Abstract
While sodium-glucose cotransporter-2 (SGLT2) inhibitors improve cardiovascular outcomes after myocardial infarction (MI), they carry the risk of euglycemic diabetic ketoacidosis (euDKA). We report the case of a 60-year-old male with type 2 diabetes mellitus who developed euDKA after a primary percutaneous coronary intervention (PCI) for ST-segment elevation myocardial infarction (STEMI). Despite exhibiting hemodynamic stability, the patient developed persistent metabolic acidosis. The diagnosis of SGLT2 inhibitor-associated euDKA was significantly delayed, as it was obscured by a combination of the patient's clinical stability, an initial normal anion gap acidosis from diarrhea, and the administration of sodium bicarbonate. This case highlights the fact that clinical stability after primary PCI might mask SGLT2 inhibitor-associated euDKA. This report also emphasizes that euDKA should be a critical diagnostic consideration in the face of persistent acidosis in STEMI patients treated with PCI and receiving SGLT2 inhibitors, even when they appear clinically stable. LEARNING OBJECTIVES: This case highlights that euglycemic diabetic ketoacidosis (euDKA) might be a critical and missed diagnosis in SGLT2 inhibitor-treated diabetic patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI). SGLT2 inhibitor-associated euDKA should be considered in diabetic patients presenting with unexplained metabolic acidosis, even if they are hemodynamically stable and their blood glucose levels are normal. Routine ketone monitoring should be considered in this setting.