LAUSR

In recent years there has been increasing interest in the measurement of lactate as one component in the assessment of metabolic status. Lactate concentration is an end metabolite of anaerobic metabolism, and is therefore elevated when there is poor perfusion of the microcirculation, for example in septic shock.1 For this reason, it is widely measured in emergency and intensive care units. Inexpensive and portable microvolume (0.5– 10 μl) lactate analyzers were developed in the early 1990s, primarily for use by athletes to evaluate the intensity of their training. There are a variety of pointofcare (POC) devices, which are all robust, produce results rapidly, and use only about onetenth of the volume of blood required for a full bloodgas analysis.2 Therefore they have been increasingly used to evaluate fetal acidemia during labor. The initial methodology of POC lactate measurement was colorimetric, where an enzymatic reaction linked the end product of the reaction to a color, and the change of color was proportional to the lactate concentration. The light wavelength change was measured and translated into a lactate concentration by an appropriate algorithm. Subsequently, electrochemical devices were developed in which the lactate in the blood sample reacts with the enzyme lactate oxidase and produces an electrical voltage measured by an embedded sensor, from which the lactate concentration can be derived from previous calibrations. The correlation between the color change method and the currently used voltage system is high (r = 0.80– 0.85). However, these measures have to be converted into a lactate concentration from a reference curve. There is no agreed standard for calibrating the measurement algorithms. The Lactate ProTM (LP1, an electrochemical device) algorithm was published 1993.3 When the meter was commercially launched in 1998, the manufacturer had modified the algorithm to increase the value of the lactate measurement by about 25% from the research prototype, probably to produce results similar to other available meters. In 2015 an updated version, Lactate Pro 2TM, was launched (Lactate Pro 2TM, LP2), in which the algorithm had again increased the lactate value outputted from a standard sample by approximately 50%.4 Because LP1 had been the only device from which a normal range of fetal blood sample lactate had been derived,5 the higher values outputted by LP2 required a conversion factor to be applied if the previous normative ranges were to be used. Erich Saling developed the technique of fetal scalp blood sampling (FBS) and studied the distribution of pH from a series of 1085 samples from 306 fetuses with uncomplicated births and with normal Apgar scores.6 He concluded from this analysis that a fetal scalp blood pH > 7.25 is normal, 7.25– 7.20 is preacidemic (with repeat sampling recommended within 30 min) and <7.20 is acidemic, suggesting intervention, ie, delivery. These values have since come to be regarded as a reference standard. When the Lactate ProTM (LP1) was introduced, FBS with pH analysis was already established as an adjunct to electronic fetal monitoring. Consequently, it was considered ethically inappropriate to perform FBS on a lowrisk population without any indication, just to provide a normal range. In 1999, an observational study by Kruger et al. was published with both pH and lactate analysis of 814 scalp blood samples performed in a population of fetuses with fetal heart rate (FHR) patterns indicating the need for further investigation.5 In this population, the 25th centile for pH was 7.21, close to the previously set acidemic value of 7.20 suggested by Bretscher and Saling.6 The 75th centile for lactate (as the corresponding measure of acidemia) was 4.8 mmol/L, which was therefore suggested as the cutoff value for acidemia, with 4.2– 4.8 representing preacidemia. The proportion of acidemia measured in any sampled population depends upon the characteristics of the population and the indications for FBS. The more liberal the sampling indications (eg, with milder FHR changes), the smaller the proportion of “acidemic” cases will be. Using the reference intervals proposed by Kruger et al.,5 a large randomized controlled multicenter trial of lactate vs pH for assessing acidemia was performed by WibergItzel et al., including 2992 women and published in 2008.7 There was no significant difference in the proportions of babies assessed to be acidemic at birth after using FBS with pH or lactate (3.6% and 3.2%, respectively) and there was a similar correlation with neonatal outcome as assessed by Apgar scores. There was, however, a large difference in failure to obtain a meaningful result— 10.4% with pH but only 1.2% with lactate. It is important that FBS measurements should not give false reassurance. The falsenegative rate for birth acidemia was reassuringly small; six babies had a pH <7.00 and 10 had metabolic acidemia at birth when fetal scalp blood pH determined within 60 min before delivery was >7.20. Corresponding figures for cases with scalp blood lactate <4.8 mmol/L were none with pH <7.00 and six with metabolic acidemia.