Traumatic Brain Injury - Epidemiology, Classification, and Pathophysiology

Traumatic brain injury: Epidemiology, classification, and pathophysiology
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2011 UpToDate
Traumatic brain injury: Epidemiology, classification, and

pathophysiology
Authors
Section Editor
Nicholas Phan, MD, FRCSC
Michael J Aminoff, MD, DSc
J Claude Hemphill, III, MD, MAS
Deputy Editor
Janet L Wilterdink, MD
Last literature review version 18.3: Setembro 2010 | This topic last updated: Janeiro 28,
2010
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.
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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 help to refine treatment approaches
[15].
Clinical severity scores TBI has traditionally been classified using injury severity scores; the
most commonly used is the Glasgow Coma Scale (GCS) (table 1) [16]. A GCS score of 13 to 15 is
considered mild injury, 9 to 12 is considered 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, and predictive value for overall prognosis. However, it is limited by confounding
factors such as medical sedation and paralysis, endotracheal intubation, and intoxication. These
confounding issues are often particularly prominent in patients with a low GCS score [17,18].
An alternative scoring system, the Full Outline of Unresponsiveness (FOUR) Score, has been
developed in order to attempt to obviate these issues, primarily by including a brainstem
examination [19,20]. However, this lacks the long track record of the GCS in predicting prognosis
and is somewhat more complicated to perform, which may be a barrier for nonneurologists [21].
Neuroimaging scales Traumatic brain injury can lead to several pathologic injuries, most of
which can be identified on neuroimaging [15]:
Skull fracture
Epidural hematoma
Subdural hematoma
Subarachnoid hemorrhage
Intraparenchymal hemorrhage
Cerebral contusion
Intraventricular hemorrhage
Focal 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 widely used in neurotrauma centers and has been shown to predict the risk of increased
intracranial pressure and outcome 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 the Marshall 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 with severe traumatic brain injury.
Different disease mechanisms (eg, closed versus penetrating injuries, blast versus blunt
trauma) may affect the type of pathologic brain injury.
Extracranial injuries are present in about 35 percent of cases [24]. Multiple systemic traumatic
injuries can further 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 related categories: primary brain injury and secondary brain injury.
Current clinical approaches to the management of TBI center around these concepts of primary
and secondary brain injury. Surgical treatment of primary brain injury lesions is central to the
initial management of severe head injury. Likewise, the identification, prevention, and treatment
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of secondary brain injury is the principle focus of neurointensive care management for patients
with severe TBI. (See "Management of acute severe traumatic brain injury".)
Primary brain Injury Primary brain injury occurs at the time of trauma. Common mechanisms
include direct impact, rapid acceleration/deceleration, penetrating injury, and blast waves.
Although these mechanisms are heterogeneous, 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 (diffuse axonal injury) along
with cerebral edema and swelling.
Shearing mechanisms lead to diffuse axonal injury (DAI), which is visualized pathologically and
on neuroimaging studies as multiple small lesions seen within white matter tracts (figure 1).
Patients with severe DAI typically present with profound coma without elevated intracranial
pressure (ICP), and often have poor outcome. This typically involves the gray-white junction in the
hemispheres, with more severe injuries affecting the corpus callosum and/or midbrain.
Focal cerebral contusions are the most frequently encountered lesions. Contusions are
commonly seen in the basal frontal and temporal areas, which are particularly susceptible due to
