2. 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.
3. 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.
4. 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).
5. 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.
6. 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.
7. Diuretics - The osmotic effect can be
prolonged by the use of loop diuretics
(Furosemide) after the osmotic agent
infusion.
8. 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
9. 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.
10. 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
11. 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.
12. 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 .
