Your activity: 250 p.v.
your limit has been reached. plz Donate us to allow your ip full access, Email:

Complications of carotid endarterectomy

Complications of carotid endarterectomy
Jeffrey Jim, MD, MPHS, FACS
Section Editors:
John F Eidt, MD
Joseph L Mills, Sr, MD
Scott E Kasner, MD
Deputy Editor:
Kathryn A Collins, MD, PhD, FACS
Literature review current through: Nov 2022. | This topic last updated: Sep 27, 2022.

INTRODUCTION — The accepted indications for carotid endarterectomy (CEA) balance the long-term benefit of stroke reduction with the risk of perioperative complications, requiring overall morbidity and mortality rates associated with CEA to be low; otherwise, the intervention cannot be justified. Complications following CEA can be related to underlying cardiovascular disease or other comorbid conditions, or to the technique of performing carotid endarterectomy.

Postoperative complications of CEA, including myocardial infarction; perioperative stroke; postoperative bleeding; and the potential consequences of cervical hematoma, nerve injury, infection, and carotid restenosis, which may require repeat carotid intervention, are reviewed here. The indications for carotid intervention are reviewed separately. (See "Management of asymptomatic extracranial carotid atherosclerotic disease" and "Management of symptomatic carotid atherosclerotic disease" and "Carotid endarterectomy".)

GENERAL CONSIDERATIONS — The accepted indications for carotid endarterectomy (CEA) balance the long-term benefit of stroke reduction with the risk of perioperative complications, requiring that overall morbidity and mortality rates associated with CEA should be low (<6 percent in symptomatic patients, <3 percent in asymptomatic patients) to justify the intervention [1,2]. The morbidity and mortality rates used by the American Heart Association (AHA) to formulate recommendations for CEA are more than 10 years old and based upon data that are even older. Two large trials likely more accurately reflect the contemporary risk of stroke or death following CEA:

The European trial (International Carotid Stenting Study [ICSS]) randomly assigned patients to receive carotid endarterectomy or carotid stenting for treatment of symptomatic carotid stenosis [3]. 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 [4]. 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 (with a rate of 1.4 percent for the 587 asymptomatic patients and 3.2 percent for the 653 symptomatic patients) [5].

Appropriate perioperative medication management is important to reduce the risk of cardiovascular and procedure-specific complications. (See "Carotid endarterectomy", section on 'Preoperative preparation' and "Overview of carotid artery stenting", section on 'Medication management'.)

PERIOPERATIVE STROKE — Stroke is the second most common cause of death following carotid endarterectomy (CEA). Stroke rates associated with CEA in large trials are generally <3 percent for asymptomatic patients and <5 percent for symptomatic patients. Rates range from less than 0.25 percent to more than 3 percent depending upon the indication for CEA and other factors, including the experience of the surgeon [6-13].

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, early postoperative neurologic changes in the patient after CEA must be considered related to problems at the endarterectomy site (eg, thrombosis, intimal flap) until proven otherwise. Technical errors must be ruled out.

The optimal time to heparinize the postoperative patient with new neurologic symptoms is also controversial [14]. 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.

Evaluation and treatment — Evaluation and treatment of new neurologic deficits that occur immediately following CEA varies. It is important to assess the operative site for technical defects, rule out intracranial hemorrhage, and identify other treatable causes of acute cerebral ischemia (eg, middle cerebral artery embolus). How these are accomplished depends largely upon on the availability of resources, surgeon experience, and preferences. Surgeons with access to high-quality duplex ultrasound may prefer to obtain a study in the recovery room or in the operating room, while others immediately return the patient to the operating room to explore the wound and directly inspect the endarterectomy site. If ultrasound shows good flow throughout the carotid artery with no thrombosis or intimal flaps, a head computed tomography (CT) scan should be obtained to rule out intracranial bleeding. A CT angiogram of the head and neck can also be obtained to identify for any treatable vascular lesion (eg, distal large vessel embolus). For surgeons who have access to a hybrid operating room, another approach may be to obtain head CT first and, if no bleeding is identified, proceed with intraoperative arteriography to identify any correctable lesions. Any technical issues found at the endarterectomy site should be corrected with preferably open surgical technique.

Carotid artery 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 arteriography and stent placement [15]. The angiographic success was 100 percent, and 11 patients had complete resolution of neurologic symptoms. In contrast, only one of five patients undergoing surgical re-exploration had neurologic recovery. Stenting, however, is not considered standard for treatment of acute complications of carotid endarterectomy. (See "Overview of carotid artery stenting".)

If distal emboli are identified during the evaluation of a perioperative stroke, then considerations should be made to pursue further treatment. Due to the recent operation, systemic intravenous thrombolytic therapy is contraindicated. However, mechanical thrombectomy or intra-arterial thrombolytic therapy may be considered. At this time, there are no controlled trials evaluating the outcomes of these interventions in post-procedure stroke. As such, the consideration of these treatment options should depend on specific patient factors and circumstances and the decision to proceed made in conjunction with a neurologist and neurointerventionalist on a case-by-case basis. (see "Approach to reperfusion therapy for acute ischemic stroke")

Intra-arterial thrombolytic therapy, in highly selected cases, may be another treatment option for patients with a postoperative stroke proven by arteriography to be embolic, presumably occurring during the CEA. The rationale for the administration of tissue-type plasminogen activator (alteplase) in this setting is based upon trials in acute stroke for which a benefit has been demonstrated if therapy is initiated within 4.5 hours in highly selected patients. However, the incidence of intracranial hemorrhage in patients treated with thrombolytic therapy for acute stroke is approximately 6 percent [16]. Furthermore, it is not known if the results obtained from the intravenous systemic administration of alteplase can be extrapolated to localized intra-arterial therapy. Intra-arterial 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, and its use is therefore not justified. Nevertheless, some neurologists advocate searching for distal thrombosis via arteriogram and, if found, proceeding with intra-arterial thrombolytic therapy.