direct impact on basal skull surfaces in the setting of acceleration/deceleration injuries (figure 2).
Coalescence of cerebral contusions or a more severe head injury disrupting intraparenchymal
blood vessels may result in an intraparenchymal hematoma.
Extra-axial (defined as outside the substance of the brain) hematomas are generally
encountered when forces 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 middle meningeal artery, and are almost always associated with a skull fracture. EDHs are
lenticular-shaped and tend not to be associated with underlying brain damage. For this reason,
patients who are found to have EDHs only on CT scan may have a better prognosis than
individuals with other traumatic hemorrhage types (figure 3) [23].
- Subdural hematomas (SDH) result from damage to bridging veins, which drain the cerebral
cortical surfaces to dural venous sinuses, or from the blossoming of superficial cortical contusions.
They tend to be 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 in the sylvian fissures and interpeduncular cisterns. Intraventricular hemorrhage or
superficial intracerebral hemorrhage may also extend into the subarachnoid space.
- Intraventricular hemorrhage is believed to result from tearing of subependymal veins, or by
extension from adjacent intraparenchymal or subarachnoid hemorrhage.
Secondary brain Injury Secondary brain injury in TBI is usually considered as a cascade of
molecular injury mechanisms that are initiated at the time of initial trauma and continue for hours
or days. These mechanisms include [25-34]:
Neurotransmitter-mediated excitotoxicity causing glutamate, free-radical injury to cell
membranes
Electrolyte imbalances
Mitochondrial dysfunction
Inflammatory responses
Apoptosis
Secondary 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 can further exacerbate the brain injury. This injury cascade shares many features of
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the ischemic cascade in acute stroke. These various pathways of cellular injury have been the
focus of extensive preclinical work into the development of neuroprotective treatments to prevent
secondary brain injury in TBI. No clinical trials of these strategies have demonstrated clear benefit
in patients.
However, a critical aspect of ameliorating secondary brain injury after TBI is the avoidance of
secondary brain insults, which would otherwise be well-tolerated but can exacerbate neuronal
injury in cells made vulnerable by the initial TBI. Examples include hypotension and hypoxia
(which decrease substrate delivery of oxygen and glucose to injured brain), fever and seizures
(which may further increase metabolic demand), and hyperglycemia (which may exacerbate
ongoing injury mechanisms). (See "Management of acute severe traumatic brain injury".)
SUMMARY Traumatic brain injury (TBI) encompasses a broad range of pathologic injuries to
the brain of varying clinical severity that result from head trauma.
Among adults, TBI is most common in the young (<25 years), although there is another,
smaller peak that occurs in elder adults (>65 years). Motor vehicle accidents are a leading cause
in younger adults, while falls are 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 Glasgow coma 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 of brain injury, and other variables. These factors individually, and in the aggregate,
influence prognosis and treatment. (See 'Classification' above.)
The pathophysiology of TBI includes primary and secondary brain injury.
- The pathoanatomical sequelae of primary TBI include intra- and extraparenchymal
hemorrhages and diffuse axonal injury. (See 'Primary brain Injury' above.)
- Secondary TBI results from a cascade of molecular injury mechanisms, that are initiated at
the time of initial trauma and continue for hours or days. It is likely that secondary brain injury
can be exacerbated by modifiable systemic events such as hypotension, hypoxia, fever, and
seizures. (See 'Secondary brain Injury' above.)
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REFERENCES
1. Rutland-Brown, W, Langlois, JA, Thomas, KE, Xi, YL. Incidence of traumatic brain injury in
the United States, 2003. J Head Trauma Rehabil 2006; 21:544.
2. Tagliaferri, F, Compagnone, C, Korsic, M, et al. A systematic review of brain injury
