180 Comprehensive Study of Posttraumatic Cerebral Energy Metabolism

Abstract

INTRODUCTION: Previous 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. METHODS: CMRs 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. RESULTS: Post-TBI CMRO2 (0.599 vs 1.391; P CONCLUSION: In 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. Language: en