12
Official reprint from UpToDate ® www.uptodate.com ©2012 UpToDate ® Authors J Claude Hemphill, III, MD, MAS Nicholas Phan, MD, FRCSC, FACS Section Editor Michael J Aminoff, MD, DSc Deputy Editor Janet L Wilterdink, MD Traumatic brain injury: Epidemiology, classification, and pathophysiology Disclosures All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Oct 2012. | This topic last updated: Jul 5, 2012. INTRODUCTION — Traumatic brain injury (TBI) is the leading cause of death in North America for individuals between the ages of 1 and 45. Many survivors live with significant disabilities, resulting in major socioeconomic burden as well. In 2000, the economic impact of TBI in the United States was estimated to be $9.2 billion in lifetime medical costs and $51.2 billion in productivity losses [1 ]. The focus of this topic is on the epidemiology, pathophysiology and classification of TBI. Other aspects of traumatic head injury are discussed separately. (See "Management of acute severe traumatic brain injury" and "Concussion and mild traumatic brain injury" and "Intracranial epidural hematoma in adults" and "Post-traumatic seizures and epilepsy" and "Subdural hematoma in adults: Etiology, clinical features, and diagnosis" and "Skull fractures in adults" .) EPIDEMIOLOGY — The overall incidence of TBI in the United States was estimated to be 538.2 per 100,000 population, or around 1.5 million new cases in 2003 [1 ]. Somewhat lower rates are reported in Europe (235 per 100,000) and Australia (322 per 100,000) [2,3 ]. Rates of TBI are highest in the very young (age group zero to four years) and in adolescents and young adults (15 to 24 years); there is another peak in incidence in the elderly (age >65 years) [1 ]. Approximately 78 percent of TBI are treated in the emergency department only; 19 percent of patients require hospitalization, and 3 percent are fatal. Most cases treated in emergency departments occur in the very young (ages zero to four years), while hospitalization rates are highest in patients older than 65 years. As with most traumatic injuries, the incidence of TBI is significantly higher in men compared to women, with ratios that vary between 2.0 to 1 and 2.8 to 1 [4,5 ]. For severe TBI, the gender ratio is more pronounced, 3.5 to 1. Lower socioeconomic status is also a risk factor for head injury. Falls are the leading cause of TBI (particularly in older patients), followed by motor vehicle accidents [6,7 ]. The proportion of TBI secondary to violence has risen over the past decade and now accounts for 7 to 10 percent of cases [8 ]. TBI related to military combat has received increased attention in the years from 2002 to 2009 [9 ]. Mechanistic aspects of combat-related trauma may differ from TBI related to other causes, as the former usually involve blast explosives. Moderate and severe TBIs are associated with neurologic and functional impairments. The prevalence of long-term disability related to TBI in the United States is variably estimated to be between 3.2 to 5.3 million, or approximately 1 to 2 percent of the population [10,11 ]. Epidemiologic trends more specific to mild TBI are discussed separately. (See "Concussion and mild traumatic brain injury", section on 'Epidemiology' .) CLASSIFICATION — TBI is a heterogeneous disease. There are many different ways to categorize patients in terms of clinical severity, mechanism of injury, and pathophysiology, each of which may impact prognosis and treatment. The best prognostic models ideally include all of the factors described below, as well as age, medical comorbidity, and laboratory parameters [12-14 ]. However, treatment decisions are likely best informed by considering these variables individually rather than as a lump score. Further efforts at improved classification are ongoing as these may

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Official reprint from UpToDate® www.uptodate.com ©2012 UpToDate®

AuthorsJ Claude Hemphill, III, MD, MASNicholas Phan, MD, FRCSC, FACS

Section EditorMichael J Aminoff, MD, DSc

Deputy EditorJanet L Wilterdink, MD

Traumatic brain injury: Epidemiology, classification, and pathophysiology

Disclosures

All topics are updated as new evidence becomes available and our peer review process is complete.Literature review current through: Oct 2012. | This topic last updated: Jul 5, 2012.

INTRODUCTION — Traumatic brain injury (TBI) is the leading cause of death in North America for individualsbetween the ages of 1 and 45. Many survivors live with significant disabilities, resulting in major socioeconomicburden as well. In 2000, the economic impact of TBI in the United States was estimated to be $9.2 billion in lifetimemedical costs and $51.2 billion in productivity losses [1].

