Carotid Endarterectomy

Updated: Jul 22, 2022
Author: Omar Haqqani, MD; Chief Editor: Vincent Lopez Rowe, MD 



The objective of carotid endarterectomy (CEA) is to prevent strokes. In the United States, stroke is the fifth leading cause of death overall, and women have a higher lifetime risk of stroke than men do.[1] Among patients suffering a stroke, 50-75% had carotid artery disease that would have been amenable to surgical treatment.

Several prospective randomized trials have compared the safety and efficacy of CEA with those of medical therapy in symptomatic and asymptomatic patients. Data from these prospective trials have confirmed that CEA offers better protection from ipsilateral strokes than medical therapy alone in patients presenting with either symptomatic or asymptomatic carotid artery disease.


CEA should be considered for any patient with carotid artery stenosis in whom surgery will improve the natural history of the disease to a greater degree than the corresponding medical treatment would.[2]

In symptomatic good-risk patients with surgical morbidity and mortality (stroke and death) of less than 6%, proven indications for CEA include the following:

  • One or more transient ischemic attacks (TIAs) in the preceding 6 months and carotid artery stenosis exceeding 50% [3]

Acceptable but not proven indications include the following:

  • Ipsilateral TIA and carotid artery stenosis exceeding 70%, combined with required coronary artery bypass grafting (CABG)
  • Progressive stroke and carotid artery stenosis exceeding 70%

In asymptomatic good-risk patients treated by surgeons with surgical mortality and morbidity of less than 3%, the proven indication for CEA is stenosis exceeding 60%.[4]

The 2014 American Heart Association (AHA)/American Stroke Association (ASA) guidelines for the prevention of stroke in patients with stroke or TIA contained the following new or updated recommendations relevant to CEA[5] :

  • Carotid angioplasty and stenting (CAS) is indicated as an alternative to CEA for symptomatic patients at average or low risk for complications associated with endovascular intervention when the diameter of the lumen of the internal carotid artery is reduced by >70% by noninvasive imaging or >50% by catheter-based imaging or noninvasive imaging with corroboration and the anticipated rate of periprocedural stroke or death is < 6% (class IIa; evidence level B)
  • It is reasonable to consider patient age in choosing between CAS and CEA; for patients older than about 70 years, CEA may be associated with improved outcome CAS, particularly when the arterial anatomy does not favor endovascular intervention; for younger patients, CAS is equivalent to CEA in terms of risk for periprocedural complications and long-term risk for ipsilateral stroke (class IIa; evidence level B)
  • CAS and CEA in the above settings should be performed by operators with established periprocedural stroke and mortality rates of < 6% for symptomatic patients (class I; evidence level B)
  • Routine, long term follow-up imaging of the extracranial carotid circulation with carotid duplex ultrasonography is not recommended (class III; evidence level B)


CEA is contraindicated if the patient’s general condition includes a serious illness that will substantially increase perioperative risk or shorten life expectancy. It is also contraindicated in patients who present acutely with a major stroke or in patients who experienced a major devastating stroke with minimal recovery or a significantly altered level of consciousness.

The traditional teaching was that emergency CEA in an acutely occluded carotid artery might convert an ischemic cerebral infarct to a hemorrhagic infarct, possibly resulting in death. The timing of the operation was considered optimal when the patient reached optimal recovery before elective CEA was performed. However, a few reports of improved neurologic outcomes with early intervention in patients with acute nonhemorrhagic strokes have emerged.[6] Careful patient selection is essential.

In a study of perioperative and long-term outcomes after CEA in hemodialysis patients, Cooper et al found that the risks of CEA in asymptomatic dialysis-dependent patients were high, possibly outweighing the benefits.[7] They also found the risk to be high in symptomatic patients and suggested that it should be offered only to a small and carefully selected cohort of these patients.

Technical Considerations

A solid understanding of the anatomy of the carotid vessels and adjacent structures (see the image below) is critical for performing CEA effectively and minimizing complications.

Anatomy of internal carotid and vertebral arteries Anatomy of internal carotid and vertebral arteries.

The aortic arch provides the great vessels, including the innominate artery, the left common carotid artery (CCA), and the subclavian artery. In the most common configuration, the innominate artery branches into the right subclavian artery and the right CCA. Vertebral arteries branch off the subclavian arteries bilaterally.

