Naslov
Drugs in Treatment of Patients with Intracranial Hypertension

Autori
Ščap, Miroslav

Izvornik
Periodicum biologorum (1849-0964) 106 (2004), Supl 1;

Vrsta, podvrsta i kategorija rada
Radovi u časopisima, kongresno priopcenje, stručni

Ključne riječi
intracranial hypertension; intracranial pressure monitoring; severe brain injury; mannitol; hypertonic saline

Sažetak
Control of increased ICP depends on effective control of cerebral tissue volume, cerebral blood volume, and CSF volume. The therapy of intracranial hypertension must either decrease the volume of the component that caused the original problem (e.g., tumor or hematoma removal) or decrease the volume of one of the other components. On an emergent basis, intracranial hypertension is most quickly treated by reducing cerebral blood volume, often by intentionally using acute hyperventilation to decrease CBF. Brain tissue volumen, often increased as a consequece of cerebral edema, can be reduced medically or surgically. Mannitol is an important therapeutic agent used in the treatment of elevated ICP. While the effects of mannitol on cerebral edema are generally ascribed to its hyperosmolality, creating an osmolar gradient between the vascular space and the brain tissue that result in net water movement out of the brain, there are other mechanisms involved as well. Mannitol decreases blood viscosity and microvasculatory vascular resistance ; additionally, it likely acts as an oxygen free-radical scaveneger. Hypertonic saline (HS) when used for acute control of elevated ICP, increased blood osmolarity, creating the driving force that pulls water out of neurons and interstitium. Effective restoration of blood pressure and cardiac output contributes to the increase of CPP. The serum sodium is not allowed to climb above approximately 155 mEq/L, nor the measured serum osmolarrity above 320 mOsm/kg H2O. Intravenous anestetics. Barbiturates appear to exert their ICP lowering and cerebral-protective effects via several mechanisms: alteration in vascular tone, decreasing metabolism, and inhibition of free radical peroxidation of cerebral lipids. Etomidate effectively decreased ICP without decreasing CPP. Decrease in ICP my be caused bay reduction of CBF (and CBV) that is induced by functional (metabolic) depressant effects of etomidate. Propofol either decreased or does not change ICP. Drugs such as furosemid, acetazolamide and even digoxin reduce CSF production and during this action can deacrease ICP, although they are uncommonly used in acute situation except furosemid administration before mannitol. Control of elevated ICP is sometimes quite difficult. Using some drugs together with other techniques like head elevation, hyperventilation, sedation and neuromuscular blocade, hypothermia, surgery and liquor drainage very good normalization of ICP can be achieved. Despite that results of all this aggressive treatment is desappointed.

Izvorni jezik
Engleski

Znanstvena područja
Kliničke medicinske znanosti

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