The focus of this topic is on the epidemiology, pathophysiology and classification of TBI. Other aspects of traumatichead injury are discussed separately. (See "Management of acute severe traumatic brain injury" and "Concussionand mild traumatic brain injury" and "Intracranial epidural hematoma in adults" and "Post-traumatic seizures andepilepsy" and "Subdural hematoma in adults: Etiology, clinical features, and diagnosis" and "Skull fractures inadults".)

EPIDEMIOLOGY — The overall incidence of TBI in the United States was estimated to be 538.2 per 100,000population, or around 1.5 million new cases in 2003 [1]. Somewhat lower rates are reported in Europe (235 per100,000) and Australia (322 per 100,000) [2,3].

Rates of TBI are highest in the very young (age group zero to four years) and in adolescents and young adults (15 to24 years); there is another peak in incidence in the elderly (age >65 years) [1]. Approximately 78 percent of TBI aretreated in the emergency department only; 19 percent of patients require hospitalization, and 3 percent are fatal.Most cases treated in emergency departments occur in the very young (ages zero to four years), whilehospitalization rates are highest in patients older than 65 years.

As with most traumatic injuries, the incidence of TBI is significantly higher in men compared to women, with ratiosthat vary between 2.0 to 1 and 2.8 to 1 [4,5]. For severe TBI, the gender ratio is more pronounced, 3.5 to 1. Lowersocioeconomic status is also a risk factor for head injury.

Falls are the leading cause of TBI (particularly in older patients), followed by motor vehicle accidents [6,7]. Theproportion of TBI secondary to violence has risen over the past decade and now accounts for 7 to 10 percent ofcases [8]. TBI related to military combat has received increased attention in the years from 2002 to 2009 [9].Mechanistic aspects of combat-related trauma may differ from TBI related to other causes, as the former usuallyinvolve blast explosives.

Moderate and severe TBIs are associated with neurologic and functional impairments. The prevalence of long-termdisability related to TBI in the United States is variably estimated to be between 3.2 to 5.3 million, or approximately 1to 2 percent of the population [10,11].

Epidemiologic trends more specific to mild TBI are discussed separately. (See "Concussion and mild traumatic braininjury", section on 'Epidemiology'.)

CLASSIFICATION — TBI is a heterogeneous disease. There are many different ways to categorize patients in termsof clinical severity, mechanism of injury, and pathophysiology, each of which may impact prognosis and treatment.

The best prognostic models ideally include all of the factors described below, as well as age, medical comorbidity,and laboratory parameters [12-14]. However, treatment decisions are likely best informed by considering thesevariables individually rather than as a lump score. Further efforts at improved classification are ongoing as these may

help to refine treatment approaches [15].

Clinical severity scores — TBI has traditionally been classified using injury severity scores; the most commonlyused is the Glasgow Coma Scale (GCS) (table 1) [16]. A GCS score of 13 to 15 is considered mild injury, 9 to 12 isconsidered moderate injury, and 8 or less as severe traumatic brain injury.

The GCS is universally accepted as a tool for TBI classification because of its simplicity, reproducibility, andpredictive value for overall prognosis. However, it is limited by confounding factors such as medical sedation andparalysis, endotracheal intubation, and intoxication. These confounding issues are often particularly prominent inpatients with a low GCS score [17,18].

An alternative scoring system, the Full Outline of Unresponsiveness (FOUR) Score, has been developed in order toattempt to obviate these issues, primarily by including a brainstem examination [19,20]. However, this lacks the longtrack record of the GCS in predicting prognosis and is somewhat more complicated to perform, which may be abarrier for nonneurologists [21].

Neuroimaging scales — Traumatic brain injury can lead to several pathologic injuries, most of which can beidentified on neuroimaging [15]:

Skull fractureEpidural hematomaSubdural hematomaSubarachnoid hemorrhageIntraparenchymal hemorrhageCerebral contusionIntraventricular hemorrhageFocal and diffuse patterns of axonal injury with cerebral edema

Two currently used CT-based grading scales are the Marshall scale and the Rotterdam scale:

The Marshall scale uses CT findings to classify injuries in six different categories (table 2) [22]. It is widelyused in neurotrauma centers and has been shown to predict the risk of increased intracranial pressure andoutcome in adults accurately, but lacks reproducibility in patients with multiple types of brain injury.

