Abstract Introduction Metformin-associated lactic acidosis (MALA) is a rare but potentially fatal complication of metformin therapy, characterized by profound metabolic acidosis and elevated lactate levels. It remains a diagnostic challenge due to overlap with other critical conditions, particularly septic shock. Failure to promptly recognize MALA can delay life-saving interventions such as renal replacement therapy. This case highlights the importance of clinical suspicion, the significance of extremely low pH survival unique to MALA, and the diagnostic pitfalls when sepsis protocols dominate early management. Case Presentation A 73-year-old woman with a history of type 2 diabetes mellitus on metformin 1000 mg twice daily, hypothyroidism, and hypertension presented to the emergency department unresponsive. She was hypothermic (93.6 °F), hypotensive (54/41 mmHg), tachycardic, and tachypneic. Initial laboratory findings showed severe metabolic acidosis with venous pH of 6.658, lactate 16.9 mmol/L, bicarbonate 2.5 mEq/L, and anion gap 41. She demonstrated acute renal failure with creatinine 8.6 mg/dL and GFR 4.5 mL/min. Despite broad-spectrum antibiotics and vasopressor support, the severity of acidosis was disproportionate to presumed septic shock. Arterial blood gas confirmed worsening acidosis (pH 6.837). Given the patient’s metformin use and renal dysfunction, MALA was strongly suspected. Using the Extracorporeal treatment and poisoning (EXTRIP) criteria, Nephrology was consulted and Continuous renal replacement therapy (CRRT) was initiated within six hours of ICU admission. The patient demonstrated rapid metabolic recovery, was weaned off vasopressors within 48 hours, extubated at 72 hours, and ultimately discharged to rehabilitation with full neurological recovery. Discussion MALA should be considered in any metformin user presenting with unexplained high anion gap metabolic acidosis and significantly elevated lactate, particularly in the setting of renal impairment. Survival at extremely low pH levels, as seen in this case, is a distinguishing feature of MALA not commonly observed in other etiologies of lactic acidosis. Early dialysis is critical due to metformin’s dialyzable nature and ongoing lactate generation. Although sepsis protocol activation is common in such presentations, reliance solely on sepsis pathways may delay MALA-specific interventions. This case reinforces the need for differentiation early in the clinical course, as delayed recognition contributes to increased mortality. Conclusion This case highlights the life-saving importance of early recognition of MALA, especially when severe acidosis is out of proportion to suspected sepsis. Metformin should be immediately discontinued, and renal replacement therapy initiated without delay. Incorporating MALA-specific considerations into existing sepsis protocols may prevent misdiagnosis and improve outcomes in this rare but highly treatable condition. This abstract is funded by: None
Fashugba et al. (Fri,) studied this question.