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ANESTHESIA FOR CAROTID ARTERY SURGERY
Ischemic cerebrovascular disease accounts for 80% of strokes; the remaining 20% are due to hemor-rhage. Ischemic strokes are usually the result of embolism or (less commonly) thrombosis in one of the blood vessels supplying the brain. Ischemic stroke may follow severe vasospasm after subarach-noid hemorrhage. By convention, a stroke is defined as a neurological deficit that lasts more than 24 h; its pathological correlate is typically focal infarction of brain. Transient ischemic attacks (TIAs), on the other hand, are neurological deficits that resolve within 24 h; they may be due to a low-flow state at a tightly stenotic lesion or to emboli that arise from an extracranial vessel or the heart. When a stroke is associated with progressive worsening of signs and symptoms, it is frequently termed a stroke inevolution. A second distinction is also often madebetween complete and incomplete strokes, based on whether the territory involved is completely affected or additional brain remains at risk for focal ischemia (eg, hemiplegia versus hemiparesis). The bifurcation of the common carotid artery (the ori-gin of the internal carotid artery) is the most com-mon site of atherosclerotic plaques that may lead to TIA or stroke. The mechanism may be embo-lization of platelet-fibrin or plaque material, ste-nosis, or complete occlusion. The last may be the result of thrombosis or hemorrhage into a plaque. Symptoms depend on the adequacy of collateral cir-culation. Emboli distal to regions lacking collateral blood flow are more likely to produce symptoms. Small emboli in the ophthalmic branches can cause transient monocular blindness (amaurosis fugax). Larger emboli usually enter the middle cerebral artery, producing contralateral motor and sen-sory deficits that primarily affect the arm and face. Aphasia also develops if the dominant hemisphere is affected. Emboli in the anterior cerebral artery territory typically result in contralateral motor and sensory deficits that are worse in the leg. It is com-mon for TIAs or minor strokes to precede a major stroke.
Indications for open surgery or intravascular interventions include TIAs associated with ipsilat-eral severe carotid stenosis (>70% occlusion), severe ipsilateral stenosis in a patient with a minor (incom-plete) stroke, and 30–70% occlusion in a patient with ipsilateral symptoms (usually an ulcerated plaque). In the past, carotid endarterectomy was recom-mended for asymptomatic but significantly stenotic lesions (>60%). Currently, stenting would often be the recommendation. Operative mortality for open surgery is 1–4% and is primarily due to cardiac com-plications (myocardial infarction). Perioperative morbidity is 4–10% and is principally neurological; patients with preexisting neurological deficits have the greatest risk of perioperative neurological events.
Studies suggest that age greater than 75 years,symptomatic lesions, uncontrolled hypertension, angina, carotid thrombus, and occlusions near the carotid siphon increase operative risk.
Most patients undergoing carotid endarterectomy are elderly and hypertensive, with generalized arte-riosclerosis. Many are also diabetic. Preoperative evaluation and management should focus on defining preexisting neurological deficits as well as optimizing the patient’s clinical status in terms of coexisting diseases. Most postoperative neurological deficits appear to be related to surgical technique. Uncontrolled perioperative hyperglycemia can increase morbidity by enhancing ischemic cerebral injury.
With the possible exception of diuretics, patients should receive their usual medications on schedule until the time of surgery. Blood pres-sure and the blood glucose concentration should be controlled. Angina should be stable and controlled, and signs of overt congestive heart failure should be absent. Because most patients are elderly, enhanced sensitivity to premedication should be expected.
The emphasis of anesthetic management dur-ing carotid surgery is on maintaining adequateperfusion to the brain and heart. Traditionally, this is accomplished by close regulation of arterial blood pressure and avoidance of tachycardia. Monitoring of intraarterial pressure is therefore nearly always done. Electrocardiographic monitoring should include the V5 lead to detect ischemia. Continuous computerized ST-segment analysis is desirable. Carotid endarterectomy is not usually associated with significant blood loss or fluid shifts.
Regardless of the anesthetic agents selected, mean arterial blood pressure should be maintained at—or slightly above—the patient’s usual range. Propofol and etomidate are popular choices for induction because they reduce cerebral metabolic rate proportionately more than cerebral blood flow. Small doses of an opioid or β-adrenergic blocker can be used to blunt the hypertensive response to endotracheal intubation. In theory, isoflurane may be the volatile agent of choice because it appears to provide the greatest protection against cerebral ischemia. Desflurane qualitatively has similar cere-bral effects but may not be as effective as isoflurane; however, desflurane is very useful in accelerating awakening and allowing immediate neurologi-cal assessment in the operating room. We do not regard the differences in neuroprotection among inhaled agents as clinically important. Some clini-cians also prefer remifentanil as the opioid for rapid emergence.
