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Brain Injury, Traumatic
Caleb J. Mentzer, DO
James R. Yon, MD
image BASICS
  • Traumatic brain injury (TBI) is defined as an alteration in brain function, or other evidence of brain pathology, caused by an external force.
  • System(s) affected: neurologic; psychiatric; cardiovascular; endocrine/metabolic; gastrointestinal
  • Synonym(s): head injury, concussion
  • 2.2 million ED visits and 280,000 hospitalizations/year
  • 50,000 deaths/year; ˜30% of all injury-related deaths
  • Incidence in males twice that of females with 4-fold risk of fatal trauma
  • Predominant age: 0 to 4 years, 15 to 19 years, and >65 years
  • Predominant gender: male > female (2:1)
  • Falls (40%)
  • Motor vehicle accidents (14%)
  • Assault (10%)
  • Child abuse (24% of TBI age 2 years and younger)
  • Recreational activities (21% of pediatric TBI, peak seasons spring/summer; peak ages 10 to 14 years)
  • Primary insult: direct mechanical damage
  • Secondary insult: actuation of complex cellular and molecular cascades that promote cerebral edema, ischemia, and apoptotic cell death
Alcohol and drug use, prior/recurrent head injury, contact sports, seizure disorder, ADHD, male sex, luteal phase of female menstrual cycle
Geriatric Considerations
Subdural hematomas are common after a fall or blow in elderly; symptoms may be subtle and not present until days after trauma. Many elderly patients are on antiplatelet or anticoagulation therapy.
  • Safety education
  • Seat belts; bicycle and motorcycle helmets
  • Protective headgear for contact sports
Pediatric Considerations
Child abuse: Consider if dropped or fell <4 feet (e.g., off bed, couch), suspicious history, significant injury present, or any retinal hemorrhages.
  • Neurologic and cognitive testing is important.
  • Repeat neurologic exams every 30 minutes until 2 hours after GCS reaches 15, then hourly for 4 hours, then every 2 hours.
  • Evidence of increased intracranial pressure (ICP) (elevated BP, decreased pulse rate, or slow/irregular breathing [Cushing triad]—only 30% have all 3)
  • Decorticate or decerebrate posturing
  • Signs of basilar skull fracture: raccoon eyes, Battle sign, hemotympanum, CSF rhinorrhea or otorrhea)
Other causes of altered mental status (e.g., toxicologic, infectious, metabolic, vascular)
Initial Tests (lab, imaging)
  • Mild TBI and concussions cognitive screening tests
    • Sports Concussion Assessment Tool V3 (SCAT3)
    • Child SCAT3
    • Concussion Recognition Tool (CRT)
    • Standardized Assessment of Concussion (SAC)
    • King-Devick Test
    • Balance Error Scoring System (BESS)
  • Evaluate for coagulopathy.
  • Type and screen for possible surgical intervention.
  • Perform drug and alcohol screening.
  • CT, noncontrast, is the study of choice to review bone windows, tissue windows, and subdural space.
  • NEXUS II study demonstrated that if all eight clinical criteria are absent, there is a low likelihood of significant TBI:
    • Evidence of significant skull fracture (depressed, basilar, or diastatic)
    • Altered level of alertness
    • Neurologic deficit
    • Persistent vomiting
    • Presence of scalp hematoma
    • Abnormal behavior
    • Coagulopathy
    • Age >65 years
Follow-Up Tests & Special Considerations
Blast-related TBI: much higher rates of postconcussive syndrome, PTSD, depression, and chronic pain. Chronic impairment is strongly correlated with psychological factors. Return to battlefield guidelines similar to return to play in sports (see “General Measures”) (1)[A]
Pediatric Considerations
Skull radiographs are not indicated unless abuse is suspected in which case they can detect fractures not seen under CT. No return to activity until they are asymptomatic, and return to school should precede return to sport/physical activity (2)[A].
Diagnostic Procedures/Other
  • CSF rhinorrhea
    • Contains glucose; nasal mucus does not.
    • Check for the double-halo sign: If nasal discharge contains CSF and blood, two rings appear when placed on filter paper—a central ring followed by a paler ring.
  • ICP monitors are associated with lower mortality, but use is not superior to nonuse (3)[A].
  • Acute management depends on injury severity. Most patients need no interventions.
