Background
Traumatic brain injury (TBI) is one of the major causes of premature death and disability worldwide1. Management of the patient with a TBI focuses on not only treating and limiting the effects of the initial primary insult or injury, but also attempting to limit the damage of secondary brain injury.
Primary brain injury refers to the sudden and profound impact to the brain that is considered to be more or less complete at the time of impact.
Secondary brain injury refers to the changes that evolve hours to days after the primary injury, as a consequence of the physiological responses to the initial trauma1,2. The impact of secondary brain injury caused by dysregulation of brain blood vessels and blood-barrier disruption can lead to the development of cerebral oedema, increased intracranial pressure (ICP) and decreased cerebral perfusion pressure (CPP)2. However, the mechanism of secondary brain injury is extremely complex and involves multiple processes, such as neurotransmitter release, mitochondrial dysfunction, neuronal apoptosis, lipid degradation and the initiation of inflammatory and immune responses3, making singular targeted treatment and prevention difficult.
In order to try and minimise the occurrence of secondary brain injury, early and aggressive control of factors that are known to be implicated in its aetiology, collectively known as neuroprotective measures2, is recommended. These measures, which collectively aim to maintain CPP, and the evidence for each, are detailed below.