Lactate blood measurement in acute cyanide poisoning: effect of preanalytical delay and hydroxocobalamin uses as treatment.

Abstract

We quantify the impact of several variables including site of blood draw, delay in measurement, and use of the cyanide antidote hydroxocobalamin on detection of both normal (<2 mmol/L) and elevated (>6 mmol/L) human plasma lactate. An in vivo study assessed effects of venous or arterial origin of blood samples. Two in vitro studies assessed the effect of a 2 h delay in measuring plasma lactate concentrations, as well as the interference of low (100 μmol/L) and high (300 μmmol/L) plasma hydroxocobalamin concentrations on detecting normal and elevated levels of lactate. A relative change of 20% in the measured lactate concentration was considered clinically significant. There was no clinically relevant effect of the site of blood draw on lactate measurements. Plasma lactate concentrations were artificially increased by a delay of 2 h between blood draw and sample measurement. Under conditions where plasma lactate levels were in a normal range, the dose equivalent to 300 μmol/L hydroxocobalamin concentration caused an artificial increase in lactate measurements that could possibly be misinterpreted clinically as an elevation. Under conditions where plasma lactate levels were elevated, as would occur in cases of acute cyanide poisoning, neither the low nor high concentration of hydroxocobalamin caused a clinically relevant change in lactate measurements. Clinicians should be cautious in interpreting lactate concentrations if there has been a significant delay between blood draw and laboratory analysis, or when blood was collected shortly after the completion of hydroxocobalamin administration.