Anesthetic Management for Carotid Endarterectomy and Current Practice in USA Chuanyao Tong, MD, Yanfu Shao, MD+

Department of Anesthesiology, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA; + Department of Anesthesiology, Ohio State University College of Medicine, Columbus, Ohio, USA Introduction Stroke or cerebral vascular accident (CVA) is the 3rd leading cause of death in the United State. Surviving from the initial life threatening events, many patients may be left with significant neurologic deficits requiring rehabilitation and medical interventions. The sequela will affect the patients quality of life, add the burden on family member, and significantly impact the social economy. The origin of the internal carotid arteries and bifurcation of the common carotid is the most common site of atherosclerosis leading to CVA. The mechanism may be embolization of plaque-fibrin or plaque material, stenosis or occlusion. The last may result from thrombosis or hemorrhage into a plaque. Therefore, the etiology of cerebral ischemia is mostly embolic in nature but may have a hemodynamic component. Several milestone clinical studies in the later 80s have demonstrated significant advantage of carotid endarterectomy (CEA) over the medical management in reducing the incidence of CVA in high-risk patients. Preoperative management The patients requiring CEA commonly have multiple co-existing diseases. The significant ones are coronary artery disease with decompensated congestive heart failure and unstable angina, hypertension (diastolic BP>110 mmHg), diabetic mellitus (glucose >200 mg/dl). If not well controlled, these co-morbidities increase postoperative morbidity and mortality although most postoperative neurologic deficits appear to be related to surgical technique. Preoperative evaluation and management should focus on defining preexisting neurologic deficits as well as optimizing the patients co-existing diseases. Adjusting medications by adding beta blocker for coronary artery disease with possible myocardial infarction and ACE inhibitor for congestive heart failure, and controlling hypertension and blood glucose level have been shown beneficial. Coumadin should be discontinued 5-7 days prior to surgery while Aspirin continues. Routine laboratory tests include CBC, basic metabolic profile and ECG. Echocardiography with stress test is valuable for evaluating patients cardiac reserve. Interventional diagnostic studies are still controversial and usually not recommended. Reviewing cerebral angiogram has proved to be helpful for the anesthesia preparations.

Monitoring and cerebral ischemia management ASA standard monitors are routinely applied. Correct placement of V5 lead of ECG is important for detecting cardiac ischemia. The use of transesophageal echocardiography is recommended for high cardiac risk patients. An arterial line is usually placed prior to induction. Central nervous system monitoring: For CEA performed with regional anesthesia, the assessment of mental status (conversing with the patient) and the contralateral motor and sensory

responses during carotid cross clamping are adequate. If CEA is performed under general anesthesia (GA), a number of special methods have been utilized for intra-operative neurologic monitoring, although those practices are not mandated as standard care. The special techniques include: 1) Electroencephalography (EEG), somatosensory evoked potential and Neurotrack (4channel processed EEG). The 16-channel raw EEG read by a neurologist on site is considered as a gold standard and a focal decrease in waveform frequency and/or amplitude is the signs for ischemia; 2) Transcranial Doppler. It measures cerebral blood flow velocity and is helpful in detecting emboli; 3) Cerebral perfusion pressure including MAP and stump pressure. The latter, however, is unreliable and less used; 4) Cerebral oximetry or Near-infrared spectroscopy (NIRS). It non-invasively measures regional cerebral O2 saturation (rSo2); It monitor rSo2 tends but lack specificity. Studies have shown that 20% of reduction in rSo 2 had high false-positive value (66%) but 97.4-100% negative predictive value, i.e., if no rSo2 decrease, cerebral ischemia is unlikely, but a decrease does not always indicate ischemia ; and 5) Jugular mixed venous O2 saturation. This is an invasive and nonspecific technique. A reading reduces to < 50% suggesting possible ischemia. Currently no single method has been infallible and shown to improve neurologic outcome. Cerebral ischemia management: If intraoperative cerebral ischemia is detected, immediate measures should be taken, including informing surgeon, releasing the clamp if carotid arterial has not been opened, placing a shunt, increasing mean arterial pressure (MAP) by 10-20%, and/or administrating neuroprotective agents. Anesthesia induction and maintenance The choice of anesthesia, regional vs. general, is mainly depending on the surgeon and anesthesiologists experience and preference. There is no data to support one technique is superior to the other in terms of clinical outcome. A balanced GA using multiple agents is a common practice, i.e., combining intravenous (propofol, thiopental or etomidate) and volatile (isoflurane, desflurane or sevoflurane) agents with narcotics (fentanyl, sulfentanil, or remifentanil). The goal is to maintain hemodynamic stability to ensure cerebral perfusion and to minimize cardiac depression. Nitric Oxide is not contraindicated; however, it increases the size of air emboli. Regional techniques include superficial or deep cervical plexus block or a field block. However, deep cervical block may be associated with more complications. Bupivacaine (0.25-0.5%) or ropivacaine (0.5%) with or without epinephrine (1:200,000) are commonly used with an equivalent clinical efficacy, which provides 2-3 hours surgical anesthesia and 4-6 hour postoperative pain relief. Supplement with 1% lidocaine is frequently performed by surgeons during a deep dissection. CEA performed under regional anesthesia requires less vasopressor support postoperatively. Anesthesia emergence and postoperative complications The goal is to have a smooth and rapid emergence with stable hemodynamics in order to facilitate immediate neurologic assessment. The associated complications are: 1) acute myocardial ischemia

