Concurrent Metformin-Associated Lactic Acidosis and Euglycemic Diabetic Ketoacidosis Without Sodium-Glucose Cotransporter 2 Inhibitor Exposure: A Case Report and Literature Review.

Document Type

Article

Publication Date

4-1-2026

Abstract

Metformin-associated lactic acidosis (MALA) and euglycemic diabetic ketoacidosis (euDKA) are distinct causes of high anion gap metabolic acidosis, but their simultaneous occurrence is rare and may be overlooked when severe hyperlactatemia dominates the presentation. We report the case of a 68-year-old man with type 2 diabetes mellitus treated with basal-bolus insulin, metformin, and linagliptin who presented with vomiting, confusion, fatigue, hypotension, and reduced level of consciousness. Initial evaluation revealed profound acidemia (arterial pH 6.75), severe high anion gap metabolic acidosis (anion gap 51 mEq/L, bicarbonate < 2 mEq/L), marked hyperlactatemia (19 mmol/L), significant ketonemia (beta-hydroxybutyrate >9.60 mmol/L), near-normal glucose (9.1 mmol/L), hyperkalemia (6.5 mEq/L), and severe acute kidney injury (creatinine 516 µmol/L). Ongoing metformin exposure in the setting of acute kidney injury supported MALA, while marked ketonemia with near-normal glucose supported concurrent euDKA, likely precipitated by vomiting and reduced oral intake. The patient was treated with intravenous fluids, vasopressors, sodium bicarbonate, insulin with concurrent dextrose, and sustained low-efficiency dialysis, with subsequent hemodynamic, metabolic, and renal recovery. This case emphasizes that marked hyperlactatemia does not exclude a concurrent ketotic process and that early ketone measurement can materially change management in metformin-treated patients with persistent high anion gap acidosis.

Publication Title

Cureus

Volume

18

Issue

4

First Page

106919

Last Page

106919

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