SESSION TITLE: Wednesday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/23/2019 09:45 AM - 10:45 AM INTRODUCTION: Physicians are facing Euglycemic Diabetic Ketoacidosis (euDKA) in patients at increasing rates. Diagnosis can be challenging as it lacks one of the criteria required to diagnose DKA: hyperglycemia. We present a case of a patient presenting with euDKA secondary to Empagliflozin use. CASE PRESENTATION: 57-year-old male with past medical history of coronary artery disease, diabetes mellitus type 2, hypertension, hyperlipidemia, COPD presented to the emergency room with complaints of fever, shortness of breath, myalgias, right sided pleuritic chest pain, mild epigastric abdominal pain, and nausea for the last 3 days. On physical exam patient was hypotensive, tachycardiac, tachypneic, hypoxic and had diminished breath sounds bilaterally with inspiratory and expiratory wheezes. ECG showed sinus tachycardia. Laboratory values were significant for acidosis with pH 7.25, WBC count of 13.2/L, anion gap of 17mmol/L and glucose 102 mg/dL. Chest X-ray was notable for increased interstitial markings. Respiratory viral panel was positive for Influenza A. Home medications included Metformin, Empagliflozin, Lantus, Lisinopril and Simvastatin. Patient was admitted on the medicine floor for the management of acute viral and suspected superimposed bacterial pneumonia. He was treated with intravenous Levofloxacin and oral Tamiflu. Acidosis was not improving despite adequate medical management and hydration. Given patients history of diabetes, serum acetone and osmolality were checked. He was found to have serum osmolality of 312 mosml/L and large level of acetone. Serum chemistry showed persistent anion gap. Urine studies revealed glucosuria and ketonuria. He was upgraded to the medical ICU for further management of euglycemic DKA likely secondary to Empagliflozin, which was held upon admission. Patient was started on intravenous insulin drip and fluids. After 24 hours the anion gap closed, and metabolic acidosis resolved. Patient was switched to subcutaneous insulin and educated to avoid further use of SGLT-2 inhibitors. DISCUSSION: Some reported causes of euDKA include fasting/starvation, pregnancy, pancreatitis, cocaine intoxication, protracted vomiting or diarrhea, use of insulin pumps, and use of SGLT2 inhibitors. SGLT2 inhibitors work by acting on the receptors in the proximal tubule of the kidney to decrease glucose reabsorption, thereby increasing glucose clearance in the kidney. This leads to glucosuria. Glucosuria contributes to the euglycemic state by causing patients to develop ketoacidosis secondary to SGLT2 inhibitor use. CONCLUSIONS: Reported cases of euDKA have included patients with Type 1 and Type DM. Even though SGLT2 inhibitors are not approved for type 1 diabetics, their off-label use is fairly common. This is an important factor to remember when diabetics present with symptoms of acidosis and dehydration, especially because a delayed diagnosis of euDKA can increase morbidity and mortality. Reference #1: Rawla P, Vellipuram AR, Bandaru SS, Raj JP. Euglycemic diabetic ketoacidosis: a diagnostic and therapeutic dilemma.Endocrinol Diabetes Metab Case Rep. 2017 Sep, EDM170081, https://doi.org/10.1530/EDM-17-0081 Reference #2: Rosenstock J, Ferrannini E. Euglycemic Diabetic Ketoacidosis: A Predictable, Detectable, and Preventable Safety Concern With SGLT2 Inhibitors. Diabetes Care. 2015 Sep;38(9):1638-42. https://doi.org/10.2337/dc15-1380. Reference #3: Bader N, Mirza L. Euglycemic Diabetic Ketoacidosis in a 27 year-old female patient with type-1-Diabetes treated with sodium-glucose cotransporter-2 (SGLT2) inhibitor Canagliflozin. Pak J Med Sci. 2016 May-Jun; 32(3): 786–788. https://doi.org/10.12669/pjms.323.9201 DISCLOSURES: No relevant relationships by Anna Abbasi, source=Web Response No relevant relationships by Sushilkumar Gupta, source=Web Response No relevant relationships by Tina Nguyen, source=Web Response No relevant relationships by Taek Sang Yoon, source=Web Response