What
interventions may reduce the risk of neurologic injury?
Ischemic neurologic insult from carotid artery
surgery may result from arterial embolization during surgical manipulation,
decreased cerebral perfusion during temporary arterial occlusion, reperfusion
injury, or unintentional arterial occlusion following surgery. Arterial
embolization during surgery is very common and often depends on sur-gical
technique and the preoperative presence of athero-sclerosis. Surgical placement
of a shunt may increase the incidence of embolization. Therefore, in many
centers shunts are inserted only if indicated by EEG ischemic changes following
carotid occlusion or other evidence of poor cerebral collateral circulation.
Although thiopental may improve outcome following focal ischemia, it is not
widely employed for maintenance of general anesthesia. This may be due to
dose-dependent delayed awakening or its hemodynamic effects. Hypothermia also
improves out-come following focal cerebral ischemia. However, it has not gained
wide acceptance for carotid artery surgery. This may be due to the deleterious
effects of hypothermia on cardiac function.
Decreased cerebral perfusion during temporary
arterial occlusion is most often treated by deliberate hypertension. In many
centers, systemic arterial pressure is increased by 10–20% during temporary
arterial occlusion. Intravenous phenylephrine is most often employed for this
purpose because of extensive evidence of improved outcome in animal models of
focal cerebral ischemia. Surgical place-ment of a temporary vascular shunt
during carotid artery occlusion will also improve cerebral blood flow. This
may, however, prolong surgical time, obscure surgical exposure, and promote
embolization.
Following reperfusion, ischemic or infarcted
brain may be at risk for reperfusion injury. Usually arterial blood pressure is
reduced to near normal prior to reperfusion.
The choice of anesthetic agent for CEA remains
contro-versial. In a randomized study comparing potent inhala-tion anesthetics,
EEG evidence of ischemia occurred at higher cerebral blood flow values in
patients anesthetized with halothane compared with isoflurane. This supports
the use of isoflurane in these patients. There is no widely accepted preference
for either a primarily opioid-based or inhalation anesthetic technique. In any
case, rapid emer-gence from general anesthesia permitting timely assess-ment of
neurologic function will facilitate diagnosis of neurologic deficit resulting
from cerebrovascular occlu-sion. This will allow for a more rapid intervention
such as therapeutic surgical re-exploration, cerebral thrombolysis, or angioplasty,
if indicated.
Control of arterial carbon dioxide tension also
remains somewhat controversial. Mild hypocapnea may reduce cerebral blood flow,
but may also preferentially shunt blood from normal brain to ischemic brain.
Most practitioners maintain arterial carbon dioxide tension near normal.
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