Assessment of traumatic brain injury, acute

Last reviewed: 20 Sep 2021

Last updated: 25 May 2021

Definitions

Traumatic brain injury (TBI) is a disruption of the normal function or structure of the brain caused by a head impact or external force.[1][2] Blunt trauma, penetrating injuries, and blast injuries may all cause TBI. Not all impacts to the head cause TBI. TBI can be classified as mild, moderate, or severe, typically based on the Glasgow Coma Scale (GCS) score and/or neurobehavioural deficits after the injury.

The term 'concussion' is often used interchangeably with mild TBI. Both the Centers for Disease Control and Prevention and the World Health Organization agree that mild TBI is due to a blunt or mechanical force that results in: some type of transient confusion, disorientation or loss of consciousness lasting not more than 30 minutes; possibly associated with transient neurobehavioural deficits; and a GCS no worse than 13.[3] CDC: heads up external link opens in a new window

Classification

TBI can be classified in numerous ways, including type, severity, location, mechanism of injury, and physiological response to injury.

TBI is extremely heterogeneous, with short and long term outcomes affected by the specific intracranial injury, concomitant extracranial injury, age, and pre-existing comorbidities. Most classification systems are based on patient symptomatology, clinical examination or diagnostic findings during the early stabilisation phase, and do not account for the evolving TBI process.

However, it has been suggested that classification based on repeated risk assessment over time would allow for the many variables that affect outcome.[4]

Classification by clinical severity

The GCS has been used extensively to classify TBI into levels of severity and prognosis.[5][6] After TBI, there is an inverse relationship between the GCS score and the incidence of positive findings on computed tomography (CT); the rate of intracranial injury (ICI) and need for neurosurgical intervention doubles when the GCS drops from 15 to 14.[7][8]

Mild TBI: GCS 13-15; mortality 0.1%
Moderate TBI: GCS 9-12; mortality 10%
Severe TBI: GCS <9; mortality 40%.

Many clinicians recommend that patients with a GCS of 13 be classified as having moderate TBI instead of mild, due to the higher incidence of ICI and poor outcomes in these patients (compared with those with a GCS of >13).[9][10][11] Clinical guidelines in Australia recognise the increased morbidity associated with a GCS of 13, and limit the classification of mild TBI to those patients with a GCS of 14 or 15.[12]

The Mayo classification system for TBI classifies patients with TBI into definite, probable, and possible, based on the patient’s clinical and CT findings.[13]

Classification by broad aetiology

May be blunt, penetrating, or blast-related.

Blunt TBI: occurs when external mechanical force leads to rapid acceleration or deceleration with brain impact. It is typically found in the setting of motor vehicle-related injury, falls, crush injuries, or physical altercations.
Penetrating TBI: occurs when an object pierces the skull and breaches the dura mater, seen commonly in gunshot and stab wounds.
Blast TBI: commonly occurs after bombings and warfare, due to a combination of contact and inertial forces, overpressure, and acoustic waves.[14]

Classification by area of involvement

TBI can be classified by area involved, as in diffuse or focal, although the two types frequently coexist.

Diffuse brain injury includes diffuse axonal injury (DAI), hypoxic brain injury, diffuse cerebral oedema, or diffuse vascular injury.[15]
Focal injury includes specific lesions such as contusions, intracranial haematomas, infarctions, axonal tears, cranial nerve avulsions, and skull fractures.[15]

Classification by injury progression: primary versus secondary

Primary injury is due to the immediate mechanical force, whether blunt, penetrating, or blast, and may include the following:

Concussion
Skull fracture
Contusion
Haematoma
Subarachnoid or focal haemorrhage
Axonal shear or laceration.

Secondary injury refers to the evolving pathophysiological consequences of the primary injury. It encompasses a multitude of complex neurobiological cascades altered or initiated at a cellular level following the primary injury, and may include the following:[15]

Cerebral oedema
Increased intracranial pressure
Haemorrhage
Seizures
Ischaemia
Infection.

Epidemiology

TBI is a substantial cause of morbidity and mortality, leading to approximately 2.5 million accident and emergency department visits annually in the US, and more than 1.4 million in the UK.[1][16] The burden of disability and death due to TBI is higher in low- and middle-income countries compared with high-income countries.[17]

Approximately 90% of patients with TBI sustain a minor head injury, and are treated and released without hospital admission or intervention.[18] About 10% have injuries that require hospitalisation and about 2% die.[1]

TBI most frequently occurs in very young children (age 0 to 4 years), and in adolescence and young adulthood (age 15 to 24 years), with a subsequent peak in incidence in older adults (over age 65).[19] Older age comprises the group with the highest rates of TBI-related hospitalisations and deaths.[1] Estimated average annual rates of TBI are higher for males than for females across all age groups.[20]

The need for neurosurgical intervention (craniotomy, elevation of skull fracture, increased intracranial pressure monitor, or ventriculostomy) doubles when the GCS drops from 15 to 14.[8]

Concussion and post-concussive symptoms

Concussion occurs in most patients with TBI, and is typically the only finding in patients with mild TBI. Patients with moderate or severe TBI typically have a combination of injuries, including concussive symptoms.