  • Immediate goal: Determine who needs further therapy, imaging studies (CT), and hospitalization to prevent further injury.
  • For the mildly injured patient
    • Early education is beneficial for recovery (4)[A].
    • Return to play (RTP)
      • Never RTP on same day.
      • Strict guidelines for graduated return to cognitive and physical activity when there are no evident signs or symptoms (physical, cognitive, emotional, or behavioral) on neuropsychological and clinical evaluation (2)[A]
  • For the moderate to severely injured patient
    • Avoid hypotension or hypoxia. Head injury causes increased ICP secondary to edema, and cerebral perfusion pressure (CPP) should be maintained between 60 and 70 mm Hg (5)[A].
    • 30-degree head elevation decreases ICP and improves CPP.
    • Hyperventilation (hypocapnia)
      • Use should be limited to patients with impending herniation while preparing for definitive treatment or intraoperatively. Risk of worsening cerebral ischemia and organ damage (5,6,7)[A]
      • Addition of tromethamine can offset deleterious effects and lead to better outcomes (7)[A].
    • Mild systematic hypothermia lowers ICP but leads to increased rates of pneumonia. Selective brain cooling may also decrease ICP with improved outcomes at 2 years post injury (7)[A].
  • Seizure prophylaxis
    • Does not change morbidity or mortality. Consider phenytoin or levetiracetam for 1 week post injury or longer for patients with early seizures, dural-penetrating injuries, multiple contusions, and/or subdural hematomas requiring evacuation (8)[A].
First Line
  • Pain
    • Morphine: 1 to 2 mg IV PRN, with caution, because it can depress mental status, further altering serial neurologic evaluations
  • Increased ICP
    • Hypertonic saline: 2 mL/kg IV decreases ICP without adverse hemodynamic status; preferred agent (5,9)[A]
    • Mannitol: 0.25 to 2 g/kg (0.25 to 1 g/kg in children) given over 30 to 60 minutes in patients with adequate renal function. Prophylactic use is associated with worse outcomes (9)[A].
  • Sedation
    • Propofol: preferred due to short duration of action. Avoid high doses to prevent propofol infusion syndrome. When combined with morphine, it can also effectively decrease ICP and decrease use of other meds (9)[A].
    • Midazolam: similar sedating effect to propofol but may cause hypotension (9)[A]
  • Seizures
    • Phenytoin (Dilantin): 15 mg/kg IV (1 mg/kg/min IV, not to exceed 50 mg/min). Stop infusion if QT interval increases by >50%.

Consult neurosurgery for:
  • All penetrating head trauma
  • All abnormal head CTs
  • Emerging therapies with limited but promising evidence: coma arousal therapy: amantadine, zolpidem, and levodopa/carbidopa; post coma therapy: bromocriptine
  • Limited role for therapeutic hypothermia with defined physiologic parameters (10)[A]
  • Early evacuation of trauma-related intracranial hematoma decreases mortality especially with GCS <6 and CT evidence of hematoma, cerebral swelling, or herniation (11)[A].
  • Decompressive craniectomy reduces ICP especially when a large bone flap is removed. ONLY for adults and ONLY with GCS >6 (7)[A].
  • Hyperbaric oxygen temporarily lowers ICP and improves mortality, but evidence is conflicting about outcomes at 6 to 12 months post injury (7)[A]. The combination of hyperbaric and normobaric hyperoxia reduces ICP and improves overall morbidity/mortality (12)[B].
  • CSF drainage reduces ICP but has not been demonstrated to have long-term benefit (7)[A].
  • CSF leakage often resolves in 24 hours with bed rest, but if not, may require surgical repair (5)[A].
Music therapy in conjunction with multimodal stimulation improves awareness in comatose TBI patients (10)[B].
Admission Criteria/Initial Stabilization
  • Abnormal GCS or CT
  • Clinical evidence of basilar skull fracture
  • Persistent neurologic deficits (e.g., confusion, somnolence)
  • Patient with no competent adult at home for observation
  • Possibly admit: LOC, amnesia, patients on anticoagulants with negative CT
  • ABCs take priority over head injury.
  • C-spine immobilization should be considered in all head trauma.
IV Fluids
Use normal saline for resuscitation fluid.
Discharge Criteria
Normal CT with return to normal mental status and responsible adult to observe patient at home (see “Patient Monitoring”)
  • Schedule regular follow-up within a week to determine return to activities.
