Throughout training and in clinical practice, pediatricians will care for children who have sustained trauma to the central nervous system (CNS), which includes traumatic brain injury (TBI) and spinal cord injury (SCI). Unique to pediatrics, these injuries occur within the context of a developing nervous system. In addition to age-dependent acute physiologic responses to injury, CNS injury has the potential to disrupt synaptogenesis, axonal sprouting and pruning, myelination, and other ongoing molecular processes critical for optimal brain growth and function. Considering the essential role of the CNS in both automatic processes (eg, breathing, blood pressure control) and more sophisticated functions (eg, motor skills, language and learning, problem solving, behaviors and personality), brain or SCI can impair every aspect of a child’s daily life.
Given the complexity of nervous system injuries, interdisciplinary teams of providers should ideally be available from the time of injury (emergency medicine, intensive care, neurosurgery, neurology) and throughout subacute and chronic periods of recovery (physical medicine and rehabilitation, neurology, physical therapy, occupational therapy, neuropsychology, behavior psychology, education). As the medical home for children and their families, pediatricians should have a comprehensive understanding of the acute and chronic aspects of CNS injuries.
This chapter will focus specifically on TBI and SCI. However, more detail on the critical care management TBI can be found in Chapter 105.
ETIOLOGY AND PATHOPHYSIOLOGY
TBI is a leading cause of death and disability in children, and the incidence of mild TBIs has significantly increased in recent years. The most common mechanism of injury in children varies by age at the time the TBI was sustained. For example, TBIs in infants and younger children are more likely to result from falls or being struck, whereas motor vehicle accidents are the most common etiology of TBI in adolescents. Common to the different mechanisms of injury, TBI results from an external impact transmitting a direct or indirect force that disrupts brain tissue. This produces the primary injury and triggers a complex cascade of cellular and metabolic changes, resulting in ongoing, or secondary, brain injury. While TBI is clinically categorized as mild, moderate, and severe, the underlying pathophysiology is similar, although the extent of primary and secondary injury reflects clinical injury severity.
Primary injury results from direct injury to brain tissue (eg, penetrating injuries, skull fractures, and hematomas), the initial acceleration–deceleration forces, and rotational forces causing axonal shearing injury. Direct injury to brain tissue can result from skull fragments or objects entering and deforming the underlying cortex as well as from movement of brain parenchyma along the bony prominences of the skull. Direct injury can occur both at the site of impact (coup) as well as the corresponding brain opposite the site of injury (countercoup). Epidural hematomas (EDHs) classically result from traumatic disruption of meningeal arteries, presenting with initial ...