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Management of cerebral oedema

Last reviewed dd mmm yyyy. Last edited dd mmm yyyy

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Clinical signs of cerebral oedema begin to appear when the intracranial pressure exceeds 30mm Hg. Failure to arrest the process results in respiratory arrest from brainstem coning. Consult neurosurgical advice. Measures include:

  • ICP monitoring with extradural transducers may allow brainstem herniation to be anticipated and prevented.

  • Osmotic diuretics: such as mannitol used for the treatment of cerebral oedema because of possible reduced cerebral perfusion. If used, urine output must be monitored hourly as mannitol is potentially nephrotoxic. Infusions may be be repeated provided plasma osmolarity does not exceed 320mOsm - mannitol, a sugar alcohol acts as an osmotic diuretic, causing sustained hyperosmolarity by dehydration, has become the most widely used hyperosmolar solution to treat elevated intracranial pressure
    • osmotic diuretics such as mannitol
    • associated with hypovolaemia and the induction of a hyperosmotic state - danger of reduced cerebral perfusion
    • hypertonic saline has emerged as an alternative hyperosmolar agent after several trials reported its relative superiority, especially for refractory intracranial pressure
      • evidence that intravenous bolus administration of hypertonic saline resulted in a sustained reduction of intracranial pressure on patients with traumatic cerebral oedema, even when elevated intracranial pressure is resistant to other intracranial pressure-lowering agents including mannitol
      • concentration and volume of hypertonic saline for clinical use range from 2% to 23.4% in concentration and 10 to 30 mL/kg in volume
      • based on limited data, there is weak evidence to suggest that hypertonic saline is no better than mannitol in efficacy and safety in the long-term management of acute traumatic brain injury (1)

  • Steroids: good for cerebral oedema secondary to tumours or abscesses - not trauma

  • Barbiturates: thiopentone has been widely accepted as a means of treating raised intracranial pressure. However, it may also cause haemodynamic disturbances and mask the clinical effects of cerebral oedema. Therefore ICP monitoring is advised.

  • Positioning: patients may be positioned with the head at no more than 30 degrees to the horizontal. Further elevation seems to produce a paradoxical increase in intracranial pressure.

  • Hyperventilation - reduce PCO2 to 3.5kPa - causes vasoconstriction


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