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Transcript
INCREASED INTRACRANIAL PRESSURE, CERE BRAL EDEMA,
AND BRAIN SWELLING
Cerebral edema is an increase in the brain's volume caused by an increase in its
water and sodium content .( It is excess accumulation of fluid in
the intracellular or extracellular spaces of the brain ).
Cerebral edema is rarely a primary disease, but commonly an accompaniment of
other diseases. Cerebral edema is commonly a transient phenomenon and may be
fatal but complete recovery or recovery with residual nervous signs also occurs. It
is manifested clinically by blindness, opisthotonos, muscle tremor, paralysis, and
clonic convulsions.
ETIOLOGY
Increased intracranial pressure results from either localized or generalized cerebral
edema. The types of cerebral edema are vasogenic, cytotoxic, or interstitial.
Increased capillary permeability causes vasogenic edema; this occurs with brain
tumor, abscess, trauma, and hemorrhage. The fluid is located primarily in the white
matter and responds to treatment with corticosteroids.
Osmotic agents have no effect on vasogenic edema, but they reduce total
intracranial pressure by decreasing normal brain volume.
Cytotoxic edema, characterized by swelling of neurons, glia, and endothelial cells,
constricts the extracellular space. The usual causes are hypoxia, ischemia, or
infection of the nervous system. Corticosteroids do not decrease edema, but
osmotic agents may relieve intracranial pressure by decreasing brain volume.
Transependymal movement of fluid causes interstitial edema from the ventricular
system to the brain; this occurs when CSF absorption is blocked and the ventricles
enlarge. The fluid collects chiefly in the periventricular white matter. Agents
intended to decrease CSF production, such as acetazolamide and furosemide, may
be useful. Corticosteroids and osmotic agents are not effective.
CLINICAL FINDINGS
There is central blindness, and periodic attacks of abnormality occur in which
opisthotonos, nystagmus, muscle tremor, and convulsions are prominent.
TREATMENT
In general terms, edema of the brain responds to parenteral treatment with
hypertonic solutions and corticosteroids.
Hypertonic solutions are most used to cytotoxic edema and corticosteroids to
vasogenic edema.
This is in addition to treatment of the primary cause of the disease.
Mannitol at 2 g/kg BW and dexamethasone at 1 mg/kg BW, both intravenously,
are recommended. The mannitol is given intravenously as a 20% solution followed
3 hours later by the dexamethasone, also intravenously.
Diuretics usually produce tissue dehydration too slowly to be of much value in
acute cases, but they may be of value as an adjunct to hypertonic solutions or in
early or chronic cases.