The still-developing nervous system holds the potential for greater recovery from traumatic brain injury while also carrying the risk of disordered development, dysplasia, and other adverse sequelae. At the same time, mechanical factors may differentiate pediatric from adult injury such as the unfused or less mineralized calvarium and the narrower subarachnoid and sulcal spaces. Pediatric head trauma also differs not only from adult but also within the childhood age spectrum. The mechanisms, including not only the velocity but also the intentionality—whether the injury was accidental— strongly affect the severity distribution. Greater impact force, as seen in vehicular (especially unrestrained)-induced injury or nonaccidental injury, skews the distribution toward more severe presentation and worse outcomes.

Trauma is the major cause of morbidity and mortality in childhood and nervous system involvement is the biggest determinant of severity. Children account for about one-half million incidents of traumatic brain injury (TBI) per year in the United States, a rate disproportionately high for their part of the overall population. Although the mechanisms and circumstances vary across the pediatric age range—with child abuse dominant in infancy and self or mutual violence, vehicular, firearm use, and other high-risk behaviors prevalent in adolescence—it remains true across the pediatric age range that the causes are to a great extent socially influenced rather than purely sporadic and therefore often at least potentially preventable. As such, the reduction of the immense toll of brain injury relies on two distinct approaches: prevention of primary injury and of secondary injury.

The former is an educational and legal as much as medical task. Initiatives such as infant car seats, bike helmets, and statewide abuse recognition and reporting systems are critical components. Although recent public attention to cumulative and late effects of concussion was largely generated by cases of prominent adult athletes, much of the response has been to change practice from middle school through college, the duration of the athletic careers of most of the public.

The pathophysiology of primary and secondary brain injury is distinct. The primary injury depends on linear and angular velocity, mechanism (penetrating or closed), biomechanical factors (contrecoup injury), trajectory, and compartment. The consequences can be considered based on the tissue impacted. Epidural and subdural bleeds contribute to injury largely due to the pressure they cause by stealing intracranial space. Gray matter architecture can be disrupted in concussion, contusion, or abrasion. Cortical projections and corticocortical connections can be interrupted by penetrating foreign bodies or bone fragments. Less obvious on initial computed tomography imaging but highly influential on outcome is the diffuse axonal injury, the shearing of fiber tracts from torsional forces. Cerebral ischemia due to vascular dissection, occlusion, and thrombosis can be as injurious as force to the parenchyma directly. In intentionally inflicted trauma, multiple mechanisms may have contributed. The injuries of the “shaken baby” can be compounded by impact, partial strangulation, or carotid compression.

Secondary injury encompasses all subsequent deleterious processes at various levels of organization (Table 146.1). On a macroscopic scale, the pediatric brain is at high risk from loss of volume. As brain growth drives skull growth in childhood and the atrophy of adulthood is not yet present, accommodation of hematoma and cerebral edema (which evolves largely over the first 3 days post injury) is poor. Although the dura and unfused calvarium of the neonate and infant flexibly allows reshaping (as required during parturition), it maintains intracranial volume nearly constant as it is inelastic to outward stretch. Consequently, babies too are subject to severe restriction of the intracranial vault. Pressure can cause herniation, compromise cerebral perfusion pressure globally, or compress adjacent cerebral vessels exacerbating tissue compromise.

Multiple factors threaten the already wounded cortical tissue. Cerebral autoregulation is less robust after injury, increasing the risk that cerebral perfusion pressure will fall beneath the compensated range. Injury to the normally well-sealed and precisely regulated blood-brain barrier implies loss of control of the neuronal microenvironment.

At the cellular level, excitotoxicity due to excessive glutamate release, calcium entry, and hyperactivated intrinsic membrane conductances place increased metabolic demands and interfere with cell volume regulation. At the same time, mitochondrial dysfunction and impaired perfusion make the cells less able to meet these increased demands, leading to cell death.

Although overlapping with mechanisms of secondary injury in the adult, the distribution of injury may differ in the child because of incomplete myelination and selective expression of transmitter and voltage-dependent conductances in specific developmental windows.