On each side, the CCA travels within the carotid sheath before branching into the ipsilateral internal carotid artery (ICA) and external carotid artery (ECA). The ECA primarily supplies blood to the face and includes branches of the superior thyroid and ascending pharyngeal arteries. The ICA has no extracranial branches.

The carotid sinus is a baroreceptor located at the carotid bifurcation (where the CCA bifurcates into the ICA and the ECA) and is innervated by the nerve of Hering, a branch from cranial nerve IX (the glossopharyngeal nerve). The carotid bifurcation also contains the carotid body, which functions as a chemoreceptor responding to low oxygen levels or high carbon dioxide levels.

The ICA has an intracranial branch called the ophthalmic artery, which collateralizes and communicates with the external carotid blood supply. The ophthalmic artery is a common location for carotid emboli, which may result in transient monocular blindness (TMB) if they dissolve quickly or central retinal artery occlusion and blindness if they do not. The intracranial circle of Willis provides further communication between the ICA, the ECA, and the vertebrobasilar system.

For more information about the relevant anatomy, see Arterial Supply Anatomy, Arteries to the Brain and Meninges, and Circle of Willis Anatomy.


A 2020 Cochrane review found CAS for symptomatic carotid stenosis to be associated with a higher risk of periprocedural stroke or death than CEA, with most of the greater risk attributable to more frequent minor, nondisabling strokes in people older than 70 years.[8] Beyond the periprocedural period, CAS was as effective as CEA in preventing recurrent stroke; however, the combination of procedural safety and long-term efficacy in preventing stroke recurrence favored CEA. In people with asymptomatic carotid stenosis, CAS may be associated with a small increase in the risk of periprocedural stroke or death.

In a study of nationwide trends in CEA and CAS in the post-CREST (Carotid Revascularization Endarterectomy Versus Stenting Trial) era,[9] Cole et al found that when were matched for characteristics and illness severity, those undergoing CEA had a higher rate of perioperative stroke than those undergoing CAS; this difference was primarily among symptomatic patients. CEA was associated with lower procedure cost and readmission rate.

Schermerhorn et al compared in-hospital outcomes of patients undergoing transcarotid artery revascularization (TCAR; n = 1182) and CEA (n = 10,797), using the Society for Vascular Surgery (SVS) Vascular Quality Initiative TCAR Surveillance Project registry and the SVS Vascular Quality Initiative CEA database, respectively.[10] The primary outcome was a composite of in-hospital stroke and death. They found that despite a substantially higher medical risk in patients undergoing TCAR, in-hospital stroke/death rates were similar for the two procedures.


Periprocedural Care

Preprocedural Planning

Carotid artery disease may be either symptomatic or asymptomatic. Symptoms include transient ischemic attack (TIA), stroke, stroke in evolution, or crescendo TIA. In symptomatic patients, imaging should begin with carotid duplex ultrasonography (US). Carotid duplex imaging uses qualitative and quantitative information to determine the severity of carotid artery stenosis with an overall accuracy of 80-97%.

If duplex imaging demonstrates severe stenosis or ulcerative plaque that correlates with clinical symptoms, no further carotid imaging is required in most cases. In patients with mild-to-moderate disease (< 50%) on duplex imaging and hemispheric TIAs, alternative causes may be sought with magnetic resonance angiography (MRA), computed tomography (CT) angiography (CTA), or catheter-based angiography of the chest, neck, and brain. These advanced imaging techniques may also be indicated for operative planning in the following situations[11] :

  • Low carotid lesion (suggested by low common carotid artery [CCA] velocities)
  • High carotid lesion (above C2)
  • Previous carotid endarterectomy (CEA)
  • History of other major neck operation (eg, radical neck dissection, laryngectomy, or tracheostomy)
  • Cervical fusion
  • Poor neck mobility
  • Previous neck irradiation

A study by Qin et al suggested that low or high preoperative serum cortisol levels may adversely affect the stability of carotid plaque in patients with carotid artery stenosis who undergo CEA, and this effect may be associated with an increased risk of stroke.[12]

Patient Preparation


Patients undergoing CEA are kept on nil per os (nothing by mouth) status from midnight the day before surgery.

Regional anesthesia using deep or superficial cervical blocks is commonly performed and allows direct observation of the patient for signs of cerebral ischemia, thereby reducing the need for intraoperative carotid shunting. However, use of regional anesthesia is contraindicated if either the patient or the surgeon has issues with anxiety or communication. Local anesthetic techniques result in less blood pressure lability.

