This is an excess accumulation of water in theintra- and/or extra cellular spaces of thebrain.Oedema can occur as the result of manythings, including head injury, allergicreaction, stroke, acute liver disease, cardiacarrest or from the lack of proper altitudeacclimatization.
Clinical signs of cerebral oedema begin toappear when the intracranial pressure exceeds30mm Hg.Failure to arrest the process results inrespiratory arrest from brainstemcompressing.If left untreated, it can lead to death.
OsmotherapyThe most rapid and effective means ofdecreasing tissue water and brain bulk isosmotherapyOsmotic therapy is intended to draw waterout of the brain by an osmotic gradient andhelp to decrease blood viscosity.These changes would decrease ICP andincrease cerebral blood flow (CBF).
Osmotic diuretics may reduce intracranialpressure in patients with reduced level ofconsciousness and raised intracranialpressure, but are short-lasting and oftenineffectiveInfusions may be repeated provided plasmaosmolarity does not exceed 320mOsm.
Mannitol is the most popular osmotic agent.Mannitol is thought to decrease brainvolume by decreasing overall watercontent, and to reduce blood volume byvasoconstriction, to reduce CSF volume bydecreasing water content. Mannitol mayalso improve cerebral perfusion bydecreasing viscosity or altering red bloodcell rheology.Lastly mannitol may exert a protectiveeffect against biochemical injury.
Diuretics - The osmotic effect can be prolonged by the use of loop diuretics (Furosemide) after the osmotic agent infusion.
Corticosteroids: Good for cerebral oedemasecondary to tumours or abscesses - nottrauma.Glucocorticoids are used for the managementof malignant brain tumours, either primary orsecondary, as adjuvant chemotherapy of someCNS tumours and perioperatively in brainsurgery.Exert their influence on brain tumours mainlyby reducing tumor-associated vasogenicedema, probably by decreasing the increasedcapillary permeability of BBB
Barbiturates: Thiopentone has been widely accepted as a means of treating raised intracranial pressure. However, it may also cause heamodynamic disturbances and mask the clinical effects of cerebral oedema. Produce a marked decrease in metabolic rate and it seems likely that the fall in cerebral blood flow and ICP is secondary.
Positioning: Patients may be positioned withthe head at no more than 30 degrees to thehorizontal. Further elevation seems to producea paradoxical increase in intracranial pressure.Blood pressure needs to be monitoredcarefully in cases with cerebral edema.Fluid restriction minimally affects cerebraledema and, if pursued to excess, may result inepisodes of hypotension, which may increaseICP andis associated with worse neurologicoutcome
Inter Cranial Pressure (ICP): Monitoring withextradural transducers may allow brainstemherniation to be anticipated and prevented.Most trusts now use ICP monitors these areusually placed into the right (non-dominant) frontal region through a smallburr hole. It is calculated as mean arterialpressure minus intracranial pressure.Cerebral perfusion pressure is the principaldeterminant of cerebral blood flow.
Recommended for large hemispherical infarcts with edema and life threatening brain-shifts. Temporary venticulostomy or craniectomy may prevent deterioration and may be lifesaving. Decompressive craniectomy in the setting of acute brain swelling from cerebral infarction is a life saving procedure and should be considered in younger patients who have a rapidly deteriorating neurological status .