Traumatic brain injury (TBI) is a disruption of the normal function of the brain caused by a head injury. Blunt trauma, penetrating injuries, and blast injuries may all cause TBI. Not all head injuries cause TBI. TBI can be classified as mild, moderate, or severe, typically based on the Glasgow Coma Scale (GCS) score and/or neurobehavioral 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 neurobehavioral deficits; and a GCS no worse than 13. CDC: heads up external link opens in a new window However, there is ongoing debate about whether patients with a GCS of 13 should instead be classified as having moderate TBI.
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. Efforts in the US and the UK to standardize 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.
Classification by clinical severity
The GCS has been used extensively to classify TBI into levels of severity and prognosis. After traumatic brain injury, there is an inverse relationship between the GCS score and the incidence of positive findings on computed tomography (CT); in fact, the rate of intracranial injury (ICI) and need for neurosurgical intervention doubles when the GCS drops from 15 to 14.
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 moderate instead of mild, due to the higher incidence of ICI and poor outcomes in these patients. Clinical guidelines in Australia recognize 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.
The Mayo classification system for TBI classifies patients with TBI into definite, probable, and possible, based on the patient’s clinical and CT findings.
Classification by broad etiology
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.
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, hypoxic brain injury, diffuse cerebral edema, or diffuse vascular injury.
Focal injury includes specific lesions such as contusions, intracranial hematomas, infarctions, axonal tears, cranial nerve avulsions, and skull fractures.
Classification by injury progression
Primary injury is due to the immediate mechanical force, whether blunt, penetrating, or blast, and may include the following:
Subarachnoid or focal hemorrhage
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:
Increased intracranial pressure
Epidemiology of TBI
TBI is a substantial cause of morbidity and mortality, leading to more than 2.5 million emergency department visits annually in the US, an increase from 1.6 million in 2006, and more than 1.4 million in the UK. The burden of disability and death due to TBI is higher in low- and middle-income countries compared with high-income countries.
Around 80% of patients with TBI sustain a minor head injury, and are treated and released without hospital admission or intervention, other than diagnostic imaging. About 10% have injuries that require hospitalization and about 2% die.
TBI is the most common cause of death in people under the age of 25. It most frequently occurs in very young children (ages 0 to 4 years) and in adolescence and young adulthood (ages 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 hospitalizations and deaths.
Males are over-represented by 3:1 in all subgroups of TBI. Neurosurgical intervention (craniotomy, elevation of skull fracture, increased intracranial pressure monitor, or ventriculostomy) is required in about 40% of patients with severe TBI, about 10% of patients with moderate TBI, and about 1% of patients with mild TBI. In 2017, 15% of high school students in the US reported at least one sports-related concussion in the past year. Approximately 30% of children and adults experience persistent post-concussive symptoms lasting more than 30 days after injury.
Epidemiology of specific injuries
Most patients have a combination of injuries.
Traumatic subarachnoid hemorrhage (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. 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.
Subdural hematomas (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 hospitalizations or deaths are most commonly secondary to motor vehicle-related injury in younger adults, and falls in older adults.
Epidural hematomas (EDH) are 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.
Axonal injury is 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. 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.
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.
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.
Blast injuries are a leading cause of TBI in active duty military personnel in war zones, accounting for about 60% of all severe TBI.
Albert J. Lauro Professor of Medicine/Emergency Medicine
Clinical Professor Medicine/Emergency Medicine
Section of Emergency Medicine
Louisiana State University Health Science Center
MJH is an author of a reference cited in this topic.
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.
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