5-Minute Pediatric Consult

Brain Injury, Traumatic

Description

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

Epidemiology

  • 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

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 from shear forces
  • Secondary:
    • 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”).
AGE-SPECIFIC PATHOPHYSIOLOGY
  • Infants/Toddler:
    • 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

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?

Physical Exam
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.

Tests

Laboratory
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

Imaging
  • 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.

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.

  • Airway, breathing, circulation
  • Pre-hospital stabilization: Avoid hypoxemia and hypotension (strong, possibly modifiable, independent predictors of outcome in TBI)

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 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.

General Measures

  • 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

Prognosis

  • 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.

ICD9

  • 854.0[05] Intracranical injury

BIBLIOGRAPHY

  1. American College of Radiology. Suspected Cervical Spine Trauma. Reston, VA: American College of Radiology; 2002.
  2. 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]
  3. 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]
  4. 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]
  5. Jayawant S, Parr J. Outcome following subdural haemorrhages in infancy. Arch Dis Child. 2007;92(4):343–347.  [PMID:17376941]
  6. Pollack MM, Ruttimann UE, Geston PR. Pediatric risk of mortality (PRISM) score. Crit Care Med. 1988;16:1110–1116.  [PMID:3048900]
  7. White JR, Farukhi Z, Bull C Predictors of outcome in severely head-injured children. Crit Care Med. 2001;29:534–540.  [PMID:11373416]
  8. Zink BJ. Traumatic brain injury outcome: Concepts for emergency care. Ann Emerg Med. 2001;37(3):318–332.  [PMID:11223769]

AUTHORS

Karen LeComte, MDJerry Larrabee, MD

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