Abstract 4145352: SGLT2 Inhibitor-Induced Euglycemic Ketoacidosis in a Non-Diabetic Patient with Ischemic Cardiomyopathy

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Introduction: Sodium-glucose cotransporter-2 (SGLT2) inhibitors are drugs designed to lower plasma glucose concentration by inhibiting Na + -glucose–coupled transport in the proximal tubule. Clinical trials demonstrate these drugs have favorable effects on cardiovascular outcomes including including slowing the progression of CKD. Although most patients tolerate these drugs, a potential complication is development of ketoacidosis, often with a normal or only a minimally elevated plasma glucose concentration mostly in diabetic patients. We present a case of SGLT-2 inhibitor induced ketoacidosis in a patient without any risk factor. Case Presentation: The patient is a 56-year-old gentleman without significant past medical history who presented to the emergency room with prolonged chest pain for more than 12 hours. He was hemodynamically stable with EKG evidence of acute Q-wave and ST elevation in the anteroseptal leads and high sensitivity troponin of about 78,000. He underwent successful PCI along with placement of two DES at mid LAD and proximal OM. Transthoracic echocardiography post catheterization showed LVEF of 25% with dyskinetic apical and apical inferior segment. Subsequently, GDMT for ischemic cardiomyopathy. Approximately after two days of initiation of GDMT, he was noted to have low bicarbonate of 18 and an AG of 16 following which ABG was drawn that showed metabolic acidosis with a nadir pH of 7.30 and an associated Pco 2 level of 29 mmHg. Despite an abnormal lab, he was clinically asymptomatic with no active complaints. His A1C was found to be 5.4. UA revealed ketones (2+) without glucose. β-Hydroxybutyrate level was elevated to 3.34 mmol/L. On further review of his chart, we saw that he had received two doses of empagliflozin. Diagnosis of euglycemic ketoacidosis, presumably related to SGLT2 inhibitor therapy was made. Endocrinologist recommended the usual management like diabetic ketoacidosis. The patient was then started on dextrose and insulin drip. Following closure of anion gap, drips were discontinued. Later, the patient was discharged home on GDMT without SGLT2 inhibitor. Conclusion: Given the tremendous benefits of SLGT-2 inhibitors in patients with diabetes, heart failure, and CKD, their use is expected to grow significantly. Providers should remain vigilant for potential evidence of the development of euglycemic ketoacidosis even in nondiabetic patients using SGLT-2 inhibitors, so that appropriate intervention is done in a timely manner.

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