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464 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E

Cerebral Venous Thrombosis
TABLE 17.5 Hunt-Hess scale for SAH Cerebral venous thrombosis is particularly important to
recognise because there is general consensus that early
Score Description anticoagulation can result in good clinical outcomes.
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0 Unruptured; asymptomatic discovery MR and CT vascular imaging has made it easier to estab-
lish the diagnosis, but close monitoring of the patient is
I Asymptomatic or minimal headache with slight
nuchal rigidity essential, as late deterioration can occur.
II Moderate to severe headache, nuchal rigidity; no
neurological deficit other than cranial nerve Collaborative Management of Stroke
deficit
Expected outcomes for patients with acute ischaemic and
III Drowsiness, confusion, or mild focal deficit (e.g. haemorrhagic stroke include prevention of secondary
hemiparesis), or a combination of these findings
injury, of airway and respiratory complications, and
IV Stupor, moderate to severe deficit, possibly early the maintenance of haemodynamic stability. Timely
decerebrate rigidity and vegetative disturbances
assessment and intervention is paramount in the man-
V Deep coma, decerebrate rigidity, moribund agement of ischaemic stroke, especially regarding inter-
appearance ventional pharmacology and prevention of cerebral
haemorrhage. See Online resources for specific protocols
related to stroke.
(hypervolaemia), and producing relative haemodilution Atrial fibrillation and deep vein thrombosis (DVT) pre-
(’triple H therapy’). 91 vention (in ischaemic stroke) requires anticoagulation
Hypovolaemia occurs in 30–50% of patients, as does control. In haemorrhagic stroke, sequential compression
excessive hyponatraemia in 30% of patients. In the first device and stockings are indicated for DVT prophylaxis as
six days, plasma volume decreases of greater than 10% anticoagulants are a risk factor for rebleeding. Mainte-
can occur following SAH, thus increasing the risk of vaso- nance of bowel and bladder function and prevention of
spasm and ischaemia. Women have been found to have integument complications, malnutrition, seizures and
more significant drops in blood volume than men fol- increasing neurological deficits are important goals. Envi-
92
lowing SAH. ‘Third space’ loss, insensible losses and ronmental precautions are implemented to provide a
blood loss account for this drop in fluid volume, as well non-stimulating environment, preventing rises in ICP
as electrolyte disturbances. and further bleeding.
Sensory perceptual and motor alterations need to be
Other aspects of management in the acute stages include assessed in regard to effective communication and pain
suitable analgesia, seizure control, and treatment with management. Rehabilitation and psychological support
nimodipine to prevent secondary ischaemia caused by for the patient and significant others are integrated into
vasospasm. Vasospasm often occurs 4–14 days after the acute care phase for a smooth transition.
initial haemorrhage when the clot undergoes lysis (dis-
solution), increasing the chances of rebleeding. It is
believed that early surgery to clip the aneurysm prevents INFECTION AND INFLAMMATION
rebleeding and that removal of blood from the basal The CNS infections of major interest in the ICU are
cisterns around the major cerebral arteries may prevent divided into those which affect the meninges (meningi-
vasospasm. 93,94 (See previous section on Management of tis) and those which affect the brain parenchyma
vasospasm.) (encephalitis). They may be viral or bacterial in aetio-
logy. There are also numerous medical conditions that
ICP monitoring and drainage of CSF via ventricul ostomy may produce an encephalopathic illness which may
89
is indicated in SAH but not in cerebral haemorrhage. mimic viral encephalitis. In patients recently returning
SAH causes increased sympathetic activation from the from abroad, particular vigilance must be paid to the
presence of haemoglobin in the subarachnoid space. This possibility of such non-viral infections as cerebral
results in elevated catecholamine levels, which may result malaria, which may be rapidly fatal if not treated early.
in focal myocardial necrosis, expla ining the presence of A number of metabolic conditions, including liver and
inverted T waves, ST dep ression, prominent U waves, and renal failure and diabetic complications, may also cause
Q-T intervals in more than 50% of pati ents. As cardiac confusion due to the manifestation of cerebral oedema.
function is one of the determinants for adequate cerebral The possible role of alcohol and drug ingestion must
blood flow, it is essential to identify such occurrences always be considered.
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early and treat them acco rdingly. Hyponatraemia occurs
from alte rations in atrial natriuretic factor (ANF) in
response to sympathetic nervous system activation. The Meningitis
syndrome of inappropriate secretion of antidiuretic The incidence of disease caused by Neisseria meningitidis
hormone (SIADH) is primarily responsible for hypona- remains an issue of public health concern in Australia
traemia in those with SAH, as is cerebral salt-wasting and New Zealand. The introduction of a publicly funded
syndrome; however, both mechanisms are still relatively program of selective vaccination with conjugate sero-
misunderstood. 90 group C meningococcal vaccine in 2004 has resulted in