The biguanide metformin is an oral antihyperglycemic drug widely used
in the management oi non-insulin-dependent diabetes mellitus (NIDDM) w
hich acts by improving hepatic and peripheral tissue sensitivity to in
sulin. Its major drawback is the possibility of developing lactic meta
bolic acidosis in patients suffering from renal failure or poor tissue
perfusion. However, the incidence is about 10- to 20-fold lower than
that reported with phenformin. We report the case of a 84-year-old wom
an with NIDDM and hypertension treated with metformin, glibenclamide,
enalapril and diuretics who presented with severe high-anion-gap metab
olic acidosis: pH 6.9, bicarbonate 5 mmol/L, potassium 7.4 mEq/L and s
erum creatinine 6.3 mg/dL. Following a first hemodialysis, performed w
ith bicarbonate and glucose dialysate, her plasma lactate level was 16
mmol per liter (normal levels: 1 to 2.2 mmol/L). A second session cor
rected these severe acid-base and electrolyte disorders. The rational
treatment of metformin-associated lactic acidosis seems to be, apart f
rom withdrawing the drug, short consecutive hemodialysis sessions and
slow intravenous infusion of 1/6 molar sodium bicarconate, avoiding Na
+ overload.