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Euglycemic DKA — ABIM Board MCQ

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ModerateEndocrinology/MetabolismEuglycemic DKAABIM Board

A 58-year-old man with type 2 diabetes mellitus treated with metformin, glipizide, basal-bolus insulin, and empagliflozin presents with 2 days of nausea, vomiting, and abdominal discomfort. He began a very-low-carbohydrate diet 1 week ago and halved his insulin doses because he was eating less. He is afebrile, blood pressure is 118/72 mm Hg, and respirations are 24/min and deep. Laboratory studies show glucose 185 mg/dL, sodium 138 mEq/L, potassium 4.2 mEq/L, chloride 102 mEq/L, bicarbonate 12 mEq/L, anion gap 24, arterial pH 7.24, lactate 1.2 mmol/L (normal), and markedly elevated serum beta-hydroxybutyrate. Which of the following mechanisms best explains his acid-base disorder?

Educational content. Not a substitute for clinical judgement or local policy.

Reveal the answer and explanation

Correct answer: D — Urinary glucose loss with a raised glucagon-to-insulin ratio driving hepatic ketogenesis

Explanation lettering: C = shown as B · B = shown as C · E = shown as D · D = shown as E

E is correct. This is euglycemic diabetic ketoacidosis: high-anion-gap acidosis, ketonemia, and glucose below 250 mg/dL. Empagliflozin produces continuous urinary glucose loss, which masks hyperglycemia and lowers insulin requirements; combined with insulin dose reduction and carbohydrate restriction, it raises the glucagon-to-insulin ratio, stimulating lipolysis and hepatic ketone production (with reduced ketone excretion). A is wrong—sulfonylurea-driven endogenous insulin excess suppresses ketogenesis and typically causes hypoglycemia, not ketoacidosis. B describes metformin-associated lactic acidosis, excluded by the normal lactate and elevated beta-hydroxybutyrate. C (mineralocorticoid excess) produces hypertension, hypokalemia, and metabolic alkalosis, not acidosis. D causes steatorrhea and fat-soluble vitamin deficiency, not acute ketoacidosis. Management: intravenous fluids, insulin with dextrose, and stopping the SGLT2 inhibitor.

Reference: US Food and Drug Administration. Drug Safety Communication: FDA revises labels of SGLT2 inhibitors for diabetes to include warnings about too much acid in the blood (ketoacidosis) and serious urinary tract infections (canagliflozin, dapagliflozin, empagliflozin), 2015/current class labeling. https://www.fda.gov/files/drugs/published/FDA-revises-labels-of-SGLT2-inhibitors-for-diabetes-to-include-warnings-about-too-much-acid-in-the-blood-and-serious-urinary-tract-infections.pdf