Cerebrovascular Pathophysiology in Pediatric Traumatic Brain Injury

Abstract

Traumatic brain injury (TBI) is the leading cause of traumatic morbidity and mortality in children. Although there is increasing information concerning TBI in adults and experimental animal models, relatively little is known regarding cerebrovascular pathophysiology specific to children. A review of the pertinent medical literature. Systemic and cerebral hemodynamic factors such as hypotension, hypoxia, hyperglycemia, and fever are associated with poor outcome in pediatric TBI. Similarly, cerebral autoregulation is often impaired after TBI and may adversely affect outcome, especially if systemic hemodynamics are altered. Furthermore, CO2 vasoreactivity may be altered after pediatric TBI and lead to either cerebral ischemia or hyperemia. Understanding the effect of pediatric TBI on the cerebral circulation is needed to potentially develop protocols to improve outcome in this vulnerable population. Specifically, changes in pediatric cerebrovascular physiology and pathophysiology, including CO2 vasoreactivity and pressure autoregulation, must be understood and their mechanism elucidated.