Traumatic brain injury

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.

• Traumatic brain injury (TBI): structural or physiological disruption of the brain resulting from a head injury ^[1][2]
• Head injury: trauma to the head that may or may not be associated with soft tissue injury, skull fractures, and TBI ^[3]
  • Closed head injury (most common): head injury with intact dura mater
  • Open head injury: head injury with a breach in the dura mater exposing the cranial contents to the environment; associated with skull fractures

• 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]

• Definition: brain injury that occurs at the time of the trauma as an immediate consequence of head injury
• Focal primary brain injury
  • Intracranial hemorrhage
    • Epidural hemorrhage (EDH)
    • Subdural hemorrhage (SDH)
    • Subarachnoid hemorrhage (SAH)
    • Intracerebral hemorrhage (ICH)
  • Cerebral contusion: focal area of heterogeneous brain injury, varying from a bruise to a focal area of necrosis ^[14]
  • Coup-contrecoup injury
    • Coup injury: injury on the side of an impact
    • Contrecoup injury: additional injury (typically a contusion) on the opposite side of impact
  • Brain parenchymal lacerations
  • Intracerebral or intracerebellar hematomas
• Diffuse primary brain injury
  • Mild traumatic brain injury (concussion)
  • Cerebral edema
  • Diffuse axonal injury (DAI)
    • Multifocal shearing tears and disruption of the axons of the brain due to rotational acceleration-deceleration trauma of the head; typically seen in high-impact road traffic accidents. ^[15][16]
    • Commonly results in severe neurological injury (e.g., coma, persistent vegetative state)

Secondary brain injury ^[12][13]

• Definition: indirect brain injury resulting from physiological changes following acute CNS insults and/or their treatment
• Examples: disrupted blood-brain barrier, hypoxic-ischemic encephalopathy (see “Pathophysiology” in “Secondary brain injury” for details)

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

• Global neurological symptoms
  • Loss of consciousness or altered consciousness (e.g., confusion, disorientation), possibly with a lucid interval
  • Headache
  • Amnesia
• Symptoms of increased intracranial pressure (ICP)
  • Altered mood and behavior (e.g., aggressive behavior)
  • Dizziness, nausea, vomiting
  • Cushing triad
  • Cerebral herniation syndromes
• Focal neurologic deficits: depending on the affected brain region (see “Stroke symptoms by affected region”)
  • Contralateral hemiparesis or hemiplegia
  • Contralateral sensory loss
  • Cranial nerve palsies (e.g., diplopia, blurred vision, unequal pupils, anosmia)
  • Slurred and/or disorganized speech
  • Impaired coordination
• Abnormal posturing: characteristic posture of the limbs that typically signifies severe brain injury (most commonly involving the brainstem) ^[17][18]

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

Symptoms of associated injuries

• General symptoms of skull fractures ^[19][20]
  • Hematoma; , local swelling, and laceration of the scalp
  • Liquorrhea: leakage of CSF from the subarachnoid space through an external opening
    • Due to a dural tear immediately or within the first few days after the trauma
    • May show a halo sign: rapidly-expanding clear ring of fluid surrounding blood
• Basilar skull fractures
  • Anterior basilar skull fracture
    • CSF rhinorrhea
    • Raccoon eyes
    • Palsies of cranial nerves I, V, VI, VII, and/or VIII
  • Posterior basilar skull fracture
    • CSF otorrhea
    • Hemotympanum
    • Battle sign ^[21]
    • Palsies of cranial nerves VI, VII, and/or VIII palsies
• Facial fractures: hematomas, facial and/or nasal swelling, epistaxis, visible deformity

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

Approach ^[22][23][24]

• Start primary survey (ABCDE survey) with simultaneous neuroprotective measures.
  • Additional prehospital trauma care (e.g., spine immobilization, analgesics)
  • Maintain or achieve normoxia, normocapnia, blood pressure control, and euglycemia
• Measure GCS and pupillary response.
• Classify TBI by severity based on GCS.
• Transfer to a neurocritical care unit if needed.
• Diagnostics and imaging (usually noncontrast CT) if indicated
• 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.