MYOCARDIAL INFARCTION — In randomized trials, myocardial infarction has occurred at a slightly higher rate for carotid endarterectomy compared with carotid artery stenting, with a reported incidence between 0 and 2 percent [3,4,17-19]. In one systematic review that collected data on over 60,000 patients who underwent CEA, the pooled absolute risk of perioperative (30 day) myocardial infarction was 0.87 percent [20]. Risk factors for myocardial infarction included older age, coronary heart disease, peripheral artery disease, and carotid restenosis. In the CREST trial, a periprocedural myocardial infarction was associated with an increased risk of death at 10-year follow-up [21]. (See "Evaluation of cardiac risk prior to noncardiac surgery" and "Perioperative myocardial infarction or injury after noncardiac surgery".)

HYPERPERFUSION SYNDROME — Cerebral hyperperfusion syndrome is an uncommon sequela of carotid endarterectomy (CEA) occurring in only a small percentage of patients after carotid revascularization (from less than 1 to as high as 3 percent in various reports) [22-25]. It 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 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. Hypertension is a frequent predecessor of the syndrome, underscoring the importance of good perioperative blood pressure control.

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 [26-29]. Reduced cerebral blood flow or cerebral vasoreactivity prior to CEA may also be a risk factor for postoperative hyperperfusion [30]. (See "Carotid endarterectomy", section on 'Risk factors for poor outcome'.)

Transcranial Doppler techniques have been used to monitor flow velocities of the middle cerebral artery in order to predict the occurrence of hyperperfusion syndrome [26,31-33], but the utility of these methods for this indication is not clearly established.

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 approximately 0.6 percent of patients after CEA, usually within two weeks of surgery [34].

Neuroimaging studies, including head computed tomography (CT) and magnetic resonance (MR) imaging with T2 or fluid-attenuated inversion recovery (FLAIR) sequences, typically show cerebral edema, petechial hemorrhages, or frank intracerebral hemorrhage. Postrevascularization ipsilateral cerebral blood flow (CBF) is markedly increased compared with preprocedure flow [35]. Ipsilateral CBF after revascularization may be two to three times that of homologous regions in the contralateral hemisphere [36]. 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) [37].

Treatment — The best management is prevention. Strict control of postoperative hypertension is important. Systolic blood pressure should be maintained at or below 150 mmHg. Aggressive measures (eg, intravenous beta blockers, nitroglycerin) may be necessary to achieve this goal. Treatment should begin at the time of restoration of internal carotid flow and be maintained during the hospital stay and for the first weeks postprocedure. Fortunately, most postoperative blood pressure lability resolves in the first 24 hours.

Any patient who complains of severe headache following CEA should be evaluated with head CT and potentially admitted for observation and blood pressure control. Seizures related to hyperperfusion are usually successfully treated with standard antiepileptic drugs such as phenytoin [38]. In addition to control of blood pressure, antithrombotic therapies should be discontinued. For patients on aspirin, platelet transfusions may be useful to reverse the antiplatelet effect. (See "Platelet transfusion: Indications, ordering, and associated risks", section on 'Platelet function disorders'.)

CERVICAL HEMATOMA — A postoperative neck hematoma can be catastrophic and result in abrupt loss of the airway. In the International Carotid Stenting trial, the overall incidence of severe hematoma following carotid endarterectomy was 3.4 percent. Hematoma was associated with cranial nerve palsy in 28 of 45 patients [39].

When a significant neck hematoma develops in the postoperative period, immediate return to the operating room and re-exploration of the neck wound is necessary and can be lifesaving.

The incidence of cervical hematoma following carotid endarterectomy (CEA) is higher for patients receiving antiplatelet therapy preoperatively or remaining on anticoagulant therapy postoperatively [39-43].

Reversal of intraoperative anticoagulation with protamine has reduced the incidence of serious bleeding that would require reoperation without a significant increase in other complications (eg, stroke, coronary events) [44].

Uncontrolled hypertension while awakening from anesthesia or in the postoperative period can also lead to hematoma formation. (See "Anesthesia for carotid endarterectomy and carotid stenting", section on 'Hematoma' and "Anesthesia for carotid endarterectomy and carotid stenting", section on 'Hemodynamic monitoring'.)

Significant bleeding is also more likely in patients who have undergone a combined CEA and coronary artery bypass graft (CABG), generally because of a coagulopathy. When these procedures are combined, the CEA is performed first, and the neck is packed and left open; CABG is then performed and, when completed, the neck wound is closed. In this way, the likelihood of achieving adequate hemostasis is maximized in these coagulopathic patients.


Frequency and distribution — Cranial nerve or other nerve injuries occur in approximately 5 percent of patients following carotid endarterectomy (CEA) [45-49]. The majority of cranial nerve injuries (CNIs) resolve after surgery, and the risk of permanent CNI is low at <1 percent [48,49]. Among the 1739 patients who underwent CEA in the European Carotid Surgery Trial (ECST), the rate of motor CNIs in the immediate postoperative period was 5.1 percent, but by hospital discharge, the CNI rate declined to 3.7 percent [49]. In the Carotid Revascularization Endarterectomy versus Stenting Trial (CREST), CNI was identified in 4.6 percent (53 of 1151) of patients. CNIs occurred in 5 percent of patients receiving general anesthesia and 0.9 percent of patients operated on under local anesthesia. The deficit resolved in 18 (34 percent) at one month and in 42 of 52 (81 percent) by one year. The group with CNIs had a negative effect in eating/swallowing parameters within the first month, but this resolved at one year [50]. In a review of 6878 patients from the Vascular Study Group of New England (VSGNE) database, the overall rate of nerve injury at discharge was 5.6 percent; 0.7 percent of patients had more than one nerve affected [48].

