INTRODUCTION — Treatment aimed at carotid atherosclerotic lesions may be beneficial for symptomatic or asymptomatic patients. This topic will review the preoperative evaluation and surgical technique of carotid endarterectomy (CEA). The indications for carotid revascularization and perioperative stroke risk assessment for patients with carotid atherosclerosis are discussed elsewhere. (See "Management of asymptomatic carotid atherosclerotic disease" and "Management of symptomatic carotid atherosclerotic disease".)
Carotid artery stenting is also discussed separately. (See "Carotid artery stenting and its complications".)
INDICATIONS — Carotid endarterectomy (CEA) is most commonly performed for symptomatic or asymptomatic high-grade (>60, 70 percent, respectively) internal carotid artery stenosis. The effectiveness of CEA has been established by large randomized clinical trials. The indications for CEA in patients with significant carotid atherosclerosis are discussed in detail elsewhere. (See "Management of symptomatic carotid atherosclerotic disease", section on 'Carotid endarterectomy' and "Management of asymptomatic carotid atherosclerotic disease", section on 'Carotid endarterectomy'.)
Special considerations
Bilateral carotid stenosis — Some patients have varying degrees of bilateral carotid disease. No randomized clinical trials have evaluated the effectiveness of bilateral CEA for such patients. However, bilateral carotid occlusive disease appears to increase the risk for complications during and after unilateral CEA [1-3]. As an example, in one study of 700 patients undergoing CEA, 15.4 percent had contralateral disease [2]. The combined death and stroke rates in these patients were almost twice that of matched patients with unilateral disease (5.6 versus 2.4 percent).
The impact of severe contralateral carotid artery stenosis or occlusion on the benefit and risk of unilateral CEA in patients with symptomatic and asymptomatic disease is discussed separately in the appropriate topic reviews. (See "Management of symptomatic carotid atherosclerotic disease", section on 'Contralateral carotid stenosis or occlusion' and "Management of asymptomatic carotid atherosclerotic disease", section on 'Contralateral carotid stenosis or occlusion'.)
When the extent of contralateral carotid disease is significant enough to warrant bilateral CEA, most surgeons stage the approach, with a delay of at least one to two weeks between operations.
The risk of respiratory compromise secondary to neck hematomas or laryngeal nerve injury, frequent difficulty with blood pressure control after manipulation of the carotid sinus, concerns about cerebral hyperperfusion syndrome and the unknown effect of bilateral cerebral ischemia (although temporary) generally contraindicates a combined approach. (See 'Complications' below.)
Prophylactic carotid endarterectomy
Coronary artery bypass surgery — Neurologic complications are second only to heart failure as a cause of morbidity and mortality following cardiac surgery. As a result, carotid endarterectomy (CEA) is often considered in conjunction with coronary artery bypass grafting (CABG) in patients with significant carotid stenosis. However, there have been no trials examining the use of CEA in patients having CABG. In addition, it is not clear if CABG should be combined with CEA or should be staged (ie, performed before or after CEA). (See "Coronary artery bypass grafting in patients with cerebrovascular disease", section on 'Prophylactic carotid intervention'.)
General surgery — The incidence of stroke appears to be lower following general (nonvascular) surgical procedures than following cardiac surgery, with a reported incidence in patients undergoing general anesthesia of less than 0.5 percent [4-6]. The risk may be slightly higher (1 percent) in asymptomatic patients with a carotid bruit who undergo general surgery [7].
There have been no randomized trials examining the use of prophylactic CEA in patients with carotid stenosis prior to general surgery. A retrospective review suggests that prophylactic CEA is probably not warranted in most patients with asymptomatic carotid disease [8]. This study was a chart review of 284 patients who had undergone nonvascular surgery requiring general anesthesia and had preoperative carotid ultrasound. While a previous history of stroke or TIA, a carotid bruit, or both were present in 250 patients, all were considered to have asymptomatic carotid stenosis [9]. Ten of 284 patients (3.5 percent) had perioperative ischemic strokes within 30 days of the index procedure, and 8 of 224 (3.6 percent) with >50 percent carotid stenosis had an ipsilateral perioperative stroke (bilateral lesions were present in three patients). While this stroke risk exceeds that of the general population and of patients with carotid bruits, the increased risk appears to be insufficient to mandate prophylactic CEA for asymptomatic carotid stenosis in the general surgical population.
Vascular procedures — Although there are no trials of prophylactic CEA prior to abdominal aortic aneurysm repair or other major peripheral vascular procedures, many vascular surgeons support performing prophylactic CEA in anticipation of a major vascular procedure that may involve significant hemodynamic fluctuations.
Endarterectomy in patients with intracranial aneurysm — Ipsilateral intracranial aneurysms that are distal to a cervical internal carotid artery stenosis may be susceptible to sudden hemodynamic changes associated with CEA leading to aneurysm rupture. On the other hand, surgical clipping of an aneurysm distal to a severe internal carotid stenosis may increase the risk of ischemic stroke.
Unfortunately, data are too sparse to allow firm conclusions as to which problem should be treated first. However, caution is advised if CEA is performed in this setting, especially if the ipsilateral aneurysm is ≥7 mm in diameter or if there is a history of subarachnoid hemorrhage from another aneurysm. (See "Unruptured intracranial aneurysms".)
Contraindications — With the advent of carotid stenting as an alternative to CEA, relative contraindications to CEA include the following:
- History of prior neck irradiation resulting in “woody infiltration” of the skin and subcutaneous tissues.
- Concurrent tracheostomy
- Prior radical neck dissection with or without radiation
- Contralateral vocal cord paralysis from prior endarterectomy
- Atypical lesion location, either high or low that is surgically inaccessible
- Severe recurrent carotid stenosis
- Unacceptably high medical risk (eg, unstable cardiac status) (see 'Perioperative risk assessment' below)
Patients with these conditions may be candidates for carotid artery stenting. (See "Carotid artery stenting and its complications".)
PREOPERATIVE EVALUATION — A thorough vascular history and physical examination are essential components of the evaluation of a patient being considered for CEA. A search should be made for evidence of atherosclerotic disease elsewhere, including abdominal aortic aneurysm and peripheral artery disease. (See "Screening for abdominal aortic aneurysm" and "Noninvasive diagnosis of arterial disease".)
Cardiac evaluation should be considered selectively since patients undergoing CEA are most likely to have morbidity that is related to coronary heart disease. This evaluation may be performed with exercise stress testing, dobutamine echocardiography, dipyridamole imaging, or, when warranted, coronary catheterization [10]. However, there is no evidence that immediate cardiac intervention alone reduces perioperative procedural risk of stroke or death for carotid endarterectomy. (See "Estimation of cardiac risk prior to noncardiac surgery", section on 'Noninvasive cardiac testing'.)
Perioperative risk assessment — Identification of risk factors for morbidity and mortality associated with CEA is important in order to avoid surgery in patients who may face unacceptably high risk for endarterectomy.