Overall morbidity and mortality are not significantly affected by the choice of anesthetic technique. Although the type of anesthesia used for CEA does not impact outcomes, regional anesthesia is associated with shorter operating times, anesthetic times, and time to discharge.[13]  In a 2021 Cochrane review, no difference in perioperative stroke or death was seen when regional and general anesthesia were compared for CEA.[14]

The main alternative to regional anesthesia in this setting is general anesthesia. General anesthesia has the advantage of reducing cerebral metabolic demand and increasing cerebral blood flow. Endotracheal intubation also provides good airway control and reduces patient and physician anxiety. Nasotracheal intubation can be used to facilitate exposure of the distal cervical segment of the internal carotid artery (ICA) in patients with high carotid artery stenosis or in patients undergoing reoperation.

Antiplatelet therapy should be continued throughout the perioperative period. Perioperative use of vasopressors or vasodilators to maintain blood pressure in the patient’s optimal physiologic range is critical.


The patient is placed in the supine position with the head turned away from the side of the operation. A beach-chair configuration offers greater comfort to awake patients and provides excellent exposure while decreasing venous pressure. The neck is moderately extended by placing a shoulder roll or by tilting back the neck extension of the bed.

The endarterectomy site is prepared and draped from the midline in an area encompassing the clavicle, the sternal notch, and the mandible. Proper lighting is essential, and loupe magnification is routine.

Monitoring & Follow-up

As a rule, if no complication occurs, patients are discharged home on postoperative day 1. They continue their antiplatelet and secondary preventative therapy.

At 2-6 weeks after CEA, carotid duplex US should be performed. If the findings from duplex imaging are satisfactory, another duplex study should be done 6 months to 1 year later, then every year thereafter. If there is evidence of moderate contralateral disease or recurrent carotid artery stenosis, scanning may be performed at intervals of 6-12 months.[15]

The 2018 guidelines from the Society for Vascular Surgery (SVS) recommended that after CEA, surveillance with duplex US should be carried out at baseline and every 6 months for 2 years and annually thereafter until the patient is stable.[16] The first duplex study should be done soon after the procedure (preferably ≤ 3 months) to establish a posttreatment baseline. Surveillance should be maintained at some regular interval (eg, every 2 years) for the life of the patient.

In the Carotid Revascularization Endarterectomy versus Stenting Trial (CREST), restenosis and occlusion occurred infrequently and rates were similar after CEA and carotid artery stenting (CAS) during 2 years of follow-up. Female sex, diabetes, and dyslipidemia independently predicted restenosis or occlusion after the two procedures, and smoking predicted an increased rate of restenosis in patients who underwent CEA but not in those who underwent CAS.[17]

In a retrospective review of SVS Vascular Registry database subjects who underwent CEA or CAS from 2004 to 2011, Geraghty et al found that the 30-day outcomes of both procedures were significantly affected by the type of symptom presentation.[18]  Presentation with stroke and TIA predicted higher rates of periprocedural complications, whereas TMB presentation with transient monocular blindness (TMB) predicted a periprocedural risk profile similar to that of asymptomatic disease.

Long-term data from the randomized International Carotid Stenting Study (ICSS) comparison of CAS and CEA in patients with symptomatic carotid stenosis indicated that the two procedures are comparable with respect to long-term functional outcome and risk of fatal or disabling stroke.[19]



Conventional Carotid Endarterectomy

The steps in a conventional carotid endarterectomy (CEA) are illustrated in the video below.

Carotid endarterectomy: operative techniques.


A cervical incision is made parallel and anterior to the sternocleidomastoid and centered over the carotid bifurcation. This incision can be extended proximally to the sternal notch for more proximal lesions of the common carotid artery (CCA) and distally to the mastoid process for higher exposure. Its upper end should be angled posterior to the earlobe to avoid the parotid gland and the greater auricular nerve. The incision is carried down through the platysma, and the sternocleidomastoid is retracted laterally with self-retaining retractors.

Exposure and mobilization

The internal jugular vein is visualized, and the carotid sheath is opened along the anterior border of the vein. The internal jugular vein is retracted laterally, and the common facial vein is ligated. Dissection is continued anterior to the CCA to keep from injuring the vagus nerve. The vagus nerve usually lies in a posterior lateral position within the carotid sheath but occasionally may spiral anteriorly, particularly in the lower end of the incision.

