pH 6.68--surviving severe metformin intoxication.
Metformin, a widely used anti-diabetic agent of the biguanide family, although generally safe,1,2,3,4 holds the risk of developing a potentially lethal acidosis.5,6

The association between lactic acidosis and metformin is well-established but rarely seen in patients taking this medication.7 Its elimination relies solely on kidneys’ excretion,8 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,9 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.

A 47-year-old, apparently previously fit, non-insulin-dependent diabetic male was brought to the Emergency Department for hypoglycemia, agitation and hyperventilation. Ambulance crew found blood glucose level at 1.33 mmol/l (24 mg/dl) and administered 20 ml of 33% glucose solution followed by other 250 ml at 5%. At the arrival in the Emergency Room, the patient was confused and agitated with no signs of respiratory distress or shock.

Arterial blood gases (ABG) and laboratory tests are summarized in Table 1 and show a clear clinical presentation of acute metabolic acidosis of unknown etiology with respiratory compensation, as a result …