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

• Focused history
  • SAMPLE history
  • Mechanism/time of injury
  • Presence/duration of amnesia
  • Presence of seizures/headache
  • Use of anticoagulant medication
• Physical examination: thourough head-to-toe examination and complete neurological examination
• Continuous monitoring
  • Vitals, SpO2
  • Serial neurological examination: GCS, pupillary exam, lateralizing signs
• Emergency consults
  • Neurosurgery (if GCS ≤ 12 or deteriorating)
  • Trauma surgery for additional major trauma
• Transfer: If GCS ≤ 12, transfer to a trauma center or neurocritical care unit if unavailable at current site

Severity classification using Glasgow coma scale (GCS) ^[33][34][35]

• Clinical applications of GCS in TBI ^[12]
  • Assessing the level of consciousness objectively
  • Guiding targeted therapies ^[12]
  • Estimating patient prognosis
  • Monitoring therapy
  • Evaluating AMS or coma of concurrent etiologies (e.g., stroke, intoxication)
• Scoring of GCS
  • Eye opening (E): spontaneous (4); to verbal instruction (3); to pain (2); unresponsive (1)
  • Verbal response (V): oriented (5); confused (4); inappropriate words (3); incomprehensible sounds (2); unresponsive (1)
  • Motor response (M): follows instruction (6); localizes pain (5); withdraws from pain (4); decorticate posturing (3); decerebrate posturing (2); unresponsive (1)
• Interpretation of GCS
  • GCS 3 (minimum score): deeply comatose or imminent brain death
  • GCS 15 (maximum score): fully conscious
• TBI severity
  • Mild TBI (mTBI): GCS 13–15; includes concussion; may or may not be associated with neuroimaging findings ^[24]
  • Moderate TBI: GCS 9–12; usually associated with structural brain lesions on neuroimaging
  • Severe TBI: GCS ≤ 8; usually an indication for intubation
• Important considerations
  • Record the score of each criterion individually (e.g., GCS 11, E(3) V(4) M(4)).
  • The score is invalid if any parameter is nontestable.
  • Alcohol and certain drugs (e.g., analgesics, antidepressants, anesthetics) may affect initial score.
  • Significant hypotension (SBP < 90 mm Hg) alters GCS. ^[24]

GCS is the standard for initial evaluation and classification of patients with traumatic brain injury.

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

Other classifications

• By mechanism of injury, e.g.:
  • Primary brain injury vs. secondary brain injury
  • Due to closed head injury or open head injury
  • Associated with blunt head injury, penetrating head injury, or blast injury
• By type of injury (usually seen on neuroimaging): e.g., EDH, SDH, traumatic SAH, traumatic ICH, traumatic IVH, DAI, cerebral contusion

General principles ^[24]

• Head CT without IV contrast is the first-line diagnostic modality.
  • Mild TBI: imaging only required for patients fulfilling criteria for neuroimaging in mTBI
  • Moderate/severe TBI: emergency neuroimaging after stabilization
• 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

• Indications: preferred first-line imaging modality in patients with TBI ^[24][37]
  • Moderate or severe TBI (GCS ≤ 12)
  • Mild TBI (GCS ≥ 13): only if any criteria for neuroimaging in mTBI are present
  • Open head injury
  • Depressed skull fracture
  • Short-term follow-up of TBI in patients with rapid deterioration of neurological symptoms
• Supportive findings
  • On brain window
    • Usually normal in mTBI ^[38]
    • Intracranial hemorrhage or hematoma: hyperdense lesions (see “Differential diagnosis of intracranial hemorrhage” for a comparison of CT findings)
    • Mass effect
      • Compression of cerebral parenchyma adjacent to hematoma
      • Midline shift to the contralateral side of the hematoma
      • Brain herniation: displacement of brain tissue from one compartment to another ^[36]
    • Diffuse axonal injury (DAI): can be normal in mild DAI; multiple punctate hyperdensities indicating small hemorrhages typically at the junction of gray and white matter, brainstem, internal capsule, and corpus callosum ^[23][36]
    • Cerebral contusion: heterogeneous lesion (mixed hemorrhagic, necrotic, and edematous tissue) surrounded by cerebral edema ^[23]
    • Cerebral edema: compression of ventricles, loss of defined sulci and gyri, and effacement of basal cisterns ^[36]
  • On bone window
    • Evidence of skull fractures: linear, depressed, or basilar skull fractures
    • Pneumocephalus: air within the cranium; typically associated with an open skull fracture
• Scrollable CT imaging examples
  • EDH and SDH
  • SDH
  • Traumatic ICH

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.

