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 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 0-14 years. Males age 0-4 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 3-5 days (see "Treatment").
- Age-specific pathophysiology:
- Infants/toddler
- Shear forces on the brain due to acceleration/deceleration avulse axons from their cell bodies (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, 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
Diagnosis
History
- 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?
- Consider use of published concussion symptom checklists.
Physical Exam
Rapid neurologic 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 4 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.
- Mild TBI can be assessed with standard neurologic exam as outlined earlier. Balanced assessment and neurocognitive assessment (short-term memory, months of the year in reverse, digits in reverse) may be useful. Use of SCAT3 in sport concussion assessment may be beneficial on sideline or emergency department.
Diagnostic Tests & Interpretation
Lab
- 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)
- Electrolytes
- Toxin screen
- Laboratory studies likely not necessary in mild TBI unless laboratory abnormality suspected as contributor to TBI.
Imaging
- In mild TBI, imaging most likely not needed. High risk for lesion includes GCS <15 at 2 hours post injury, suspicion of open skull fracture, worsening headache, and irritability. Medium risk for lesion includes large, boggy hematoma, signs of basal skull fracture, and dangerous mechanism of injury.
- 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, CT scan initially with consideration for MRI of the spine to rule out noncontiguous unstable ligamentous injury.
- Long bone films if degree of injury is not consistent with history or history of fall from unclear height
- Consider EEG and lumbar puncture if a nontraumatic etiology for altered mental status is suspected, if CT normal.
Differential Diagnosis
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.
Treatment
- Airway, breathing, circulation
- Cervical spine stabilization in unconscious patient with unclear mechanism of injury
- Prehospital stabilization: Avoid hypoxemia and hypotension (strong, possibly modifiable, independent predictors of outcome in TBI).
Additional Therapies
General Measures
- For acute mild TBI, recommend physical rest and reducing cognitive stress while symptomatic.
- AAP guidelines set conditions for return to play depending on symptoms:
- An AAP concussion statement outlines graduated return to activity if no return of symptoms and suggests (a) no same-day return; (b) and medical clearance needed before initiating return to activity progression.
- A rapid neurologic exam repeated over time is instrumental in directing the patient's care.
- For more severe trauma or in infants
- Secondary survey: external evidence of head injury/deformities, ecchymoses (periorbital-orbital roof fracture; mastoid-petrous temporal fracture), lacerations, penetrations. CSF leak nasal/otic
- Seizures: lorazepam 0.05-0.1 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 increased ICP, neurotoxicity, hypoxia
- No evidence that seizure prophylaxis >1 week post trauma prevents late seizures
- No evidence that steroids improve outcome
- Hypothermia may be protective in severe TBI, no difference in long-term outcome.
- No evidence for prophylactic use of mannitol, although 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 3% saline IV 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
Inpatient Considerations
Initial Stabilization
- 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 first 24 hours.
- Increased ICP managed by bed elevation of 30 degrees, 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: ā†‘HR, ā†“capillary refill, ā†“urine output
- Fluid resuscitation: 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 neurologic exams precluded by sedation.
Ongoing Care
Prognosis
- Majority of mild TBI patients recovery without significant sequelae
- 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 neurologic 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, and disinhibition.
- Monitoring for cognitive difficulties, hyperactivity, seizures, hydrocephalus, movement disorders, paralysis, visual/hearing disturbance, headache; psychologists, neurologists, neurosurgeons, ophthalmologists, audiologists, and physical therapists may be helpful.
- Refer any patient with known skull fracture who manifests a new swelling in area of old fracture to neurosurgery for 3-D CT imaging of the head.
- ~10% of patients with severe head injury will develop epilepsy.
Additional Reading
- Adelson PD, Bratton SL, Carney NA, 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. [View Abstract]
- Centers for Disease Control and Prevention: www.cdc.gov/concussion/HeadsUp/high_school.html
- Halstead ME, Walter KD; Council on Sports Medicine and Fitness. Clinical report-sport-related concussion in children and adolescents. Pediatrics. 2010;126(3):597-615. [View Abstract]
- Hymel KP, Makoroff KL, Laskey AL, et 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. [View Abstract]
- Jagannathan J, Okonkwo DO, Dumont AS, et al. 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. [View Abstract]
- Osmond MH, Klassen TP, Wells GA, et al. CATCH: a clinical decision rule for the use of computed tomography in children with minor head injury. CMAJ. 2010;182(4):341-348. [View Abstract]
- White JR, Farukhi Z, Bull C, et al. Predictors of outcome in severely head-injured children. Crit Care Med. 2001;29(3):534-540. [View Abstract]
Codes
ICD09
- 854.00 Intracranial injury of other and unspecified nature without mention of open intracranial wound, unspecified state of consciousness
- 854.06 Intracranial injury of other and unspecified nature without mention of open intracranial wound, with loss of consciousness of unspecified duration
- 854.09 Intracranial injury of other and unspecified nature without mention of open intracranial wound, with concussion, unspecified
- 854.01 Intracranial injury of other and unspecified nature without mention of open intracranial wound, with no loss of consciousness
ICD10
- S06.9X0A Unsp intracranial injury w/o loss of consciousness, init
- S06.9X9A Unsp intracranial injury w LOC of unsp duration, init
- S06.9X1A Unspecified intracranial injury with loss of consciousness of 30 minutes or less, initial encounter
SNOMED
- 127295002 traumatic brain injury (disorder)
- 127298000 traumatic brain injury with loss of consciousness (disorder)
- 127302008 traumatic brain injury with no loss of consciousness (disorder)
- 28188001 Brain injury with open intracranial wound