However, the data are conflicting regarding risk factors for morbidity following CEA. One or more of the following characteristics have been associated with an increased risk of poor outcome (stroke, myocardial infarction, or death) at 30 days after CEA in some [11-17] but not all [18-21] studies:
- Age 80 years or older
- Severe heart disease
- Severe pulmonary dysfunction
- Renal insufficiency or failure
- Stroke as the indication for endarterectomy
- Anatomic issues, including limited surgical access, prior cervical irradiation, prior ipsilateral CEA, and contralateral carotid occlusion (see 'Contraindications' above)
As already noted, a number of reports have NOT confirmed the independent association of these proposed risk factors with poor outcome after CEA [18,19,21-23]:
- One of the largest studies queried the database of the National Surgical Quality Improvement Program of the American College of Surgeons and analyzed a sample of 3949 patients who had CEA as the primary procedure in 2005 and 2006 [23]. Patients with one or more "high risk" factors (age >80 years, major cardiac disease or chronic obstructive pulmonary disease) made up 30 percent of the population. Neither the indication for CEA (symptomatic versus asymptomatic disease) nor anatomic risk factor status (eg, prior neck radiation therapy) was available in the database. The following observations were reported [23]:
- The 30-day stroke rate was similar for patients with and without "high risk" criteria (1.4 versus 1.7 percent). In contrast, the 30-day mortality was significantly higher for patients with "high risk" criteria (1.3 versus 0.4 percent). However, when individual "high risk" criteria were analyzed, only major cardiac disease was associated with a higher 30-day mortality; age >80 was not.
- In multivariate analysis, independent risk factors for stroke at 30 days were intraoperative transfusion, baseline hemiplegia, shorter height (likely a surrogate for smaller artery size), and increased intraoperative anesthesia time. Independent risk factors for 30-day mortality were baseline critical limb ischemia and poor functional status.
- A single center series of 2236 consecutive isolated CEA operations reported a 30-day stroke and death rate of 1.4 percent [22]. No single clinical variable was significantly associated with perioperative complications.
- Another single center study of 1370 consecutive CEAs found that patients with two or more risk factors had significantly higher mortality compared with those who had no risk factors [13].
Advances in perioperative management have led at least some surgeons to conclude that the proportion of patients with unacceptable risk is extremely small and continues to shrink [18,24]. Others have challenged the concept of a high-risk group of patients for CEA [21]. Modifications in surgical practice, refinement of anesthetic techniques, refinement and use of vasoactive medications in the perioperative period and the declining use of routine preoperative contrast angiography may all be driving a reduction in the perioperative complication rates for CEA [22]. In the series of 2236 CEAs discussed above, the investigators noted that morbidity and mortality in the last five years of the study compared with the previous five years had declined by 36 percent [22].
Patients deemed unfit for general anesthesia can undergo CEA with regional anesthesia, a technique that has shown equally good perioperative outcomes after CEA in patients with and without risk factors such as advanced age, diabetes, coronary artery disease, and contralateral internal carotid occlusion [25]. (See 'Choice of anesthesia' below.)
Preoperative imaging — Patients suspected of having carotid atherosclerosis are typically evaluated with carotid duplex ultrasound as the initial test to assess the severity and extent of carotid stenosis. Other useful noninvasive methods to assess the degree of stenosis of the internal carotid artery include computed tomography angiography, magnetic resonance angiography (MRA) and contrast enhanced magnetic resonance angiography. The utility of these noninvasive methods and cerebral angiography in the initial evaluation of carotid stenosis is discussed in detail separately. (See "Evaluation of carotid artery stenosis".)
In patients with a hemodynamically significant atherosclerotic lesion identified on duplex ultrasound, it remains controversial if further imaging is needed prior to endarterectomy in asymptomatic patients to verify the degree of stenosis or further evaluate arterial anatomy.
Duplex ultrasound — Some surgeons may feel the sensitivity of carotid duplex at their institution is not sufficient to reliably determine the degree of internal carotid artery stenosis [26,27]. In support of this point of view is a lack of uniformly applied, prospectively-validated criteria in some settings for quantifying the degree of internal carotid artery stenosis with duplex ultrasound. Against this point of view are the risks and costs associated with catheter-based angiography, the known tendency of MRA to overestimate the degree of stenosis, and CTA to potentially underestimate the degree of stenosis [28-30].
Experts in carotid ultrasound addressed this issue and developed consensus recommendations for using duplex-derived velocity and imaging parameters to quantify internal carotid artery stenosis with duplex ultrasound [31].
The recommendations are by consensus and it is suggested the utility of the recommendations be verified in individual vascular laboratories, and that these parameters should not replace duplex parameters that are locally well documented as providing accurate assessment of carotid stenosis. As such, it may be reasonable for the surgeon who has access to a certified vascular laboratory with ongoing quality assurance programs and staffed by registered vascular technologists to use duplex ultrasound as a sole imaging modality of the cervical internal carotid artery prior to performing carotid endarterectomy.
Other imaging — In the symptomatic patient, the preoperative evaluation should also include computed tomography (CT) or magnetic resonance imaging (MRI) of the brain to assess the degree of cerebral infarction, if any, and to exclude other disorders that might be responsible for symptoms (eg, subdural hematoma, tumor).
The added risk and costs of catheter-based arteriography probably outweigh the benefit of obtaining more anatomic detail. The Asymptomatic Carotid Atherosclerosis Study (ACAS) found a 1.6 percent incidence of stroke associated with routine arteriography, although the risk was less in other reports [32]. However, arteriography is the gold standard for evaluating intracranial atherosclerotic disease, which is present, to some degree, in 20 to 50 percent of patients with stenosis of the extracranial internal carotid artery.
In an analysis of a subset of patients from NASCET, the relative risk of stroke associated with intracranial atherosclerotic disease in medically-treated patients was 1.3 for extracranial stenosis <50 percent, and 1.8 for extracranial stenosis 85 to 99 percent [33]. CEA reduced this risk, suggesting that detection of intracranial atherosclerotic disease, particularly in those with moderate extracranial carotid stenosis, may help stratify patients into a group that is more likely to achieve benefit from CEA. Of the available noninvasive tests (ie, transcranial Doppler, CTA, MRA), CTA may be more accurate for identifying intracranial large artery stenosis. The diagnosis of intracranial stenosis is discussed elsewhere. (See "Intracranial large artery atherosclerosis", section on 'Diagnosis'.)
Laryngoscopy — Otolaryngologic examination, which may include laryngoscopy, should be performed in patients who have a residual vocal disturbance (tone change, hoarseness) after a prior neck surgery (eg, CEA, thyroid surgery). (See "Hoarseness in adults", section on 'Neurologic dysfunction'.)
PREOPERATIVE PREPARATION
Medication management
Aspirin — Antiplatelet therapy with aspirin reduces the risk of stroke of any cause in patients undergoing carotid endarterectomy (CEA) [34,35]. In addition, lower-dose aspirin (81 to 325 mg daily) is more effective than higher-dose aspirin (650 to 1300 mg daily).
- In a randomized, controlled trial involving 232 patients, aspirin 75 mg daily or placebo treatment was started preoperatively and continued for six months [36]. Patients assigned to aspirin had significantly fewer strokes at one month and six months than those assigned to placebo. However, this study was likely underpowered [37].
