Abstract
Euglycemic diabetic ketoacidosis (DKA) is a rarely reported side effect of sodium-glucose cotransporter-2 inhibitor (SGLT2i) empagliflozin. A 51-year-old female with Gitelman syndrome and type 2 diabetes mellitus (DM) presented with abdominal pain after a recent hospitalization for acute pancreatitis. Her diabetes medications included metformin, pioglitazone, and empagliflozin. Diabetic ketoacidosis was suspected; however, glucose levels were below the cutoff for DKA; therefore, she was diagnosed with euglycemic DKA. Her pancreatitis workup was insignificant. Severe symptomatic hypokalemia despite aggressive repletion limited the management of DKA with insulin infusion therapy. As her ketonemia resolved, she was initiated on subcutaneous insulin with a small but acceptable decrease in potassium. The therapeutic dilemma of managing euglycemic DKA due to SGLT2i in a patient with Gitelman syndrome has not been previously described.
Highlights
Euglycemic diabetic ketoacidosis (DKA) is a clinical syndrome characterized by normal blood glucose level, severe metabolic acidosis, and ketonemia
We report a case of euglycemic ketoacidosis due to Sodium-glucose cotransporter-2 inhibitors (SGLT2i) in a patient with Gitelman syndrome
Euglycemic DKA is generally managed on the same principles as conventional DKA, with insulin infusion and intravenous resuscitation
Summary
Euglycemic diabetic ketoacidosis (DKA) is a clinical syndrome characterized by normal blood glucose level (less than 250 mg/dL), severe metabolic acidosis, and ketonemia. We report a case of euglycemic ketoacidosis due to SGLT2i in a patient with Gitelman syndrome. This case demonstrates an approach to the management of ketoacidosis complicated by severe baseline hypokalemia. Empagliflozin was added to her antihyperglycemic regimen three months ago, and she was tolerating it well Her family history was significant for Gitelman syndrome in her grandmother. After 24 hours of aggressive potassium repletion, her potassium level raised up to 3.0 mmol/L As her ketonemia and anion gap acidosis improved with intravenous hydration, she was started on subcutaneous insulin with a small but acceptable decrease in potassium.
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