The five major subtypes of concussion include headache, cognitive, vestibular, mood and ocular-motor. One meta-analysis demonstrated that headache and cognitive are the most common subtypes in both adults and children.[21]

The World Health Organization’s definition of post-concussive syndrome includes the presence of 3 or more of the following symptoms after a head injury: headache, dizziness, fatigue, irritability, difficulty with concentrating and performing mental tasks, impairment of memory, insomnia and reduced tolerance to stress, emotional excitement, or alcohol.[22]

In 2017, 15% of high school students in the US reported at least one sports-related concussion in the past year.[23] Approximately 30% of children and adults experience persistent post-concussive symptoms lasting more than 30 days after injury.[24][25]

Haemorrhage

Traumatic subarachnoid haemorrhage (SAH) is one of the most common CT findings in TBI, occurring in about 30% to 40% of patients with moderate to severe TBI, and 5% of patients with mild TBI.[6][26][27] SAH is frequently associated with other injuries. SAH is associated with a poorer outcome in patients with moderate or severe TBI, although it is unclear whether the SAH is simply a marker of severity of injury, or if the poorer outcomes are due to subsequent vasospasm.[28]

Subdural haematomas (SDH) are the most common type of mass lesion in TBI, seen in about 20% of patients with moderate to severe TBI, and in about 30% of fatal TBI. SDH occur in only 3% of patients with mild TBI. SDH that lead to hospitalisations or deaths are most commonly secondary to motor vehicle-related injury in younger adults, and falls in older adults.[6][29]

Epidural haematoma (EDH) is seen in about 10% of patients with moderate to severe TBI and about 1% of patients with mild TBI. The incidence of EDH is highest among adolescents and young adults, most commonly between 20 and 30 years of age. Most cases of EDH are caused by traffic accidents, falls, and assaults.[6][26]

Intracerebral haematomas occur in 10% to 30% of patients with moderate to severe TBI, and <1% of patients with mild TBI.[6][15]

Cerebral contusions

Occur in 20% to 30% of patients with moderate to severe TBI, and 6% of patients with mild TBI.[6][27][30]

Axonal injury

Probably present in a majority of patients with TBI to some degree, although low-grade axonal injury is usually microscopic and not detected by CT.

Diffuse axonal injury (DAI) is thought to be present to some degree in all TBI-related fatalities and those resulting in a persistent vegetative state. The presence of DAI increases the likelihood of a poor outcome.[31] The initial CT is normal in 50% to 80% of patients ultimately diagnosed with DAI, but magnetic resonance imaging shows evidence of axonal injury in 70% of patients with moderate to severe TBI.[32]

Skull fractures

Occur in about 5% of patients with mild TBI and up to 50% of those with severe TBI. Most skull fractures are due to falls, assaults, or motor vehicle-related injuries. The most common fractures are simple linear fractures, comprising >50% of all skull fractures. Less than 1% of patients with mild TBI have a depressed skull fracture.[6]

Penetrating or blast injury

Penetrating injuries are classified as high- or low-velocity, and may be self-inflicted, non-intentional, or related to an assault. A single gunshot wound to the head has 50% mortality.[33]

Blast injuries are a leading cause of TBI in active duty military personnel in war zones, accounting for about 60% of all severe TBI.[34]

Differentials

Common

Skull fracture (excl. base of skull)
Base of skull fracture
Cerebral contusion
Intracerebral haemorrhage
Subdural haematoma
Epidural haematoma
Intraventricular haemorrhage
Traumatic subarachnoid haemorrhage
Penetrating injuries
Diffuse axonal injury
Mild traumatic brain injury

Full details

Contributors

Authors

Micelle J. Haydel, MD

Albert J. Lauro Professor of Medicine/Emergency Medicine

Clinical Professor Medicine/Emergency Medicine

Section of Emergency Medicine

Louisiana State University Health Science Center

New Orleans

Disclosures

MJH is an author of a reference cited in this topic.

Acknowledgements

Dr Micelle J. Haydel would like to gratefully acknowledge Dr Victoria E. Johnson, Dr Marek Ma, Dr Nathan Ranalli, and Dr Douglas H. Smith, previous contributors to this topic.

Disclosures

VEJ, MM, NR, and DHS declare that they have no competing interests.

Peer reviewers

David W. Wright, MD

Director of Research

Department of Emergency Medicine

Emory University

Atlanta

Disclosures

DWW declares that he has no competing interests.

David Sharp, MBBS, BA, MRCP, PhD

Senior Lecturer In Neurology

Imperial College

London

Disclosures

DS declares that he has no competing interests.

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Definitions

Classification

Epidemiology

Differentials

Common

Contributors

Authors

Micelle J. Haydel, MD

Disclosures

Acknowledgements

Disclosures

Peer reviewers

David W. Wright, MD

Disclosures

David Sharp, MBBS, BA, MRCP, PhD

Disclosures

Guidelines

Calculators

Videos

Assessment of traumatic brain injury, acute

Summary

Definitions

Classification

Epidemiology

Differentials

Common

Contributors

Authors

Micelle J. Haydel, MD

Disclosures

Acknowledgements

Disclosures

Peer reviewers

David W. Wright, MD

Disclosures

David Sharp, MBBS, BA, MRCP, PhD

Disclosures

Guidelines

Calculators

Videos