Pediatric Traumatic Brain Injury

Published on 10/02/2015 by admin

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Last modified 10/02/2015

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24 Pediatric Traumatic Brain Injury

Epidemiology

An estimated 615,000 traumatic brain injuries (TBIs) occur each year in patients younger than 19 years; this figure accounts for 26% of pediatric hospitalizations and 15% of all pediatric deaths.1 Children 0 to 4 years of age and older adolescents 15 to 19 years of age are most likely to sustain a TBI. Mild traumatic brain injury (mTBI), or concussion, represents the predominant form of acquired brain injury and accounts for 75% to 90% of all instances.2,3

Pathophysiology

The mechanisms of pediatric TBI are similar to those in adults, with falls being the most common cause. However, child abuse must be considered as an occult mechanism of head injury in preverbal children because abusive head trauma remains the most common cause of traumatic death in infancy. Findings in such patients may be subtle, with nonspecific symptoms (vomiting, fussiness) and no history of trauma. Clinicians must maintain a high index of suspicion for inflicted injury in young children. In older adolescents, sports are a common cause of concussive injury, and return to sports should be addressed in the discharge instructions.

As in adults, the pathophysiology of pediatric head trauma is related to the degree of force. With moderate force, injury can occur to the brain parenchyma, which primarily results in nonoperative lesions, or can involve vascular structures, which typically results in operative lesions.

Patients younger than 2 years are at higher risk for skull fractures, with the most common type being linear fractures. In infants, fractures may occur even after short falls (≤3 to 4 feet). The majority of fractures have an overlying hematoma or swelling; only 15% to 30% are associated with an intracranial injury.4 In general, linear skull fractures heal without incident. Rarely, in children with open fontanelles (<2 years old) and fractures with greater than 3-mm separation, a tear in the dura allows pulsation of cerebrospinal fluid (CSF) or herniated meninges, which impedes fracture healing and extends the fracture over time.5 This may become apparent months to years after the initial injury and usually requires surgical correction. Depressed skull fractures with greater than 5 mm of depression generally require surgical correction. Basilar skull fractures have classic findings on physical examination (raccoon eyes, Battle sign, hemotympanum) and may be associated with cranial nerve palsies (facial palsy, nystagmus, diplopia, and facial numbness), CSF rhinorrhea or otorrhea, and hearing loss.

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