked beta cell insufficiency. It is thus highly recommended to initially treat these patients with insulin rather than oral agents. Presentation: Thursday, June 15, 2023