- The ACE trial randomly assigned 2849 patients scheduled for endarterectomy to aspirin at doses of 81, 325, 650, or 1300 mg daily [38]. Aspirin was started before surgery and continued for three months. At three-month follow-up, the primary end point (stroke, MI, vascular death) was significantly reduced in the lower-dose (81 or 325 mg daily) aspirin group compared with the higher-dose group (6.2 versus 8.4 percent).
Consensus guidelines from the American Academy of Neurology (AAN) and the American College of Chest Physicians (ACCP) recommend aspirin for symptomatic and asymptomatic patients undergoing CEA [37,39]. We recommend starting aspirin (81 to 325 mg daily) prior to CEA and continuing indefinitely in the absence of contraindications. (See "Antiplatelet therapy for secondary prevention of stroke".)
For patients taking extended release dipyridamole/aspirin combinations (eg, Aggrenox, Asasantin), the need to continue combination therapy depends upon the original indication. One study of 102 patients undergoing CEA found no significant difference in perioperative bleeding in patients taking dipyridamole/ASA (n = 39), dipyridamole/ASA plus dextran (n = 30) or dipyridamole/ASA plus clopidogrel (n = 33) [40]. There was also no difference in the number of postoperative microembolic signals as detected by transcranial Doppler. Given these results, it may be reasonable to allow patients who are placed on dual antiplatelet therapy for other indications to continue on these throughout the perioperative period. However, for patients on triple oral antithrombotic therapy (ASA, thienopyridine, oral anticoagulation), the management of warfarin is individualized. (See "Management of anticoagulation before and after elective surgery" and "Triple antithrombotic therapy in patients with cardiovascular disease".)
For patients who are allergic or sensitive to aspirin, clopidogrel can be used as an alternative agent. (See "Benefits and risks of aspirin in secondary and primary prevention of cardiovascular disease", section on 'Aspirin sensitivity' and "Antiplatelet therapy for secondary prevention of stroke".)
Statins — The use of statins in symptomatic patients undergoing CEA may be associated with improved outcomes. In a retrospective observational study of 3360 CEAs, statin use was associated with reduced in-hospital mortality and combined in-hospital ischemic stroke or death (adjusted odds ratio 0.25, 95% CI 0.07-0.90 and 0.55, 95% CI 0.32-0.95, respectively), but in-hospital cardiac outcomes were not significantly improved [41]. In contrast, statin use by patients with asymptomatic carotid stenosis was not associated with significantly different outcomes.
Similar results were reported in another retrospective study involving 1566 patients with symptomatic and asymptomatic disease who received statins for at least one week before CEA [42]. These findings require confirmation in randomized clinical trials.
Evidence is also emerging that statins may be of benefit in the perioperative period, and that this benefit might be lost if statins are discontinued. This issue is discussed elsewhere. (See "Perioperative medication management", section on 'Non-statin hypolipidemic agents'.)
Prophylactic antibiotics — We recommend administration of antibiotics prior to carotid endarterectomy to control surgical site infection due to the frequent use of prosthetic material (table 1). (See "Overview of control measures to prevent surgical site infection", section on 'Vascular surgery'.)
SURGICAL ANATOMY AND PHYSIOLOGY
Carotid artery — The left common carotid artery (CCA) originates from the aortic arch, whereas the right CCA originates from the innominate artery (figure 1). The CCA divides into the internal carotid artery (ICA) and external carotid artery (ECA) at the level of the superior border of the thyroid cartilage corresponding to the C3/C4 disc space. The vagus nerve is located posteriorly to the common carotid artery in most individuals, although it may be located anteriorly in 5 to 10 percent of cases.
External carotid artery — The ECA has multiple branches that supply the face and scalp and provide collateral circulation to the brain (figure 2). These branches include (caudal to cranial) the superior thyroid, lingual, facial, ascending pharyngeal, occipital, posterior auricular, maxillary, and superficial temporal arteries. The ascending pharyngeal artery arises very near the bifurcation of the carotid artery. In one anatomic study, the ascending pharyngeal artery originated from the ECA in 80 percent of specimens (56 percent medially, 44 percent posteriorly) [43]. In the other 20 percent, the ascending pharyngeal artery originated from the internal carotid artery (5 percent), carotid bifurcation (5 percent), occipital artery (5 percent), and a trunk common to the lingual and facial arteries (5 percent).
Internal carotid artery — The ICA normally has no branches in the neck (figure 3). The cervical segment of the internal carotid extends from the carotid bifurcation until it enters the carotid canal anterior to the jugular foramen. The internal carotid artery runs cranially within the carotid sheath and lies posterior and lateral to the external carotid artery beneath the medial border of the sternocleidomastoid muscle. In its distal (cranial) course, it passes beneath the hypoglossal nerve, the digastric muscle, the stylohyoid muscle, the occipital artery and the posterior auricular artery. More cranially, the styloglossus and stylopharyngeus muscles, the tip of the styloid process and the stylohyoid ligament, the glossopharyngeal nerve and the pharyngeal branch of the vagus nerve separate the internal from the external carotid artery.
Carotid baroreceptor — Baroreceptors are stretch-sensitive mechanoreceptors that respond to alterations in blood pressure. The carotid sinus baroreceptors are located within the adventitia of the origin of the internal carotid artery and are innervated by the sinus nerve of Hering, which is a branch of glossopharyngeal nerve. In response to low blood pressure, the nerve fibers decrease their firing rates stimulating the sympathetic nervous system and inhibiting of the parasympathetic nervous system via a centrally-acting mechanism. Carotid sinus reactivity may be altered in patients with carotid atherosclerosis. (See "Pathophysiology of symptoms from carotid atherosclerosis", section on 'Impaired vasoreactivity'.)
Patients display varying degrees of heart rate or blood pressure alterations during manipulation of the carotid bifurcation, carotid clamping or postoperatively following CEA [44]. Endarterectomy, removal of atheromatous debris and reconstruction of the carotid artery may increase tension on the carotid sinus baroreceptor increasing activity. The opposite is also possible if damage to the carotid sinus or sinus nerve occurs.
CHOICE OF ANESTHESIA — The use of general anesthesia for CEA or performing awake carotid surgery with local anesthesia (with or without cervical block) is generally decided by individual surgeon preference and patient characteristics and preference. Ideally, surgical and anaesthetic teams should be competent in both techniques because a patient might prefer, or there might be a medical reason to choose, one rather than the other [45]. The available evidence suggests that the choice of anesthetic technique has no significant impact on clinically important outcomes after CEA. Anesthetic techniques are discussed in detail elsewhere. (See "Overview of anesthesia and anesthetic choices", section on 'Types of anesthesia' and "Peripheral nerve block: Techniques", section on 'Superficial cervical plexus block'.)
A systematic review and meta-analysis of randomized trials comparing locoregional with general anesthesia identified ten trials that included 4335 operations of which 3526 were from the General Anesthesia versus Local Anesthesia (GALA) trial [46]. The primary outcome measure of the GALA trial was a composite of stroke (including retinal infarction), myocardial infarction (MI) or death between randomization and 30 days after surgery [45]. There was no statistically significant difference in the primary outcome between the local and general anesthesia groups (4.4 versus 4.8 percent). However, 9.5 percent of patients randomized to one arm received the opposite treatment. An as-treated analysis was performed removing the crossovers for the composite outcome (no differences) but individual outcomes (stroke, death, MI) were not assessed.
