C49-06 Metformin Associated Severe Lactic Acidosis Causing Multiorgan Dysfunction Requiring Continuous Renal Replacement Therapy (CRRT)

Abstract Introduction Metformin-associated lactic acidosis (MALA) is a rare yet potentially life-threatening complication of metformin therapy. The lactic acidosis resulting from toxic metformin levels can often mimic other common causes of shock. We present a case of MALA that manifested with severe acidemia and multiorgan dysfunction, necessitating continuous renal replacement therapy (CRRT). Case Description A 37-year-old woman with type 2 diabetes mellitus (on metformin), hypertension, peripheral artery disease (status post left above-knee amputation) and schizophrenia was found unresponsive at home and presented with altered mental status. On arrival, she was obtunded and required emergent intubation. Vitals revealed hypotension and tachycardia, necessitating vasopressor support. Laboratory workup showed severe metabolic acidosis (pH 7.0, bicarbonate 5 mEq/L, anion gap 32), lactic acidosis (lactate 13 mmol/L), acute kidney injury (creatinine 10.2 mg/dL; baseline 1.8 mg/dL) and hyperkalemia (5.4 mEq/L). Leukocytosis (18.9 x10³/μL) and baseline anemia (Hgb 9.2 g/dL) were also noted. Toxicology screening and serum ketones were negative. Blood culture negative. Imaging ruled out pulmonary embolism and intracranial pathology but revealed basilar patchy opacities consistent with aspiration. EKG demonstrated ST depressions consistent with demand ischemia. Despite fluid resuscitation, broad-spectrum antibiotics, bicarbonate therapy, and multiple vasopressors (norepinephrine, vasopressin, epinephrine), the patient remained in refractory shock. Ventilator settings were optimized to enhance pCO2 clearance, with a respiratory rate of 38 breaths/min and tidal volume of 450 mL while maintaining plateau pressures 30 cm H2O. Due to persistent acidosis and hemodynamic instability, CRRT (Continuous Veno-Venous Hemodialysis modality) was initiated, resulting in rapid clearance of metformin and correction of acid-base status, decreasing lactate, and resolution of shock. A delayed serum metformin level returned markedly elevated at 48 mcg/mL (therapeutic 2 mcg/mL), confirming MALA. The patient was successfully weaned off vasopressors and extubated. Discussion MALA is rare but carries a high mortality rate, and its clinical presentation is often nonspecific, making timely diagnosis challenging. Metformin toxicity develops when decreased renal clearance leads to drug accumulation, causing inhibition of mitochondrial oxidative phosphorylation and excessive lactate production. Laboratory findings of severe metabolic acidosis, elevated lactate in renal dysfunction in patients on metformin should prompt consideration of MALA in the differential diagnosis, even before confirmatory metformin levels are available. Our case highlights the importance of maintaining high clinical suspicion for MALA in any patient on metformin presenting with unexplained severe lactic acidosis and renal impairment. Early initiation of dialysis either intermittent hemodialysis or CRRT is associated with improved survival in MALA. This abstract is funded by: None