Resection (see also chapter 4)
The anesthetic must be chosen to lower ICP and minimize seizure risk (especially during cortical stimulation mapping). The patient's hepatic, renal and cardiopulmonary status will also impact on the anesthetic chosen .
Volatile anesthetics are highly halogenated molecules with an unknown mechanism of action. The group includes halothane, enflu-rane, isoflurane, desflurane and sevoflurane. Halogenated anesthetics provide amnesia, analgesia, and muscle relaxation at higher dosage. The newer agents have a low solubility, permitting rapid adjustment of anesthetic depth and prompt awakening. Halogenated anesthetics decrease cerebral metabolic rate and oxygen consumption (CMRO2) while increasing the CBF, hence producing a metabolic decoupling. They all preserve CO2 reactivity. Volatile anesthetics can increase ICP, this effect being more prominent with halothane and desflurane, but this rise may be prevented by hyperventilation.
Nitrous oxide (N2O) is a poorly soluble agent permitting rapid achievement of alveolar and brain partial pressure, and hence has a rapid onset and termination of action. It possesses weak amnestic properties, but provides prominent analgesia with no muscle relaxation. N2O increases ICP, this effect being completely reversed by hyperventilation. In addition, since N2O readily diffuses into sealed air pockets, it may cause a severe and rapid increase in ICP in the presence of a pneumocephalus. However, as shown by Domino et al. in craniotomies, it is usually not necessary to discontinue its use prior to dural closure . CO2 reactivity appears maintained when N2O is used alone or added to propofol, but may be reduced when used with isoflurane.
The site of action of barbiturates is located on the GABA receptor complex. Thiopental is a fast-onset short-acting drug, producing unconsciousness in 10-20 seconds. The short duration of action is explained by the rapid redistribution half-life of 7 minutes. Thiopental is principally used as an induction agent. Thiopental decreases CMRO2 and CBF and can produce EEG suppression at clinical doses. It also decreases the intracranial pressure (ICP) of patients with intracranial hypertension to a greater extent than it decreases the mean arterial pressure (MAP), thus improving the cerebral perfusion pressure (CPP). CO2 reactivity of brain vasculature is preserved with thiopental and does not change over time.
Like barbiturates, etomidate possesses a GABA-mimetic activity. Etomidate is a fastonset drug producing loss of consciousness in 10 seconds. Etomidate is used as an induction drug, but it can also be used as an infusion. Etomidate decreases CMRO2 by 45% and CBF by 35% and can produce a flat EEG. It decreases ICP, while increasing, or at least maintaining, the CPP. CO2 reactivity of the cerebral vascula-ture is maintained with etomidate. The brain-protecting effect of etomidate was also shown to be a dose-dependent phenomenon with deleterious effect at higher doses, presumably because of the induction of spiking EEG activity without further depression of CMRO2. In humans, a recent study showed that etomidate may even cause cerebral hypoxia at doses sufficient to induce burst-suppression. Although still widely used for neuroanesthesia, etomidate may not possess the brain-protecting virtues it was once thought to have.
Propofol is administered in an egg-oil-glycerol emulsion, and probably exerts its pharmacological effect by enhancing GABA-activated
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