Assessment of traumatic brain injury, acute

Last reviewed:September 2019

Last updated:November 2018

Summary

Definitions

Head injury is defined as any trauma to the head, with or without injury to the brain. The head injury can be described as minimal, minor, moderate, or severe, based on symptoms after the injury. Patients with minimal head injury are those with trauma to the head and no loss of consciousness, a normal Glasgow Coma Scale (GCS) score, and no symptoms of head injury. Minor head injury patients have a GCS of 13 to 15 after head injury.[1]

Traumatic brain injury (TBI) is a non-specific term describing blunt, penetrating, or blast injuries to the brain. TBI can be classified as mild, moderate, or severe, typically based on the GCS and/or neurobehavioural deficits after the injury.

The term 'concussion' is often used interchangeably with mild TBI and minimal or minor head injury in the sports literature. 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, and possibly associated with transient neurobehavioural deficits and a GCS no worse than 13 to 15.[2] CDC: heads up However, there is ongoing debate about whether patients with a GCS of 13 should instead be classified as having moderate TBI.

Classification

TBI can be classified in numerous ways, including type, severity, location, mechanism of injury, and physiological response to injury. This heterogeneity is considered to be one of the most significant barriers to establishing effective therapeutic interventions in TBI.[3] Efforts in the US and the UK to standardise the naming, definitions, and classification of TBI subgroups have the potential to reduce the variability in data coding and improve the quality of data gathering in TBI research.[4][5][6]

Classification by clinical severity

The GCS has been used extensively to classify TBI into levels of severity and prognosis.[7][8] After traumatic brain injury, there is an inverse relationship between the GCS score and the incidence of positive findings on CT; in fact, the rate of intracranial injury (ICI) and need for neurosurgical intervention doubles when the GCS drops from 15 to 14.[9][10]

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

Many authors recommend that patients with a GCS of 13 be classified as moderate instead of mild or minor, due to the higher incidence of ICI and poor outcomes in these patients.[11][12][13][14] 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.[15]

The Mayo classification system for TBI classifies patients with TBI into definite, probable, and possible, based on the patient’s clinical and CT findings.[16]

Classification by broad aetiology

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.[17]

Classification by 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.[18]
Focal injury includes specific lesions such as contusions, intracranial haematomas, infarctions, axonal tears, cranial nerve evulsions, and skull fractures.[18]

Classification by injury progression

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

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

Secondary injury refers to the evolving pathophysiological consequences of the primary injury and encompasses a multitude of complex neurobiological cascades altered or initiated at a cellular level following the primary injury, and may include the following:[18]

Cerebral oedema
Increased intracranial pressure (ICP)
Haemorrhage
Seizures
Ischaemia
Infection.

Epidemiology of TBI

TBI is a substantial cause of morbidity and mortality, leading to more than 2 million accident and emergency department visits annually in the US,[19] and more than 1 million in the UK.[20] A 2017 review highlighted the higher burden of disability and death due to TBI in low- and middle-income countries compared with high-income countries.[21]

Around 80% of patients with TBI have minor head injury, and are treated and released without hospital admission or intervention other than diagnostic imaging.[22] About 20% have injuries that require hospitalisation, 6% suffer permanent disability, and about 3% die.[23][24]

TBI is the most common cause of death in people under the age of 25. It 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). Older age comprises the group with the highest rates of TBI-related hospitalisations and deaths.[25][26]

Males are over-represented by 3:1 in all subgroups of TBI. Neurosurgical intervention (craniotomy, elevation of skull fracture, ICP monitor, or ventriculostomy) is required in about 40% of patients with severe TBI, about 10% of patient with moderate TBI, and about 1% of patients with minor TBI.[8][27] Post-concussive syndrome is the neurobehavioural sequelae of even mild TBI, which encompasses somatic, cognitive, and affective domains, and patients commonly report headache, dizziness, difficulty concentrating, and depression. Approximately 30% of children and adults experience persistent post-concussive symptoms more than 30 days after injury.[28][29]

Medical costs and losses due to either temporary or permanent gaps in productivity are estimated to annually exceed £15 billion in the UK[30][31] and $70 billion in the US.[32] Even in mild TBI, persistent neurocognitive dysfunction can occur, exacting a significant emotional toll on patients and families, and a financial toll on society. Some patients with a discharge diagnosis of mild TBI will have symptoms at 3 months post-injury. [33]

Epidemiology of specific injuries

Most patients have a combination of injuries.

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 minor TBI.[8][34][35] 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.[36]

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 minor TBI. SDH that lead to hospitalisations or deaths are most commonly secondary to motor vehicle-related injury in younger adults, and to falls in older adults.[8][27]

Epidural haematomas (EDH) are seen in about 10% of patients with moderate to severe TBI and about 1% of patients with minor 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.[8][34]

Contusions occur in 20% to 30% of patients with moderate to severe TBI, and 6% of patients with minor TBI.[8][35][37]

Intracerebral haematomas occur in 10% to 30% of patients with moderate to severe TBI, and <1% of patients with minor TBI.[8][18]

Diffuse axonal injury (DAI) is probably present in a majority proportion of patients with TBI to some degree, although low grade axonal injury is usually microscopic and not detected by CT. The initial CT is normal in 50% to 80% of patients ultimately diagnosed with DAI, but MRI shows evidence of axonal injury in 70% of patients with moderate to severe TBI. Axonal injury is detected in <1% of patients with minor TBI on CT, although the degree of microscopic injury is greater on MRI. Some degree of DAI is thought to be present in all TBI-related fatalities and those resulting in a persistent vegetative state.[8][38]

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 minor TBI have a depressed skull fracture.[8]

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.[39]

Blast injuries are a leading cause of TBI in active duty military personnel in war zones, accounting for about 60% of all severe TBI.[40][41]

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

AuthorsVIEW ALL 

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

Peer reviewersVIEW ALL 

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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Summary

Definitions

Classification

Classification by clinical severity

Classification by broad aetiology

Classification by involvement

Classification by injury progression

Epidemiology of TBI

Epidemiology of specific injuries

Differentials

Common

Contributors

AuthorsVIEW ALL 

Micelle J. Haydel, MD

Disclosures

Acknowledgements

Peer reviewersVIEW ALL 

David W. Wright, MD

Disclosures

David Sharp, MBBS, BA, MRCP, PhD

Disclosures

Guidelines

Calculators

Procedural videos

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