There was no difference between the groups (intention to treat) in the risk of postoperative stroke within 30 days of surgery, but locoregional anesthesia was associated with a trend towards decreased mortality, odds ratio (OR) 0.62 (95% CI 0.36-1.07). No significant differences were found for other measures including myocardial infarction, postoperative bleeding, pulmonary complications, or length of stay.
Blood pressure in the perioperative period is affected by the method of anesthesia. General anesthesia reduces blood pressure following induction often necessitating the use of pressor agents. Overall, the use of local anesthesia appears to be associated with fewer alterations in blood pressure compared with general anesthesia. (See 'Labile blood pressure' below.)
SURGICAL TECHNIQUE
Endarterectomy procedure — Carotid endarterectomy (CEA) is performed through a neck incision, either bordering the sternocleidomastoid muscle, or, more esthetically, with a transverse incision in a skin crease at the level of carotid bulb. For the latter incision, preoperative imaging and palpation of the neck will guide the surgeon to the optimal placement of the incision.
The underlying platysma muscle and subcutaneous tissues are divided, the carotid sheath exposed, and the internal carotid artery (ICA) is carefully identified and dissected. The extent of exposure of the artery is dependent upon the distribution of disease determined by intraoperative findings. Typically, dissection is needed from the common carotid artery (CCA) to a point distal to the bifurcation of the ICA and ECA that is beyond palpable ICA plaque to allow for clamping of normal soft artery.
After proximal and distal control of the artery is obtained, the patient is given a bolus of heparin, intravenously. Monitoring of the activated clotting time (ACT) is not usually needed owing to the short duration of carotid clamping, typically less than an hour. The internal, common, and external arteries are then clamped sequentially; the internal carotid artery is usually clamped first to prevent embolization. A longitudinal arteriotomy is performed below the level of the bifurcation and extended proximally and distally.
With general anesthesia and mandatory shunting, the shunt is placed after the vessel is opened and prior to the endarterectomy. For patients who are undergoing general anesthesia, some surgeons routinely place a carotid shunt while others used cerebral perfusion monitoring to guide the need for selective shunt placement. For these patients and those undergoing awake carotid endarterectomy using local anesthesia (with or without cervical block), the endarterectomy is often completed prior to the need to place a shunt, as indicated by brain monitoring. (See 'Carotid shunting' below and 'Assessing brain perfusion' below.)
The carotid plaque, which is consistently found at the carotid bifurcation and the origin of the internal carotid artery, is then freed and removed through a dissection plane developed in the layers of the deep media. Great care is taken to create a smoothly tapered transition between the endarterectomized portion of the artery and its normal distal extent. This maneuver avoids intimal flaps that might lead to arterial dissection after flow is reestablished.
After meticulous inspection of the endarterectomized surface to remove any residual plaque or debris, attention is directed at repair. Some surgeons choose to repair primarily, while others patch the artery with saphenous vein or prosthetic material such as polyester (eg, Dacron®), polytetrafluoroethylene (PTFE, eg, Gore-Tex®) or bovine pericardium. (See 'Patch angioplasty versus primary closure' below.)
Just prior to completion of the arterial closure, the carotid clamps are sequentially briefly released and re-clamped to back bleed (ECA, ICA) and forward flush (CCA) the vessel which is then irrigated and suctioned of any residual debris. After the suture line is completed, flow is restored first to the ECA, then to the ICA.
A topical hemostatic agent may be used over the suture line to slow any oozing of blood. In a retrospective analysis of 4587 patients in a regional registry, reversal of heparin with protamine was associated with a lower incidence of serious bleeding requiring reoperation (0.64 versus 1.7 percent) compared with no reversal, without increasing the risk of MI, stroke, or death [47]. Although a small Jackson Pratt drain can be placed, drains are generally not required if heparin is reversed. The platysma and skin are closed and the wound dressed.
A completion study to assess patency of the repair can be performed using duplex ultrasound or by performing a contrast arteriogram, depending on operator preference.
High access — More distal (cranial) access may be needed. As the internal carotid artery is dissected, the hypoglossal nerve will be seen to cross anteriorly. The nerve is isolated and gently retracted.
The ansa hypoglossus nerve, which innervates the strap muscles of the neck, is typically seen coursing along the carotid sheath. The ansa can be divided without clinically significant consequence when dissection needs to be carried more cranially. The posterior belly of the digastric muscle can also be divided. Subluxation of the jaw is rarely warranted.
Eversion endarterectomy — Eversion endarterectomy is a variant of carotid endarterectomy. The internal carotid is transected at its origin from the carotid bulb and then the artery everted, or turned inside-out, to create the exposure otherwise not afforded by a traditional vertical arteriotomy. This technique may be quicker to perform and a lower the incidence of restenosis has been reported in randomized trials in comparison with conventional endarterectomy [48-51]. Insertion of a shunt can be more difficult with this procedure since the plaque must be completely removed before shunt insertion.
Patch angioplasty versus primary closure — As noted above, some surgeons choose to repair to the carotid artery primarily, while others patch the artery with saphenous vein or prosthetic material. We prefer patch closure for all patients undergoing carotid endarterectomy (non-eversion).
The trials that have been performed suggest two benefits from use of a patch: a marked reduction in the frequency of ≥50 percent restenosis and a lower rate of ipsilateral stroke [52,53].
A systematic review of patch angioplasty versus primary closure during CEA was published in 2002 and updated in 2009 [53,54]. The review identified ten eligible randomized controlled trials involving 1967 patients undergoing 2157 operations. Many of the trials were limited by significant methodological flaws; most were small, and none could be analyzed on a true intention-to-treat basis because of losses to follow-up. The use of a patch is associated with:
- A reduction in the risk of ipsilateral stroke in the perioperative period (odds ratio (OR) 0.31, 95% CI 0.1-0.63 and long-term OR 0.32, 95% CI 0.16-0.63).
- A reduced risk of perioperative arterial occlusion (OR 0.18, 95% CI 0.08-0.41).
- Decreased restenosis during long-term follow-up in eight trials (OR 0.24, 95% CI 0.17-0.34). These results are more certain than those of the previous review since the number of operations and events have increased. However, the sample sizes are still relatively small, data were not available from all trials, and there was significant loss to follow-up.
- No significant correlation was found between use of patch angioplasty and the risk of either perioperative or long-term all-cause death rates.
In the prior metaanalysis, seven trials that compared different patch types showed no difference in the risk for stroke, death, or recurrent arterial stenosis during perioperative or one-year follow-up time points [54]. The only high-quality trial that compared use of Dacron® and PTFE in CEA found that Dacron® was associated with increased risk for perioperative stroke and increased risk for both perioperative and late recurrent stenosis, compared with PTFE [55,56]. The additional studies added in the updated review did not compare types of patch material [57,58]. Clearly, more data are needed to establish differences between various patch materials.
