Description

Traumatic brain injury (TBI): damage to the brain from accidental or nonaccidental trauma

• Children >1 year: Glasgow Coma Scale (GCS) <14, amnesia >15 minutes for event, penetrating head injury (see Appendix, Table 5)
• Children <1 year: any loss of consciousness (LOC), protracted emesis, suspected abuse (see Appendix, Table 6)
• Mild brain injury: GCS >14
• Severe brain injury: usually initial GCS <9

Epidemiology

• Trauma, number 1 cause of death of children >1 year; head injury most common contributor to morbidity and mortality
• Almost 500,000 emergency department visits each year for TBI for those aged 0 to 14 years; males age 0 to 4 years highest rate of TBI emergency department visits
• 75% of TBIs each year are mild.
• <2 years old: Nonaccidental trauma is principal cause of TBI.
• >2 years old: Falls (~37%) are most common cause of trauma.
• For severe TBI, nonaccidental trauma remains principal cause in young children.
• Motor vehicle accidents in older children, although penetrating injuries becoming more common

Pathophysiology

• Primary
  • Focally applied forces: lacerations, penetration injuries, skull fractures
  • Contusions, intracerebral hematomas uncommon; epidurals, classic subdurals <10% in children
  • Acceleration–deceleration/shearing forces: cervical spine injuries, diffuse axonal injury (DAI), nonaneurysmal subarachnoid hemorrhage, subdural hematoma (SDH) from shear forces
• Secondary
  • Extension of injury to viable tissue/entire brain
  • Dysautoregulation of cerebral blood flow, neuroexcitotoxicity, and inflammatory mediators. In severe TBI, CT or MRI signs of edema may progress over 3 to 5 days (see “Treatment”).
• Age-specific pathophysiology:
  • Infants/toddler
    • Shear forces on the brain due to acceleration/deceleration avulse axons from their cell bodies causing DAI; often compounded by tearing and bleeding of dural veins
    • Unmyelinated infant brain absorbs rather than transfers impact. Immature, distensible skull renders brain less likely to contuse or herniated but more likely to sustain diffuse secondary injuries, with swelling.
    • Subgaleal hematoma, cephalohematoma (below the periosteum), and caput succedaneum (confined to the superficial scalp) at birth do not predict brain injury.
    • More severe birth trauma can result in SDH.
    • Bilateral interhemispheric SDH suggests nonaccidental trauma.
    • Diffuse injuries secondary to shaken impact syndrome can lead to cerebral swelling with secondary infarction and/or decreased central respiratory control, leading to apnea, hypoxia, seizures, and cerebral edema.
    • Suspect nonaccidental trauma with growing skull fracture, if >1 cranial bone involved or if other injuries are present.
  • Older children/adolescents
    • Mild TBI likely due to neuronal disruption, potassium efflux with release of glutamate; increases demand of ATP and glucose
    • Still more subject to DAI than adults due to incomplete myelination
    • Projectile injuries in adolescent population may cause prolonged brain swelling (particularly close-range gunshot wounds).