epidemiology in Europe. Acta Neurochir (Wien) 2006; 148:255.
3. Hillier, SL, Hiller, JE, Metzer, J. Epidemiology of traumatic brain injury in South Australia.
Brain Inj 1997; 11:649.
4. Langlois, JA, Keyl, PM, Guralnik, JM, et al. Characteristics of older pedestrians who have
difficulty crossing the 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:
emergency department visits, hospitalizations, and deaths. Centers for Disease Control and
Prevention, Atlanta, GA 2006.
7. Jennett, B, Frankovyski, RF. The epidemiology of head injury. In: Handbook of Clinical
Neurology, Vol 13, Braakman, R (Ed), Elsevier, New York 1990. p.1.
24/02/2011 16:42
5 de 14
8. Butcher, I, McHugh, GS, Lu, J, et al. Prognostic value of cause of injury in traumatic brain
injury: results from the IMPACT study. J Neurotrauma 2007; 24:281.
9. Summers, CR, Ivins, B, Schwab, KA. Traumatic brain injury in the United States: an
epidemiologic overview. Mt Sinai J Med 2009; 76:105.
10. Thurman, DJ, Alverson, C, Dunn, KA, et al. Traumatic brain injury in the United States: A
public health perspective. J Head Trauma Rehabil 1999; 14:602.
11. Zaloshnja, E, Miller, T, Langlois, JA, Selassie, AW. Prevalence of long-term disability from
traumatic brain injury in the civilian population of the United States, 2005. J Head Trauma
Rehabil 2008; 23:394.
12. Steyerberg, EW, Mushkudiani, N, Perel, P, et al. Predicting outcome after traumatic brain
injury: development and international validation of prognostic scores based on admission
characteristics. PLoS Med 2008; 5:e165; discussion e165.
13. Menon, D, Harrison, D. Prognostic modelling in traumatic brain injury. BMJ 2008; 336:397.
14. MRC CRASH Trial, Collaborators, Perel, P, Arango, M, et al. Predicting outcome after
traumatic brain injury: practical prognostic models based on large cohort of international
patients. BMJ 2008; 336:425.
15. Saatman, KE, Duhaime, AC, Bullock, R, et al. Classification of traumatic brain injury for
targeted therapies. J Neurotrauma 2008; 25:719.
16. Teasdale, G, Jennett, B. Assessment of coma and impaired consciousness. A practical scale.
Lancet 1974; 2:81.
17. Balestreri, M, Czosnyka, M, Chatfield, DA, et al. Predictive value of Glasgow Coma Scale after
brain trauma: change in trend over the past ten years. J Neurol Neurosurg Psychiatry 2004;
75:161.
18. Stocchetti, N, Pagan, F, Calappi, E, et al. Inaccurate early assessment of neurological severity
in head injury. J Neurotrauma 2004; 21:1131.
19. Stead, LG, Wijdicks, EF, Bhagra, A, et al. Validation of a new coma scale, the FOUR score, in
the emergency department. Neurocrit Care 2009; 10:50.
20. Wijdicks, EF, Bamlet, WR, Maramattom, BV, et al. Validation of a new coma scale: The FOUR
score. Ann Neurol 2005; 58:585.
21. Eken, C, Kartal, M, Bacanli, A, Eray, O. Comparison of the Full Outline of Unresponsiveness
Score Coma Scale 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 and combinations of computed tomographic predictors.
Neurosurgery 2005; 57:1173.
24. Maas, AI, Stocchetti, N, Bullock, R. Moderate and severe traumatic brain injury in adults.
Lancet Neurol 2008; 7:728.
25. Bki, A, Koizumi, H, Povlishock, JT. Moderate posttraumatic hypothermia decreases early
calpain-mediated proteolysis and concomitant cytoskeletal compromise in traumatic axonal
injury. Exp Neurol 1999; 159:319.
26. Coles, JP, Minhas, PS, Fryer, TD, et al. Effect of hyperventilation on cerebral blood flow in
traumatic head injury: clinical relevance and monitoring correlates. Crit Care Med 2002;
30:1950.
27. Diringer, MN, Videen, TO, Yundt, K, et al. Regional cerebrovascular and metabolic effects of
hyperventilation after severe traumatic brain injury. J Neurosurg 2002; 96:103.
28. Kroemer, G, Galluzzi, L, Brenner, C. Mitochondrial membrane permeabilization in cell death.
Physiol Rev 2007; 87:99.
29. Morganti-Kossmann, MC, Rancan, M, Stahel, PF, Kossmann, T. Inflammatory response in
acute traumatic brain injury: a double-edged sword. Curr Opin Crit Care 2002; 8:101.
30. Oertel, M, Boscardin, WJ, Obrist, WD, et al. Posttraumatic vasospasm: the epidemiology,
24/02/2011 16:42
6 de 14
severity, and time course of an underestimated phenomenon: a prospective study performed