Very few arterial complications, including hemorrhage, infection, cranial nerve palsies and pseudo-aneurysm formation have been evaluated with patch compared with primary closure but the available data suggest no significant differences.
Assessing brain perfusion — The benefit derived from CEA is partially dependent upon low perioperative morbidity. Although 80 to 85 percent of patients tolerate clamping of the carotid artery without consequence, assessment of the ability of the collateral circulation via the circle of Willis should be performed in all patients who do not undergo mandatory shunting. Assessing cerebral perfusion in selectively shunted patients can be accomplished with a variety of methods that are determined in part by the type of anesthesia chosen. Methods that have been studied include awake monitoring, transcranial Doppler, somatosensory evoked potentials, raw electroencephalographic (EEG) monitoring, processed EEG monitoring, carotid stump pressure, jugular venous oxygen saturation and others. The most commonly used methods are discussed below. The author prefers EEG monitoring. (See 'Choice of anesthesia' above and 'Carotid shunting' below.)
Data from randomized trials on which neurologic monitoring method should be used to select patients for shunting are limited. A single trial comparing EEG to carotid stump pressure monitoring showed a benefit to EEG monitoring [59]. Other methods of assessing brain perfusion have not been evaluated in randomized trials.
Awake endarterectomy — Patients who undergo local/regional anesthesia can be followed clinically throughout the procedure by monitoring mental status, speech and extremity function. A disadvantage of awake surgery is that it is frequently uncomfortable for the patient and may necessitate urgent conversion to general anesthesia or urgent shunt placement.
A neurologic assessment is performed at the beginning of the procedure and repeated every ten to fifteen minutes during carotid dissection, immediately prior to carotid clamping and continuously during carotid clamping. Agitation, slurred speech, disorientation, and extremity weakness are indications for shunt placement. (See 'Carotid shunting' below.)
Clinical assessment of the patient undergoing awake carotid endarterectomy is consistently associated with the lower rates of shunt use. With awake carotid endarterectomy, a carotid shunt is needed in <5 percent of patients. In a metaanalysis of ten trials, five evaluated shunt use and found significantly less use for local anesthesia compared with general anesthesia (odds ratio 0.27, 95% CI 0.23-0.31) [46]. However, there were no significant differences in the rates of stroke or death.
EEG monitoring — When general anesthesia is used, raw EEG monitoring is more commonly used. A neurologist monitors the tracings during the course of the procedure for cerebral ischemia as indicated by the presence of theta and delta waves or disorganized rhythms that indicate the need for shunting [60]. (See 'Carotid shunting' below.)
Processed EEG monitoring (eg, bispectral index) has been used to correlate cerebral ischaemia with processed EEG monitor values [61-63]. Bispectral index monitoring for depth of anesthesia and normal BIS values during general anesthesia are presented elsewhere (table 2). (See "Awareness with recall following anesthesia", section on 'Brain monitoring'.)
In one study, bispectral index (BIS) monitoring used during awake carotid endarterectomy found that the percent reduction in BIS values from baseline was significantly greater in patients shunted on the basis of clinical neurologic status compared with non-shunted patients (14 versus 4 percent). No trials are available using processed EEG prospectively in patients undergoing general anesthesia.
Stump pressure — Although stump pressures have been used to determine the need for carotid shunting in the past, EEG monitoring is more commonly used in patients undergoing general anesthesia when mandatory shunting is not chosen.
Carotid stump pressures are obtained after clamping the proximal common and external carotid arteries. A needle attached to a transducer is introduced into the common carotid artery to obtain a waveform. Mean pressures greater than 30 to 50 mmHg imply adequate collateralization via the circle of Willis down the ipsilateral carotid artery. Lower stump pressures are an indication for shunt placement and higher pressures are associated with stroke rates <0.5 percent [64].
Critics of this technique caution that pressures are only obtained after initial clamping, and, therefore, represent a "snapshot" in time. In addition, the above criteria should be used with caution in patients who have suffered prior ipsilateral strokes since there is a poor correlation between adequate perfusion pressures and outcomes in this setting. The accuracy of the pressure in the face of a preocclusive (string) lesion may also be questionable.
Carotid shunting — Any patient who demonstrates evidence of cerebral ischemia by any of the monitoring techniques discussed above should be shunted. A temporary shunt is placed beyond the proximal and distal extent of the arteriotomy from the common to the internal carotid artery. Blood flows through the shunt providing continuous cerebral perfusion during the procedure. Neurologic reassessment is then performed.
Although some surgeons prefer to use carotid shunts routinely to avoid the need for intraoperative neurologic monitoring, it should be recognized that shunting is unnecessary in approximately 90 percent of patients and exposes patients to the risks of shunting that may include the following:
- Formation of an intimal flap during shunt insertion, resulting in arterial dissection
- Dislodgement of plaque emboli during vessel manipulation
- Air embolism due to bubbles in the shunt
On the other hand, surgeons who routinely shunt feel that shunt complications are more likely to occur when shunting is rarely performed and feel the advantages of routine shunting include:
- Minimization of the risks associated with shunt placement because the surgeon and surgical team are familiar with technique
- Cerebral flow is assured with a properly placed shunt without need for neurological monitoring (EEG, stump pressure, awake neurological examination)
Studies targeted at defining the best approach in this regard have been equivocal with respect to demonstrating any difference in important clinical outcomes, and given that there is no consensus, neurologic monitoring with selective shunting versus routine shunting has been largely a matter of surgeon preference [65-67]. Based on this study, some feel that if general anesthesia is needed, mandatory shunting is best.
A key question is whether shunting at all results in lower rates of perioperative stroke and other morbidity. A systematic review that identified three trials involving 686 patients found no significant differences in the rates of all stroke, ipsilateral stroke or death up to 30 days for patients that were routinely shunting compared with no shunting [68].
Similarly, there are insufficient data to support one type of carotid shunt over another [67]. Many shunts are available for use (Argyle™, Pruitt-Inahara, Brenner, Burbank, Sundt) and each have their advantages and disadvantages. The features (stiff versus flexible, inline Doppler, balloons for occlusion), and use of these shunts can be found on proprietary websites. The selection of a particular shunt by a vascular surgeon is based on their experience. Most vascular surgeons become comfortable using one particular shunt.
POSTOPERATIVE CARE — Upon recovering from anesthesia, a neurologic assessment is performed and repeated every hour during recovery.
Because blood pressure lability is common in the first 12 to 24 hours postoperatively, it is standard care for CEA patients to be placed in a monitored setting with an arterial line in place.
Labile blood pressure — Manipulation of the carotid bulb during carotid endarterectomy not infrequently results in hemodynamic instability intraoperatively and in the early postoperative period. Adequate cerebral perfusion pressure should be maintained during periods of hemodynamic instability to avoid low cerebral blood flow and cerebral ischemia.
Systolic blood pressure should be maintained between 100 to 150 mmHg in the postoperative period. Hypertension may increase the likelihood of neck hematoma or suture line disruption, while relative hypotension compared with the patient's baseline value will increase the likelihood of inadequate cerebral perfusion and potential thrombosis of the endarterectomy site. Hypotension is more likely to result in cerebral ischemia and neurologic deficits in those patients who also have intracerebral small vessel disease. Patients may require pressor or antihypertensive drips to maintain the target blood pressure. (See "Drug treatment of hypertensive emergencies", section on 'Nitroglycerin'.)
