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 ( ), , , , , and is discussed in separate articles.
- Traumatic brain injury (TBI): structural or physiological disruption of the brain resulting from a head injury 
- Head injury: trauma to the head that may or may not be associated with soft tissue injury, skull fractures, and TBI 
- Blunt head injury (common): injury caused by blunt force trauma to the head
- Penetrating head injury (less common): injury caused by penetrative trauma to the head 
- Blast injuries: injury caused by the high pressure wave (blast wave) generated from an explosion; common in active military or war zones 
Primary brain injury 
- Definition: brain injury that occurs at the time of the trauma as an immediate consequence of head injury
Focal primary brain injury
- Intracranial hemorrhage
- Cerebral contusion: focal area of heterogeneous brain injury, varying from a bruise to a focal area of necrosis 
- 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
- concussion) (
- Diffuse axonal injury (DAI)
- Definition: indirect brain injury resulting from physiological changes following acute CNS insults and/or their treatment
- Examples: disrupted blood-brain barrier, (see “Pathophysiology” in “Secondary brain injury” for details)
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”.
- Global neurological symptoms
- Symptoms of increased intracranial pressure (ICP)
- Focal neurologic deficits: depending on the affected brain region (see “Stroke symptoms by affected region”)
Abnormal posturing: characteristic posture of the limbs that typically signifies severe brain injury (most commonly involving the brainstem) 
- Decorticate posturing (flexor posturing)
- Decerebrate posturing (extensor posturing)
In deCORticate posture, the arms are flexed towards the CORe of the body.
Symptoms of associated injuries
- General symptoms of skull fractures 
- hematomas, facial and/or nasal swelling, epistaxis, visible deformity :
- Start primary survey (ABCDE survey) with simultaneous .
- Measure GCS and pupillary response.
- GCS. by severity based on
- 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.
Neuroimaging should not delay transfer to centers that can provide definitive neurosurgical care if required. 
Primary survey 
|Key aspects for primary survey in TBI |
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).
- Focused history
- Physical examination: thourough head-to-toe examination and complete neurological examination
- Continuous monitoring
- Emergency consults
- Transfer: If GCS ≤ 12, transfer to a trauma center or neurocritical care unit if unavailable at current site
Severity classification using (GCS) 
- Clinical applications of GCS in TBI 
- 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
- TBI severity
- Important considerations
By mechanism of injury, e.g.:
- vs. s
- Due to or
- Associated with , , or
- By type of injury (usually seen on neuroimaging): e.g., , , , traumatic , traumatic , ,
General principles 
- 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.
Head CT without IV contrast
- Indications: preferred first-line imaging modality in patients with TBI 
- On brain window
- Usually normal in mTBI 
- Intracranial hemorrhage or hematoma: hyperdense lesions (see “Differential diagnosis of intracranial hemorrhage” for a comparison of CT findings)
- Mass effect
- 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 
- Cerebral contusion: heterogeneous lesion (mixed hemorrhagic, necrotic, and edematous tissue) surrounded by cerebral edema 
- Cerebral edema: compression of ventricles, loss of defined sulci and gyri, and effacement of basal cisterns 
- On bone window
- On brain window
MRI head without IV contrast 
- Acute TBI with symptoms unexplained by CT (in hemodynamically stable patients) 
- 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) 
- Supportive findings: Microhemorrhages, DAI, and contusions are better visualized on MRI than on CT.
Additional imaging 
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) 
- CT maxillofacial and/or temporal bone without IV contrast: in suspected CSF leak
- CT or MR angiography: in suspected intracranial arterial injury 
- CT or MR venography: suspected cerebral venous thrombosis: 
Laboratory studies 
- In patients with altered consciousness
- In patients with suspected coagulopathies : coagulation panel
- In patients with moderate TBI, severe TBI, and/or extensive blood loss from other injuries : blood
- In women of childbearing age: urine/serum pregnancy test
- 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”.
|Overview of TBI management |
|Severity of TBI||Treatment||Supportive care|
|Mild (GCS ≥ 13)|
|Moderate TBI (GCS 9–12)|| || |
|Severe TBI (GCS ≤ 8)|
Surgical treatment 
- Skull fracture surgery can be indicated for depressed skull fracture with one of the following:
- Craniotomy and evacuation of hematomas
- Surgical management of ↑ ICP (See “ICP management” for details.)
- Extraventricular drain (EVD)
- Decompressive craniectomy 
Additional treatment and monitoring
- Antifibrinolytic therapy: Consider TXA.
- Supportive care:
- 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:
- Pain: Use self-reported or behavior-based pain scales.
- Sedation: Use standardized scales to assess agitation and level of sedation (e.g., ).
- Follow-up neuroimaging
- Disposition: admission/urgent transfer to definitive neurosurgical care or neurocritical care unit
Prevention of complications in brain injuries
Secondary bleeding or hematoma expansion
Anticoagulant reversal 
- Indication: all patients with intracranial hemorrhage who are on anticoagulant medication
- Contraindication: concomitant cerebral venous thrombosis 
- Target INR: ≤ 1.4 
- Stop further doses of anticoagulants.
- Administer .
- Resumption of anticoagulant therapy should be individualized. 
- Antiplatelet therapy, thrombocytopenia, and platelet dysfunction 
- DIC monitoring: repeat INR, platelets, and hemoglobin
Additional prophylactic measures
- DVT prophylaxis 
CNS Infection prophylaxis: not routinely recommended 
- Routine monitoring of serum inflammatory markers or ventricular fluid WBC count is not recommended. 
- Indications for empiric antibiotic therapy include: 
- Regimens should provide coverage for Staphylococci, gram-negative bacteria, and anaerobes 
- Seizure prophylaxis and treatment
- Maintenance of vitals and nutrition: See .
- ABCDE survey and immediate initiation of 
- Additional cervical spine control, analgesics, fluid resuscitation) as needed (e.g.,
- Rapid neurological examination, including assessment for
- Assess severity of TBI (see ).
- Consider intubation if GCS ≤ 8 (high-risk situation, recommend expert consultation)
- Consider tranexamic acid if GCS 9–13 and < 3 hours have elapsed since injury.
- Administer 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
- Permanent focal neurological deficits, including persistent vegetative state
- Chronic CSF rhinorrhea
- Intracranial infection (e.g., meningitis, encephalitis, brain abscess secondary to open head injury or neurosurgery) 
- Surgical site infections (e.g., bone flap osteomyelitis, shunt infections in patients who undergo neurosurgery) 
We list the most important complications. The selection is not exhaustive.
Paroxysmal sympathetic hyperactivity (PSH)
- Traumatic brain injury (most common)
- Anoxic brain injury
- Patient repositioning or extraction of endotracheal tube
- Brain tumors
- Infections (e.g., encephalitis)
- 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
- Supportive care (e.g., antipyretics for fever, adequate hydration, analgesia, remove or reduce stimuli that may trigger symptoms)
Special patient groups
- 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.
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
- Inpatient observation indications
Overview of common brain lesions
|Overview of common brain lesions|
|Location of lesion||Clinical features|
|Frontal eye fields|| |
|Mammillary bodies (bilateral)|
|Medial longitudinal fasciculus|
|Paramedian pontine reticular formation|
Middle and inferior cerebellar peduncles
|Nucleus and fibers of the hypoglossal nerve|
Overview of intracranial hemorrhage
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.
|Overview of intracranial hemorrhage|
|Epidural hematoma||Subdural hematoma||Subarachnoid hemorrhage||Intracerebral hemorrhage|
|Characteristic clinical features|
|Typical findings on noncontrast CT head|| |