The Rotterdam scale is a more recent CT-based classification developed to overcome the limitations of theMarshall scale (table 3). It has shown promising early results but requires broader validation [23].

Other considerations — There are other important considerations for prognosis and treatment in individuals withsevere traumatic brain injury.

Different disease mechanisms (eg, closed versus penetrating injuries, blast versus blunt trauma) may affectthe type of pathologic brain injury.

Extracranial injuries are present in about 35 percent of cases [24]. Multiple systemic traumatic injuries canfurther exacerbate brain injury because of associated blood loss, hypoxia, and other related complications.

PATHOPHYSIOLOGY — The pathophysiology of TBI-related brain injury is divided into two separate but relatedcategories: primary brain injury and secondary brain injury.

Current clinical approaches to the management of TBI center around these concepts of primary and secondary braininjury. Surgical treatment of primary brain injury lesions is central to the initial management of severe head injury.Likewise, the identification, prevention, and treatment of secondary brain injury is the principle focus ofneurointensive care management for patients with severe TBI. (See "Management of acute severe traumatic braininjury".)

Primary brain Injury — Primary brain injury occurs at the time of trauma. Common mechanisms include directimpact, rapid acceleration/deceleration, penetrating injury, and blast waves. Although these mechanisms areheterogeneous, they all result from external mechanical forces transferred to intracranial contents. The damage that

results includes a combination of focal contusions and hematomas, as well as shearing of white matter tracts (diffuseaxonal injury) along with cerebral edema and swelling.

Shearing mechanisms lead to diffuse axonal injury (DAI), which is visualized pathologically and onneuroimaging studies as multiple small lesions seen within white matter tracts (figure 1). Patients with severeDAI typically present with profound coma without elevated intracranial pressure (ICP), and often have pooroutcome. This typically involves the gray-white junction in the hemispheres, with more severe injuriesaffecting the corpus callosum and/or midbrain.

Focal cerebral contusions are the most frequently encountered lesions. Contusions are commonly seen in thebasal frontal and temporal areas, which are particularly susceptible due to direct impact on basal skullsurfaces in the setting of acceleration/deceleration injuries (figure 2). Coalescence of cerebral contusions or amore severe head injury disrupting intraparenchymal blood vessels may result in an intraparenchymalhematoma.

Extra-axial (defined as outside the substance of the brain) hematomas are generally encountered whenforces are distributed to the cranial vault and the most superficial cerebral layers. These include epidural,subdural, and subarachnoid hemorrhage.

In adults, epidural hematomas (EDH) are typically associated with torn dural vessels such as the middlemeningeal artery, and are almost always associated with a skull fracture. EDHs are lenticular-shaped andtend not to be associated with underlying brain damage. For this reason, patients who are found to haveEDHs only on CT scan may have a better prognosis than individuals with other traumatic hemorrhagetypes (figure 3) [23].

Subdural hematomas (SDH) result from damage to bridging veins, which drain the cerebral corticalsurfaces to dural venous sinuses, or from the blossoming of superficial cortical contusions. They tend tobe crescent-shaped and are often associated with underlying cerebral injury (figure 4).

Subarachnoid hemorrhage (SAH) can occur with disruption of small pial vessels and commonly occurs inthe sylvian fissures and interpeduncular cisterns. Intraventricular hemorrhage or superficial intracerebralhemorrhage may also extend into the subarachnoid space.

Intraventricular hemorrhage is believed to result from tearing of subependymal veins, or by extensionfrom adjacent intraparenchymal or subarachnoid hemorrhage.

Approximately one-third of patients with severe TBI develop a coagulopathy, which is associated with an increasedrisk of hemorrhage enlargement, poor neurologic outcomes and death [25-29]. While the coagulopathy may resultfrom existing patient medications such as warfarin or antiplatelet agents, acute TBI is also thought to produce acoagulopathy through the systemic release of tissue factor and brain phospholipids into the circulation leading toinappropriate intravascular coagulation and a consumptive coagulopathy [30].

