SUN-176 Euglycemic Diabetic Ketoacidosis withSGLT2 Inhibitor Presenting as Chest Pain in a Patient with Coronary Artery Disease on a Ketogenic Diet

Background: Euglycemic diabetic ketoacidosis (DKA) is a known complication of sodium-glucose cotransporter 2 (SGLT2) inhibitors. We report an unusual case of euglycemic DKA caused by an SGLT2 inhibitor during self-introduction of a ketogenic diet; initial concern was for acute coronary syndrome. Clinical Case: A 61-year-old man with a history of type 2 diabetes with a hemoglobin A1c of 8.3%, coronary artery disease, hypertension, and hyperlipidemia presented to the emergency room with nausea and chest pain. The patient had a 30-year history of diabetes and was on oral therapy for years before starting insulin with an average daily dosage of 28 units. Three years ago, he started an SGLT2 inhibitor, improved his lifestyle and glycemic control, and was able to stop insulin. His home medications included empagliflozin 10 mg daily, metformin 500 mg twice a day, liraglutide 1.8 mg subcutaneously daily, rosuvastatin 5 mg daily, ezetimibe 10 mg daily, and omeprazole 40 mg daily. He reported several weeks of atypical chest pain and computed tomography angiography showed total occlusion of the mid-right coronary artery. He underwent an exercise stress test that showed echocardiographic changes that were positive for ischemia and subsequently was scheduled to undergo a left heart catheterization in 1 week. In the interim, he was highly motivated to change his lifestyle. He adopted a ketogenic diet, significantly limiting his daily carbohydrate. Five days later, he developed persistent and increased right-sided chest pain along with nausea, and presented to the emergency room. On review of systems, he reported hunger and his wife reported an odd breath odor. His vitals were stable. His troponin was negative and EKG showed inferior Q waves similar to prior EKGs. Given concern for acute coronary syndrome, he underwent cardiac catheterization, which showed the known complete total occlusion of RCA with collaterals, for which intervention was not performed. Review of additional labs showed: glucose 110 [70-100 mg/dL], bicarbonate 17 [22-29 mmol/L], anion gap 17 [6-14 mmol/L], betahydroxybutyric acid 4.1 [<0.3 mmol/L], large quantity of urinary ketones and glucose. He was diagnosed with euglycemic DKA and treated with insulin, fluids, and dextrose with resolution of ketoacidosis and chest pain. Conclusion: The use of SGLT2 inhibitors is increasingly favored in those with established cardiovascular disease, and carbohydrate-restrictive diets are a popular form of nutritional therapy. This case highlights severe carbohydrate restriction as an important risk factor that may predispose patients on SGLT2 inhibitors to euglycemic DKA that demonstrated with an unusual presentation of chest pain.