Intraoperative hypertension is common and generally necessitates the use of an intravenous vasodilator. Nitroglycerin is usually a good choice for mild to moderate hypertension because of its beneficial effects on the coronary circulation. Marked hypertension requires a more potent agent, such as nicardipine, nitroprusside, or clevidipine. β-Adrenergic blockade facilitates management ofthe hypertension and prevents reflex tachycardia from vasodilators, but should be used cautiously. Hypotension should be treated with vasopressors. Many clinicians consider phenylephrine the vaso-pressor of choice; if selected, it should be admin-istered in small increments to prevent excessive hypertension.
Pronounced or sustained reflex bradycardia or heart block caused by manipulation of the carotid baroreceptor can be treated with atropine. To pre-vent this response, some surgeons infiltrate the area of the carotid sinus with lidocaine, but the infiltra-tion itself can induce bradycardia. Arterial CO 2 tension should be maintained in the normal range because hypercapnia can induce intracerebral steal, whereas extreme hypocapnia decreases cerebral perfusion. Ventilation should be adjusted to main-tain normocapnia. Maintenance intravenous fluids should consist of glucose-free solutions because of the potentially adverse effects of hyperglycemia. Heparin (5000–7500 units intravenously) is usually administered prior to occlusion of the carotid artery. Some clinicians routinely use a shunt . Protamine, 50–150 mg, is usually given to reverse heparin prior to skin closure.
Rapid emergence from anesthesia is desir-able because it allows immediate neurologicalassessment, but the clinician must be prepared to treat hypertension and tachycardia. Postoperativehypertension may be related to surgical dener-vation of the ipsilateral carotid baroreceptor. Denervation of the carotid body blunts the ven-tilatory response to hypoxemia. Following extu-bation, patients should be observed closely for the development of a wound hematoma. When an expanding wound hematoma compromises the airway, the initial treatment maneuver may require opening the wound to release the hematoma. Transient postoperative hoarseness and ipsilateral deviation of the tongue may be noted; they are due to intraoperative retraction of the recurrent laryn-geal or hypoglossal nerves, respectively.
Unless regional anesthesia is used , indirect methods must be relied upon to assess the adequacy of cerebral perfusion during carotid cross-clamping. Some surgeons routinely use a shunt, but this practice may increase the incidence of postop-erative neurological deficits; shunt insertion can dis-lodge emboli. Carotid stump pressure distal to the cross-clamp, EEG, somatosensory evoked poten-tials (SSEPs), and cerebral oximetry have been used in some centers to determine whether a shunt is needed. A distal stump pressure of less than 50 mm Hg has traditionally been used as an indication for a shunt. Electrophysiological signs of ischemia (or a marked decline in cerebral oxygen saturation) after cross-clamping dictate the use of a shunt; changes lasting more than 10 min may be associated with a new postoperative neurological deficit. Although multichannel recordings and computer processing can enhance the sensitivity of the EEG, neither EEG nor SSEP monitoring is sufficiently sensitive or spe-cific to reliably predict the need for shunting or the occurrence of postoperative deficits. Other techniques, including measurements of regional cerebral blood flow with radioactive xenon-133, transcranial Doppler mea-surement of middle cerebral artery flow velocity, cerebral oximetry, jugular venous oxygen satura-tion, and transconjunctival oxygen tension, are also not sufficiently reliable.
Carotid surgery may be performed under regional anesthesia. Blockade of the superficial cervical plexus effectively blocks the C2–C4 nerves and allows the patient to remain comfortably awake during sur-gery. Deep cervical plexus block is not required. A substantial fraction of patients will require admin-istration of local anesthetic by the surgeon into the carotid sheath (whether or not a deep cervical block is performed). The principal advantage of regional anesthesia (and it is a tremendous advantage) is that the patient can be examined intraoperatively; thus, the need for a temporary shunt can be assessed and any new neurological deficits diagnosed immedi-ately during surgery. In fact, intraoperative neuro-logical examination may be the most reliable method for assessing the adequacy of cerebral perfusion dur-ing carotid cross-clamping. The examination mini-mally consists of level of consciousness, speech, and contralateral handgrip. Experienced clinicians use minimal sedation and “cocktail conversation” with the patient to monitor the neurological status. Some studies also suggest that when compared with gen-eral anesthesia, regional anesthesia results in more stable hemodynamics but outcomes appear similar. Regional anesthesia for carotid surgery requires the cooperation of the surgeon and patient.
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