Severe lactic acidosis except for shock states

Abstract

The development of lactic acidosis in a patient admitted in the intensive care unit (ICU) usually indicates a severe clinical situation. Etiologies of lactic acidosis are multiple and classified as A-type in relation to tissue hypoxia and B-type including all cases related to underlying primary diseases, poisonings and iatrogenic events as well as inborn errors of metabolism. Circulatory failure is clearly the most typical situation associated with lactic acidosis in the ICU; however, this cause will not be discussed in this review. Increase in blood lactate concentrations results from an unbalance between lactate production (stimulation of anaerobic glycolysis or dysfunction of mitochondria respiratory chain) and clearance. Toxic exposures represent a major cause of lactic acidosis, including intoxications with metformin, cyanide, valproic acid, nucleoside/tide reverse transcriptase inhibitors, and adrenergic stimulants. In the presence of ICU-acquired lactic acidosis, iatrogenic hypotheses should be suggested like propofol infusion syndrome, propylene glycol intoxication, as well as beta-adrenergic catecholamine- and linezolid-related side-effect. Other etiologies, sometimes obvious and sometimes more difficult to assess, include liver insufficiency and seizures or status epilepticus especially if tonic or clonic. More rarely, lactic acidosis leads to the identification of an underlying solid cancer or blood malignancy. Finally, in selected patients at risk, vitamin deficiencies like thiamine and biotin as well as inborn errors of sugar metabolism should be suspected. In all lactic acid cases as no specific treatment of increased blood lactate exist, patient management should rely on the treatment of the underlying etiology and be prompt once the diagnosis is assessed, since this severe condition is usually associated with a bad final outcome.