Attention should be paid to cranial nerves IX (glossopharyngeal nerve), X (vagus nerve), XI (accessory nerve), and XII (hypoglossal nerve), as well as the marginal mandibular branch of VII (facial nerve) and the rare nonrecurrent laryngeal nerve that comes directly off the vagus to innervate the vocal cords. This nerve can cross anterior to the carotid artery and can be mistaken for a part of the ansa cervicalis; if it is inadvertently divided, cord paralysis results. A nonrecurrent laryngeal nerve is most often noted on the right side of the neck.

The CCA is mobilized proximal to the carotid lesion. Dissection is continued upward to isolate the external carotid artery (ECA). The internal carotid artery (ICA) is mobilized up to a point where the vessel is completely normal.

Because the hypoglossal nerve may be injured by retraction, every effort should be made to minimize traction on this nerve. Mobilization of the hypoglossal nerve may require division of the tethering artery and vein to the sternocleidomastoid, the descending hypoglossal branch of the ansa cervicalis, or the occipital artery in order to expose the distal ICA.

Careful attention should also be given to the superior laryngeal nerve, which is usually located medial to the ICA. This nerve divides into external and internal branches that pass posterior to the superior thyroid artery and may be harmed while the surgeon is attempting to control either this vessel or the ICA. The glossopharyngeal nerve crosses the ICA near the base of the skull and is best protected by maintaining dissection close to the anterior surface of the ICA.

Excessive or prolonged retraction of the upper aspect of the incision may cause temporary compression injuries either to the greater auricular nerve laterally or to the marginal mandibular branch of the facial nerve medially.

In patients with a high carotid bifurcation or an extensive lesion, mobilizing the ICA distally can be achieved through several maneuvers, as follows:

  • The skin incision can be extended up to the mastoid process, with complete mobilization of the sternocleidomastoid toward its tendinous insertion on the mastoid process; care must be taken not to injure the accessory nerve, which enters the substance of the sternocleidomastoid at that level
  • The digastric muscle can be mobilized anteriorly or, if necessary, divided
  • If further exposure is needed, the styloid process can be transected, and the mandible can be subluxated anteriorly

Control of the CCA is obtained proximal to the level of disease by surrounding the vessel with an umbilical tape. If sinus bradycardia develops, 1-2 mL of 1% lidocaine is injected into the tissues of the carotid bifurcation to correct reflex sympathetic bradycardia. Once proximal control is obtained, dissection is continued distally around the ECA and its first branch, the superior thyroid artery. Subsequently, control is obtained distally at the ICA.

Throughout the dissection, it is important to minimize manipulation of the carotid artery so as to reduce the risk of embolization. Dissection must be carried out with extreme care taken to avoid injuring surrounding nerves, most notably the vagus and hypoglossal nerves. The ansa cervicalis, a branch of the hypoglossal nerve, may have to be divided to facilitate the dissection; this is acceptable.

Arteriotomy and shunting

Heparin (5000-7000 U) is administered intravenously (IV). The ICA, the CCA, and the ECA are occluded, in that order. An arteriotomy is made with a No. 11 blade, starting anteriorly on the CCA proximal to the lesion and extending cephalad through the plaque opposite the flow divider, then continued into the ICA with Potts scissors. Distal to the plaque, the arteriotomy is extended until it reaches a point where the ICA is relatively normal.

When general anesthesia is used without cerebral monitoring or when neurologic changes are noted during monitoring, a shunt is placed by inserting the distal end of the shunt into the normal ICA distal to the lesion. Back-bleeding the shunt clears any air or debris, and the proximal end of the shunt is then placed well into the CCA, proximal to the plaque.

Removal of plaque

The endarterectomy proper is begun with a Penfield elevator. The optimal endarterectomy plane is that between the inner and outer medial layers.

The proximal endpoint is obtained by sharply dividing the plaque in the CCA. The plaque can be elevated under full vision while the endarterectomy is continued into the carotid bulb. Carotid plaque that extends a short distance into the ICA may be teased medially toward the origin of the ECA to achieve an adequate endpoint. The plaque can also be divided in the bulb so that the ICA and ECA endarterectomies can be conducted independently.

Once the plaque is divided, the device (clamp or loop) used to control the ECA is loosened, and an eversion endarterectomy is performed. In the ICA, the divided plaque is feathered so that a smooth taper is achieved in the transition to the normal distal intima. If a smooth distal taper is not achieved, placement of interrupted 7-0 monofilament tacking sutures may be necessary to secure the endpoint.

