Brain Injury, Traumatic
Traumatic brain injury (TBI): Damage to the brain from accidental or nonaccidental trauma:
- Children >1 year, i.e., GCS <14, amnesia >15 min for event, penetrating head injury
- Children <1 year: any LOC, protracted emesis, suspected abuse
- Severe brain injury: Usually initial GCS <9
- Trauma, number 1 cause of death of children >1 year. Head injury most common contributor to morbidity and mortality.
- Between 29,000 and 50,000 children in the US <19 suffer permanent disability from TBI each year.
- Age-dependent mechanism of injury and pathophysiology
- <2 years old: Nonaccidental trauma is principle cause of TBI.
- >2 years old: Falls (~37%) are most common cause of trauma.
- For severe TBI, nonaccidental trauma remains principle cause in young children.
- Motor vehicle accidents in older children, although penetrating injuries becoming more common
- 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 from shear forces
- Extension of injury to viable tissue/entire brain.
- Dysautoregulation of cerebral blood flow, neuroexcitotoxicity and inflammatory mediators. CT or MRI signs of edema may progress over 3–5 days (see “Treatment”).
- Shear forces on the brain due to acceleration/deceleration avulses axons from their cell bodies (DAI); often compounded by tearing and bleeding of dural veins.
- Unmyelenated 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 don’t predict brain injury.
- More severe birth trauma can result in subdural hematoma.
- 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, and cerebral edema.
- Children <3 at risk of growing skull fracture when leptomeningeal cyst protrudes through a dural tear (late effect)
- Suspect nonaccidental trauma with growing skull fracture, if more than one cranial bone involved, or if other injuries are present.
- Older children/adolescents:
- Still more subject to DAI than adults due to incomplete myelination
- Projectile injuries in adolescent population
- Can result from nonaccidental trauma (usually with other stigmata of assault)
Signs and Symptoms
- Eyewitness accounts are invaluable.
- Details of who was caring for the child
- Falls: Did loss of consciousness precede fall? Height of fall, surface of impact
- History of epilepsy, cardiac problems
- History of previous concussions (consider “second impact syndrome”) or trauma
- Intoxication (of child, caregiver, others in the environment)
- Prior physical abuse/neglect?
- Restrained motor vehicle passenger? Angle of impact
- How did patient act or change over time? Unresponsive? Confused? Headache? Visual changes? Vomiting? Seizure?
Rapid neurological exam in trauma:
- Can derive some of these by observation. Note presence of neuromuscular blockers:/sedation
- Level of arousal: Awake, lethargic, stuporous, unresponsive
- Resting posture: Spontaneous, restless, still normal, flexor, extensor
- Respiration: In context of arousal and posture, hyperpnea or Cheyne-Stokes respiration
- Response to stimulation: Voice, pain (of earlobe to avoid spinal withdrawal response); note localization, withdrawal, posturing
- Pupils: Equal, anisocoria >1 mm, unequal/sluggish pupil, unequal/wide/fixed pupil
- Extraocular movements: Disconjugate gaze nonlocalizing with drugs/trauma, 3rd nerve palsy uncal herniation sign, 4th nerve palsy common in head injuries, 6th nerve palsy from trauma or increased ICP
- Brainstem reflexes: Corneals (V & VII ), oculocephalic if patient unable to cooperate with eye exam and cervical spine cleared. Avoid gag—raises ICP.
- Muscle reflexes/motor exam: Lateralizing signs may indicate contralateral hemispheric lesion, with ipsilateral dilated pupil may indicate uncal herniation
- Sensory: Brief for four limbs/spinal level if indicated
- This exam should be repeated often according to the patient’s level of acuity. A more detailed exam tailored to degree of arousal can be done as the patient is stabilized.
In all patients with suspected TBI, consider:
- 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)
- Toxin screen
- Unenhanced CT scan of the brain is the imaging study of choice for initial evaluation of a patient with suspected TBI.
- Abnormal CT: Lesion density, midline shift, compression of cisterns, bone fragments
- MRI: Useful for DAI (with a negative head CT) as well as showing small lesions (e.g., punctate contusions)
- In suspected cervical spine injury where patient is unresponsive, MRI of the spine to R/O noncontiguous unstable ligamentous injury
- Long-bone films if degree of injury is not consistent with history or history of fall from unclear height
- With CT scan showing normal brain/ventricular spaces: Consider EEG and lumbar puncture if a nontraumatic etiology for altered mental status is suspected.
Neurologic presentation varies in severity from a normal examination through coma similar to hypoxic-ischemic brain injuries (e.g., near-drowning), other causes of stupor/coma, seizure activity (postictal encephalopathy):
- Distinction between simple concussion, DAI, and hypoxic-ischemic injury may be difficult at initial presentation, becoming clear as clinical picture/neuroimaging evolves.
- Airway, breathing, circulation
- Pre-hospital stabilization: Avoid hypoxemia and hypotension (strong, possibly modifiable, independent predictors of outcome in TBI)
- Cervical spine stabilization and clearance; in severe TBI, entire spine is stabilized:
- If necessary, orotracheal intubation with rapid sequence induction; avoid hypotension.
- Hyperventilation may induce regional cerebral ischemia in children, especially in 1st 24 hours.
- Increased ICP managed by bed elevation 30°, hypertonic fluids, sedation
- Hemodynamic stabilization (normal high systolic BP (~135) predictor of better outcome in TBI [Median systolic BP = 90 mm Hg + (2 × age in years)].
