Lactate clearance in the acutely traumatized patient.

1162 December 2012 W HEN oxygen delivery falls below a critical threshold, the anaerobic threshold, the amount of oxygen available for consumption is not able to meet the needs of cells. These imbalances result in cellular hypoxia, resulting in the failure of mitochondrial oxidative phosphorylation, and as a result energy metabolism becomes wholly dependent on anaerobic glycolysis.1 Anaerobic glycolysis sharply increases the production of cellular lactate, which diffuses into the blood during prolonged cell ischemia. Elevated circulating lactate concentration thus often indicates widespread inadequate tissue oxygenation due to inadequate oxygen delivery and/ or consumption.2 In this issue of ANESTHESIOLOGY, Regnier et al.3 present a prospective cohort analysis of the utility of lactate and lactate clearance measurements in the setting of the acutely traumatized patients. Numerous previous studies have documented the utility of lactate as a prognostic indicator in shock states.2,4 The use of lactate measurements is gaining recognition in critical care settings as a potential indicator of tissue hypoperfusion.5,6 Furthermore, lactate screening as a method of risk stratification and prognosis has been shown to be beneficial in hemodynamically stable patients with suspected infection.5,7 Underscoring the importance of these data is the fact that point-of-care testing performed at the patient’s bedside is becoming more common.8,9 There are many evidence based, data-driven, and logical arguments why lactate clearance monitoring is a superior therapeutic target than oxygen-derived variables. First, the published experimental (randomized trial) evidence supporting the use of lactate clearance as a therapeutic target is more robust in terms of the number of multicenter studies.10,11 Unlike oxygen-derived variables, the ability to clear lactate has consistently predicted better survival in published studies of resuscitation.12–15 Second, elevated lactate levels reflect the total picture of energy metabolism in the acutely stressed patient. Elevated blood lactate level has long been known to reflect anaerobic metabolism from tissue hypoxia in critically ill patients.2 However, besides these anaerobic processes, aerobic (metabolic) mechanisms that affect the host’s efficiency of energy transfer also contribute to lactate production. Cytokine-mediated glucose uptake and catecholamine-stimulated Na-K pump overactivity both can result in increased pyruvate production that eventually will overwhelm the catalytic capacity of pyruvate dehydrogenase and result in increased lactate due either to mass effect, sepsis-induced pyruvate dehydrogenase dysfunction, or both. In addition, reduced lactate clearance may reflect globally impaired metabolic function by the liver and kidney, both of which normally contribute to systemic lactate disposal through anaplerosis, a mechanism that carboxylates lactate and delivers it to the tricarboxylic acid cycle, independent of the action of pyruvate dehydrogenase.16 Thus, lactate clearance biologically reflects more of the general homeostasis of the host and provides more meaningful data about the overall adequacy of the resuscitative processes. Lactate clearance has previously been shown to be of value in monitoring several critically ill populations including those with sepsis10,12 and cardiac arrest.17 With the present publication by Regnier et al. we now have Lactate Clearance in the Acutely Traumatized Patient