and/or infarct, cardiac complications are still the number one cause of perioperative mortality; 2) hyper- or hypotension which may require treatment with vasoactive agents; 3) ipsilateral hyperperfusion syndrome; 4) perioperative stroke; 5) an emergency obstructive airway related to surgical bleeding; and 6) cranial nerves injury. Special issues Emergency Airway (EA): It does present as a real challenge. This usually happens: 1) intraoperatively, the loss of airway is due to poor tolerance of carotid clamping that causes significant cerebral ischemia and mental status change. This only occurs when CEA performed under regional anesthesia; 2) postoperatively, surgical site hematoma compressing the trachea, thereby leading to severe tracheal deviation and airway obstruction. At those critical moments, think about fast-track LMA, awake fiberoptic intubation, or spontaneous breathing inhalational induction, etc. Shunt: The placement of shunt is to maintain cerebral blood floor (CBF) during carotid artery cross-clamping. It seems to provide maximal nueroprotection. But the risks of insertion of shunt are associated with dislodging emboli and intimal wall dissection. Blood pressure: In this patients population, the CBF is more likely pressure-dependent. Maintaining MAP 10-20% above baseline is recommended during carotid clamping to augment the collateral cerebral perfusion; while keeping systolic BP <160 mmHg is extremely important to prevent cerebral hyperemia (hyper-perfusion), excessive surgical bleeding and stressing the heart. PaCO2: Maintaining normocarbia is recommended. Either hypo- or hypercarbia should be avoided. Hypercarbia may only be able to dilate the vessels in normal areas while the vessels in ischemic areas are already maximally dilated. This results in the steal effect, i.e., diverting blood from ischemic to normal areas. Conversely, hypocarbia may cause vessels in the ischemic and marginally perfused areas to undergo constrict, converting the marginally perfused areas to truly ischemic areas (the Robin Hood or inversed steal effect). Pharmacologic cerebral protection: Sodium thiopental is the only agent may provide cerebral protection for focal ischemia when used properly (initial dose of 10-15 mg/kg, and 5 mg/kg every 10-15 min, or guided by EEG of burst suppression). Inotrope and pressors are frequently required to counteract its effect of hemodynamic suppression. Cerebral hyperemia: The post-stenosis epithelia layer is vulnerable to post-CEA high pressure shear force. Complain of ipsilateral headache, blurred vision, and facial or eye pain are suggesting of brain hyperemia and demanding an urgent management. Hyperglycemia: Serum glucose >200 mg/dl is associated with adverse neurologic outcome. Avoid glucose contain fluid and use insulin if necessary. Carotid Stent: Carotid stent is becoming popular and more accepted. Its short-term effect is equivalent to CEA, while the long-term benefit is still under evaluation. The newly deployed distal intercept filter device has significantly decreased stenting related complications. Conclusions In 2005, the American Academy of Neurology published its evidence-based review which reconfirmed the benefit effect of CEA in CVA prevention: CEA is indicated for symptomatic patients with stenosis>70%, while CEA for stenosis of 70-99% asymptomatic is depending on surgical complication rate (should be <6%), and stenosis <60% should be best managed medically with Aspirin (81-325 mg/day).

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