MON-646 Profound Acidosis In Shock: Metformin Toxicity Or Multifactorial? A Diagnostic Dilemma Prompting Rethink Of Metformin Use In Primary Care.
Year: 2025
Type: article
Abstract: Disclosure: N. Tara: None. H. Marasandra Ramesh: None. R. Subramani: None. T. Hammad: None. A. Kauser: None. A. Karki: None. Profound Acidosis in Shock: Metformin Toxicity or Multifactorial? A Diagnostic Dilemma Prompting Rethink of Metformin Use in Primary Care. Introduction: Metformin-associated lactic acidosis (MALA) is a rare but life-threatening complication, often triggered by renal or hepatic dysfunction impairing metformin clearance. We present a case of young female with type 2 diabetes mellitus (T2DM) on metformin with profound high anion gap metabolic acidosis (HAGMA) with severe lactic acidosis. Case description. A 40-year-old female with T2DM on 1500 mg metformin, alcohol (ETOH) dependence with hepatic steatosis and a history of recurrent pancreatitis presented with 4 days of worsening chest pain, dyspnea and vomiting. On arrival, she was in profound shock requiring three vasopressors and had severe metabolic acidosis (pH 6.78, Anion Gap 48, lactate 27.6 mmol/L, bicarbonate 5.2mEq/L). Labs significant of AKI (Creatinine 3.5mg/dL), transaminitis (AST/ALT 300s U/L, leukocytosis (40.0 x 103/L, high blood ETOH levels (162 mg/dL), hyperglycemia (401 mg/dL), and ketonuria. CT imaging revealed bilateral pulmonary dependent ground glass opacities. She was intubated after failing BiPAP, admitted to intensive care unit, started on an insulin and bicarbonate infusion, broad-spectrum antibiotics, ETOH withdrawal management and continuous renal replacement therapy (RRT) for metformin clearance. pH, bicarbonate and lactate corrected to normal after 24 hours. She was extubated after 2 days and shock resolved. On discharge her metformin and empagliflozin was held. Discussion and Conclusion: This case illustrates a critically ill patient with profound HAGMA in the context of MALA, compounded by ETOH liver disease and AKI—both contributing to impaired lactate clearance and increased production. MALA generally occurs in the setting of renal or hepatic impairment, as metformin inhibits mitochondrial respiration, increasing anaerobic metabolism and lactate production. While diabetic or alcoholic ketoacidosis, and sepsis-related lactic acidosis are all potential contributors to her acidemia, the disproportionately elevated lactate level raises strong suspicion for metformin toxicity, especially considering ongoing metformin use and AKI impairing metformin clearance. Given that mortality in severe lactic acidosis can reach up to 50%, particularly when associated with shock and multi-organ failure, early and aggressive intervention, including RRT facilitating the clearance of metformin, is essential to improve outcomes. Management in such scenarios requires a multifaceted approach as above. While renal function is commonly assessed, liver functions are often overlooked, despite their role in increasing the risk of MALA. Ongoing hepatic dysfunction and ETOH dependence should prompt primary care providers to reconsider metformin prescription to prevent lactic acidosis. Presentation: Monday, July 14, 2025
Source: Journal of the Endocrine Society
Institution: Guthrie Robert Packer Hospital
Language: English
Subfield: Endocrinology, Diabetes and Metabolism
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $3,255
OpenAlex ID: W7093324835
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