Lactic acidosis update for critical care clinicians

Lactic acidosis is a broad-anion gap metabolic acidosis caused by lactic ac id overproduction or underutilization. The quantitative dimensions of these two mechanisms commonly differ by I order of magnitude. Overproduction of lactic acid, also termed type A lactic acidosis, occurs when the body must regenerate ATP without oxygen (tissue hypoxia). Circulatory, pulmonary, or hemoglobin transfer disorders are commonly responsible. Overproduction of l actate also occurs with cyanide poisoning or certain malignancies. Underuti lization involves removal of lactic acid by oxidation or conversion to gluc ose. Liver disease, inhibition of gluconeogenesis, pyruvate dehydrogenase ( thiamine) deficiency, and uncoupling of oxidative phosphorylation are the m ost common causes. The kidneys also contribute to lactate removal. Concerns have been raised regarding the role of metformin in the production of lact ic acidosis, on the basis of individual case reports. The risk appears to b e considerably less than with phenformin and involves patients with underly ing severe renal and cardiac dysfunction. Drugs used to treat lactic acidos is can aggravate the condition. NaHCO3 increases lactate production. Treatm ent of type A lactic acidosis is particularly unsatisfactory. NaHCO3 is of little value. Carbicarb is a mixture of Na,CO, and NaHCO3 that buffers simi larly to NaHCO3 but without net generation of CO2. The results from animal studies are promising; however, clinical trials are sparse. Dichloroacetate stimulates pyruvate dehydrogenase and improves laboratory values, but unfo rtunately not survival rates, among patients with lactic acidosis. Hemofilt ration has been advocated for the treatment of lactic acidosis, on the basi s of anecdotal experiences. However, kinetic studies of lactate removal do not suggest that removal can counteract lactate production in any meaningfu l way. The ideal treatment is to stop acid production by treating the under lying disorder.