Abstract

Traumatic brain injury is the number one cause of death and disability among the pediatric population in the USA. The heterogeneity of the pediatric population is reflected by both the normal cerebral maturation and the age differences in the causes of TBI, which generate unique age-related pathophysiology responses and recovery profiles. This review will address the normal changes in cerebral glucose metabolism throughout developmental phases and how TBI alters glucose metabolism. Evidence has shown that TBI disrupts the biochemical processing of glucose to energy. This brings to question, "What is the optimal substrate to manage a pediatric TBI patient?" Issues related to glycemic control and alternative substrate metabolism are addressed specifically in regard to pediatric TBI. Research into pediatric glucose metabolism after TBI is limited, and understanding these age-related differences within the pediatric population have great potential to improve support for the injured younger brain.

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