Traumatic brain injury: an evidence-based review of management

Abstract

Traumatic brain injury (TBI) is the leading cause of death and disability in young adults in the developed world. In the UK about 1.4 million patients per year suffer head injuries. Although the majority of injuries are mild, around 10.9% are classified as moderate or severe and many patients are left with significant disability. The incidence is increasing in lower income countries, with the World Health Organization predicting that TBI and road traffic accidents will be the third greatest cause of disease and injury worldwide by 2020. In our ageing population the number of elderly patients presenting with TBI has increased and age appears to be an independent risk factor for poor outcome. Consequently TBI presents a major health and socioeconomic problem. TBI is a heterogeneous condition in terms of aetiology, severity, and outcome. The most useful classification of severity is based on the level of consciousness as assessed by the Glasgow Coma Scale (GCS) after resuscitation. The GCS comprises the sum score of the values from three components: eye, motor, and verbal scales (Table 1). TBI is classified as mild (GCS 15–13), moderate (GCS 13–9), and severe (GCS , 8). However, factors such as hypoxia, hypotension, and alcohol intoxication can all affect GCS, leading to diagnostic confusion. Therefore the patient should be resuscitated and reversible causes corrected before GCS assessment. The ability to assess eye opening and verbal response is influenced by sedative agents or tracheal intubation, leading some to suggest the use of the motor score alone. TBI can be divided into primary and secondary brain injury. The primary injury occurs as a consequence of the initial physical insult. The pattern and extent of damage will depend on the nature, intensity, and duration of the impact. Compression and shearing forces may result in skull fracture, contusions, intracranial haematoma, cerebral oedema, and diffuse brain injury. Microscopically there is cell wall disruption and increased membrane permeability disrupting ionic homeostasis. Axonal tissue is particularly susceptible to injury. Neurological injury progresses over hours and days, resulting in a secondary injury. Inflammatory and neurotoxic processes result in vasogenic fluid accumulation within the brain, contributing to raised intracranial pressure (ICP), hypoperfusion, and cerebral ischaemia. Much of this secondary injury may be amenable to intervention, as almost one-third of patients who die after a TBI will talk or obey commands before their death. Secondary injury also occurs as a result of further physiological insults. Hypoxia, hypotension, hyperor hypocapnia, hyperor hypoglycaemia have all been shown to increase the risk of secondary brain injury.