Case report pH 6.68—surviving severe metformin intoxication*

Metformin, a widely used anti-diabetic agent of the biguanide family, although generally safe, holds the risk of developing a potentially lethal acidosis. The association between lactic acidosis and metformin is well-established but rarely seen in patients taking this medication. Its elimination relies solely on kidneys’ excretion, so its accumulation is feasible in just two circumstances: renal failure (RF) and acute overdosage. At normal dosage, a toxic accumulation of drug requires time after the development of RF, due to metformin high clearance. About 90% of the drug is eliminated by glomerular filtration and tubular secretion (serum half-life of 1.5–5 h). Moreover, RF is itself associated with acidosis as it impairs kidneys’ ability to excrete protons. Acute intoxication on the other hand is a viable option in those cases where renal function is normal and can correlate with a psychiatric disorder. The mechanism thought to be responsible for lactic acidosis is suppression of gluconeogenesis forming lactate, pyruvate, glycerol and amino acids leading to lactate accumulation, a risk that is increased by either chronic or acute RF (ARF). Usually hyperlactatemia is the most common finding leaving lactic acidosis for the most severe intoxications.