A systematic review identified nine trials that recorded blood pressure during and after carotid endarterectomy. Blood pressure dropped significantly in the general anesthesia group after induction of anesthesia and in one trial, more patients in the general anesthesia group had significant hypotension during or after the operation (25 versus 7 percent) [68]. The GALA trial found that more patients undergoing general anesthesia required manipulation of blood pressure compared with patients receiving local anesthetic (72 versus 54 percent) [45]. However, blood pressure responses intraoperatively and postoperatively are highly variable with hypertension and hypotension reported for local and general anesthesia.
Bleeding — Postoperative bleeding, resulting in neck hematoma, occasionally occurs after CEA. It is easy to underestimate the size of a neck hematoma and the patient can rapidly lose their airway. There must be a low threshold to reexplore the neck and search for a surgically correctable source of bleeding.
Close observation and judgment are critical in deciding when to open a neck wound and drain a hematoma. The airway may be lost if clinical signs such as hoarseness and stridor are relied upon. Diagnostic studies are generally not helpful in making this clinical decision. If there is any question about the significance of a hematoma, the patient should be returned to the OR for re-exploration
COMPLICATIONS — While a number of controlled trials have highlighted the patient population most likely to benefit from carotid endarterectomy (CEA), this operation is not without risk [69]. The perioperative mortality associated with CEA ranges from <0.5 to 3 percent. Mortality rates may be higher when this procedure is performed at non-tertiary care centers [70-72]. Surgeons are encouraged to keep accurate records of their individual stroke rates to ensure that standards are upheld. Low patient volume (<3 CEAs performed every two years) and a greater number of years since licensure of the surgeon are associated with worse outcomes following CEA [73].
The American Heart Association (AHA) consensus statement states that indications for surgery are proven in symptomatic patients in whom morbidity and mortality rates associated with CEA are less than 6 percent and in the asymptomatic patient when the rates are less than 3 percent [74,75]. These recommendations are, however, more than 10 years old and based upon data that are up to 20 years old. The AHA recommendations are under revision. Two large randomized trials likely reflect more accurately the contemporary risk of stroke or death following carotid endarterectomy:
- The European trial (International Carotid Stenting Study [ICSS]) randomly assigned patients to receive carotid endarterectomy or carotid stenting for treatment of symptomatic carotid stenosis [76]. The 120 day all-cause mortality for the 857 symptomatic patients in the endarterectomy group was 0.8 percent. The 120 day combined any stroke or procedural death rate was 4.2 percent.
- In North America, the Carotid Revascularization Endarterectomy versus Stenting Trial (CREST) reported combined results for symptomatic and asymptomatic patients [77]. In 1240 patients assigned to endarterectomy (47.3 percent asymptomatic), the 30-day death rate was 0.3 percent and the rate of any periprocedural (30-day) stroke or death or postprocedural ipsilateral stroke was 2.3 percent.
Myocardial infarction — The majority of deaths following CEA are due to cardiac events, placing emphasis on the appropriate cardiac workup and perioperative management in these patients. (See 'Perioperative risk assessment' above and "Perioperative myocardial infarction after noncardiac surgery".)
Postoperative stroke — Stroke is the second most common cause of death following CEA. The rate of perioperative stroke (30 day) associated with CEA ranges from less than 0.25 to more than 3 percent, with the experience of the surgeon again being important.
Multiple factors can contribute to postoperative stroke in patients who have undergone CEA. These include:
- Plaque emboli
- Platelet aggregates
- Improper flushing
- Poor cerebral protection
- Relative hypotension
However, neurologic changes in the patient after CEA must be considered secondary to thrombosis at the operative site until proven otherwise. Technical errors must be ruled out.
Evaluation and treatment — Evaluation of the CEA patient with new neurologic deficits varies among surgeons. Some advocate recovery room or intraoperative ultrasound to assess potential thrombosis, while others immediately return to the operating room and open the endarterectomy site for direct visual inspection.
The optimal time to heparinize the symptomatic postoperative patient is also controversial [78]. Some surgeons heparinize immediately upon suspicion of the diagnosis, while others first obtain a head CT to rule out hemorrhagic stroke. Head CT performed immediately after an embolic event is frequently normal; follow-up CT in a few days may reveal injury.
Percutaneous transluminal carotid angioplasty with stenting is an alternative therapy for elective treatment of carotid artery disease. Carotid stenting may also be effective for managing perioperative stroke after CEA, particularly if the cause is a flow-limiting dissection. As an example, one study evaluated 13 patients with major or minor neurologic complications after CEA who underwent emergency carotid angiography and stent placement [79]. The angiographic success was 100 percent and 11 patients had complete resolution of neurologic symptoms. In contrast, only one of five patients undergoing surgical reexploration had neurologic recovery. Stenting, however, is not considered standard for treatment of acute complications of carotid endarterectomy. (See "Carotid artery stenting and its complications".)
Intraarterial thrombolytic therapy, in highly selected cases, may be another treatment option in patients with a postoperative stroke proven by arteriography to be due to distal emboli that, presumably, occurred during the course of the endarterectomy. The rationale for the administration of tissue-type plasminogen activator (alteplase) in this setting is based upon trials in acute stroke in which benefit has been demonstrated if therapy is initiated within 4.5 hours in highly selected patients. (See "Reperfusion therapy for acute ischemic stroke".)
However, the incidence of intracranial hemorrhage in patients treated with thrombolytic therapy for acute stroke has been in the range of 6 percent [80]. Furthermore, it is not known if the results obtained from the intravenous systemic administration of alteplase can be extrapolated to localized intraarterial therapy.
Intraarterial thrombolysis for patients with postoperative stroke has only been described in case reports and retrospective studies and is, currently, experimental. There are, as yet, no controlled trials. Some neurologists advocate searching for distal thrombosis via arteriogram and, if found, proceeding with intraarterial thrombolytic therapy.
Hyperperfusion syndrome — The cerebral hyperperfusion syndrome is probably the cause of most postoperative intracerebral hemorrhages and seizures in the first two weeks after CEA. The clinical manifestations of hyperperfusion occur in only a small percentage of patients after carotid revascularization (from less than 1 to as high as 3 percent in various reports) [81-84].
The mechanism of hyperperfusion is related to changes that occur in the ischemic or low-flow carotid vascular bed. To maintain sufficient cerebral blood flow, small vessels compensate with chronic maximal dilatation.
After surgical correction of the carotid stenosis, blood flow is restored to a normal or elevated perfusion pressure within the previously hypoperfused hemisphere. The dilated vessels are thought to be unable to vasoconstrict sufficiently to protect the capillary bed because of a loss of cerebral blood flow autoregulation. Breakthrough perfusion pressure then causes edema and hemorrhage, which in turn results in the clinical manifestations.
The hyperperfusion syndrome is characterized by the following clinical features:
- Headache ipsilateral to the revascularized internal carotid, typically improved in upright posture, may herald the syndrome in the first week after endarterectomy.
