Traumatic brain injury (TBI) is a significant cause of pediatric morbidity and mortality in the United States. More than 6000 children die each year as a result of traumatic brain injury, another 60,000 are hospitalized, and an additional 630,000 seek care in emergency departments (EDs).¹ The Centers for Disease Control (CDC) reports that TBI-related ED visits have increased for all age groups from 2001 to 2010, with pediatric ED visits in 2010 ranging from 900 per 100,000 for children aged 5 to 14 years to greater than 2000 visits per 100,000 for children aged less than 4 years.² Among children who die from trauma, 90% have an associated brain injury.³ Hospitalization rates for mild traumatic brain injury have decreased significantly in the past 20 years, while rates for moderate and severe injuries are relatively unchanged.⁴ Pediatric brain injury leads to major morbidity from physical disability, seizures, and developmental delay. The most common cause of head injury in younger children is falls, while adolescents are more frequently injured as a result of assault, sports activities, or motor vehicle crashes.^1,5 Deaths in all pediatric age groups related to TBI are more commonly caused by motor vehicle collisions and assault.¹ Boys are injured more commonly than girls, and in particular, boys aged 0 to 4 years have the highest rates of head injury–related ED visits compared with all other age groups.²

Primary brain injury occurs as a result of direct mechanical damage inflicted during the traumatic event. Secondary injuries occur from metabolic events such as hypoxia, ischemia, or increased intracranial pressure. The prognosis for recovery depends on the severity of the injuries. Anatomic features, specific injuries, and intracranial pressure physiology are important components in the pathophysiology of pediatric brain injury.

The scalp is the outermost structure of the head and adjacent to the galea (Fig. 24-1). Beneath the galea is the subgaleal compartment where large hematomas may form, especially in infants and young children. The outer and inner tables of the skull are separated by the diploic space. The thin, fibrous dura is next, and it contains few blood vessels compared with the underlying leptomeninges, the arachnoid and pia. Small veins bridge the subdural space and drain into the dural sinuses. Dural attachments partially compartmentalize the brain. In the midline, the falx cerebri divides the right and left hemispheres of the brain. The tentorium divides the anterior and middle fossa from the posterior fossa, with an opening for the brain stem. Cerebrospinal fluid surrounds the brain within the subarachnoid space.

The outer structures protect the brain during everyday movements and minor trauma; however, these features can inflict damage when significant force is applied or sudden movement occurs. Movement of the brain within the vault along the uneven base of the skull may injure brain tissue. The unyielding, mature skull can contribute to brain injury when brain edema or an expanding hematoma develops. Subsequently, herniation across compartments can cause compression of vital structures, ischemia from vascular occlusion, and infarction.

In infants, the open sutures and thin calvarium produce a more flexible skull capable of absorbing greater impact. Incomplete myelinization contributes to greater plasticity of the brain as well. This flexibility permits more severe distortion between skull and dura and cerebral vessels and brain, increasing susceptibility to hemorrhage. Finally, the disproportionately large size and weight of the head compared with the rest of the body of infants and young children contribute to an increased likelihood of head injury.

The scalp is richly vascularized and if injured can bleed profusely. This can lead to hemodynamically significant blood loss from relatively small lacerations, especially in infants and very young children. Carefully explore open scalp wounds for skull integrity, depressions, or foreign bodies. The presenting sign of a subgaleal hematoma is an extensive soft-tissue swelling that occurs several hours or days after the traumatic event and is commonly associated with a skull fracture. A subgaleal hematoma can persist for several days to weeks.

Linear nondepressed skull fractures are estimated to comprise 75% of all skull fractures, and occur at the point of impact.³ The presence of a skull fracture indicates a significant blow to the head, and children with skull fractures are more likely to have an associated intracranial injury. However, the absence of a skull fracture does not exclude the presence of intracranial injury.^3,6 “Growing fractures” are unique to infants and young children. They may occur after a skull fracture in children younger than 2 years of age when associated with a dural tear. Rapid brain growth post-injury may be associated with the development of a leptomeningeal cyst, which is an extrusion of cerebrospinal fluid or brain tissue through the dural defect. Thus, children younger than 2 years with a skull fracture require follow-up to detect a growing fracture.

