Brain Injury, Traumatic

Brain Injury, Traumatic is a topic covered in the 5-Minute Pediatric Consult.

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Basics

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).

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