skip to main content

Lactic acidosis from metformin accumulation — FFICM MCQ

Instant feedback + full explanation. One question, done properly.

HardRenal and MetabolicLactic acidosis from metformin accumulationFFICM

A 73-year-old man with type 2 diabetes is admitted with diarrhoea, AKI and shock. He takes metformin and ramipril. ABG shows pH 7.02, lactate 11.5 mmol/L and bicarbonate 7 mmol/L. CT abdomen shows no ischaemic bowel and cultures are pending. What is the most appropriate management?

Educational content. Not a substitute for clinical judgement or local policy.

Reveal the answer and explanation

Correct answer: BStop metformin, support perfusion and discuss renal replacement therapy

The correct answer is B, stop metformin, support perfusion and discuss renal replacement therapy. This patient has profound type B lactic acidosis (lactate 11.5 mmol/L, pH 7.02, bicarbonate 7 mmol/L) in the context of AKI and diarrhoeal illness, the classic setting for metformin accumulation because the drug is renally excreted and AKI removes its clearance route, precipitating metformin associated lactic acidosis (MALA). Diagnosis is clinical (metformin exposure plus AKI plus unexplained severe lactic acidosis with no ischaemic bowel on imaging) rather than reliant on a single confirmatory test, so the priority is to withhold the culprit drug, aggressively resuscitate to restore renal perfusion, and involve critical care early for renal replacement therapy (RRT), which both corrects the severe acidosis and clears accumulated metformin. This matches standard critical care and BNF guidance that metformin must be stopped in acute illness with dehydration or renal impairment because of the lactic acidosis risk. Why the other options are wrong: A. Serum amylase: This investigates pancreatitis, which is not suggested by the clinical picture (diarrhoea, AKI, shock with a metabolic, not epigastric, presentation) and does not address the immediate life threatening acidosis. C. Lumbar puncture before resuscitation: Performing an invasive procedure before stabilising a shocked, profoundly acidotic patient risks cardiovascular collapse and is not indicated here as there is no suggestion of meningitis; resuscitation always precedes non-emergent invasive tests. D. D-dimer: This is used to help exclude venous thromboembolism, not to exclude MALA or lactic acidosis, and a raised D-dimer would be non-specific in a critically unwell septic/shocked patient. E. HbA1c: This reflects glycaemic control over the preceding 2 to 3 months and has no role in guiding management of acute severe lactic acidosis or AKI. Key point: Severe lactic acidosis with AKI in a patient on metformin should trigger immediate drug cessation, perfusion optimisation and early consideration of renal replacement therapy rather than pursuit of alternative single diagnostic tests.

Reference: BNF (NICE/BNF), Metformin hydrochloride, Cautions and Lactic acidosis: metformin should be stopped in patients with conditions that may cause tissue hypoxia or acute deterioration in renal function, such as dehydration, severe infection or shock; https://bnf.nice.org.uk/drugs/metformin-hydrochloride/