After completion of the endarterectomy, all residual debris and medial fibers are excised because of their potential contribution to embolization or hyperplastic restenosis. The endarterectomy surface is irrigated with heparinized saline solution to facilitate visualization and removal of all debris. Before the clamps are removed, flushing must be done from each direction. The ICA is unclamped last.


As a rule, a conventional CEA is closed with a patch angioplasty. Although patch angioplasty closure is routine in all patient groups, its benefits are most apparent in women, patients with small ICAs, current smokers, and patients who have previously undergone ipsilateral carotid surgery. Various patch materials have been used with excellent results, including the following:

  • Autogenous saphenous vein
  • Internal jugular vein
  • Polytetrafluoroethylene (PTFE)
  • Dacron
  • Bovine pericardium

Double-armed 6-0 polypropylene sutures are typically used, though when PTFE patches are used, PTFE suture seems to reduce needle-hole bleeding.

Before closure is completed, heparinized saline solution is used to flush the ECA, the ICA, and the CCA. The shunt is removed, and the final few stitches are placed. Flow is then reestablished to the ECA and subsequently to the ICA. Complete hemostasis is obtained. In combined CEA–coronary artery bypass grafting (CABG) procedures, a closed suction drain is placed and is removed the following morning. The wounds are closed with subcuticular stitches.

Eversion Endarterectomy

Eversion CEA (eCEA) is an alternative to conventional CEA (see Eversion Carotid Endarterectomy). In an eCEA, preparation and exposure are identical to those in a conventional CEA, except that the carotid bifurcation and the ICA are more completely mobilized.

Instead of being opened with a longitudinal arteriotomy, the ICA is obliquely transected through the bifurcation in such a way as to include a small portion of the CCA. The endarterectomy is started from the cut end of the ICA; the artery is rolled back over the plaque, allowing the diseased intima and media to be removed intact.

The arteriotomy can be extended onto the CCA to allow removal of CCA plaque. The ICA is then anastomosed to the CCA in an end-to-side fashion. If the CCA arteriotomy was extended, a corresponding extension up the ICA will be necessary. Drawing the ICA down to the CCA to create an anastomosis effectively foreshortens the ICA and eliminates redundancy. This technique allows shunt placement, does not require patch angioplasty, and is ideal for patients with ICA redundancy.

Postoperative Care

Patients are awakened in the operating room, where the surgeon ensures that no neurologic deficit is present. They are then transferred to the recovery room and observed for approximately 6 hours. Postoperative care should include monitoring of the patient’s neurologic status, blood pressure control, and wound observation for hematoma.



Carotid baroreceptor stimulation after CEA may cause hypotension. Removal of the carotid plaque causes the carotid bulb to transmit increased arterial pulsation to the carotid sinus nerve, sometimes resulting in reflex bradycardia and hypotension.

Bradycardia during CEA is treated with local infiltration of lidocaine around the nerve and carotid sinus. Blocking the reflex arc by administering atropine sulfate while volume deficits are corrected frequently returns the blood pressure to the normal range. Postoperative pressor support may be necessary; if such support is required, it should last no longer than 6-24 hours in most patients.


Interference with the baroreceptor mechanisms of the carotid sinus may contribute to postoperative blood pressure fluctuation, as may cerebral renin production during carotid clamping and the use of halogenated fluorocarbon general anesthesia.

Adequate preoperative management of patients with hypertension is critical to minimize the deleterious effect on myocardial function and to decrease the incidence of neurologic deficit and hyperperfusion in these patients. Perioperative hypertension should be promptly treated with sodium nitroprusside or other vasoactive agents.

Wound hematoma

The incidence of wound hematomas requiring reoperation is lower than 1%. The use of antiplatelet agents and intraoperative heparin anticoagulation contribute to this bleeding risk. However, these agents are required to reduce the risk of coronary or cerebrovascular thrombotic events. A meta-analysis by Kakisis et al found that heparin reversal with protamine apparently lowered the risk of wound hematoma without increasing the risk of procedural stroke; however, they noted that further studies would be needed to confirm this finding.[20]

A large cervical hematoma may compress the ICA and adjacent cranial nerves; it also may compromise the airway and be a potential nidus of infection. Significant perioperative hematomas should be surgically drained.

