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Trauma is the leading cause of death in the first four decades of life, with head injury being implicated in at least half the number of cases. In the UK, 1500 per 100 000 of the population (total one million) attend accident and emergency departments with a head injury, 300 per 100 000 per year are admitted to hospital, 15 per 100 000 per year are admitted to neurosurgical units, and 9 per 100 000 per year die from head injury. Recent advances in the management of head injury have occurred at several levels including prevention, pre-hospital care, immediate hospital care, acute hospital care, and rehabilitation. This synopsis aims to outline the principles of the treatment of head injury in the acute phase.
PATHOPHYSIOLOGY
Fundamental processes occur at a cellular level following brain injury, which culminate in cell death.1 These processes include the release of excitotoxic quantities of the amino acids, glutamate and aspartate, production of free radicals, and increased production of lactate and hydrogen ions. One of the final common pathways of these processes is the entry of calcium ions into cells, which results in cell swelling. This swelling, within the confines of the rigid cranium, results in an increase in intracranial pressure (ICP) and reduction in cerebral perfusion pressure (CPP, defined as mean arterial blood pressure − intracranial pressure), with cerebral ischaemia and reduced delivery of oxygen to the tissues, provoking further acidosis, and glutamate and free radical release to potentiate the above cycle. The goal of treatment in these patients is to intervene in this cycle by reducing intracranial pressure and increasing cerebral perfusion pressure.2
The structural changes following head injury can be divided into two main groups:
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diffuse injury—this ranges from mild injury with concussion to major injury with diffuse axonal injury characterised by histological …