Current concepts in the treatment of acute head-trauma

Citation
C. Werner et K. Engelhard, Current concepts in the treatment of acute head-trauma, ANASTH INTM, 42(6), 2001, pp. XI-XX
Citations number
33
Categorie Soggetti
Aneshtesia & Intensive Care
Journal title
ANASTHESIOLOGIE & INTENSIVMEDIZIN
ISSN journal
01705334 → ACNP
Volume
42
Issue
6
Year of publication
2001
Pages
XI - XX
Database
ISI
SICI code
0170-5334(200106)42:6<XI:CCITTO>2.0.ZU;2-7
Abstract
Normal to high cerebral perfusion pressure, normoxia, and surgical decompre ssion are by far the most important and effective neuroprotective treatment s in patients following severe head injury. Interventions to increase CBF i n the ischemic territory, reduction of cerebral metabolism, lactic acidosis and excitatory neurotransmitter activity, prevention of Ca++-influx, inhib ition of lipidperoxidation, and free radical scavenging have been proposed to be protective in cerebral ischemia, However, only few of these treatment s have been proven to be efficacious in the setting of experimental or clin ical head neurotrauma, With the current knowledge the following physical an d pharmacological interventions seem to be justified in head injured patien ts: Normoventilation (paCO(2): 36 - 40 mmHg) in patients with normal or moderat ely elevated ICP. Avoid prophylactic hyperventilation but transiently hyper ventilate (paCO(2): 30 - 34 mmHg) during episodes of acute intracranial hyp ertension (plateau waves) until other interventions Rill reduce ICP. In patients,vith head injury mild to moderate hypothermia cannot be recomme nded as a standard rather than an option when other treatment strategies fa il to reduce ICP. In contrast, immediate and aggressive treatment of hypert hermia will reduce secondary injury. Barbiturates may decrease elevated ICP and improve neurologic outcome. Hyperglycemia is associated with worsened outcome following neurotrauma and plasma glucose concentrations should be assayed every 2 hours and maintain ed within the range of 100 - 150 mg/dl. Patients suffering from head injury or traumatic subarachnoid hemorrhage do not benefit from the administration of nimodipine. Rapid evacuation of epidural, subdural, or parenchymal mass lesions is an e ffective and causal intervention in the treatment of secondary insults. Sur gical decompression is currently ranked as a second tier treatment to avoid ischemic neuronal injury from sustained intracranial hypertension.