Secondary brain Injury — Secondary brain injury in TBI is usually considered as a cascade of molecular injurymechanisms that are initiated at the time of initial trauma and continue for hours or days. These mechanisms include[25,31-39]:

Neurotransmitter-mediated excitotoxicity causing glutamate, free-radical injury to cell membranesElectrolyte imbalancesMitochondrial dysfunctionInflammatory responsesApoptosisSecondary ischemia from vasospasm, focal microvascular occlusion, vascular injury

These lead in turn to neuronal cell death as well as to cerebral edema and increased intracranial pressure that canfurther exacerbate the brain injury. This injury cascade shares many features of the ischemic cascade in acutestroke. These various pathways of cellular injury have been the focus of extensive preclinical work into thedevelopment of neuroprotective treatments to prevent secondary brain injury in TBI. No clinical trials of thesestrategies have demonstrated clear benefit in patients.

However, a critical aspect of ameliorating secondary brain injury after TBI is the avoidance of secondary braininsults, which would otherwise be well-tolerated but can exacerbate neuronal injury in cells made vulnerable by theinitial TBI. Examples include hypotension and hypoxia (which decrease substrate delivery of oxygen and glucose toinjured brain), fever and seizures (which may further increase metabolic demand), and hyperglycemia (which mayexacerbate ongoing injury mechanisms). (See "Management of acute severe traumatic brain injury".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, “The Basics” and

“Beyond the Basics.” The Basics patient education pieces are written in plain language, at the 5th to 6th gradereading level, and they answer the four or five key questions a patient might have about a given condition. Thesearticles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond theBasics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the

10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable withsome medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail thesetopics to your patients. (You can also locate patient education articles on a variety of subjects by searching on“patient info” and the keyword(s) of interest.)

Basics topics (see "Patient information: Closed head injury (The Basics)")

SUMMARY — Traumatic brain injury (TBI) encompasses a broad range of pathologic injuries to the brain of varyingclinical severity that result from head trauma.

Among adults, TBI is most common in the young (<25 years), although there is another, smaller peak thatoccurs in elder adults (>65 years). Motor vehicle accidents are a leading cause in younger adults, while fallsare the most likely cause of TBI in the older age group. (See 'Epidemiology' above.)

TBI is classically categorized as mild, moderate, and severe according to clinical severity using the Glasgowcoma scale (GCS) (table 1). (See 'Clinical severity scores' above.)

TBI can also be classified according to the type and severity of neuroimaging findings, the mechanism ofbrain injury, and other variables. These factors individually, and in the aggregate, influence prognosis andtreatment. (See 'Classification' above.)

The pathophysiology of TBI includes primary and secondary brain injury.

The pathoanatomical sequelae of primary TBI include intra- and extraparenchymal hemorrhages anddiffuse axonal injury. (See 'Primary brain Injury' above.)

Secondary TBI results from a cascade of molecular injury mechanisms, that are initiated at the time ofinitial trauma and continue for hours or days. It is likely that secondary brain injury can be exacerbated bymodifiable systemic events such as hypotension, hypoxia, fever, and seizures. (See 'Secondary brainInjury' above.)

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street. Am J Public Health 1997; 87:393.5. Kraus JF, McArthur DL. Epidemiologic aspects of brain injury. Neurol Clin 1996; 14:435.

6. Langlois JA, Rutland-Brown W, Thomas KE. Traumatic brain injury in the United States: emergencydepartment visits, hospitalizations, and deaths. Centers for Disease Control and Prevention, Atlanta, 2006.

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and the Glasgow Coma Scale in an emergency setting population. Eur J Emerg Med 2009; 16:29.22. Marshall LF, Marshall SB, Klauber MR, et al. The diagnosis of head injury requires a classification based on

computed axial tomography. J Neurotrauma 1992; 9 Suppl 1:S287.23. Maas AI, Hukkelhoven CW, Marshall LF, Steyerberg EW. Prediction of outcome in traumatic brain injury with

computed tomographic characteristics: a comparison between the computed tomographic classification andcombinations of computed tomographic predictors. Neurosurgery 2005; 57:1173.

