Beyond Glucose Levels: Redefining Diabetic Ketoacidosis-A Case of Hypoglycemic Diabetic Ketoacidosis

Abstract

Background/objective: Diabetic ketoacidosis (DKA) is a life-threatening condition typically diagnosed by the presence of hyperglycemia, acidemia, and ketonemia. A subset of patients may develop ketoacidosis without the traditionally increased glucose levels in a condition known as euglycemic DKA. This article describes an atypical presentation of DKA with concomitant hypoglycemia in a condition termed hypoglycemic DKA.

Case report: A 74-year-old woman with a history of hypertension, type 2 diabetes mellitus (treated with empagliflozin), and hypothyroidism, presented from an outlying hospital due to concern for acute gallstone pancreatitis and choledocholithiasis. On arrival, laboratory evaluation revealed an anion gap of 16 mEq/L (reference range, 6-12 mEq/L), bicarbonate level of 11 mEq/L (reference range, 21-31 mEq/L), serum glucose level of 57 mg/dL (reference range, 70-105 mg/dL), beta-hydroxybutyrate level of 1.7 mmol/L (reference range, <0.6 mmol/L), and urinalysis demonstrating a ketone level of >80 mg/dL (reference range, <3.49 mg/dL). The patient was treated according to the institution DKA protocol, with resolution of her DKA.

Discussion: The case presented highlights a manifestation of DKA characterized by a concurrent state of hypoglycemia in a patient treated with a sodium-glucose cotransporter 2 inhibitor, an atypical and likely underreported phenomenon.

Conclusion: Clinicians should maintain a high level of suspicion for DKA in patients with metabolic acidosis and ketosis, irrespective of their glucose levels, in particular in those treated with sodium-glucose cotransporter 2 inhibitors. Additionally, redefining these cases as drug-induced ketoacidosis may assist in preventing delayed diagnosis and management.

Keywords: diabetic ketoacidosis (DKA); drug-induced ketoacidosis (DiKA); euglycemic DKA (EDKA); hypoglycemic DKA (HDKA); sodium-glucose cotransporter 2 (SGLT2) inhibitors.

Fig

Hypothesis of sodium-glucose cotransporter 2 (SGLT2) inhibitor–induced hypoglycemic diabetic ketoacidosis.