• CT cervical spine: consider in patients with history suggesting vertebral fracture (e.g., motor vehicle accident) ^[39]
• CT maxillofacial and/or temporal bone without IV contrast: in suspected CSF leak
• CT or MR angiography: in suspected intracranial arterial injury ^[37]
  • CTA spot sign
  • Signs of BCVI and penetrating injuries ^[36]
• CT or MR venography: suspected cerebral venous thrombosis: ^[37]

Laboratory studies ^[23][24]

• In patients with altered consciousness
  • Blood glucose
  • Blood alcohol level
  • Urine toxicology screen
  • Serum electrolyte levels
  • ABG analysis
• In patients with suspected coagulopathies : coagulation panel
• In patients with moderate TBI, severe TBI, and/or extensive blood loss from other injuries : blood type and screen
• In women of childbearing age: urine/serum pregnancy test

Overview

• After the initial management of TBI, the severity of injury and neuroimaging findings determine further management.
• The goal is to prevent secondary brain injury and provide surgical treatment if necessary.
• For surgical management of intracranial lesions see “Treatment” in “EDH”, “SDH”, “SAH”, “ICH”, and “Elevated intracranial pressure and brain herniation”.

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).

• Skull fracture surgery can be indicated for depressed skull fracture with one of the following:
  • Open fracture with dural penetration or significant depression
  • Significant cranial hematoma
  • Frontal sinus involvement
  • Gross contamination/wound infection
  • Pneumocephalus
  • Major cosmetic deformity
• Craniotomy and evacuation of hematomas
  • EDH and acute SDH meeting criteria for surgery should have evacuation done as soon as possible.
  • See “SDH” and “EDH” for details on indications and methods.
• Surgical management of ↑ ICP (See “ICP management” for details.)
  • Extraventricular drain (EVD)
  • Decompressive craniectomy ^[26]
    • Indicated in traumatic intraparenchymal hemorrhages and posterior fossa hemorrhages with:
      • Mass effect
      • Neurological deterioration attributable to the lesion
      • High ICP refractory to medical therapy
    • Approach (e.g., suboccipital, subtemporal, frontotemporoparietal) depends on lesion location.

Additional treatment and monitoring

• Antifibrinolytic therapy: Consider TXA.
  • Moderate TBI: Consider TXA if < 3 hours have elapsed since the injury ^{[40][41][42][43][44]}
  • Severe TBI: benefit of TXA unlikely because of potentially extensive intracranial hemorrhage at presentation ^[40]
• Supportive care:
  • ICP management
  • Intubated patients: See “Adjunctive care of ventilated patients”.
  • Pain management: Treat pain and agitation with analgesics and sedatives.
  • Antiemetics (in patients with significant nausea/vomiting)
• Monitoring
  • Continuous or frequent monitoring of vitals.
  • Frequent assessment of GCS
  • Frequent monitoring of blood glucose and serum electrolyte levels as needed.
  • Consider invasive ICP monitoring in patients with risk factors for elevated ICP, including:
    • GCS ≤ 8 and signs of high ICP on CT scan
    • Normal CT scan and ≥ 2 of the following:
      • Age > 40 years
      • Unilateral or bilateral motor posturing
      • SBP < 90 mm Hg
  • Pain: Use self-reported or behavior-based pain scales.
  • Sedation: Use standardized scales to assess agitation and level of sedation (e.g., RASS).
• Follow-up neuroimaging
  • Moderate TBI: consider after 12–24 hours or before discharge if any of the following are present: ^[45][46]
    • Clinical deterioration
    • Initial neuroimaging showed abnormalities
    • Elevated ICP
    • Coagulopathy
    • Hypotension
  • Severe TBI: usually obtained 6 hours after initial neuroimaging ^[47]
• Disposition: admission/urgent transfer to definitive neurosurgical care or neurocritical care unit

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

• Anticoagulant reversal ^[50][51]
  • Indication: all patients with intracranial hemorrhage who are on anticoagulant medication
  • Contraindication: concomitant cerebral venous thrombosis ^[50]
  • Target INR: ≤ 1.4 ^[24]
  • Treatment
    • Stop further doses of anticoagulants.
    • Administer anticoagulant reversal.
  • Resumption of anticoagulant therapy should be individualized. ^[52][53]
• Antiplatelet therapy, thrombocytopenia, and platelet dysfunction ^[2][23]
  • Stop further doses of antiplatelet agents.
  • Patients planned for neurosurgery or invasive procedures: Consider platelet transfusion if platelet count is < 80–100,000/μL. ^[31][54]
  • Resumption of antiplatelet therapy should be individualized.
• DIC monitoring: repeat INR, platelets, and hemoglobin