In the VSGNE study discussed above, the hypoglossal nerve was most frequently involved, occurring in 2.7 percent, followed the facial nerve at 1.9 percent, and the vagus nerve and glossopharyngeal nerve each at 0.7 percent [48]. This cited distribution of injuries was similar in the ECST, with injuries involving the hypoglossal nerve (27/1739), marginal mandibular nerve (a branch of the facial nerve; 17/1739), recurrent laryngeal nerve (a branch of the vagus nerve; 17/1739), accessory nerve (1/1739), and sympathetic chain injury leading to Horner syndrome (3/1739). Duration of surgery longer than two hours was the only independent risk factor for CNI. In the vascular registry study, patients who suffered a perioperative stroke had a significantly increased risk of CNI. Other factors that significantly increased the risk of CNI included urgent procedures (odds ratio [OR] 1.6, 95% CI 1.2-2.1), immediate re-exploration after closure under the same anesthetic (OR 2.0, 95% CI 1.3-3.0), and return to the operating room for a neurologic event or bleeding (OR 2.3, 95% CI 1.4-3.8). Redo CEA or prior cervical radiation were not associated with an increased risk.

In a meta-analysis combining 26 published studies between 1970 and 2015, CNI most frequently involved the vagus nerve (pooled incidence 3.99 percent) followed by the hypoglossal nerve (pooled incidence 3.79 percent). Fewer than 1 in 7 of the injuries were permanent [45]. The authors noted that the rates of cranial nerve injuries have significantly decreased over the 35-year study period. Furthermore, urgent procedures as well as return to the operating room were associated with an increased risk of nerve injury.

Specific nerves — The most commonly encountered nerves during CEA including the following:

Hypoglossal nerve — The hypoglossal nerve supplies motor function to the tongue. It is routinely identified during CEA with exposure of the distal internal carotid artery. Injury to this nerve is one of the more frequent cranial nerve injuries associated with CEA and can result from inadvertent retraction or, rarely, transection. On physical examination, hypoglossal nerve injury is manifested as tongue deviation toward the side of injury (ie, ipsilateral to the CEA).

Facial nerve/mandibular nerve — 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 ipsilateral to the CEA may be identified during bedside examination as an asymmetric smile with a drooped lip.

Vagus/laryngeal nerves — The vagus nerve, which usually lies posterolaterally in the carotid sheath, may be injured during dissection of the carotid from the internal jugular vein. The vagus nerve may be stretched, inadvertently clamped, or cut at this level, leading to hoarseness. The laryngeal nerves are branches of the vagus nerve (figure 1A-B). The recurrent laryngeal nerve is generally distal to the area of carotid artery dissection; however, a nonrecurrent right laryngeal nerve can occur (<1 percent; left side even rarer) crossing transversely from the vagus nerve and behind the common carotid artery, increasing its risk for injury during CEA. Injury to the recurrent laryngeal nerve results in unilateral vocal cord paralysis. The superior laryngeal nerve is rarely injured during CEA; the internal branch supplies sensation to the larynx, while the external branch innervates the cricothyroid muscle. Changes in voice quality may result from superior laryngeal nerve injury.

Glossopharyngeal nerve — 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, is clinically important since it innervates the carotid sinus and is responsible for the bradycardic and hypotensive responses that can be seen with manipulation of baroreceptors at this structure. Excessive dissection in the carotid bifurcation can injure this nerve branch.

Sympathetic nerves — Injury to the sympathetic nerves can result in Horner’s syndrome or, rarely, an entity called "first bite syndrome." Horner syndrome can be complete (miosis, ptosis, anhydrosis) or partial (no anhydrosis). (See "Horner syndrome".)

First bite syndrome is characterized by unilateral pain in the parotid region after the first bite of each meal felt to be due to sympathetic denervation of the parotid gland [51]. Local botulinum toxin injection is a potential treatment option. Only a handful of cases have been reported following CEA.


Surgical site/patch infection — Wound infections rarely occur following carotid endarterectomy (CEA), and, when they occur, most are superficial and self-limiting with antibiotic treatment. Although some proponents of primary repair cite reports of an increased incidence of infection when a prosthetic patch has been used, there are no definitive data to support this conclusion. Nevertheless, all patients undergoing CEA should receive antibiotic prophylaxis to prevent surgical site infection. (See "Carotid endarterectomy", section on 'Patch angioplasty versus primary closure' and "Carotid endarterectomy", section on 'Prophylactic antibiotics'.)

Most of the information regarding deep wound infections involving a carotid patch, which are rare, comes from small case series [52-62]. There are insufficient data to determine whether a specific type of nonautogenous carotid patch material is more prone to infection. Deep wound infection following CEA can present early or in a delayed fashion (85 months in one series) [52]. When these present early in the postoperative course, the patient typically has neck swelling and drainage from the neck incision, while those occurring later may present with a draining sinus tract or pulsatile neck mass indicative of a carotid pseudoaneurysm.

Initial management includes wound drainage and antibiotic therapy, which is initially empiric and directed at the most common organisms, Staphylococcus and Streptococcus, until definitive culture and sensitivity results are available. In one case series, 13 of 25 patients were successfully managed in a conservative manner [52]. However, if infection persists, patch excision is indicated with either carotid artery ligation, reconstruction with autogenous vein, or bypass [63].

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. The evaluation and management of parotitis is discussed elsewhere. (See "Suppurative parotitis in adults".)