- Focal motor seizures are common, sometimes with postictal Todd's paralysis mimicking post-endarterectomy stroke from carotid thrombosis.
- Intracerebral hemorrhage is the most feared complication, occurring in about 0.6 percent of patients after CEA, usually within two weeks of surgery [85].
Neuroimaging studies, including head CT and MRI with T2 or FLAIR sequences, typically show cerebral edema, petechial hemorrhages, or frank intracerebral hemorrhage. Post-revascularization ipsilateral cerebral blood flow (CBF) is markedly increased compared with preprocedure flow [86]. Ipsilateral CBF after revascularization may be two to three times that of homologous regions in the contralateral hemisphere [87]. However, hyperperfusion syndrome may develop in the presence of only moderate (20 to 44 percent) increases in ipsilateral cerebral blood flow, as measured by perfusion magnetic resonance imaging, and in the absence of increases in middle cerebral artery flow velocity, as measured by transcranial Doppler (TCD) [88].
The hyperperfusion syndrome appears to be more likely with revascularization of a high-grade (80 percent or greater stenosis) carotid lesion, and it may be more likely when CEA is performed after recent cerebral infarction [89]. Reduced CBF or cerebral vasoreactivity prior to CEA may also be a risk factor for postoperative hyperperfusion [90].
Transcranial Doppler techniques have been used to monitor flow velocities of the middle cerebral artery in order to predict the occurrence of hyperperfusion syndrome [91-93], but the utility of these methods for this indication is not clearly established.
Treatment — The best remedy for cerebral hyperperfusion is prevention. Strict control of postoperative hypertension is paramount. Systolic blood pressure must be maintained at or below 150 mmHg. Aggressive measures including intravenous labetalol, nitroprusside, and nitroglycerin may be necessary to achieve this goal. Therapy should begin at the time of restoration of internal carotid flow and be maintained vigilantly during the hospital stay and for the first 10 to 14 days postprocedure. Fortunately, most postoperative blood pressure lability resolves in the first 24 hours. (See 'Labile blood pressure' above.)
Seizures related to hyperperfusion are usually successfully treated with standard antiepileptic drugs such as phenytoin [94].
Intracerebral hemorrhage from hyperperfusion is often devastating. Hypertension must be strictly controlled and anticoagulant and antithrombotic drugs should be discontinued. For patients on aspirin, platelet transfusions may be useful to reverse the antiplatelet effect. (See "Clinical and laboratory aspects of platelet transfusion therapy".)
Nerve injury — A number of nerve injuries can complicate CEA:
- The vagus nerve, which usually lays posterolaterally in the carotid sheath, is identified during dissection of the carotid from the internal jugular vein and is at risk for injury.
- The recurrent laryngeal nerve branches of the vagus are distal to the area of carotid artery dissection; injury to this nerve may result in unilateral vocal cord paralysis. The occasionally nonrecurrent nerve places this branch at even higher risk.
- The facial nerve exits the stylomastoid foramen and courses along the inferior portion of the ear. The most common branch affected during CEA is the marginal mandibular branch, which may be damaged during improper or prolonged retraction. The resulting paresis of the lateral aspect of the orbicularis oris muscle may be exacerbated during bedside examination with a revealing asymmetric smile.
- The glossopharyngeal nerve is more cephalad than the extent of the typical neck dissection during CEA. A branch of this nerve, the nerve of Hering, has great clinical significance since it innervates the carotid sinus and is responsible for the bradycardic and hypotensive responses that may be seen with manipulation of this structure. Some surgeons anesthetize the carotid sinus with lidocaine to avoid this complication, which is typically manifested intraoperatively.
- Damage to the hypoglossal nerve, also identified routinely during a CEA, is the complication with which most are familiar. Injury to this nerve may result from inadvertent retraction or, rarely, transection; it results in tongue deviation to the side of injury.
- Branches of the trigeminal nerve may be transected during dissection, resulting in sensory loss in the area of distribution
- The ansa hypoglossus nerve innervates the strap muscles of the neck and is typically seen coursing along the carotid sheath. Unlike the other nerves, this nerve may be divided without clinically significant consequence.
- The superior laryngeal nerve is rarely injured during CEA. The internal branch supplies sensation to the larynx, while the external branch innervates the cricopharyngeal muscle. Changes in voice quality may result from nerve injury.
The vast majority of cranial nerve injuries associated with CEA resolve over the first few months after surgery, and the risk of permanent cranial nerve deficit is very low. Among the 1739 patients who had CEA in the European Carotid Surgery Trial (ECST), immediate motor cranial nerve injury occurred in 5.1 percent, all ipsilateral to the side of the operation [95]. By hospital discharge, the cranial nerve injury rate had declined to 3.7 percent, and the involved cranial nerves included hypoglossal (n = 27), marginal mandibular (n = 17), recurrent laryngeal (n = 17), accessory (n = 1), and Horner syndrome (n = 3). The rate of persistent cranial nerve injury at four-month follow-up declined to 0.5 percent. Duration of surgery longer than two hours was the only independent risk factor for cranial nerve injury.
Parotitis — Parotitis is an unusual complication after CEA that results from manipulation of the parotid gland during the procedure. For this reason, most surgeons use this landmark as the cephalad extent of their dissection.
FOLLOW-UP CARE — Following carotid endarterectomy, patients are typically discharged within one to three days. The most common delay in discharge is due to difficulties controlling blood pressure.
Wound care — The postoperative dressing is removed on the first postoperative day. If a drain has been placed, it should be removed as soon as possible in the postoperative period (day one or two) to decrease the potential for wound infection provided there is no significant drainage. Antibiotics are limited to perioperative prophylaxis. (See 'Prophylactic antibiotics' above.)
Duplex surveillance — Repeat duplex ultrasonography should be obtained three to six weeks following carotid endarterectomy to establish a new baseline for future comparison. Duplex surveillance is performed at six months and annually. More frequent intervals may be warranted if a contralateral stenosis is being observed.
CAROTID RESTENOSIS — Historical rates of carotid artery restenosis after CEA were as high as 20 percent [96]. Lower values (2.6 to 10 percent at five years) are reported in more contemporary series [1,97].
Pathology — The pathology of the restenotic lesion is related to the time of presentation after initial surgery [98].
"Early" restenosis is that which occurs within two to three years after CEA. Patients with early restenosis frequently have highly cellular and minimally ulcerated intimal hyperplasia, similar to that which occurs after angioplasty or with stent placement. As a result, there is a low likelihood of symptomatic embolization.
"Late" restenosis occurs more than two to three years after CEA and generally results from progression of atherosclerotic disease. It is frequently associated with irregular plaques that may serve as an embolic source.
Risk factors — Patients at increased risk for restenosis include those below age 65, smokers, and women, probably due to the smaller size of their carotid arteries [98,99]. Elevated creatinine has been associated with the development of early restenosis, and elevated serum cholesterol with late restenosis [97]. Lipid lowering drugs may be protective for both early and late restenosis [97], although this finding requires confirmation.
