SAT-636 - “From Polyuria to Cardioversion: An Atypical Presentation of Metformin‑Associated Lactic Acidosis.”

Introduction

Despite a central role in treating type 2 diabetes, metformin carries a small but significant risk of metformin‑associated lactic acidosis (MALA), a rare complication with high morbidity. Diagnosis may be challenging when presentation is dominated by cardiovascular or metabolic instability rather than classic gastrointestinal or toxic features. We report an atypical case of severe MALA presenting primarily with hemodynamically unstable tachyarrhythmia and marked hyperglycemia.

Case Presentation

An 80‑year‑old man with two‑vessel CAD, HTN and type 2 diabetes on metformin, glipizide, and empagliflozin presented with several days of dizziness and rising home glucose values. He was tachycardic to the 180s with a wide‑complex supraventricular tachycardia unresponsive to adenosine and diltiazem. Laboratory evaluation showed CO₂ 9 mmol/L, potassium 5.9 mmol/L, anion gap 28, glucose 474 mg/dL, serum osmolality 314 mOsm/kg and creatinine 2.6 mg/dL (Baseline 1.4mg/dl). Arterial blood gas revealed pH 7.14 and lactate 13.8 mmol/L. He continued to deteriorate hemodynamically despite aggressive fluid resuscitation, ultimately requiring etomidate‑assisted cardioversion. An insulin infusion was started for suspected DKA; however, beta‑hydroxybutyrate later returned at only 1 mmol/L. Persistent severe acidosis prompted bicarbonate therapy. Nephrology was consulted emergently, and hemodialysis was initiated promptly, resulting in a rapid decline in lactate from 14.2 to 4 mmol/L within two hours and to 1.3 mmol/L shortly thereafter. With ongoing treatment, his anion gap corrected, and his clinical symptoms fully improved. Once stabilized, he provided additional history, denying new medication initiation, noncompliance, overdose, illness, or toxin/contrast exposure, stating only that “I was peeing more than usual the last week.”

Discussion

Although classic triggers were absent and metformin level wasn't available, profound acidemia, elevated lactate, acute kidney injury, and rapid improvement with dialysis supported MALA as the primary diagnosis. SGLT2 inhibitor–induced osmotic diuresis, chronic thiazide use, and angiotensin receptor blockade likely contributed to subtle volume depletion and reduced renal perfusion, impairing metformin clearance. Severe acidosis may also have precipitated tachyarrhythmia and a preserved post‑cardioversion ejection fraction (>52%) makes a primary cardiogenic source of his lactic acidosis unlikely.

Conclusion

This case highlights the need to consider MALA in patients with unexplained high‑anion‑gap acidosis, particularly when multiple mild stressors—such as SGLT2 inhibitors, diuretics, and transient renal hypoperfusion—converge. Early recognition and prompt initiation of renal replacement therapy are essential to reversing life‑threatening metabolic derangements.

*Unless otherwise noted, all abstracts presented at ENDO must not be released to the press or the public until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.*