CAROTID RESTENOSIS — Restenosis of the carotid artery after carotid endarterectomy (CEA) was reported in up to 20 percent of patients in early studies [64], although lower values (2.6 to 10 percent at five years) have been reported in later studies [53,65-80]. The pathology of the restenotic lesion is related to the time of presentation after initial surgery [81,82]. Most patients with restenosis are asymptomatic and are identified with routine follow-up carotid imaging.

"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 females (probably due to the smaller size of their carotid arteries) [76,81,83]. Elevated creatinine has been associated with the development of early restenosis and elevated serum cholesterol with late restenosis [84]. Lipid-lowering drugs may be protective for both early and late restenosis [84], 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 [85]. 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, whereas the lesions were rich in lymphocytes and macrophages in those who did not develop neointima [86].

Patch angioplasty appears to be associated with a decreased risk of long-term recurrent stenosis compared with primary closure [87]. (See "Carotid endarterectomy", section on 'Patch angioplasty versus primary closure'.)

Indications for reintervention — Once the diagnosis of restenosis has been established, a decision for or against reintervention needs to be made. There is variability in practice regarding who should be intervened upon for recurrent stenosis following carotid endarterectomy. For patients who have neurologic symptoms referable to the carotid with >50 percent stenosis and those with asymptomatic carotid restenosis >80 percent, we consider intervention. As with the primary intervention, reintervention should address management of ongoing risk factors (hypertension, hyperglycemia, smoking, hyperlipidemia). (See "Carotid endarterectomy", section on 'Medical risk assessment'.)

A systematic review identified 50 studies reporting on the indications for carotid intervention in patients with recurrent stenosis after CEA or carotid artery stenting (CAS). The majority (3478/3525) underwent CEA as the initial intervention [88]. Patients were generally treated when the degree of recurrent stenosis exceeded 80 percent. Just over one half (55 percent) of the patients were treated for any symptoms, but only 23 percent (444/1926) of symptomatic patients had documented ipsilateral symptoms. None of the studies reported whether the patients were evaluated for other sources of emboli. The remaining 45.3 percent of patients had asymptomatic restenosis. Reintervention was by redo CEA in 68 percent of patients and by CAS in 32 percent. The time to repeat intervention was significantly longer in patients with recurrent atherosclerosis, in asymptomatic patients, and in patients undergoing CEA.

Approach to reintervention — The best approach to intervention for restenosis when it is indicated has not been definitively established. As with selecting the best approach for index carotid intervention, each approach, carotid endarterectomy (CEA), transfemoral carotid artery stenting (TF-CAS), and transcarotid artery revascularization (TCAR) has its advantages and disadvantages.

Reoperative CEA may be associated with a significant incidence of complications, although much of the evidence is retrospective and conflicting, with some authors reporting good outcomes for redo surgery [89]. The following studies illustrate the range of findings reported for redo CEA:

An early series described 69 patients (48 percent men, 66 percent symptomatic) who had 82 reoperative CEA procedures [90]. 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) were nearly twice as high as reported for a first CEA [90].

A later series described 145 patients (56 percent men, 36 percent symptomatic) who had 153 reoperative CEA procedures [91]. The incidence of perioperative stroke (1.9 percent) and death (0) 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.

There are concerns that there are no controlled studies of redo carotid intervention in patients with restenosis. The presumed benefits of intervention in this group of patients are an extrapolation of the results of trials performed on patients at initial presentation, which generally have favored CEA. CAS is evolving to be the treatment of choice when intervention is deemed appropriate because recurrent lesions are typically smooth intimal hyperplasia amenable to percutaneous intervention, which also avoids complications related to repeat neck dissection. For relatively young patients, redo CEA may also appropriate.

Prior to the introduction of TCAR, one systematic review identified 59 studies involving 4399 patients who underwent redo carotid intervention for restenosis following CEA [92]. There were no significant differences in the perioperative (30 day) rates for mortality, stroke, or transient ischemic attack (TIA) when comparing redo CEA with TF-CAS performed for restenosis. Patients undergoing redo CEA had significantly increased incidence of cranial nerve injury compared with those undergoing CAS, but most patients recovered within three months. However, the risk of stenosis after intervention for restenosis was greater in TF-CAS patients compared with redo CEA patients. In a later review of patients who underwent intervention for restenosis (479 CEA, 653 transfemoral CAS), the primary endpoint of stroke and death for TF-CAS was also similar (2.7 and 2.3 percent) [93].

In reviews of the Vascular Quality Initiative (VQI) since the introduction of TCAR, TCAR for restenosis following CEA is associated with decreased risk of perioperative ischemic events compared with TF-CAS or redo CEA [65,94]. The later of these reviews identified 4425 patients operated on between September 2016 and April 2020 and who underwent redo CEA (21.8 percent), TF-CAS (40.4 percent), or TCAR (37.9 percent) after ipsilateral CEA [65]. Compared with redo CEA, TCAR was associated with lower risk of stroke/TIA (1.31 versus 3.53 percent) and stroke (1.02 versus 2.49 percent), which remained significant after adjustment for other risk factors. Mortality was not significantly different between the groups (0.54 percent and 0.42 percent, respectively). TCAR was also associated with lower risk of stroke/TIA compared with TF-CAS (1.3 versus 3.1 percent). Other differences between TCAR and TF-CAS were not significant after adjustment. Data regarding the risk for restenosis after TCAR either performed as the index operation or for restenosis following CEA are not available. However, although the technique for placement of the stent differs for TCAR compared with TF-CAS, once the stent is in place, any long-term problems seen with TF-CAS may also occur with TCAR.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Occlusive carotid, aortic, renal, mesenteric, and peripheral atherosclerotic disease".)


