Empagliflozin induced euglycemic diabetic ketoacidosis. A case reports

ElsevierVolume 84, December 2022, 104879Annals of Medicine and SurgeryHighlights•

SGLT2 inhibitors have demonstrated benefits for cardiorenal outcomes in type 2 diabetic patients with cardiorenal comorbidities.

The normal blood glucose level in EDKA delays the recognition of the problem by both the patients and the physician.

Euglycemic diabetic ketoacidosis should be considered when evaluating a patient using an SGLT2 inhibitor.

AbstractIntroduction

Diabetic ketoacidosis (DKA) is one of the most serious acute complications of diabetes. Its defining features are hyperglycemia and ketoacidosis. Euglycemic DKA (EDKA) affects patients whose serum glucose levels are within the normal range. The use of sodium-glucose cotransporter 2 (SGLT2) inhibitors is one of the newly identified risks for this condition.

Case presentation

A 75-year-old woman with type 2 diabetes mellitus presented to our emergency department with decreased consciousness and decreased oral intake for two days. She had been diagnosed with a cerebrovascular accident for 12 days, and empagliflozin was added to her medications. Laboratory evaluation revealed metabolic acidosis, despite a minimally elevated serum glucose concentration. The patient was admitted to the intensive care unit with EDKA secondary to empagliflozin and treated with intravenous rehydration therapy and intravenous insulin infusion.

Conclusions

Empagliflozin (SGLT2 inhibitor) is a new anti-hyperglycemic medication that is associated with an increased risk of DKA. Several patients present with normal or minimally elevated serum glucose concentration, which frequently leads to a delay in diagnosis. EDKA should be considered when evaluating a patient with unexplained metabolic acidosis while taking an SGLT2 inhibitor, and SGLT2 inhibitors should be discontinued if acidosis is confirmed.

Keywords

Euglycemic diabetic ketoacidosis

Empagliflozin

Sodium-glucose cotransporter-2 inhibitor

Type 2 diabetes

© 2022 The Author. Published by Elsevier Ltd on behalf of IJS Publishing Group Ltd.

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