Raised Intracranial Pressure

TREATMENT (cont'd)

Methods of reducing intracranial pressure

Mannitol infusion: An i.v. bolus of 100 ml of 20% mannitol infused over 15 minutes reduces intracranial pressure by establishing an osmotic gradient between the plasma and brain tissue. This method 'buys' time prior to craniotomy in a patient deteriorating from a mass lesion. Mannitol is also used 6 hourly for a 24-48 hour period in an attempt to reduce raised ICP. Repeated infusions, however, lead to equilibration and a high intracellular osmotic pressure, thus counteracting further treatment. In addition, repeated doses may precipitate lethal rises in arterial blood pressure and acute tubular necrosis. Its use is therefore best reserved for emergency situations.

Controlled hyperventilation: Bringing the PC02 down to 3.5kPa by hyperventilating the sedated or paralysed patient causes vasoconstriction. Although this reduces intracranial pressure, the resultant reduction in cerebral blood flow may in itself cause brain damage. Maintaining the blood presssure and the cerebral perfusion pressure (CPP) (> 70 mmHg) appears to be as, if not more, important than lowering intracranial pressure. Only by monitoring the amount of oxygen extracted from the brain can one determine whether or not the brain tissue can withstand further vasoconstriction caused by hyperventilation (see page 227).

CSF withdrawal: Removal of a few millilitres of CSF from the ventricle will immediately reduce the intracranial pressure. Within minutes, however, the pressure will rise and further CSF withdrawal will be required. In practice, this method is of limited value, since CSF outflow to the lumbar theca results in a diminished intracranial CSF volume and the lateral ventricles are often collapsed. Continuous CSF drainage may make most advantage of this method.

Sedatives: If intracranial pressure fails to respond to standard measures then sedation may help under carefully controlled conditions.

Propofol, a short acting anaesthetic agent, reduces intracranial pressure but causes systemic vasodilatation. If this occurs pressor agents may be required to prevent a fall in blood pressure and a reduction in cerebral perfusion.

Barbiturates (thiopentone) reduce neuronal activity and depress cerebral metabolism; a fall in energy requirements theoretically protects ischaemic areas. Associated vasoconstriction can reduce cerebral blood volume and intracranial pressure but systemic hypotension and myocardial depression also occur. Clinical trials of barbiturate therapy have not demonstrated any improvement in outcome.

Etomidate also provides cerebral protection by reducing cerebral metabolism and intracranial pressure without producing cardiodepression. It inhibits endogenous steroid synthesis, and therefore requires steroid cover.

Steroids: There is no doubt that steroids play an important role in treating patients with intracranial tumours and surrounding oedema. Cell membranes are stabilised, but it is not certain that their beneficial effect in tumour management is a result of reducing ICP. Steroids appear to be of no value in the treatment of traumatic or ischaemic damage. Experimental evidence suggests that they may help if administered before the damage occurs, but clearly this is seldom of practical value.

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