The accepted indications for carotid endarterectomy (CEA) balance the long-term benefit of stroke reduction with the risk of perioperative complications, which can be related to the technique of performing carotid endarterectomy or to underlying cardiovascular disease and other comorbid conditions. Postoperative complications diminish the overall long-term benefit of performing the procedure. (See 'Introduction' above and 'General considerations' above.)

Myocardial infarction occurs at a low rate (0 to 2 percent) following CEA. Stroke rates range from less than 0.25 to more than 3 percent depending upon the indication for CEA (asymptomatic, symptomatic) and other factors, including the experience of the surgeon. Although neurologic changes following CEA can be related to physiologic changes, or intracerebral etiologies, technical problems related to the carotid surgery must be identified and corrected. (See 'Myocardial infarction' above and 'Perioperative stroke' above.)

Cerebral hyperperfusion syndrome is an uncommon sequela of CEA. Risk factors include perioperative hypertension, high-grade carotid stenosis, and possibly recent cerebral infarction. The mechanism of hyperperfusion is related to loss of autoregulation that impairs the ability of the brain to accommodate to restored blood flow. Clinical manifestations may include headache, seizures, and stroke. The best management is prevention with strict control of postoperative hypertension through the first weeks postprocedure. (See 'Hyperperfusion syndrome' above.)

Cervical hematoma can become life-threatening due to airway compromise. The main risk factor for cervical hematoma is perioperative antithrombotic therapy. When a significant neck hematoma develops in the postoperative period, immediate return to the operating room and re-exploration of the neck wound is mandatory. (See 'Cervical hematoma' above.)

Nerve injuries can occur following CEA. The majority of cranial nerve injuries resolve after surgery, and the risk of permanent cranial nerve deficit is low. The most common nerves injured include the hypoglossal nerve, recurrent laryngeal (vagus nerve), and marginal mandibular branch of facial nerve. Risk factors for nerve injury include prolonged procedure duration, urgent procedure, the need for re-exploration (immediate or delayed), and perioperative stroke. (See 'Nerve injury' above.)

Wound infection rarely occurs following CEA, and when it occurs, most are superficial and self-limited, resolving with antibiotic therapy. Deep wound infections involving a carotid patch can present early or in a delayed fashion months after the procedure. Initial management includes wound drainage and empiric antibiotic therapy until definitive culture and sensitivity results are available. (See 'Infection' above.)

Carotid restenosis after CEA occurs in 2 to 10 percent of patients at five years. Early restenosis CEA is frequently a highly cellular intimal hyperplasia and minimally ulcerated with a low likelihood of symptomatic embolization, whereas late restenosis occurring more than two to three years after CEA is due to progression of atherosclerotic disease. Risk factors for restenosis include age <65, smoking, female sex, and possibly primary closure of the carotid artery at the time of CEA. Lipid-lowering drugs may be protective for both early and late restenosis. Treatment options for significant restenosis include repeat CEA, transfemoral carotid artery stenting, or transcarotid artery stenting. (See 'Carotid restenosis' above.)

ACKNOWLEDGMENTS — The UpToDate editorial staff acknowledges Emile R Mohler, III, MD (deceased), who contributed to an earlier version of this topic review.

The editorial staff at UpToDate also acknowledges Ronald M Fairman, MD, who contributed to an earlier version of this topic review.

