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‚Äď20% 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.