Many patients attend accident and emergency departments with head injury. Approximately 300 per 100 000 of the population per year require hospital admission; of these 9 per 100 000 die, i.e. 5000 patients per year in Britain. Some of these deaths are inevitable, some are potentially preventable.
The principal causes of head injury include road traffic accidents, falls, assaults and injuries occurring at work, in the home and during sports. The relative frequency of each cause varies between different age groups and from place to place throughout the country.
Head injuries from road traffic accidents are most common in young males; alcohol is frequently involved. Road traffic accidents, although only constituting about 25% of all patients with head injury, are the cause of more serious injuries. This cause contributes to 60% of the deaths from head injury; of these, half die before reaching hospital.
In many countries preventative and punitative measures controlling alcohol levels and the use of seat belts, air bags and crash helmets have reduced the incidence. Once a head injury has occurred, nothing can alter the impact damage. The aim of head injury management is to minimise damage arising from secondary complications.
Brain damage occurs both at impact and as a result of the development of secondary complications.
IMPACT DAMAGE is of two types, which may coexist:
1. Cortical contusions and lacerations These may occur under or opposite (contre-coup) the site of impact, but most commonly involve the frontal and temporal lobes. Contusions are usually multiple and may occur bilaterally. Multiple contusions do not in themselves contribute to depression of conscious level, but this may arise when bleeding into the contusions produces a space-occupying haematoma.
This type of brain damage occurs as a result of mechanical shearing following deceleration, causing disruption and tearing of axons. Depending on the severity of injury its immediate effects range from mild confusion to coma and even death. Recent studies show that the full extent of the axonal damage takes some time to evolve.
The macrosopic appearance may appear entirely normal but in some patients pathological sections reveal small haemorrhagic tears, particularly in the corpus callosum or in the superior cerebellar peduncle.
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