  1. Moore WS, Barnett HJ, Beebe HG, et al. Guidelines for carotid endarterectomy. A multidisciplinary consensus statement from the Ad Hoc Committee, American Heart Association. Circulation 1995; 91:566.
  2. Biller J, Feinberg WM, Castaldo JE, et al. Guidelines for carotid endarterectomy: a statement for healthcare professionals from a Special Writing Group of the Stroke Council, American Heart Association. Circulation 1998; 97:501.
  3. International Carotid Stenting Study investigators, Ederle J, Dobson J, et al. Carotid artery stenting compared with endarterectomy in patients with symptomatic carotid stenosis (International Carotid Stenting Study): an interim analysis of a randomised controlled trial. Lancet 2010; 375:985.
  4. Brott TG, Hobson RW 2nd, Howard G, et al. Stenting versus endarterectomy for treatment of carotid-artery stenosis. N Engl J Med 2010; 363:11.
  5. Silver FL, Mackey A, Clark WM, et al. Safety of stenting and endarterectomy by symptomatic status in the Carotid Revascularization Endarterectomy Versus Stenting Trial (CREST). Stroke 2011; 42:675.
  6. Wu TY, Anderson NE, Barber PA. Neurological complications of carotid revascularisation. J Neurol Neurosurg Psychiatry 2012; 83:543.
  7. Hill MD, Brooks W, Mackey A, et al. Stroke after carotid stenting and endarterectomy in the Carotid Revascularization Endarterectomy versus Stenting Trial (CREST). Circulation 2012; 126:3054.
  8. Saedon M, Singer DR, Pang R, et al. Registry report on kinetics of rescue antiplatelet treatment to abolish cerebral microemboli after carotid endarterectomy. Stroke 2013; 44:230.
  9. Heyer EJ, Mergeche JL, Bruce SS, et al. Statins reduce neurologic injury in asymptomatic carotid endarterectomy patients. Stroke 2013; 44:1150.
  10. Faggioli G, Pini R, Mauro R, et al. Perioperative outcome of carotid endarterectomy according to type and timing of neurologic symptoms and computed tomography findings. Ann Vasc Surg 2013; 27:874.
  11. Sfyroeras GS, Bessias N, Moulakakis KG, et al. New cerebral ischemic lesions after carotid endarterectomy. Ann Vasc Surg 2013; 27:883.
  12. Barbetta I, Carmo M, Mercandalli G, et al. Outcomes of urgent carotid endarterectomy for stable and unstable acute neurologic deficits. J Vasc Surg 2014; 59:440.
  13. Goldberg JB, Goodney PP, Kumbhani SR, et al. Brain injury after carotid revascularization: outcomes, mechanisms, and opportunities for improvement. Ann Vasc Surg 2011; 25:270.
  14. Chamorro A, Vila N, Saiz A, et al. Early anticoagulation after large cerebral embolic infarction: a safety study. Neurology 1995; 45:861.
  15. Anzuini A, Briguori C, Roubin GS, et al. Emergency stenting to treat neurological complications occurring after carotid endarterectomy. J Am Coll Cardiol 2001; 37:2074.
  16. National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. Tissue plasminogen activator for acute ischemic stroke. N Engl J Med 1995; 333:1581.
  17. Liu ZJ, Fu WG, Guo ZY, et al. Updated systematic review and meta-analysis of randomized clinical trials comparing carotid artery stenting and carotid endarterectomy in the treatment of carotid stenosis. Ann Vasc Surg 2012; 26:576.
  18. Liu Z, Shi Z, Wang Y, et al. Carotid artery stenting versus carotid endarterectomy: systematic review and meta-analysis. World J Surg 2009; 33:586.
  19. Blackshear JL, Cutlip DE, Roubin GS, et al. Myocardial infarction after carotid stenting and endarterectomy: results from the carotid revascularization endarterectomy versus stenting trial. Circulation 2011; 123:2571.
  20. Boulanger M, Camelière L, Felgueiras R, et al. Periprocedural Myocardial Infarction After Carotid Endarterectomy and Stenting: Systematic Review and Meta-Analysis. Stroke 2015; 46:2843.
  21. Jones MR, Howard G, Roubin GS, et al. Periprocedural Stroke and Myocardial Infarction as Risks for Long-Term Mortality in CREST. Circ Cardiovasc Qual Outcomes 2018; 11:e004663.
  22. Youkey JR, Clagett GP, Jaffin JH, et al. Focal motor seizures complicating carotid endarterectomy. Arch Surg 1984; 119:1080.
  23. Reigel MM, Hollier LH, Sundt TM Jr, et al. Cerebral hyperperfusion syndrome: a cause of neurologic dysfunction after carotid endarterectomy. J Vasc Surg 1987; 5:628.
  24. Naylor AR, Ruckley CV. The post-carotid endarterectomy hyperperfusion syndrome. Eur J Vasc Endovasc Surg 1995; 9:365.
  25. Coutts SB, Hill MD, Hu WY. Hyperperfusion syndrome: toward a stricter definition. Neurosurgery 2003; 53:1053.
  26. Kablak-Ziembicka A, Przewlocki T, Pieniazek P, et al. Predictors of cerebral reperfusion injury after carotid stenting: the role of transcranial color-coded Doppler ultrasonography. J Endovasc Ther 2010; 17:556.
  27. Bouri S, Thapar A, Shalhoub J, et al. Hypertension and the post-carotid endarterectomy cerebral hyperperfusion syndrome. Eur J Vasc Endovasc Surg 2011; 41:229.
  28. Pennekamp CW, Tromp SC, Ackerstaff RG, et al. Prediction of cerebral hyperperfusion after carotid endarterectomy with transcranial Doppler. Eur J Vasc Endovasc Surg 2012; 43:371.
  29. Clagett, GP, Robertson, JT. Surgical considerations in symptomatic disease. In: Stroke: Pathophysiology, diagnosis and management, Barnett, HJM, Mohr, JP, Stein, BM, Yatsu, FM (Eds), Churchill Livingstone, New York 1998. p.1209.
  30. Hosoda K, Kawaguchi T, Ishii K, et al. Prediction of hyperperfusion after carotid endarterectomy by brain SPECT analysis with semiquantitative statistical mapping method. Stroke 2003; 34:1187.
  31. Powers AD, Smith RR. Hyperperfusion syndrome after carotid endarterectomy: a transcranial Doppler evaluation. Neurosurgery 1990; 26:56.