Additional prophylactic measures

• DVT prophylaxis ^[26]
  • Mechanical prophylaxis: recommended in patients with an active intracranial bleed
  • Pharmacological prophylaxis: consider LMWH or low-dose unfractionated heparin in stable TBI after individual risk-benefit evaluation
• Antibiotic prophylaxis ^[26][51]
  • Not routinely recommended
  • Consider in select patients with open head injuries.
  • See “CNS infection prophylaxis for open head injury” for details.
• Seizure prophylaxis and treatment
  • Prophylaxis ^[23][26]
    • Indicated in severe TBI for 7 days postinjury to prevent early post-traumatic seizures
    • Preferably with phenytoin or levetiracetam ^[2][26][48]
    • See “Seizure prophylaxis after TBI” for dosages.
  • Treat acute seizures.
• Maintenance of vitals and nutrition: See neuroprotective measures.

• ABCDE survey and immediate initiation of neuroprotective measures ^[22][23][24]
• Additional prehospital trauma care as needed (e.g., cervical spine control, analgesics, fluid resuscitation)
• Rapid neurological examination, including assessment for signs of ↑ ICP
• Assess severity of TBI (see GCS).
• Consider intubation if GCS ≤ 8 (high-risk; see “Intubation of patients with high ICP.”)
• Consider tranexamic acid if GCS 9–13 and < 3 hours have elapsed since injury.
• Administer anticoagulant reversal as needed.
• Assessment for other life-threatening or limb-threatening injuries
• Continuous monitoring of vitals, pulse oximetry, and capnography
• Urgent neurosurgical consult if GCS ≤ 12
• Urgent transfer to a neurocritical care unit if GCS ≤ 12
• Serial neurological examination and assessment of GCS

• Cerebral edema
• Post-concussion syndrome
• Coma
• Seizures ^[55]
  • Early post-traumatic seizure: occurs within one week of inciting trauma
  • Late post-traumatic seizure: occurs a week after the inciting trauma
• Permanent focal neurological deficits, including persistent vegetative state
• Acute traumatic coagulopathy
• Chronic CSF rhinorrhea
• Intracranial infection (e.g., meningitis, encephalitis, brain abscess secondary to open head injury or neurosurgery) ^[56]
• Surgical site infections (e.g., bone flap osteomyelitis, shunt infections in patients who undergo neurosurgery) ^[57]
• Irreversible loss of brain function (brain death)

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

• Traumatic brain injury (most common)
• Anoxic brain injury
• Stroke
• Patient repositioning or extraction of endotracheal tube
• Brain tumors
• Infections (e.g., encephalitis)
• Hydrocephalus

Clinical features

• Usually occur 1 week after the injury
• Recurrent episodes of excessive sympathetic activity (e.g., fever, tachycardia, tachypnea, hypertension)
• Rapid onset; typically last up to 30 minutes then self-resolve
• Muscle spasms and, possibly, dystonia with posturing

Diagnostics

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

Treatment ^[58]

• Supportive care (e.g., antipyretics for fever, adequate hydration, analgesia, remove or reduce stimuli that may trigger symptoms)
• Pharmacological
  • Depends on patient symptoms
  • Abortive and preventive agents
    • Opioids (e.g., morphine, fentanyl)
    • Sympatholytics (e.g., clonidine, propranolol)
    • Benzodiazepines (e.g., diazepam, lorazepam)
    • Muscle relaxants (e.g., dantrolene, baclofen)

References: ^[59][60]

• Mild TBI: Most (80–90%) patients make a full recovery within 2 weeks ^[23][61]
• Moderate TBI ^[24][62]
  • 90% patients improve but ∼ 44% have moderate disability.
  • 10% deteriorate to severe TBI.
• Severe TBI: mortality rate of approx. 35% ^[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
    • Skull fracture > 3 mm separation or depressed
    • Evidence of traumatic brain injury on imaging (e.g.., intracranial hemorrhage)
    • Signs of ↑ ICP (e.g., headache, altered mental status)
    • Suspected physical abuse
    • Caregivers who are unreliable or unable to return if neurological deficits develop within 24 hours after release.
  • 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:^[64][65]

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

The following table focuses on traumatic causes of intracranial hemorrhage, which all have nontraumatic causes as well. See “Overview of stroke” for a comparison of nontraumatic cerebral ischemia and intracranial hemorrhage.