managementof cerebral edema

Management of Cerebral Edema

By : CHARAN TEJASVIML-608

This is an excess accumulation of water in the intra- and/or extra cellular spaces of the brain. Oedema can occur as the result of many things, including head injury, allergic reaction, stroke, acute liver disease, cardiac arrest or from the lack of proper altitude acclimatization.

Cerebral edema

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 compressing.

If left untreated, it can lead to death.

Management of Cerebral Oedema

Osmotherapy

The most rapid and effective means of decreasing tissue water and brain bulk is osmotherapy

Osmotic therapy is intended to draw water out of the brain by an osmotic gradient and help to decrease blood viscosity.

These changes would decrease ICP and increase cerebral blood flow (CBF).

Management

Osmotic diuretics may reduce intracranial pressure in patients with reduced level of consciousness and raised intracranial pressure, but are short-lasting and often ineffective Infusions may be repeated provided plasma osmolarity does not exceed 320mOsm.

Management

Mannitol is the most popular osmotic agent.Mannitol is thought to decrease brain volume by decreasing overall water content, and to reduce blood volume by vasoconstriction, to reduce CSF volume by decreasing water content. Mannitol may also improve cerebral perfusion by decreasing viscosity or altering red blood cell rheology. Lastly mannitol may exert a protective effect 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 oedema secondary to tumours or abscesses - not trauma. Glucocorticoids are used for the management of malignant brain tumours, either primary or secondary, as adjuvant chemotherapy of some CNS tumours and perioperatively in brain surgery. Exert their influence on brain tumours mainly by reducing tumor-associated vasogenic edema, probably by decreasing the increased capillary 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 with the head at no more than 30 degrees to the horizontal. Further elevation seems to produce a paradoxical increase in intracranial pressure.Blood pressure needs to be monitored carefully in cases with cerebral edema.Fluid restriction minimally affects cerebral edema and, if pursued to excess, may result in episodes of hypotension, which may increase ICP andis associated with worse neurologic outcome

Management

Inter Cranial Pressure (ICP): Monitoring with extradural transducers may allow brainstem herniation to be anticipated and prevented. Most trusts now use ICP monitors these are usually placed into the right (non-dominant) frontal region through a small burr hole. It is calculated as mean arterial pressure minus intracranial pressure. Cerebral perfusion pressure is the principal determinant of cerebral blood flow.

Measure ICP

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 .

SURGERY