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.