References for this Review were identified through searches of PubMed, by use of the search terms “traumatic brain injury” or “head injury” and other appropriate targets, such as “epidemiology”, “pathophysiology”, and “guidelines”, up to May, 2008. Papers were also identified from the authors' own files and from references cited in relevant articles. An electronic search of resources, such as international and national guidelines and book chapters, was also done. The final reference list
ReviewModerate and severe traumatic brain injury in adults
Introduction
Traumatic brain injury (TBI) constitutes a major health and socioeconomic problem throughout the world.1, 2 It is the leading cause of mortality and disability among young individuals in high-income countries, and globally the incidence of TBI is rising sharply, mainly due to increasing motor-vehicle use in low-income and middle-income countries. WHO has projected that, by 2020, traffic accidents will be the third greatest cause of the global burden of disease and injury.3 In higher income countries, traffic safety laws and preventive measures have reduced the incidence of TBI due to traffic accidents,4 whereas the incidence of TBI caused by falls is increasing as the population ages, leading to a rise in the median age of TBI populations (table 1). This has consequences for the type of brain damage currently seen, and contusions (falls in older patients) are becoming more frequent than diffuse injuries (high-velocity traffic accidents in younger patients).
Violence is now reported as the cause of closed head injury in approximately 7–10% of cases,9, 10 a substantial increase from earlier studies. The incidence of penetrating brain injury is also increasing, particularly in the USA, due to the use of firearms in violence-related injuries. Worldwide, armed conflicts and terrorist activities are causing more brain injuries, often due to improvised explosive devices, to the extent that blast injuries of the brain are now recognised as a specific entity. The changing patterns of injury and treatment approaches have challenged current concepts of classification. Moreover, basic research has greatly advanced our knowledge of what happens in the brain after TBI, offering opportunities to limit processes involved in secondary brain damage. However, translating advances from basic research into clinical benefit has proven complex. Here, we discuss current knowledge and novel insights and controversies in the study of adults with moderate and severe TBI, with the aim of integrating basic science and clinical research to provide guidelines on the epidemiological monitoring of TBI, trauma organisation, and management at the acute stage.
Section snippets
Epidemiology and cost
In the USA, monitoring by the Centers for Disease Control and Prevention shows the annual incidence of emergency department visits and hospital admissions for TBI to be 403 per 100 000 and 85 per 100 000, respectively.11 Epidemiological data on TBI from the European Union are scarce, but do indicate an annual aggregate incidence of hospitalised and fatal TBI of approximately 235 per 100 000,12 similar to that found in Australia,13 although substantial variation exists between European
Classification
TBI can be isolated, but is associated with extracranial injuries (limb fractures, thoracic or abdominal injuries) in about 35% of cases,19 which increases the risk of secondary brain damage due to hypoxia, hypotension, pyrexia, and coagulopathy. The recording of the severity of extracranial injuries should therefore form an integral part of TBI classification (panel).
Traditionally, TBI has been classified by mechanism (closed vs penetrating), by clinical severity (Glasgow coma scale [GCS]20),
Primary damage
TBI is a heterogeneous disorder with different forms of presentation. The unifying factor is that brain damage results from external forces, as a consequence of direct impact, rapid acceleration or deceleration, a penetrating object (eg, gunshot), or blast waves from an explosion. The nature, intensity, direction, and duration of these forces determine the pattern and extent of damage.
On the macroscopic level, damage includes shearing of white-matter tracts, focal contusions, haematomas
Diagnosis
Head injury does not always implicate TBI. A diagnosis of TBI is established on the basis of clinical symptoms: for example, the presence of any documented loss of consciousness and/or amnesia (retrograde or post-traumatic). Additional clinical investigations can be driven by the patient's level of awareness, presence of risk factors, and mechanisms of injury (figure 2).
CT is the preferred method of assessment on admission to determine structural damage and to detect (developing) intracranial
Guidelines and individualised management
Over the past 10 years, much of the treatment of TBI has evolved towards standardised approaches that follow international and national guidelines (table 2). International guidelines for severe head injury are mostly evidence based, and address specific aspects of management. National guidelines focus more on organisational issues, such as admission and referral policy; however, these remain limited to the constraints of existing trauma systems, and clear statements on the best trauma
Pre-hospital emergency care
The main goals of prehospital management are to prevent hypoxia and hypotension, because these systemic insults lead to secondary brain damage.68, 81 When assessed before hospital admission (by ambulance or helicopter crews), oxygen saturation below 90% is found in 44–55% of cases and hypotension in 20–30%.81, 82, 83 Trauma renders the brain more vulnerable to these insults,84 and hypoxia and hypotension are strongly associated with poor outcome (hypoxia: odds ratio [OR] 2·1, 95% CI 1·7–2·6;
Outcome and prognosis
Outcome after head injury is generally assessed at 6 months after injury, representing a compromise between true final outcome and logistic limitations. Experience shows that about 85% of recovery occurs within this time period, but further recovery can occur later. Accurate and consistent outcome determination at a fixed timepoint is a prerequisite for any TBI study. The most frequently used global outcome measure in TBI is the Glasgow outcome scale. More specific tools are required for
Neuroprotection and clinical trials
The original concept of neuroprotection involved the initiation of treatment before the onset of the event, and was aimed at minimising the intensity of an insult or its immediate effects on the brain by interrupting the harmful cascades of biochemical events. A major new focus of neurobiology now revolves around cell replacement, aimed at promoting neuroplasticity, and regeneration or replacement of lost neuronal and glial cells and neuronal circuits. Over the past 25 years, over 20 agents
Future directions
Here, we have illustrated the seriousness and complexity of the problems posed by TBI to patients, relatives, doctors, authorities, and society alike. Great advancements have been achieved over the past 10–15 years, but advances in basic science have not yet led to new treatments of clinically proven benefit, and advanced monitoring has not routinely resulted in individualised management. Current classification systems are no longer sufficient and not all patients have access to the best care.
Search strategy and selection criteria
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