  32. Dalman JE, Beenakkers IC, Moll FL, et al. Transcranial Doppler monitoring during carotid endarterectomy helps to identify patients at risk of postoperative hyperperfusion. Eur J Vasc Endovasc Surg 1999; 18:222.
  33. Fujimoto S, Toyoda K, Inoue T, et al. Diagnostic impact of transcranial color-coded real-time sonography with echo contrast agents for hyperperfusion syndrome after carotid endarterectomy. Stroke 2004; 35:1852.
  34. Piepgras DG, Morgan MK, Sundt TM Jr, et al. Intracerebral hemorrhage after carotid endarterectomy. J Neurosurg 1988; 68:532.
  35. Sundt TM Jr, Sharbrough FW, Piepgras DG, et al. Correlation of cerebral blood flow and electroencephalographic changes during carotid endarterectomy: with results of surgery and hemodynamics of cerebral ischemia. Mayo Clin Proc 1981; 56:533.
  36. Kidwell CS, Saver JL, Mattiello J, et al. Diffusion-perfusion MRI characterization of post-recanalization hyperperfusion in humans. Neurology 2001; 57:2015.
  37. Karapanayiotides T, Meuli R, Devuyst G, et al. Postcarotid endarterectomy hyperperfusion or reperfusion syndrome. Stroke 2005; 36:21.
  38. Kieburtz K, Ricotta JJ, Moxley RT 3rd. Seizures following carotid endarterectomy. Arch Neurol 1990; 47:568.
  39. Doig D, Turner EL, Dobson J, et al. Incidence, impact, and predictors of cranial nerve palsy and haematoma following carotid endarterectomy in the international carotid stenting study. Eur J Vasc Endovasc Surg 2014; 48:498.
  40. Payne DA, Twigg MW, Hayes PD, Naylor AR. Antiplatelet agents and risk factors for bleeding postcarotid endarterectomy. Ann Vasc Surg 2010; 24:900.
  41. Comerota AJ, Difiore R, Tzilinis A, Chahwan S. Cervical hematoma following carotid endarterectomy is morbid and preventable: a 12-year case-controlled review. Vasc Endovascular Surg 2012; 46:610.
  42. Rosenbaum A, Rizvi AZ, Alden PB, et al. Outcomes related to antiplatelet or anticoagulation use in patients undergoing carotid endarterectomy. Ann Vasc Surg 2011; 25:25.
  43. Morales Gisbert SM, Sala Almonacil VA, Zaragozá García JM, et al. Predictors of cervical bleeding after carotid endarterectomy. Ann Vasc Surg 2014; 28:366.
  44. Stone DH, Nolan BW, Schanzer A, et al. Protamine reduces bleeding complications associated with carotid endarterectomy without increasing the risk of stroke. J Vasc Surg 2010; 51:559.
  45. Kakisis JD, Antonopoulos CN, Mantas G, et al. Cranial Nerve Injury After Carotid Endarterectomy: Incidence, Risk Factors, and Time Trends. Eur J Vasc Endovasc Surg 2017; 53:320.
  46. Tamaki T, Node Y, Saitoum N, et al. Vernet's syndrome after carotid endarterectomy. Perspect Vasc Surg Endovasc Ther 2013; 25:65.
  47. Grieff AN, Dombrovskiy V, Beckerman W, et al. Anesthesia Type is Associated with Decreased Cranial Nerve Injury in Carotid Endarterectomy. Ann Vasc Surg 2021; 70:318.
  48. Fokkema M, de Borst GJ, Nolan BW, et al. Clinical relevance of cranial nerve injury following carotid endarterectomy. Eur J Vasc Endovasc Surg 2014; 47:2.
  49. Cunningham EJ, Bond R, Mayberg MR, et al. Risk of persistent cranial nerve injury after carotid endarterectomy. J Neurosurg 2004; 101:445.
  50. Hye RJ, Mackey A, Hill MD, et al. Incidence, outcomes, and effect on quality of life of cranial nerve injury in the Carotid Revascularization Endarterectomy versus Stenting Trial. J Vasc Surg 2015; 61:1208.
  51. Wang TK, Bhamidipaty V, MacCormick M. First bite syndrome following ipsilateral carotid endarterectomy. Vasc Endovascular Surg 2013; 47:148.
  52. Stone PA, Srivastava M, Campbell JE, et al. A 10-year experience of infection following carotid endarterectomy with patch angioplasty. J Vasc Surg 2011; 53:1473.
  53. Léonore FT, Elsa F, David PC, et al. Short- and Long-Term Outcomes Following Biological Pericardium Patches Versus Prosthetic Patches for Carotid Endarterectomy: A Retrospective Bicentric Study. Ann Vasc Surg 2021; 72:66.
  54. Haddad F, Wehbe MR, Hmedeh C, et al. Bilateral Carotid Patch Infection Occurring 12 years Following Endarterectomy. Ann Vasc Surg 2020; 65:285.e11.
  55. Azouz V, Fahmy JN, Kornbau C, Petrinec D. Recurrent pseudoaneurysm after carotid endarterectomy. J Vasc Surg Cases Innov Tech 2019; 5:128.
  56. Fatima J, Federico VP, Scali ST, et al. Management of patch infections after carotid endarterectomy and utility of femoral vein interposition bypass graft. J Vasc Surg 2019; 69:1815.
  57. Hillman Terzian WT, Schadt S, Sheth SU. Right carotid-cutaneous fistula and right carotid pseudoaneurysm formation secondary to a chronically infected polyethylene terephthalate patch. Int J Crit Illn Inj Sci 2018; 8:48.
  58. Varetto G, Trevisan A, Barile G, et al. Carotid Pseudoaneurysm After Eversion Endarterectomy: A Case Report and Review of the Literature. Vasc Endovascular Surg 2018; 52:309.
  59. Xu JH, Altaf N, Tosenovsky P, Mwipatayi BP. Management challenges of late presentation Dacron patch infection after carotid endarterectomy. BMJ Case Rep 2017; 2017.
  60. Naylor R. Management of prosthetic patch infection after CEA. J Cardiovasc Surg (Torino) 2016; 57:137.
  61. Menna D, Ruggiero M, Speziale F. Infected pseudoaneurysm after carotid endarterectomy: mismatch between clinical presentation and origin. Ann Vasc Surg 2014; 28:740.e17.
  62. Le L, Charlton-Ouw K, Safi HJ, Azizzadeh A. Late expulsion of a Dacron patch after carotid endarterectomy. J Vasc Surg 2012; 56:1721.
  63. Mann CD, McCarthy M, Nasim A, et al. Management and outcome of prosthetic patch infection after carotid endarterectomy: a single-centre series and systematic review of the literature. Eur J Vasc Endovasc Surg 2012; 44:20.
