Page 476 - ACCCN's Critical Care Nursing
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Neurological Alterations and Management 453
promotes a synergistic action, particularly in patients Corticosteroids
refractory to mannitol alone. Recent studies now suggest Excessive inflammation has been implicated in the pro-
that mannitol and frusemide have antiepileptic proper- gressive neurodegeneration that occurs in multiple
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ties and that mannitol has a role in ischaemic stroke.
neurological diseases, including cerebral ischaemia. The
Intravenous hypertonic saline (HTS) increases cerebral efficacy of glucocorticoids is well established in amelio-
perfusion and decreases brain swelling and inflammation rating oedema associated with brain tumours and in
more effectively than conventional resuscitation fluids. improving the outcome in subsets of patients with bacte-
HTS behaves like 20% mannitol in acute cerebral oedema rial meningitis. Despite encouraging experimental results,
but maintains haemodynamic status. However, unlike clinical trials of glucocorticoids in ischaemic stroke, intra-
HTS, mannitol induces a diuresis, which is relatively con- cerebral haemorrhage, aneurysmal subarachnoid haem-
traindicated in patients with both TBI and hypovolaemia orrhage and traumatic brain injury have not shown a
as it may worsen intravascular volume depletion and definite therapeutic effect. Furthermore, the CRASH (cor-
decrease cerebral perfusion. Therefore, despite theoretical ticosteroid randomisation after significant head injury)
advantages of HTS resuscitation in patients with TBI, an trial demonstrated an increased risk of death from use of
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Australian randomised controlled trial found no differ- steroids from all causes within two weeks of injury, and
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ence in outcome between HTS and other resuscitation was stopped early. Consequently, the BTF Guidelines
fluids in prehospital resuscitation. However, in many Aus- state that the use of steroids is not recommended
tralian and New Zealand intensive care units, HTS is used for TBI. 32
as a preferred alternative to mannitol in patients with The evidence supporting glucocorticoid therapy for spinal
raised ICP. cord injury is controversial; however, methylpredniso-
lone continues to be widely employed in this setting
Normothermia (this is discussed further below under Spinal injury
Hyperthermia occurs in up to 40% of patients with isch- management).
aemic stroke and intracerebral haemorrhage and in
40–70% of patients with severe TBI or aneurysmal sub- Barbiturates and sedatives
arachnoid haemorrhage. Hyperthermia is independently The BTF Guidelines state that high-dose barbiturate
associated with increased morbidity and mortality after therapy may be considered in haemodynamically-
ischaemic and haemorrhagic stroke, and in subarachnoid salvageable severe TBI patients with intracranial hyper-
haemorrhage and TBI patients temperature elevation tension refractory to maximal medical and surgical
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has been linked to raised intracranial pressure. Tempe- interventions. The utilisation of barbiturates for the
rature elevations as small as 1–2°C above normal can prophylactic treatment of ICP has not been indicated.
aggravate ischaemic neuronal injury and exacerbate Barbiturates exert cerebral protective and ICP-lowering
brain oedema. Mild hypothermia protects numerous effects through alteration in vascular tone, suppression
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tissues from damage during ischaemic insult. The use of of metabolism and inhibition of free radical-mediated
paracetamol, cooling blankets, ice packs, evaporative lipid peroxidation. Barbiturates may effectively lower
cooling and new cooling technologies may be useful cerebral blood flow and regional metabolic demands.
in maintaining normothermia. Hyperaemia (increased The lower metabolic requirements decrease cerebral
blood flow) may occur during rewarming, resulting in blood flow and cerebral volume. This results in benefi-
acute brain swelling and rebound intracranial hyperten- cial effects on ICP and global cerebral perfusion. Barbi-
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sion. In an original study, Marion and colleagues. turates within the BTF guidelines are now included
demonstrated a higher mortality rate than in more recent under the heading of Anaesthetics, Analgesics and Seda-
trials, possibly due to rapid rewarming and rebound tives and these also recommend (Level II) that it is ben-
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hyperaemia and cerebral oedema. eficial to minimise painful or noxious stimuli as well as
agitation as they may potentially contribute to eleva-
Maintenance of body temperature at 35°C may be tions in ICP. Therefore propofol is recommended for the
45
optimal. Intracranial pressure falls significantly at brain control of ICP, but does not improve mortality or six-
temperatures below 37°C but no difference was observed month outcome. High dose propofol should be avoided
at temperatures below 35°C. Cerebral perfusion pressure as it can produce significant morbidity. 49
peaks at 35–36°C and decreases with further falls in
45
temperature. At a temperature below 35°C, both oxygen Surgical interventions
delivery and oxygen consumption decrease. Cardiac The European TBI Guidelines suggest that operative man-
output decreases progressively with hypothermia. There- agement be considered for large intracerebral lesions
fore, cooling to 35°C may reduce intracranial hyperten- within the first four hours of injury. The use of unilateral
sion and maintain sufficient CPP without associated craniectomy after the evacuation of a mass lesion, such
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cardiac dysfunction or oxygen debt. As the temperature as an acute subdural haematoma or traumatic intracere-
is lowered from 34°C to 31°C, the volume of IV fluid bral haematoma, is accepted practice. Surgery is also
infusion and inotrope requirements increase substan- recommended for open compound depressed skull frac-
tially and, despite such interventions, mean arterial pres- tures that cause a mass effect. 50
sure decreases. At 31°C serum potassium, white blood
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cell count and platelet counts are diminished. Thus, it Decompressive craniectomy, for refractory intracranial
seems that hypothermia to 35°C may be optimal. hypertension, has been performed since 1977, with a

