• Joshua Robert Dusick, Thomas C Glenn, Paul M Vespa, and Neil A Martin.
• Neurosurgery. 2015 Aug 1;62 Suppl 1:226.

IntroductionPrevious studies have documented dysfunctional cerebral metabolism following traumatic brain injury (TBI), characterized by reduction in cerebral metabolic rates (CMRs) of glucose and oxygen. In our largest series to date, here, we provide further evidence and time courses of these metabolic changes.MethodsCMRs for oxygen, glucose, and lactate were determined in 74 TBI subjects over 6 postinjury days by a modified Kety-Schmidt method and in 35 normal subjects. Comparison to normal, and time courses, utilized a mixed-effects model, accounting for repeated measurements in the trauma group. Time courses are represented as a restricted cubic spline with 3 interior knots placed at the quartiles of postinjury hours. A random intercept for subject was used as the random-effects structure.ResultsPost-TBI CMRO2 (0.599 vs 1.391; P < .001), CMRglucose (0.193 vs 0.296; P < .001), CMRlactate (0.002 vs -0.024, respectively; P = .004), and metabolic ratio (3.92 vs 4.931; P = .006) all differed significantly from normal. After initial increase in glucose utilization within 24 hours, CMRglucose is depressed and time courses demonstrate persistently depressed glucose and oxygen metabolism. Oxygen metabolic depression is out of proportion to that of glucose, demonstrated by diminished metabolic ratio. Most patients demonstrate cerebral lactate uptake, contrary to the traditional view and what would be expected for cerebral ischemia/anaerobic metabolism. This is consistent with our prior observations that lactate may be used as a fuel by the injured brain.ConclusionIn our largest series of patients to date, we have demonstrated that posttraumatic cerebral metabolism is characterized by depressed glucose and oxygen metabolism that is persistent for at least 6 days postinjury. There is mismatch between glucose and oxygen utilization, indicated by diminished metabolic ratio, and frequent lactate uptake. Further study is required to fully characterize the dysfunctional metabolism, which may be a source of further secondary injury in the early postinjury period.

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