  • Rehabilitation indicated following a significant acute injury. Set realistic goals.
  • For patients on anticoagulants, net benefit to restarting therapy after discharge despite increased bleeding risk.
Patient Monitoring
Patient should be discharged to the care of a competent adult with clear instructions on signs and symptoms that warrant immediate evaluation (e.g., changing mental status, worsening headache, focal findings, or any signs of distress). Patients should be monitored but not awakened from sleep.
As tolerated, monitor for signs of nausea.
Proper counseling, symptomatic management, and gradual return to normal activities are essential.
  • Gradual improvement may continue for years.
  • 30-50% of severe head injuries may be fatal.
  • Predicting outcome is difficult; many with even minor to moderate injuries have moderate to severe disability at 1 year, whereas prolonged coma may be followed by satisfactory outcome.
  • Patients may have new-onset seizures over 2 years following trauma.
  • Poor prognostic factors: low GCS on admission, nonreactive pupils, old age, comorbidity, midline shift
1. Rosenfeld JV, McFarlane AC, Bragge P, et al. Blast-related traumatic brain injury. Lancet Neurol. 2013;12(9):882-893.
2. McCrory P, Meeuwisse WH, Aubry M, et al. Consensus statement on concussion in sport: the 4th International Conference on Concussion in Sport held in Zurich, November 2012. Br J Sports Med. 2013;47(5):250-258.
3. Yuan Q, Wu X, Sun Y, et al. Impact of intracranial pressure monitoring on mortality in patients with traumatic brain injury: a systematic review and meta-analysis. J Neurosurg. 2015;122(3): 574-587.
4. Nygren-de Boussard C, Holm LW, Cancelliere C, et al. Nonsurgical interventions after mild traumatic brain injury: a systematic review. Results of the International Collaboration on Mild Traumatic Brain Injury Prognosis. Arch Phys Med Rehabil. 2014;95(3)(Suppl):S257-S264.
5. Tsang KK, Whitfield PC. Traumatic brain injury: review of current management strategies. Br J Oral Maxillofac Surg. 2012;50(4):298-308.
6. Curley G, Kavanagh BP, Laffey JG. Hypocapnia and the injured brain: more harm than benefit. Crit Care Med. 2010;38(5):1348-1359.
7. Meyer MJ, Megyesi J, Meythaler J, et al. Acute management of acquired brain injury part I: an evidence-based review of non-pharmacological interventions. Brain Inj. 2010;24(5):694-705.
8. Agrawal A, Timothy J, Pandit L, et al. Posttraumatic epilepsy: an overview. Clin Neurol Neurosurg. 2006;108(5):433-439.
9. Meyer MJ, Megyesi J, Meythaler J, et al. Acute management of acquired brain injury part II: an evidence-based review of pharmacological interventions. Brain Inj. 2010;24(5):706-721.
10. Crossley S, Reid J, McLatchie R, et al. A systematic review of therapeutic hypothermia for adult patients following traumatic brain injury. Crit Care. 2014;18(2):R75.
11. Kim YJ. The impact of time to surgery on outcomes in patients with traumatic brain injury: a literature review. Int Emerg Nurs. 2014;22(4):214-219.
12. Rockswold SB, Rockswold GL, Zaun DA, et al. A prospective, randomized phase II clinical trial to evaluate the effect of combined hyperbaric and normobaric hyperoxia on cerebral metabolism, intracranial pressure, oxygen toxicity, and clinical outcome in severe traumatic brain injury. J Neurosurg. 2013;118(6):1317-1328.
  • S06.9X0A Unsp intracranial injury w/o loss of consciousness, init
  • S06.5X0A Traum subdr hem w/o loss of consciousness, init
  • S06.6X0A Traum subrac hem w/o loss of consciousness, init
Clinical Pearls
  • TBI involves two distinct phases: the primary mechanical insult and secondary dysregulation of the cerebrovascular system with cerebral edema, ischemia, and cell-mediated death.
  • Indications for imaging include evidence of skull fracture, altered consciousness, neurologic deficit, persistent vomiting, scalp hematoma, abnormal behavior, coagulopathy, age >65 years.
  • Strict criteria exist for patients to return to normal sport activity following head injury to avoid the second-impact syndrome, which has 50% mortality.