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Neurological Alterations and Management 455

neuroprotection, but this is still to be confirmed in clini- population. Approximately 90,211 Australians 58,59 and
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cal trials. Magnesium, however, does not cross the 16,000–22,500 New Zealanders are hospitalised for
intact BBB easily, limiting its effect to injury and disease TBI every year. Males aged 15–19 years have the highest
with leaky BBB. A randomised clinical trial of aneurys- incidence rates and suffer TBI at a rate almost three times
mal SAH patients receiving magnesium found that IV that of women. The very young (0–4 years) and the
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magnesium infusion reduced the frequency of delayed very old (over 85 years) are also at increased risk. Indig-
cerebral ischaemia in patients with aneurysmal SAH and enous Australians suffer TBI at almost three times the rate
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subsequent poor outcome. 55 (410 per 100,000) of non-Indigenous Australians. It is
estimated that 40,000 Australians are living with a dis-
In SAH, more aggressive intravascular volume expansion ability as a result of TBI. Despite definition issues relat-
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and induced hypertension are used in conjunction with ing to TBI epidemiology, there was an average annual
haemodynamic monitoring. By maintaining haematocrit decline of 5% in the TBI rate to 1997/98 but the inci-
at 30–33%, a shift in the oxygen dissociation curve is dence has increased since then. An Australian and new
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avoided. Haemodilutional therapy increases collateral Zealand epidemiological study of TBI (see Research
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circulation at the site of haemorrhage, while reducing vignette) found that the mean age was 41.6 years; 74.2%
aggregation of erythrocytes where small vessel spasm has were men; 61.4% were due to vehicular trauma, 24.9%
occurred. However, there is some emerging physiological were falls in elderly patients, and 57.2% had severe TBI
data suggesting that normovolaemic hyperten sion may (Glasgow Coma Scale score ≤8). Twelve-month mortality
be the component most likely to increase cerebral blood was 26.9% in all patients and 35.1% in patients with
flow after subarachnoid haemorrhage. In contrast, hyper- severe TBI.
volaemic haemodilution is associated with increased
complications and might also lower the haemoglobin
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to excessively low levels. Also in aneurysmal SAH, Aetiology
endovascular therapies, such as intra-arterial papaverine In Australia, motor vehicle-related trauma accounts
infusion, are employed. Papaverine acts immediately and for about two-thirds of moderate and severe TBI, with
increases arterial calibre and cerebral blood flow, but its falls and assaults being the next most common causes.
effects are short-lived. Balloon angioplasty is particularly New Zealand has a higher proportion of recreational
effective as a durable means of alleviating arterial nar- in juries compared to vehicle-related trauma. Sporting
rowing and preventing stroke in patients with symptom- accidents and falls account for a far greater percentage
atic vasospasm after aneurysmal SAH. The timing of of mild injuries. Alcohol is associated with up to half of
endovascular intubation and use of inotropes in patients all cases of TBI. In Australia and New Zealand, blunt
with cardiac dysfunction are unresolved issues. 57 trauma (falls and vehicle-related), rather than penetrat-
ing (stabbing and firearms) or blast, is the predominant
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Other Neuroprotective Measures mechanism of injury. The transfer of energy to the
brain tissue actually causes the damage and is a signifi-
Many promising animal studies have not transferred cant determinant in the severity of injury (and routinely
to successful human clinical trials and there have been noted in ED on admission). In the past 10 years, the
a plethora of different mechanisms that block single introduction of safer car designs, airbags and other road
molecular processes but do not address the complex traffic initiatives (e.g. redesigning hazardous intersec-
molecular processes involved in brain injury. Currently tions, driver education campaigns, random breath
there is interest in antioxidants (Tirilazad mesylate), leu- testing and reducing speed limits) have decreased the
kocyte adhesion inhibition (Enlimomab), and continued overall number of road fatalities; improvements in
interest in erythropoietin, progesterone and their meta- retrieval, neurosurgery and intensive care in the past few
bolites and receptors as neuroprotective targets and decades have enabled many people to survive injuries
treatments. that would previously have been fatal. Research into
and prevention of falls and shaken-baby syndromes has
CENTRAL NERVOUS SYSTEM had a small impact on incidence reduction. 65,66
DISORDERS
Pathophysiology of TBI
CNS disorders include brain and/or spinal injury from
trauma, infection or immune conditions. The pathophys- TBI is a heterogeneous pathophysiological process (see
iology and aetiology of these disorders are discussed here, Figure 17.5). The mechanisms of injury forces inflicted
including management of these conditions. on the head in TBI produce a complex mixture of diffuse
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and focal lesions within the brain. Damage resulting
TRAUMATIC BRAIN INJURY from an injury can be immediate (primary) or secondary
in nature. Secondary injury results from disordered
Head injury is a broad classification that includes injury autoregulation and other pathophysiological changes
to the scalp, skull or brain. Traumatic brain injury (TBI) within the brain in the days immediately after injury.
is the most serious form of head injury. The range of Urgent neurosurgical intervention for intracerebral, sub-
severity of TBI is broad, from concussion through to post dural or extradural haemorrhages can mitigate the
coma unresponsiveness. The Australian age-standardised extent of secondary injury. Scalp lesions can bleed pro-
incidence rate of TBI in 2004/5 was about 150 per 100,000 fusely and quickly lead to hypovolaemic shock and brain