SAT-633 - Beyond Diabetic Ketoacidosis: A Case of Metformin-Associated Lactic Acidosis

Introduction
Metformin-associated lactic acidosis (MALA) represents a rare but potentially catastrophic complication. The incidence of this condition is estimated at less than 10 cases per 100,000 patient-years. We present a case of fulminant MALA with extreme metabolic derangement that highlights the diagnostic challenges and critical importance of early recognition of this potentially fatal condition.
Case Presentation
A 59-year-old man with atrial fibrillation, hypertension, and type 2 diabetes mellitus presented to the emergency department with four days of progressive lower abdominal pain, melena, nausea, vomiting, and dyspnea. On presentation, he was critically ill, toxic-appearing, and in acute respiratory failure. Initial laboratory evaluation revealed profound high–anion gap metabolic acidosis with venous pH 6.86, bicarbonate < 5 mmol/L, severe lactic acidosis (lactate 18 mmol/L), hyperkalemia (6.4 mmol/L), transaminitis, hyperglycemia (432 mg/dl) and an elevated osmolal gap. Computed tomography angiography of the chest, abdomen, and pelvis demonstrated no acute pathology. He was admitted to the medical intensive care unit and started continuous renal replacement therapy (CRRT). Given the severity of acidosis, initial concern for diabetic ketoacidosis (DKA) prompted aggressive intravenous fluid resuscitation and insulin infusion; however, hyperglycemia resolved quickly and later DKA was subsequently excluded and insulin discontinued. Despite maximal supportive care, metabolic and lactic acidosis progressed. On ICU arrival, neurologic examination revealed fixed and dilated pupils with absent gag reflex on minimal sedation. Poison control was consulted, raising concern for metformin-associated lactic acidosis versus toxic alcohol ingestion. Empiric therapy with fomepizole, thiamine, and vitamin K was initiated. Serum methanol, ethylene glycol, beta-hydroxybutyrate, and metformin levels were obtained. Metformin levels returned markedly elevated 33 mcg/dl (0.10 mcg/dl), while acetaminophen and salicylate levels, methanol and ethylene glycol were negative. Despite CRRT and aggressive supportive measures, severe lactic acidosis persisted, consistent with fulminant metformin-associated lactic acidosis.
Discussion/ Conclusion
This case underscores that despite the overall safety profile of metformin in appropriately selected patients, clinicians must maintain vigilance for MALA in patients presenting with severe lactic acidosis and metabolic acidosis, particularly when risk factors such as acute kidney injury, advanced age, or acute illness are present. Early recognition, immediate metformin discontinuation, and timely initiation of extracorporeal therapy remain the cornerstones of management for this rare but potentially devastating complication.

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