  64. Zierler RE, Bandyk DF, Thiele BL, Strandness DE Jr. Carotid artery stenosis following endarterectomy. Arch Surg 1982; 117:1408.
  65. Elsayed N, Ramakrishnan G, Naazie I, et al. Outcomes of Carotid Revascularization in the Treatment of Restenosis After Prior Carotid Endarterectomy. Stroke 2021; 52:3199.
  66. Goodney PP, Nolan BW, Eldrup-Jorgensen J, et al. Restenosis after carotid endarterectomy in a multicenter regional registry. J Vasc Surg 2010; 52:897.
  67. Lal BK, Beach KW, Roubin GS, et al. Restenosis after carotid artery stenting and endarterectomy: a secondary analysis of CREST, a randomised controlled trial. Lancet Neurol 2012; 11:755.
  68. Hertzer NR, Bena JF. Patching plus extended exposure and tacking of the common carotid cuff may reduce the late incidence of recurrent stenosis after carotid endarterectomy. J Vasc Surg 2013; 58:926.
  69. Pavela J, Ahanchi S, Steerman SN, et al. Grayscale median analysis of primary stenosis and restenosis after carotid endarterectomy. J Vasc Surg 2014; 59:978.
  70. Chan RC, Chan YC, Cheung GC, Cheng SW. Predictors of restenosis after carotid endarterectomy: 17-year experience in a tertiary referral vascular center. Vasc Endovascular Surg 2014; 48:201.
  71. Li Q, Liu B, Zhao Y, et al. Echolucent carotid plaque is associated with restenosis after carotid endarterectomy. J Neurosurg 2020; 134:1203.
  72. Dakour-Aridi H, Mathlouthi A, Locham S, et al. Predictors of midterm high-grade restenosis after carotid revascularization in a multicenter national database. J Vasc Surg 2020; 71:1972.
  73. Edenfield L, Blazick E, Eldrup-Jorgensen J, et al. Outcomes of carotid endarterectomy in the Vascular Quality Initiative based on patch type. J Vasc Surg 2020; 71:1260.
  74. Jeong MJ, Kwon SU, Kim MJ, et al. Effects of patient age on outcomes after carotid endarterectomy: A retrospective, single-center study in Korea. Medicine (Baltimore) 2019; 98:e16781.
  75. Paraskevas KI, Gloviczki P. The jury is still out on optimal management of restenosis after carotid interventions. J Vasc Surg 2019; 70:339.
  76. Dulai M, Tawfick W, Hynes N, Sultan S. Female Gender as a Risk Factor for Adverse Outcomes After Carotid Revascularization. Ann Vasc Surg 2019; 60:254.
  77. Edenfield L, Blazick E, Healey C, et al. Long-term impact of the Vascular Study Group of New England carotid patch quality initiative. J Vasc Surg 2019; 69:1801.
  78. Okazaki T, Kanematsu Y, Shimada K, et al. A Single-center Retrospective Study with 5- and 10-year Follow-up of Carotid Endarterectomy with Patch Graft. Neurol Med Chir (Tokyo) 2019; 59:231.
  79. Texakalidis P, Tzoumas A, Giannopoulos S, et al. Risk Factors for Restenosis After Carotid Revascularization: A Meta-Analysis of Hazard Ratios. World Neurosurg 2019; 125:414.
  80. Texakalidis P, Giannopoulos S, Jonnalagadda AK, et al. Carotid Artery Endarterectomy versus Carotid Artery Stenting for Restenosis After Carotid Artery Endarterectomy: A Systematic Review and Meta-Analysis. World Neurosurg 2018; 115:421.
  81. Sadideen H, Taylor PR, Padayachee TS. Restenosis after carotid endarterectomy. Int J Clin Pract 2006; 60:1625.
  82. Fokkema M, de Borst GJ, Nolan BW, et al. Carotid stenting versus endarterectomy in patients undergoing reintervention after prior carotid endarterectomy. J Vasc Surg 2014; 59:8.
  83. Ladowski JS, Shinabery LM, Peterson D, et al. Factors contributing to recurrent carotid disease following carotid endarterectomy. Am J Surg 1997; 174:118.
  84. LaMuraglia GM, Stoner MC, Brewster DC, et al. Determinants of carotid endarterectomy anatomic durability: effects of serum lipids and lipid-lowering drugs. J Vasc Surg 2005; 41:762.
  85. Hellings WE, Moll FL, De Vries JP, et al. Atherosclerotic plaque composition and occurrence of restenosis after carotid endarterectomy. JAMA 2008; 299:547.
  86. Pauletto P, Puato M, Faggin E, et al. Specific cellular features of atheroma associated with development of neointima after carotid endarterectomy: the carotid atherosclerosis and restenosis study. Circulation 2000; 102:771.
  87. Bond R, Rerkasem K, Naylor AR, et al. Systematic review of randomized controlled trials of patch angioplasty versus primary closure and different types of patch materials during carotid endarterectomy. J Vasc Surg 2004; 40:1126.
  88. Bekelis K, Moses Z, Missios S, et al. Indications for treatment of recurrent carotid stenosis. Br J Surg 2013; 100:440.
  89. Coscas R, Rhissassi B, Gruet-Coquet N, et al. Open surgery remains a valid option for the treatment of recurrent carotid stenosis. J Vasc Surg 2010; 51:1124.
  90. Mansour MA, Kang SS, Baker WH, et al. Carotid endarterectomy for recurrent stenosis. J Vasc Surg 1997; 25:877.
  91. Stoner MC, Cambria RP, Brewster DC, et al. Safety and efficacy of reoperative carotid endarterectomy: a 14-year experience. J Vasc Surg 2005; 41:942.
  92. Tu J, Wang S, Huo Z, et al. Repeated carotid endarterectomy versus carotid artery stenting for patients with carotid restenosis after carotid endarterectomy: Systematic review and meta-analysis. Surgery 2015; 157:1166.
  93. Fokkema M, Vrijenhoek JE, Den Ruijter HM, et al. Stenting versus endarterectomy for restenosis following prior ipsilateral carotid endarterectomy: an individual patient data meta-analysis. Ann Surg 2015; 261:598.
  94. Chang H, Rockman CB, Veith FJ, et al. Outcomes of transfemoral carotid artery stenting and transcarotid artery revascularization for restenosis after prior ipsilateral carotid endarterectomy. J Vasc Surg 2022; 75:561.
Topic 15843 Version 20.0