Lactic acidosis is a relatively frequent
acid-base disorder in a hospital setting. It is defined by the association of an arterial pH inferior to 7.35 and an arterial
lactate level superior to 5 mmol/l. Classically, 2 types of
acidosis are distinguished on the basis of their mechanisms of onset: the type A, with evident clinical signs of tissue hypoperfusion and the type B, more are, without apparent
hypoxia. This last category is observed in various circumstances such as diabetes,
acute liver failure,
poisoning and, more rarely, inborn errors of carbohydrate metabolism. Treatment aims primarily at the correction of the cause. The efficacy of
sodium bicarbonate is presently debated, considering the risk to worsen
hyperlactatemia and to induce hyperosmolarity or rebound
alkalosis. The administration of dichloroacetate, an activator of
pyruvate dehydrogenase, permits to correct partially the
lactic acidosis but is not harmless especially in case of prolonged administration. Other therapeutic modalities are evoked. Arterial
lactate level is a reliable prognostic index of
shock, because blood values do not depend only of the
oxygen debt but also of the efficacy of hepatic and renal
lactate uptake. Sequential measurements are recommended.