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26. Allard CB, Scarpelini S, Rhind SG, et al. Abnormal coagulation tests are associated with progression oftraumatic intracranial hemorrhage. J Trauma 2009; 67:959.

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course of an underestimated phenomenon: a prospective study performed in 299 patients. J Neurosurg 2005;103:812.

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38. Yi JH, Hazell AS. Excitotoxic mechanisms and the role of astrocytic glutamate transporters in traumatic braininjury. Neurochem Int 2006; 48:394.

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Topic 4825 Version 8.0

GRAPHICS

Glasgow coma scale

Score

Eye opening

Spontaneous 4

Response to verbal command 3

Response to pain 2

No eye opening 1

Best verbal response

Oriented 5

Confused 4

Inappropriate words 3

Incomprehensible sounds 2

No verbal response 1

Best motor response

Obeys commands 6

Localizing response to pain 5

Withdrawal response to pain 4

Flexion to pain 3

Extension to pain 2

No motor response 1

Total

The GCS is scored between 3 and 15, 3 being the worst, and 15 the best. It iscomposed of three parameters: best eye response (E), best verbal response (V), andbest motor response (M). The components of the GCS should be recorded individually;for example, E2V3M4 results in a GCS score of 9. A score of 13 or higher correlateswith mild brain injury; a score of 9 to 12 correlates with moderate injury; and a scoreof 8 or less represents severe brain injury.

Marshall CT classification

Category Definition

Diffuse injury I(no visiblepathology)

No visible intracranial pathology seen on CT scan

Diffuse injury II Cisterns are present with midline shift of 0-5 mm and/or lesions densitiespresent; no high or mixed density lesion >25 cm3 may include bone fragmentsand foreign bodies

Diffuse injuryIII (swelling)

Cisterns compressed or absent with midline shift 0-5 mm; no high or mixeddensity lesion >25 cm3

Diffuse injuryIV (shift)

Midline shift >5 mm; no high or mixed density lesion >25 cm3

Evacuatedmass lesion V

Any lesion surgically evacuated

Non-evacuatedmass lesion VI

High or mixed density lesion >25 cm3; not surgically evacuated

Reproduced with permission from: Adelson PD, Bratton SL, Carney NA, et al. Guidelines for the acutemedical management of severe traumatic brain injury in infants, children, and adolescents. Chapter 1:Introduction. Pediatr Crit Care Med 2003; 4:S2. Copyright © 2003 Lippincott Williams & Wilkins.

Rotterdam CT classification

Predictor value Score

Basal cisterns

Normal 0

Compressed 1

Absent 2

Midline shift

No shift or shift ≤5 mm 0

Shift >5 mm 1

Epidural mass lesion

Present 0

Absent 1

Intraventricular blood or subarachnoid hemorrhage

Absent 0

Present 1

Sum score Total + 1

Reproduced with permission from: Maas Al, Hukkelhoven CW, Marshall LF, Steyerberg EW. Predictionof outcome in traumatic brain injury with computed tomographic characteristics: a comparisonbetween the computed tomographic classification and combinations of computed tomographicpredictors. Neurosurgery 2005; 57:1173. Copyright © 2005 Lippincott Williams & Wilkins.

Diffuse axonal injury

CT scan of the brain showing diffuse axonal injury (DAI). Notethe deep shearing-type injury in or near the white matter of theleft internal capsule (arrow).Reproduced with permission from: J Claude Hemphill II, MD and NicholasPhan, MD, FRCSC.

Frontal cerebral contusion

CT scan of the brain depicting cerebral contusions. The basalfrontal areas (as shown) are particularly susceptible.Reproduced with permission from: J Claude Hemphill III, MD and NicholasPhan, MD, FRCSC.

TBI epidural hematoma

CT scan demonstrating a right epidural hematoma (EDH, arrow).Note the lenticular shape.Reproduced with permission from: J Claude Hemphill III, MD and NicholasPhan, MD, FRCSC.

TBI subdural hematoma

CT scan showing a left acute subdural hematoma (SDH, arrow).Subdural hematomas are typically crescent-shape. In this casethe SDH is causing significant mass effect and shift of midlinestructures to the right.Reproduced with permission from: J Claude Hemphill III, MD and NicholasPhan, MD, FRCSC.

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