Infection and false aneurysm

Wound infection after CEA is extremely rare. Infected false aneurysms occur at a rate of only 0.15%. Infected false aneurysms should be treated with excision of all infected vascular tissues and surrounding soft tissue infection. Ideally, the carotid circulation should be reestablished with an interposition vein graft.

When the carotid bifurcation is excised, the authors usually make no effort to reconstruct the ECA. In cases where reconstruction may be technically challenging (eg, prior neck irradiation or extensive infection), ligation and resection without reconstruction may be necessary. In such cases, the authors perform preoperative angiography with test balloon occlusion of the ICA with the patient awake to obtain information on the potential consequences of carotid ligation.

Cranial nerve dysfunction

The reported incidence of cranial nerve injury after CEA ranges from a few percent up to 39%. Approximately 60% of these injuries are symptomatic, mostly related to superior laryngeal and recurrent laryngeal nerve dysfunction. Hoarseness is the most common finding; fortunately, it is temporary in most cases.

In the Carotid Revascularization Endarterectomy vs Stenting Trial (CREST), cranial nerve injury occurred in 4.6% of the CREST patients who underwent CEA; however, there was a 80% rate of resolution at 1 year, and there was no statistical difference in health-related quality-of-life outcomes between patients who had cranial nerve injury and those who did not.[21]

Injury to vagus nerve and branches (recurrent and superior laryngeal nerves)

Injury to the vagus nerve or the recurrent laryngeal nerve can be caused by retractors or by direct trauma from the use of forceps, electrocauterization, or the application of arterial clamps. Paralysis of the ipsilateral vocal cord usually results in hoarseness and loss of an effective cough mechanism. Unilateral injury to the vagus nerve or recurrent laryngeal nerve can be asymptomatic but becomes significant when bilateral carotid reconstruction is planned.

Routine laryngoscopic visualization of the vocal cords is recommended when staged bilateral CEA is planned. The superior laryngeal nerve is responsible for the quality of the voice, especially higher pitches.

Injury to hypoglossal nerve

Mobilization of the hypoglossal nerve is commonly necessary, especially when a high carotid bifurcation is present. Division of small veins that tent the nerve downward, along with the branches of the ECA to the sternocleidomastoid, facilitates mobilization, as does division of the ansa cervicalis as it comes off the hypoglossal nerve. Injury to this nerve is manifested by deviation of the tongue to the ipsilateral side; on occasion, however, a mastication problem, deglutition, or speech impairment may be noted.

Injury to glossopharyngeal nerve

In a normal CEA dissection, the glossopharyngeal nerve usually is not seen; however, it can be injured when the dissection is continued upward because of a high carotid bifurcation or a high ICA lesion. This nerve can be injured with improper clamping, during division of the digastric muscle, or by mandibular subluxation and detachment of the styloid process during high carotid dissection. Injury causes paralysis of the middle pharyngeal constrictor muscle, and this may cause difficulty in swallowing solid foods.

Horner syndrome

Horner syndrome may be produced by injury to the ascending sympathetic fibers in the area of the glossopharyngeal nerve.

Injury to facial nerve branch

The marginal mandibular branch of the facial nerve can be injured when the incision is close to the jaw; more commonly, it may be injured by upward pressure of a retractor against the mandible. Trauma to this nerve causes sagging of the ipsilateral corner of the mouth. Injury can be prevented by curving the upper portion of the incision toward the mastoid process and by using retractors carefully, with intermittent release of tension.

Hyperperfusion and cerebral hemorrhage

The classic presentation of hyperperfusion and cerebral hemorrhage syndrome is unilateral headache, seizure, and cerebral hemorrhage, peaking at postoperative days 2-7. The incidence of hyperperfusion is 2-3%, which progresses to cerebral hemorrhage in 0.2-0.8% of cases.[22] This serious complication can be minimized by good preoperative blood pressure control and staged treatment of severe bilateral stenosis.



Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Antidysrhythmics, Ib

Class Summary

Antidysrhythmic Ib agents increase the electrical stimulation threshold of the ventricle by suppressing automaticity of conduction.

Lidocaine hydrochloride (Xylocaine)

Lidocaine hydrochloride is a class IB antiarrhythmic that increases the electrical stimulation threshold of the ventricle, suppressing the automaticity of conduction through the tissue.

If sinus bradycardia develops, 1-2 mL of 1% lidocaine is injected into the tissues of the carotid bifurcation to correct reflex sympathetic bradycardia.

