8

INCREASED INTRACRANIAL PRESSURE, CERE BRAL EDEMA,

AND BRAIN SWELLING
Cerebral edemais an increase in the brain's volume caused by an increase in its water and HYPERLINK "http://www.sciencedirect.com/topics/page/Sodium" \o "Learn more about sodium" sodiumcontent .( Itis excess accumulation of fluid in the HYPERLINK "https://en.wikipedia.org/wiki/Intracellular" \o "Intracellular" intracellularor HYPERLINK "https://en.wikipedia.org/wiki/Extracellular" \o "Extracellular" extracellularspaces of the HYPERLINK "https://en.wikipedia.org/wiki/Brain" \o "Brain" 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 generalizedcerebral edema. The types ofcerebral edemaare vasogenic, HYPERLINK "http://www.sciencedirect.com/topics/page/Cytotoxic" \o "Learn more about cytotoxic" cytotoxic, or interstitial.
Increased capillary permeability causes vasogenic edema; this occurs with HYPERLINK "http://www.sciencedirect.com/topics/page/Brain_tumor" \o "Learn more about brain tumor" brain tumor, abscess, trauma, and hemorrhage. The fluid is located primarily in the HYPERLINK "http://www.sciencedirect.com/topics/page/White_matter" \o "Learn more about white matter" white matterand responds to treatment with HYPERLINK "http://www.sciencedirect.com/topics/page/Corticosteroids" \o "Learn more about corticosteroids" corticosteroids.
 HYPERLINK "http://www.sciencedirect.com/topics/page/Osmotic" \o "Learn more about Osmotic" Osmoticagents have no effect on vasogenic edema, but they reduce total intracranial pressure by decreasing normal brain volume.
 HYPERLINK "http://www.sciencedirect.com/topics/page/Cytotoxic" \o "Learn more about Cytotoxic" Cytotoxicedema, characterized by swelling of HYPERLINK "http://www.sciencedirect.com/topics/page/Neurons" \o "Learn more about neurons" neurons, glia, and HYPERLINK "http://www.sciencedirect.com/topics/page/Endothelial" \o "Learn more about endothelial" endothelialcells, constricts the extracellular space. The usual causes are hypoxia, HYPERLINK "http://www.sciencedirect.com/topics/page/Ischemia" \o "Learn more about ischemia" ischemia, or infection of the HYPERLINK "http://www.sciencedirect.com/topics/page/Nervous_system" \o "Learn more about nervous system" 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 HYPERLINK "http://www.sciencedirect.com/topics/page/Ventricular_system" \o "Learn more about ventricular system" ventricular systemto the brain; this occurs when CSF absorption is blocked and the ventricles enlarge. The fluid collects chiefly in the periventricular HYPERLINK "http://www.sciencedirect.com/topics/page/White_matter" \o "Learn more about white matter" white matter. Agents intended to decrease CSF production, such as HYPERLINK "http://www.sciencedirect.com/topics/page/Acetazolamide" \o "Learn more about acetazolamide" acetazolamideand HYPERLINK "http://www.sciencedirect.com/topics/page/Furosemide" \o "Learn more about furosemide" furosemide, may be useful. HYPERLINK "http://www.sciencedirect.com/topics/page/Corticosteroids" \o "Learn more about Corticosteroids" Corticosteroidsand HYPERLINK "http://www.sciencedirect.com/topics/page/Osmotic" \o "Learn more about osmotic" osmoticagents 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.