• Rapid acceleration/deceleration injuries, causing contusions, skull fractures, diffuse axonal injury (DAI), subdural hematoma, and cervical spine injuries; penetration injuries, causing brain lacerations; intracerebral hemorrhage; brain fungus
• Secondary phenomena (e.g., as a result of circulatory failure in the setting of body trauma or as a result of air/fat emboli after body/extremity trauma)

• A large head causes vulnerability to injury.
• A deformable, expansile skull usually protects from herniation due to cerebral edema or hematoma.
• The most commonly seen injuries are shear injuries and subdural hematoma (SDH) secondary to venous sinus tears in nonaccidental trauma.
• Diffuse axonal injury secondary to shaken impact syndrome can lead to cerebral swelling with secondary infarction and/or decreased central respiratory control, leading to apnea, hypoxia, and cerebral edema.
• Birth trauma commonly results in subgaleal hematoma, cephalhematoma, and caput succedaneum.
• More severe birth trauma can result in SDH due to tearing of the dura of falx.

• Usually due to motor vehicle accidents
• Projectile injuries in adolescent population
• Can result from nonaccidental trauma (usually correlated with other stigmata of assault)

• Incidence of general trauma is approximately 86 per 1,000, of which, 50% is head trauma.
• In children, 2 years of age, falls are the most common cause of trauma.

• Intoxications (of child, caretaker, others in the environment)
• Physical abuse/neglect
• Epilepsy

• Neurologic presentation is similar to that of other hypoxic—ischemic brain injuries (e.g., near-drowning), other causes of stupor/coma (see chapter), seizure activity (postictal encephalopathy).
• Distinction between simple concussion, DAI, and hypoxic—ischemic injury may be difficult at initial presentation but will clear as clinical picture/neuroimaging evolves.

• Eyewitness accounts are invaluable.
• A history of previous concussions or seizures, and details of who was caring for the child and when are all useful.
• Try to determine if the patient fell and injured the head or collapsed from a neurologic problem and fell with no additional injury.
• Laboratory testing depends on the problem list, but may include:
  • MRI: to evaluate posttraumatic hydrocephalus, or to evaluate extent and nature of injury for prognosis
  • EEG: to evaluate suspected seizures
  • Audiometry: especially with speech delay after head trauma
  • CSF tracer study: for suspected CSF leak
• Other complications
  • Infants can sustain growing fractures due to prolapse of meninges into the skull fracture, leading to formation of a leptomeningeal cyst.
  • The pediatrician should refer any patient with a known skull fracture who manifests a new swelling in area of old fracture to neurosurgery for three-dimensional CT imaging of the head.
  • Approximately 2% of persons with severe head injury will develop seizures.
  • Studies in adults showed no prophylactic benefit to phenytoin beyond 1 week postinjury.
  • Mild head injury (Glasgow coma score [GCS] of 13–15) was found to have no long-term effects on cognition in a large British study (n = 513,000).
  • Patients who have sustained moderate-to-severe head injury (GCS,13) often have academic difficulties, memory abnormalities, disinhibition, and other complications as described above.
  • Moderate-to-severe injury (with associated hemiplegia) can, in rare instances, cause symptomatic dystonia.
  • Static encephalopathy after head injury can be manifested as any combination of learning disabililities, seizure disorder, speech disorder, memory disturbance, and visual/hearing loss.

• Stabilization of neck to avoid exacerbation of potential spine injury is an immediate concern once airway, breathing, and circulation are ensured.
• Elevation of the head to 30 degrees may help to alleviate intracranial hypertension.
• Vital sign changes indicative of Cushing reflex (bradycardia, hypertension, irregular respirations) suggest intracranial pressure/impending brain herniation; these signs warrant prompt intubation and IV access.
• A C-spine collar should be worn until x-ray studies are done and found to be negative.
• HEENT examination for ecchymoses, retinal hemorrhages, bullet holes, penetrating bone fragments, herniating brain, hemotympanum, CSF leak (nasal or otic)
• Neurologic examination should document responsiveness (to voice, touch, pain), resting posture (flaccid, extensor, flexor), spontaneous movements (convulsions, writhing/agitated movements, purposeful), and oculomotor findings (see below).
• When carefully documented over time, these observations provide far more useful information to other caretakers than do coma scores.
• Papilledema may take 6 hours or more to develop if there is intracranial hypertension.
• Pupils: Marked asymmetry suggests brain herniation causing third-nerve palsy (see Follow-Up section, Pitfalls). Reactivity of pupils is best examined through an otoscope.
• Eye movements: Dysconjugate gaze is common in the unconscious patient and may not indicate a focal structural problem or elevated ICP. Absence of contraversive, lateral movement of eyes with passive head-turning (doll’s-eyes maneuver—if cervical spine has been cleared) suggests midbrain damage due to hemorrhage or axonal shear.
• Heart: Narrow pulse pressure or hypotension may be due to shock or pericardial tamponade. Bradycardia or irregular respirations may be due to intracranial hypertension.
• Careful examination for trauma or other clues: ecchymoses, open fractures, hematuria

