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Traumatic brain injury

Last updated: September 21, 2021

Summarytoggle arrow icon

Traumatic brain injury (TBI) is defined as a structural injury to the brain or a disruption in the normal functioning of the brain as a result of a blunt or penetrating head injury. Head injury refers to trauma to the head that may or may not be associated with TBI, soft tissue injury, or skull fractures. Primary brain injury occurs as an immediate consequence of head injury at the time of the trauma. Secondary brain injury is indirect and results from physiological changes triggered by the initial impact and/or acute management measures; it is preventable to a certain degree. TBI is most frequently seen in young children, teenagers, and individuals older than 65 years, with falls and motor vehicle accidents being the leading causes. The Glasgow coma scale (GCS) is a commonly used scoring system used to assess the severity of TBI and guide management. Clinical features of TBI depend on the severity, type, and location of brain injury. Impaired consciousness is common in severe TBI, whereas patients with mild TBI may only present with transient confusion and headache. Neuroprotective measures to prevent or minimize secondary brain injury should be the main focus of initial management of all patients with TBI. Patients with moderate TBI or severe TBI should be transferred to a neurocritical care unit at the earliest. After initial resuscitation, a head CT without contrast should be obtained to identify the type and extent of injury. Definitive management varies depending on the type and severity of injury.

The specific management of mild TBI (concussion), elevated intracranial pressure and brain herniation, EDH, SDH, SAH, and ICH is discussed in separate articles.

  • Incidence: ∼ 800/100,000
  • Age: especially children 0–4 years, teenagers and young adults 15–24 years, and adults > 65 years
  • Sex: >

References: [4][5][6]

Epidemiological data refers to the US, unless otherwise specified.

  • Blunt head injury (common): injury caused by blunt force trauma to the head
    • Falls: leading cause of TBI; more common in children, adolescents, and the elderly [7]
    • Motor vehicle accidents: second most common cause of TBI [7]
    • Contact sports (e.g., football)
  • Penetrating head injury (less common): injury caused by penetrative trauma to the head [8]
    • High-velocity missile injury: gunshot wounds
    • Low-velocity nonmissile injury: assault or accidental injury with a penetrating foreign body to the head or face (e.g., knife, screwdriver, nail gun) [9][10]
  • Blast injuries: injury caused by the high pressure wave (blast wave) generated from an explosion; common in active military or war zones [11]

TBI is categorized pathophysiologically into primary and secondary brain injury depending on whether the brain injury is a direct or indirect result of the inciting trauma.

Primary brain injury [12][13]

Secondary brain injury [12][13]

Secondary brain injury is preventable. Neuroprotective measures to prevent or minimize secondary brain injury should be initiated as early as possible in all patients with acute neurological insults.

Clinical features vary depending on the severity, location, and type of TBI. Patients require neurological examination and assessment of sensorium and cognition. For details see “Clinical features” in “EDH”, “SDH”, “SAH”, “ICH” and “Mild TBI”.

General symptoms

In deCORticate posture, the arms are flexed towards the CORe of the body.

Symptoms of associated injuries

Skull fractures, (worsening) neurological impairment, repeated vomiting, and seizures are indicative of more severe trauma or intracranial hemorrhage.

Approach [22][23][24]

  1. Primary survey (ABCDE survey) with simultaneous initiation of neuroprotective measures to prevent or minimize secondary brain injury
  2. Severity assessment (GCS) and monitoring
  3. Transfer to a neurocritical care unit if needed.
  4. Diagnostics and imaging (usually noncontrast CT) if indicated
  5. Treatment and further management based on severity scores and CT findings.

Resuscitative measures to achieve normoxia, normocapnia, normotension, and euglycemia take precedence in the acute management of TBI and should not be delayed for diagnostic steps.

Neuroimaging should not delay transfer to centers that can provide definitive neurosurgical care if required. [24]

Hypotension in TBI significantly worsens the prognosis and should be identified and treated. Permissive hypotension is harmful in TBI. [23]

Primary survey [24]

The primary survey should follow the ATLS algorithm (ABCDE). The goal is to identify and treat any life-threatening conditions and avoid secondary brain injury.

Key aspects for primary survey in TBI [22][23][24]
Airway
Breathing
Circulation
Disability
Exposure
  • Assess for other life-threatening or limb-threatening injuries (e.g., spinal cord injuries, solid organ injuries, hollow viscous injuries, and injuries to extremities)
  • Avoid hypothermia and cover the patient as early as possible.

Patients with moderate or severe TBI (GCS ≤ 12) require emergency neuroimaging with noncontrast head CT after stabilization even if potential additional causes for mental obtundation are present (e.g., alcohol intoxication).

Secondary survey

  • Definition: a neurological injury severity score used to assess the state of consciousness of a patient [33][34][35]
  • Indications
    • Standard for initial evaluation and classification of patients with traumatic brain injury [12]
      • Determination of targeted therapies (therapeutic value) [12]
      • Estimation of patient outcome (prognostic value)
      • Monitoring of therapy
    • Evaluation and monitoring of patients with altered consciousness regardless of etiology (e.g., stroke, poisoning)
Glasgow coma scale (GCS) [33]
Criteria Rating Score
Eye opening Spontaneously 4
To verbal command 3
To pain 2
No response 1
Closed due to local factor (e.g., ocular injury) Nontestable
Verbal response
Appropriate words and oriented 5
Appropriate words but confused 4
Inappropriate words 3
Incomprehensible sounds 2
No response 1
Other factor(s) interfering with communication (e.g., intubation) Nontestable
Best motor response Obeys commands 6
Localizes pain stimulus 5
Withdraws from pain (normal flexion to pain) 4
Decorticate posturing (abnormal flexion to pain) 3
Decerebrate posturing (extension to pain) 2
No motor response 1
Other or preexisting factor(s) causing paralysis Nontestable

Interpretation

  • Important considerations

Significant hypotension alters GCS. Reassess GCS after correction of hypotension [24]

Approach [24]

  • Head CT without IV contrast is the first-line diagnostic modality
  • The goal of diagnostics is timely identification of lesions that require neurosurgical intervention.
  • Imaging should not delay transfer to centers that can provide definitive neurosurgical care if required.
  • Obtain imaging of other potential sites of injury (e.g., CT cervical spine).