The cellular features of the atheroma at the time of CEA may predict the occurrence of restenosis. In a prospective study of 500 patients that examined target lesion atherosclerotic plaque composition from specimens obtained at carotid endarterectomy, both low macrophage infiltration and a small or absent lipid core were associated with an increased risk of restenosis at one year [100]. In another study of 150 patients, an abundance of smooth muscle cells and a scarcity of macrophages were seen in the primary lesion of those who had neointima development six months after surgery; in those who did not develop neointima, the lesions were rich in lymphocytes and macrophages [101].
Patch angioplasty appears to be associated with a decreased risk of long-term recurrent stenosis compared with primary closure (see 'Patch angioplasty versus primary closure' above) [54].
Reoperation — Once the diagnosis of restenosis has been made, a decision has to be made about the need for reoperation. This decision is not one to be made lightly since reoperative CEA may be associated with a significant incidence of complications, although the evidence is retrospective and conflicting. The following studies illustrate the range of perioperative complications reported for redo CEA:
- An earlier series described 69 patients (48 percent men, 66 percent symptomatic) who had 82 reoperative CEA procedures [102]. Nine patients had two reoperative CEAs and two patients had three reoperative CEAs for either bilateral recurrence or a second recurrence on the same side. The average time to presentation with recurrent carotid stenosis was 6.5 years. The incidence of postoperative stroke (4.8 percent), transient ischemic attack (7.3 percent), and hematomas (7.3 percent) was nearly twice as high as reported for a first CEA [102].
- In a series of 401 reoperative CEAs in 10 states in the United States, the 30-day combined risk of stroke or death from mid-1998 to mid-1999 was 5.7 percent [103].
- A subsequent series described 145 patients (56 percent men, 36 percent symptomatic) who had 153 reoperative CEA procedures [104]. The incidence of perioperative stroke (1.9 percent) and death (O) was very low. While the average time from primary to reoperative CEA was 6.1 years in this series, 41 percent of the cohort were patients with early (<2 years) restenosis, which is typically due to intimal hyperplasia and carries a low risk of symptomatic disease compared with late restenosis (see 'Pathology' above).
- A study of 31 patients who underwent carotid surgery for a secondary recurrent carotid stenosis required resection of the carotid and placement of an interposition graft in about 30 percent of the patients. No perioperative strokes were reported and peripheral nerve injury occurred in 10 percent of the patients [105]
An additional major concern is that there are no controlled studies establishing the efficacy of reoperative CEA in patients with restenosis. The presumed benefits of surgery in this group of patients are an extrapolation of the results of trials performed on patients at initial presentation.
PREDICTORS OF LONG-TERM OUTCOME — The predictors of long-term outcome after surgical therapy for atherosclerotic occlusive disease of the carotids were evaluated in one study of 1982 patients who underwent surgery at a single center and were followed for ≥25 years. Predictors of mortality included [106]:
- Age, with a relative risk of 1.51 for each 10 year increase in age
- Male sex, relative risk 1.58
- Diabetes mellitus, relative risk 1.48
- Systemic hypertension, relative risk 1.31
- Cigarette smoking, relative risk 1.13
Predictors of recurrence of symptoms or progression of disease were established by analysis of a subset of 886 patients who underwent one or more postoperative angiograms; these included [106]:
- Total cholesterol, with a relative risk of 1.13 for each 50 mg/dL (1.3 mmol/L) increase
- Systemic hypertension, relative risk 1.42
- Cigarette smoking, relative risk 1.47
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SUMMARY AND RECOMMENDATIONS
- The effectiveness of carotid endarterectomy (CEA) for moderate to severe asymptomatic or symptomatic carotid artery stenosis has been established by large randomized clinical trials. Prophylactic carotid endarterectomy in patients with asymptomatic carotid stenosis prior to non-cardiac surgery has no demonstrated benefit. For patients with indications for bilateral carotid endarterectomy, a staged rather that combined procedure is performed. (See "Management of symptomatic carotid atherosclerotic disease" and "Management of asymptomatic carotid atherosclerotic disease" and 'Introduction' above and 'Indications' above.)
- Prior to carotid endarterectomy for asymptomatic carotid stenosis, duplex ultrasound may be sufficient to reliably determine the degree of internal carotid artery stenosis and assess local anatomy when performed in a certified vascular laboratory using validated criteria. If these standards cannot be met, additional imaging to verify the degree of stenosis should be performed. (See 'Duplex ultrasound' above.)
- Prior to carotid endarterectomy, we recommend starting aspirin (81 to 325 mg daily) and continuing indefinitely (Grade 1B). For patients who are sensitive to aspirin, clopidogrel is an alternative agent. (See 'Aspirin' above.)
- For patients with symptomatic carotid stenosis, we suggest initiation of statin therapy prior to carotid endarterectomy (or maintenance in patients already being treated) (Grade 2B). The use of statins in symptomatic patients is associated with reduced morbidity and mortality following CEA. For patients with asymptomatic carotid stenosis undergoing CEA, statin therapy has not shown the same benefit but may be indicated for other medical reasons. (See 'Statins' above.)
- We recommend administration of antibiotics prior to carotid endarterectomy to reduce the risk of surgical site infection due to the frequent use of prosthetic material (Grade 1B). Antibiotics should be discontinued within 24 hours. (See 'Prophylactic antibiotics' above.)
- Carotid endarterectomy can be performed using general anesthesia or local anesthesia (with or without cervical block). Statistically significant differences for major endpoints (perioperative stroke, myocardial infarction, and death) have not been consistently shown for differing anesthetic approaches. The choice of anesthesia technique is largely dependent on the preferences of the patient, the anesthesiologist and the surgeon. (See 'Choice of anesthesia' above.)
- No one technique for plaque removal has been found to be superior over another with respect to the incidence of stroke, death or other morbidity. However, eversion endarterectomy appears to be associated with a reduced incidence of re-stenosis in the long-term. (See 'Endarterectomy procedure' above.)
- Prior to carotid artery clamping, the patient is systemically anticoagulated. At the completion of the procedure, we suggest reversal of heparin with protamine (Grade 2B). (See 'Endarterectomy procedure' above.)
- Following carotid plaque removal, we recommend patch closure of the carotid artery over no patch (Grade 1B). Carotid patch techniques are associated with decreased rates of stroke and carotid restenosis. No one patch material (synthetic, vein, bovine pericardium) has been shown to be superior over another.
- After the completion of the procedure, the patient’s neurologic status and blood pressure are carefully monitored. We keep the systolic blood pressure between 100 and 150 mmHg. Hypotension and hypertension are both associated with adverse outcomes. (See 'Postoperative care' above.)
- Complications following CEA include perioperative stroke, myocardial infarction, cerebral hyperperfusion syndrome, cranial nerve injury and parotitis. The cerebral hyperperfusion syndrome is probably the cause of most postoperative intracerebral hemorrhages and seizures in the first two weeks after CEA. The mechanism of hyperperfusion is related to loss of cerebral autoregulation. Patients complaining of severe ipsilateral headache (same side as CEA) within two weeks of CEA should be evaluated for hyperperfusion syndrome. (See 'Complications' above.)
ACKNOWLEDGEMENT — The authors and editors would like to thank Dr. James P Greelish for his contribution to previous versions of this topic review.
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