• Plain films and CT scans are the imaging studies of choice on initial evaluation of a patient with suspected traumatic brain injury. They usually are readily accessible and provide key information for emergent patient management.
• C-spine plain film to evaluate bones from base of skull to C7 in whiplash injury or suspected shaken impact injuries
• Skull film (and long-bone films) if degree of injury is not consistent with history or history of fall from unclear height
• CT scan to evaluate for head and/or spine injury, including SDH as well as basilar, depressed, or facial bone fractures
• CT scan showing normal brain/ventricular spaces: observation only; may want to consider EEG and lumbar puncture
• In all patients with suspected traumatic brain injury, one should obtain:
  • CBC (infants can have a large amount of intracranial blood loss)
  • PT/PTT (to evaluate a possible bleeding disorder as a possible preoperative laboratory test)
  • Electrolytes (to look for evidence of impending SIADH, which can be seen in patients with cerebral edema as well as meningitis)

• Once laboratory values are obtained, appropriate corrective measures should be undertaken as needed (e.g., packed RBC or platelet transfusion, fluid restriction).
• Anticonvulsants may be used in those with persistent coma and elevated intracranial pressure (ICP), and in those with intracranial hemorrhage, since seizures cause ICP spikes. Otherwise, anticonvulsant therapy is reserved for children with documented seizure(s).
• Radiologic findings may prompt specific interventions, including:
  • CT scan showing focal hematoma or skull films showing hairline fracture over the middle meningeal artery: neurosurgery consultation, close monitoring overnight with frequent neurologic checks, seizure precautions
  • CT scan showing structural injury, including cerebral edema, hemorrhage, hypodense white matter: Transport to ICU for medical management of elevated ICP; measures may include fluid restriction, heart monitoring, SIADH monitoring with frequent electrolyte checks and strict fluid balance, mannitol, and hyperventilation as needed for progression of neurologic symptoms; neurosurgery consult for evaluation of hematoma and consideration of placement of ICP monitor.
  • Normal neuroimaging in coma due to trauma may still be present in the setting of major CNS injury and attendant complications; alternate diagnoses (meningitis, epilepsy) and other laboratory investigation (spinal tap, EEG) should be considered if the traumatic basis of stupor/coma remains in doubt.
  • Immobilize C-spine as necessary.

• Pupil asymmetry in an awake patient may be due to pharmacologic treatment (i.e., mydriatic agents for examination).
• Bacterial meningitis in a child who has had TBI may signal a CSF leak.
• Basilar skull fracture may be missed on routine CT scan—review bone windows or skull films.
• Witnesses and or primary caregivers may have personal reasons to conceal part or all of the circumstances regarding the child’s injury.

Q: What are the specific signs of increased intracranial pressure?:
A: Cushing’s reflex in association with deterioration in mental status. A change in pupils or ocular motility, or onset of posturing may also indicate increased ICP.

Q: When is mannitol used?:
A: In patients with increased ICP in the absence of intracranial hemorrhage, mannitol may exacerbate elevated ICP if extravascular blood is present.

Bijur PE, Haslum M, Golding J. Cognitive and behavioral sequelae of mild head injury in children. Pediatrics 1990;86:337–344.

Duhaime A-C, Gennarelli TA, Thibault LE, et al. The shaken baby syndrome. J Neurosurg 1987;66:409–415.

Lee MS, Rinne JO, Ceballos-Baumann A, et al. Dystonia after head trauma. Neurology 1994;44:1374–1378.

Zimmerman RA, Bilaniuk LT. Pediatric head trauma. Neuroimag Clin North Am 1994;4:349–366.