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Brain Injury, Traumatic

Brain Injury, Traumatic: Excerpt from The 5-Minute Pediatric Consult

Karen LeComte, MDJerry Larrabee, MD

Brain Injury, Traumatic - BASICS

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

Brain Injury, Traumatic - 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

Brain Injury, Traumatic - 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)

Brain Injury, Traumatic - DIAGNOSIS

Brain Injury, Traumatic - signs & symptoms

Brain Injury, Traumatic - 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?

Brain Injury, Traumatic - 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.

Brain Injury, Traumatic - tests

Brain Injury, Traumatic - 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

Brain Injury, Traumatic - 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.

Brain Injury, Traumatic - differencial 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.

Brain Injury, Traumatic - TREATMENT

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

Brain Injury, Traumatic - 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.

Brain Injury, Traumatic - 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

Brain Injury, Traumatic - FOLLOW UP

Brain Injury, Traumatic - 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.

Brain Injury, Traumatic - bibliography

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

Brain Injury, Traumatic - CODES

Brain Injury, Traumatic - icd9

854.0[05] Intracranical injury

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Book Source Details

  • Book Title: The 5-Minute Pediatric Consult
  • Author(s): M. William Schwartz MD; et al.
  • Year of Publication: 2008
  • Copyright Details: The 5-Minute Pediatric Consult, Copyright © 2008 Lippincott Williams & Wilkins.

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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.




More About This Book:
Title: The 5-Minute Pediatric Consult
Authors: M. William Schwartz MD; et al.
Publisher: Lippincott Williams & Wilkins
Copyright: 2008
ISBN: 0-7817-7577-9

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