Anticoagulants, Cardiovascular

Class Summary

Anticoagulants are required to reduce the risk of coronary or cerebrovascular thrombotic events.


Heparin (5000-7000 U) is administered intravenously (IV). Heparin augments activity of antithrombin III and prevents conversion of fibrinogen to fibrin. It does not actively lyse but is able to inhibit further thrombogenesis. It prevents recurrence of a clot after spontaneous fibrinolysis.

Antiplatelet Agents

Class Summary

These agents can be considered to help prevent future ischemic strokes. As with anticoagulation, aspirin is of unproven benefit in moyamoya disease; its use is considered empirical.

All patients resume their antiplatelet drugs, primarily aspirin, immediately after surgery; clopidogrel is given if aspirin is contraindicated. Maximal medical therapy, including statins and beta blockers, should be given.

Aspirin (Ecotrin, Ascriptin Maximum Strength, Ascriptin, Bayer Aspirin)

Aspirin's efficacy in preventing stroke relies on the inhibitory effect of aspirin on platelet function. This presumably helps to prevent thrombus formation and propagation.

Clopidogrel (Plavix)

Clopidogrel selectively inhibits adenosine diphosphate (ADP) binding to platelet receptor and subsequent ADP-mediated activation of glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation.

Clopidogrel may have a positive influence on several hemorrhagic parameters and may exert protection against atherosclerosis, not only through inhibition of platelet function but also through changes in the hemorrhagic profile.


Questions & Answers


What is the efficacy of carotid endarterectomy (CEA) for the prevention of stroke in patients with carotid artery disease?

Which patients should consider carotid endarterectomy (CEA)?

What are the indications for carotid endarterectomy (CEA)?

What are the AHA/ASA guidelines for use of carotid endarterectomy (CEA) in stroke prevention?

What are the contraindications for carotid endarterectomy (CEA)?

What is the anatomy relevant to performing carotid endarterectomy (CEA)?

Periprocedural Care

What is the role of imaging in preprocedural planning for carotid endarterectomy (CEA)?

How do preoperative serum cortisol levels affect the outcome of carotid endarterectomy (CEA)?

How is anesthesia administered for carotid endarterectomy (CEA)?

How is the patient positioned for carotid endarterectomy (CEA)?

What is included in monitoring and follow-up care after carotid endarterectomy (CEA)?


What video demonstrates the steps in a conventional carotid endarterectomy (CEA)?

How is the initial incision made in a carotid endarterectomy (CEA)?

What is the steps for exposure and mobilization in a conventional carotid endarterectomy (CEA)?

How is the internal carotid artery (ICA) mobilized in conventional carotid endarterectomy (CEA) in patients with a high carotid bifurcation or an extensive lesion?

How is control of the common carotid artery (CCA) maintained during a conventional carotid endarterectomy (CEA)?

How is arteriotomy and shunting accomplished during a conventional carotid endarterectomy (CEA)?

How is plaque removed in a conventional carotid endarterectomy (CEA)?

How is a conventional carotid endarterectomy (CEA) closed?

What is eversion carotid endarterectomy (eCEA)?

What is the postoperative care for carotid endarterectomy (CEA)?

What causes hypotension during carotid endarterectomy (CEA) and how is it managed?

What caused hypertension following carotid endarterectomy (CEA) and how is it treated?

What are the risk factors for wound hematoma following carotid endarterectomy (CEA)?

What causes infected false aneurysms from carotid endarterectomy (CEA)?

What is the prevalence of cranial nerve injury after carotid endarterectomy (CEA)?

What causes injury to the vagus nerve or the recurrent laryngeal nerve during carotid endarterectomy (CEA)?

What causes injury to hypoglossal nerve during carotid endarterectomy (CEA)?

What causes injury to glossopharyngeal nerve during carotid endarterectomy (CEA)?

What causes Horner syndrome during carotid endarterectomy (CEA)?

What causes injury to facial nerve branch during carotid endarterectomy (CEA)?

What are the signs and symptoms of hyperperfusion and cerebral hemorrhage following carotid endarterectomy (CEA)?


What are the goals of drug treatment during carotid endarterectomy (CEA)?

Which medications in the drug class Antiplatelet Agents are used in the treatment of Carotid Endarterectomy?

Which medications in the drug class Anticoagulants, Cardiovascular are used in the treatment of Carotid Endarterectomy?

Which medications in the drug class Antidysrhythmics, Ib are used in the treatment of Carotid Endarterectomy?