Basilar skull fractures typically occur at the petrous portion of the temporal bone, although they may occur anywhere along the base of the skull. Clinical signs suggesting a basilar skull fracture include hemotympanum, cerebrospinal fluid otorrhea, cerebrospinal fluid rhinorrhea, periorbital ecchymosis (raccoon eyes), or postauricular ecchymosis (Battle’s sign). Plain skull radiographs or routine head CT scans may be insufficient for diagnosis and require detailed CT imaging of the temporal bone.

Acute subdural hematomas are the most common TBIs, followed by subarachnoid hemorrhage, and cerebral contusion with variability according to GCS score and age. Children commonly have more than one TBI.⁵ Subdural hematomas usually result from tearing of the bridging veins and typically occur over the cerebral convexities. Acute interhemispheric subdural hematomas may be caused by shaking/impact injuries of abuse. Subdural hematomas are often associated with more diffuse brain injury. They may progress more slowly than epidural bleeds, with symptoms commonly including irritability, vomiting, and alterations in mental status.

Epidural hematomas occur less commonly, but may be life threatening. Prompt diagnosis and surgical intervention make an excellent outcome possible. Most occur in combination with a temporal skull fracture and meningeal artery bleeding; the remainder are venous in origin. Signs and symptoms include headache, vomiting, and altered mental status, which may progress to signs and symptoms of uncal herniation with pupillary changes and hemiparesis. Patients classically present with an initial lucid period followed by a rapid deterioration in mental status as the hemorrhage increases in size (Fig. 24-2).

Subarachnoid hemorrhages are more commonly associated with lower GCS scores, and they are frequently associated with skull fractures, parenchymal contusions, and cerebral edema.^5,7 Parenchymal contusions are bruises or tears of brain tissue. Bony irregularities of the skull cause these cerebral contusions as the brain moves within the skull. A coup injury occurs at the site of impact, whereas a contrecoup injury occurs at a site remote from the impact. Intraparenchymal hemorrhages may also occur from shearing injury or penetrating wounds. They often occur in association with intracranial hematomas or skull fractures. Signs and symptoms may include decreased level of consciousness, focal neurologic findings, and seizures.

Penetrating injuries result from sharp object penetration or gunshot wounds. Extensive brain injury is common, and severity depends on the path of the object and location and degree of associated hemorrhage.

A concussion is defined as a rapid onset of short-lived neurologic dysfunction with or without loss of consciousness following a traumatic event.⁸ Concussions occur in the absence of abnormalities on standard neuroimaging. Symptoms resolve spontaneously or after a brief period of rest, although a small number of concussion patients will have symptoms that persist for a prolonged period as a postconcussive syndrome.^9,10 One study reported symptom duration of 21 to 28 days after concussion for athletes.¹⁰ Symptoms may include amnesia, vomiting, headache, dizziness, visual changes, instability of balance, as well as cognitive impairments, emotional changes, and abnormal sleep patterns.

Diffuse brain swelling occurs more often in children than in adults. The swelling usually results from a shearing or acceleration–deceleration injury. Prolonged coma or death may occur.

Nonaccidental trauma in infants and young children may result in the constellation of subdural hematoma, subarachnoid hemorrhage, and localized or diffuse brain edema (Fig. 24-3). Retinal hemorrhages, rib fractures, long-bone fractures, and external signs of injury may also be present. Symptoms of nonaccidental traumatic brain injury in infants may be nonspecific but severe and include lethargy, vomiting, irritability, seizures, apnea, and alteration in consciousness.^11,12

The total volume of the intracranial vault is constant. Approximately 70% of this volume is brain, 20% is cerebrospinal and interstitial fluid, and 10% is blood. If any one of these three components increases in volume, then the other two compartments must decrease or intracranial pressure rises. The main component of compensation is a displacement of cerebrospinal fluid into the spinal canal. Once this compensatory mechanism is maximized, any additional increases in volume cause elevation of intracranial pressure to abnormal levels (>15–20 mmHg). Cerebral perfusion becomes impaired and irreversible ischemic damage to the brain ensues.