in 299 patients. J Neurosurg 2005; 103:812.
31. Vespa, P, Bergsneider, M, Hattori, N, et al. Metabolic crisis without brain ischemia is common
after traumatic brain injury: a combined microdialysis and positron emission tomography
study. J Cereb Blood Flow Metab 2005; 25:763.
32. Yi, JH, Hazell, AS. Excitotoxic mechanisms and the role of astrocytic glutamate transporters
in traumatic brain injury. Neurochem Int 2006; 48:394.
33. Harhangi, BS, Kompanje, EJ, Leebeek, FW, Maas, AI. Coagulation disorders after traumatic
brain injury. Acta Neurochir (Wien) 2008; 150:165.
34. Stein, SC, Chen, XH, Sinson, GP, Smith, DH. Intravascular coagulation: a major secondary
insult in nonfatal traumatic brain injury. J Neurosurg 2002; 97:1373.
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GRAPHICS
Glasgow coma scale
Eye opening
Spontaneous
Response to verbal command
Response to pain
No eye opening
Best verbal response

Oriented
Confused
Inappropriate words
Incomprehensible sounds
No verbal response
Best motor response

Obeys commands
Localizing response to pain
Withdrawal response to pain
Flexion to pain
Extension to pain
No motor response
The GCS is scored between 3 and 15, 3 being the worst, and 15 the best. It is composed of
three parameters: best eye response (E), best verbal response (V), and best 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 correlates with mild brain
injury; a score of 9 to 12 correlates with moderate injury; and a score of 8 or less
represents severe brain injury.
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Marshall CT classification
Category
Definition
Diffuse injury I (no

visible pathology)
No visible intracranial pathology seen on CT scan
Diffuse injury II
Cisterns are present with midline shift of 0-5 mm and/or lesions

densities present; no high or mixed density lesion >25 cm3 may include
bone fragments and foreign bodies
Diffuse injury III

(swelling)
Cisterns compressed or absent with midline shift 0-5 mm; no high or

mixed density lesion >25 cm3
Diffuse injury IV (shift)
Midline shift >5 mm; no high or mixed density lesion >25 cm3
Evacuated mass lesion

V
Any lesion surgically evacuated
Non-evacuated mass
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 acute
medical 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.
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Rotterdam CT classification
Predictor value
Score
Basal cisterns
Normal
Compressed
Absent
Midline shift
No shift or shift 5 mm
Shift >5 mm
Epidural mass lesion

Present
Absent
Intraventricular blood or subarachnoid hemorrhage

Absent
Present
Sum score
Total + 1
Reproduced with permission from: Maas, Al, Hukkelhoven, CW, Marshall, LF, Steyerberg, EW. Prediction of
outcome in traumatic brain injury with computed tomographic characteristics: a comparison between the
computed tomographic classification and combinations of computed tomographic predictors. Neurosurgery
2005; 57:1173. Copyright 2005 Lippincott Williams & Wilkins.
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Diffuse axonal injury
CT scan of the brain showing diffuse axonal injury (DAI). Note

the deep shearing-type injury in or near the white matter of the
left internal capsule (arrow). Reproduced with permission from: J
Claude Hemphill II, MD and Nicholas Phan, MD, FRCSC.
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Frontal cerebral contusion
CT scan of the brain depicting cerebral contusions. The basal

frontal areas (as shown) are particularly susceptible. Reproduced
with permission from: J Claude Hemphill III, MD and Nicholas Phan, MD,
FRCSC.
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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 Nicholas Phan, MD, FRCSC.
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TBI subdural hematoma
CT scan showing a left acute subdural hematoma (SDH, arrow).

Subdural hematomas are typically crescent-shape. In this case
the SDH is causing significant mass effect and shift of midline
structures to the right. Reproduced with permission from: J Claude
Hemphill III, MD and Nicholas Phan, MD, FRCSC.
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