MON-694 EDKA and MALA in the Setting of Severe Heart Failure and Acute Renal Failure, Due to SGLT2-i

Abstract

Background: EDKA is a reported potential side effect of SGLT-2i that presents a unique challenge for diagnosis and management in the setting of HF and concurrent AKI. Literature encourages wide use of SGLT-2i’s, however this case demonstrates the need of proper evaluation before initiating therapy. Case: A 53 year old male with PMH of T2DM, Atrial fibrillation, HFrEF, presented to the Emergency Dept after a week of confusion, nausea, vomiting, and diarrhea. These symptoms were presumed due to gastroenteritis and our patient continued working on his farm in the summer heat. Following 3 days of intractable vomiting, he began to develop confusion, took his medications and presented to the ED. He was on metformin and had recently started empagliflozin following a heart failure exacerbation. Upon arrival the patient was noted to have a severe AKI with Cr of 15, hyperkalemia with potassium of 7.7, Anion gap of 45, bicarbonate of 4. Lactic acid was noted to be 7.7 and BHB was later noted to be 10.5 with a serum blood glucose of 155.Pt was determined to have Euglycemic Diabetic Ketoacidosis with an additional Metformin associated lactic acidosis. He was started on an insulin drip with a concurrent D20 infusion to minimize fluid intake. Dextrose was titrated up to maintain a goal BG of 150-180 while on a stable insulin rate of 5u/hour, while monitoring serum ketones to resolution of DKA. Due to excess fluid intake he required intubation and later, hemodialysis due to metformin associated lactic acidosis and acute renal failure. Following 3 days of dialysis he was able to successfully wean from vent and pressors, making a complete recovery.Conclusion:We present a patient with EDKA likely resulting from dehydration induced AKI compounded by SGLT2i induced diuresis. As he developed his kidney injury, metformin was able to build up to toxic levels inducing lactic acidosis. Treatment in this patient was based on the underlying physiology providing glucose to allow resolution of ketosis. Treatment is not well studied, but given the origin of the pathology should resemble a standard DKA protocol with glucose repletion. SGLT2i and metformin combinations have shown an increased risk of metabolic acidosis1 and lactic acidosis2. This case highlights a potential risk of the combination in the setting of renal insufficiency and tenuous fluid states.