Possible traumatic brain injury should always be considered in a patient with a decreased or altered consciousness.

Neuroprotective measures take precedence over diagnostics.

Imaging [23][24][36]

Head CT without IV contrast


MRI head without IV contrast [37]

  • Indications
    • Acute TBI with symptoms unexplained by CT (in hemodynamically stable patients) [24][36]
    • Short-term follow-up of acute TBI in patients with rapid deterioration of neurological symptoms (alternative to CT)
    • Subacute or chronic TBI with new, persistent, or worsening of neurological or cognitive deficits (preferred modality) [36][37]
  • Supportive findings: Microhemorrhages, DAI, and contusions are better visualized on MRI than on CT.

Additional imaging [36][37]

Consider additional imaging based on the patient's history and clinical features or if initial imaging modality findings are inconsistent with neurological symptoms.

Laboratory studies [23][24]

Overview

Overview of TBI management [23][24]
Severity of TBI Treatment Supportive care
Mild (GCS ≥ 13)
  • Check criteria for admission (e.g., GCS < 15 after two hours)
  • Observation in the ED is often sufficient.
  • See “Mild TBI” for details.
Moderate TBI (GCS 9–12)
Severe TBI (GCS ≤ 8)
  • Additionally to the measures in moderate TBI: seizure prophylaxis for 7 days postinjury [2][26][48]

Surgical treatment [23][24]

Consult neurosurgery and initiate treatment as needed based on the underlying condition (see “Treatment” in “EDH”, “SDH”, “SAH”, and “ICH” for details).

Additional treatment and monitoring

Continuing neuroprotective measures to avoid secondary brain injury is crucial for the management of moderate and severe TBI.

Pain and agitation increase SBP and ICP and contribute to secondary brain injury and should be managed adequately (see ICP management). [49]

Prevention of complications in brain injuries

Secondary bleeding or hematoma expansion

Additional prophylactic measures

We list the most important complications. The selection is not exhaustive.

Definition

A complication of acute brain injury characterized by recurrent episodes of excessive sympathetic activity.

Pathophysiology

Loss of cortical inhibition of the sympathetic system subsequent to acute brain injury → exaggerated sympathetic response to stimulation

Causes

Clinical features

Diagnostics

  • Clinical diagnosis
  • EEG and imaging (head CT/MRI) to rule out other conditions

Treatment [61]

References: [62][63]

When evaluating children and infants with TBI, a number of special issues must be observed.

  • Causes
    • Falls (most common)
    • The possibility of child abuse must always be considered.
  • Clinical features: : esp. bulging anterior fontanelle (↑ ICP)
  • Diagnosis: cranial CT without contrast
    • Identify patients with significant TBI but avoid unnecessary radiographic testing
    • CT recommended for signs of skull fractures, ↑ ICP, major neurologic symptoms (e.g., impaired consciousness, seizures), suspected child abuse
    • Consider CT: if less severe symptoms (e.g., changes in behavior, self-limited vomiting) are present.
  • Management
    • Inpatient observation indications
    • Release and at-home observation for 24 hours
      • Patients without neurological deficits and non-depressed linear skull fracture < 3 mm separation
      • Requires a caregiver who can reliably recognize new clinical neurological deficits and return the patient to the hospital if such manifestations arise

References:[67][68]

Overview of common brain lesions
Location of lesion Clinical features

Cortex

Frontal lobe
Frontal eye fields
  • Gaze deviation toward the affected side and away from the side of hemiplegia
Parietal lobe
Occipital lobe
Temporal lobe
Watershed border-zone

Posterior limb of the internal capsule

Thalamus

Basal ganglia Putamen
Substantia nigra
Striatum
Subthalamic nucleus
Hippocampus (bilateral)
Mammillary bodies (bilateral)
Amygdala (bilateral)
Medial longitudinal fasciculus
Paramedian pontine reticular formation

Dorsal midbrain

Red nucleus

Reticular activating system

Cerebellum General
Cerebellar vermis
Cerebellar hemisphere

Pons

Lateral spinothalamic tract

Middle and inferior cerebellar peduncles

Spinal trigeminal nerve nucleus

Facial nerve nuclei

Vestibulocochlear nerve nuclei

Sympathetic fibers

Pyramidal tracts

Abducens nerve

Facial nerve

Ventral pons

Medulla oblongata

Nucleus and fibers of the hypoglossal nerve

Corticospinal tract

Medial lemniscus

Nucleus ambiguus (CN IX, X, XI)

Vestibular nuclei

Lateral spinothalamic tract

Spinal trigeminal nucleus

Inferior cerebellar peduncle

Sympathetic fibers

Discrete brain lesions are typically caused by nontraumatic events, especially hemorrhagic, embolic, and neoplastic processes.

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