- Hemodynamic instability indicative of systemic hemorrhage (abdomen, long bone fractures). Pericardial tamponade (narrow pulse pressure). Neurogenic shock.
- Hypotension late sign. Early: ↑HR, ↓capillary refill, ↓urine output
- Fluid resuscitate: Consider hypertonic saline. Mounting evidence of improved outcomes especially with hemorrhagic shock and TBI (titrate continuous 3% saline infusion 0.1–1 mL/kg/h).
- Fluid bolus may worsen intracranial hypertension (ICP).
- Consider monitoring ICP to maintain <20 mm Hg) for abnormal admission CT scan, and GCS 3–8 after CPR, or normal CT and GCS 3–8, and posturing, or hypotension, or if serial neurological exams precluded by sedation.
- Maintenance of CPP >50 positively influences outcome in TBI (MAP – ICP = CPP) especially in 1st 48 hours.
- A rapid neurological exam repeated over time is instrumental in directing the patient’s care.
- Secondary survey: External evidence of head injury/deformities, ecchymoses (periorbital-orbital roof fracture; mastoid-petrous temporal fracture), lacerations, penetrations. CSF leak nasal/otic.
- Seizures: Ativan 0.1–0.2 mg/kg IV at 2 mg/min or rectal Diastat 0.3–0.5 mg/kg if no IV access. Then load fosphenytoin 15–20 mg/kg IV. Important to treat to avoid increase ICP, neurotoxicity, hypoxia.
- No evidence that seizure prophylaxis >1 week posttrauma prevents late seizures
- No evidence that steroids improve outcome
- Hypothermia may be protective, no difference in long-term outcome.
- No evidence for prophylactic use of mannitol, though it is effective for control of increased ICP. Bolus doses 0.25 g/kg of body weight to 1 g/kg of body weight to goal ICP <20 mm Hg
- Hypertonic saline for increased ICP as above under fluid resuscitation
- The postresuscitation GCS score should be recorded in all trauma patients.
- Involvement of neurosurgery with moderate GCS <13 injury, even if patient initially stable
- Survival for children with severe TBI is greater when treated in pediatric ICU.
- Decompressive craniectomy may be considered given the following conditions:
- Diffuse cerebral swelling on cranial CT imaging
- Within 48 hours of injury
- No episodes of sustained ICP >40 mm Hg before surgery
- GCS >3 at some point subsequent to injury
- Secondary clinical deterioration
- Evolving cerebral herniation syndrome
- Presence of both hypoxemia and hypotension on arrival to ER bode poorly.
- 24-hour GCS better predictor of outcome than postresuscitation, PRISM score also helpful
- GCS <3 poor prognosis unless secondary to epidural hematoma, rapid evacuation can minimize permanent deficits
- Diffuse white matter, subcortical gray or brainstem lesions on MRI portend long periods of coma and poorer outcome
- Somatosensory evoked potentials (VEPS or BAEPs) are less sensitive but have high specificity in predicting neurological outcome.
- Degree of injury on head CT can be predictive
- Patients who have sustained moderate-to-severe head injury (GCS = 13) often have academic difficulties, memory abnormalities, disinhibition
- Monitoring for cognitive difficulties, hyperactivity, seizures, hydrocephalus, movement disorders, paralysis, visual/hearing disturbance, headache; psychologists, neurologists, neurosurgeon, ophthalmologists, audiologists, and physical therapists may be helpful.
- Leptomeningeal cyst (especially in children <3 years old) almost always develops within 6 months of injury.
- Refer any patient with known skull fracture who manifests a new swelling in area of old fracture to neurosurgery for 3D CT imaging of the head.
- ~10% of patients with severe head injury will develop epilepsy.
- 854.0 Intracranical injury
- American College of Radiology. Suspected Cervical Spine Trauma. Reston, VA: American College of Radiology; 2002.
- Adelson PD, et al. Critical pathway for the treatment of established intracranial hypertension in pediatric traumatic brain injury. Pediatr Crit Care Med. 2003;4(3 Suppl):S65–S67. [PMID:12847353]
- Hymel KP, Makoroff KL, Laskey AL Mechanisms, clinical presentations, injuries, and outcomes from inflicted versus noninflicted head trauma during infancy: Results of a prospective, multicentered, comparative study. Pediatrics. 2007;119(5):922–929. [PMID:17473092]
- Jagannathan J, Okonkwo DO, Dumont AS Outcome following decompressive craniectomy in children with severe traumatic brain injury: A 10-year single-center experience with long-term follow-up. J Neurosurg. 2007;106(4 Suppl):268–275. [PMID:17465359]
- Jayawant S, Parr J. Outcome following subdural haemorrhages in infancy. Arch Dis Child. 2007;92(4):343–347. [PMID:17376941]
- Pollack MM, Ruttimann UE, Geston PR. Pediatric risk of mortality (PRISM) score. Crit Care Med. 1988;16:1110–1116. [PMID:3048900]
- White JR, Farukhi Z, Bull C Predictors of outcome in severely head-injured children. Crit Care Med. 2001;29:534–540. [PMID:11373416]
- Zink BJ. Traumatic brain injury outcome: Concepts for emergency care. Ann Emerg Med. 2001;37(3):318–332. [PMID:11223769]
Karen LeComte, MDJerry Larrabee, MD
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