EMERGENCY DRUG-THERAPY OF CLOSED-HEAD INJURY

Citation
J. Albanese et C. Martin, EMERGENCY DRUG-THERAPY OF CLOSED-HEAD INJURY, CNS DRUGS, 3(5), 1995, pp. 337-350
Citations number
37
Categorie Soggetti
Neurosciences,"Pharmacology & Pharmacy
Journal title
ISSN journal
11727047
Volume
3
Issue
5
Year of publication
1995
Pages
337 - 350
Database
ISI
SICI code
1172-7047(1995)3:5<337:EDOCI>2.0.ZU;2-X
Abstract
Preventing and treating cerebral ischaemia and secondary brain damage are the most important goals of trauma care in patients with head inju ry, At present, there are no therapies available for treating cerebral ischaemia and, therefore, the intensive therapy of severe head trauma is based on preventing or protecting against ischaemia and providing optimal conditions for tissue repair processes. This is achieved by th e maintenance of an adequate cerebral perfusion pressure. A large numb er of drugs can be considered and should be used in a stepwise fashion . Relevant monitoring parameters can help in the selection of adequate and effective treatments. An adequate cerebral perfusion pressure is greater than or equal to 70mm Hg. This is achieved in patients with he ad injury by restoring to the normal range both intracranial pressure (less than or equal to 20 to 25mm Hg) and mean arterial blood pressure (greater than or equal to 90mm Hg). All patients with a Glasgow Coma score less than or equal to 8 are considered at risk of increased intr acranial pressure. Sedation and mechanical ventilation are mandatory f or these patients. Normoxia [oxyhaemoglobin saturation recorded using a pulse oximeter (SpO(2)) greater than or equal to 95%] and moderate h ypocapnia (35 to 38mm Hg) are desirable goals, and hypo-osmolarity and hyperglycaemia must be avoided. A strict control of volaemia is requi red and in some patients hypervolaemia may be needed to maintain blood pressure. When intracranial pressure starts to increase, treatment in cludes (in a stepwise fashion): deepening of sedation, hyperventilatio n in patients with a suspected increase in cerebral blood flow, mannit ol or hypertonic saline (7.5%) and, in some patients, continuous infus ion of barbiturates. Cerebrospinal fluid removal can be considered in some patients, as well as skull vault removal to decompress widespread and uncontrollable cerebral oedema. Current research for future treat ments of cerebral ischaemia has focused on inhibition of lipid peroxid ative reactions and the use of glutamate antagonists. Inhibition of fr ee radicals is also under investigation.