Cerebral extracellular lactate increase is predominantly nonischemic in patients with severe traumatic brain injury

Growing evidence suggests that endogenous lactate is an important substrate for neurons. This study aimed to examine cerebral lactate metabolism and its relationship with brain perfusion in patients with severe traumatic brain injury (TBI). A prospective cohort of 24 patients with severe TBI monitored with cerebral microdialysis (CMD) and brain tissue oxygen tension (PbtO(2)) was studied. Brain lactate metabolism was assessed by quantification of elevated CMD lactate samples (>4 mmol/L); these were matched to CMD pyruvate and PbtO(2) values and dichotomized as glycolytic (CMD pyruvate >119 mu mol/L vs. low pyruvate) and hypoxic (PbtO(2)