Figure 89-5. A carotid angiogram with digital subtraction angiography reveals a patch repair after prior endarterectomy.

Timing of intervention after stroke continues to be debated. Traditionally, surgeons waited >6 weeks

prior to intervention but there is a chance of recurrent stroke which is highest in the short term.

Performing the surgery too soon can also have devastating consequences such as hemorrhagic

conversion of an ischemic lesion. In patients that have returned to baseline from their symptoms, the

current thought is to undergo surgery somewhere between around 2 days and 2 weeks after the event.17

If the patient doesn’t return to normal or has a dense lesion on imaging, it is best to wait a few weeks.

Crescendo TIA and evolving stroke are different entities and although the risk of stroke with

intervention is slightly higher, urgent revascularization is warranted to prevent a large stroke.

ASYMPTOMATIC

4 Treatment for patients with symptomatic disease is well established in the literature, however, the

treatment of asymptomatic carotid disease is not so clear-cut. Detection of a carotid stenosis is typically

based on a DUS finding or evidence of a carotid bruit. The rate of neurologic symptoms with an

asymptomatic bruit was estimated to be 4% per year.18 One of the first and most important trials

regarding asymptomatic patients was the Asymptomatic Carotid Atherosclerosis Study (ACAS) trial. In

ACS, asymptomatic patients with >60% stenosis were randomly assigned to either medical

management or CEA. After 5 years, best medical therapy was found to be inferior to surgery in regard

to ipsilateral CVA (11% for medical management vs. 5.1% for CEA over 5 years). Therefore with

endarterectomy, there was a risk reduction in stroke of 53%.19 In Europe, the Asymptomatic Carotid

Surgery Trial (ACST) showed similar results, with a benefit in patients undergoing surgery over medical

management in patients with ≥60% stenosis.20 The biggest benefit comes from severe stenosis and it is

generally accepted that surgical intervention be pursued for stenosis ≥80%, with 60% to 79%

remaining controversial. Antiplatelet therapy is also recommended in the form of aspirin for

asymptomatic stenosis.21 There does not appear to be a benefit to the addition of clopidogrel.22 Best

medical management with risk factor modification is mandatory for all patients with severe carotid

stenosis, whether symptomatic or asymptomatic. Currently, several clinical trials are comparing carotid

intervention versus best medical management for the treatment of asymptomatic carotid stenosis.

CAROTID ENDARTERECTOMY VERSUS CAROTID STENTING

The choice for intervention in symptomatic (>50% stenosis) and asymptomatic (>80% stenosis)

patients is currently widely accepted. The next decision is to which treatment modality should be

undertaken. CEA traces back to the 1950s and is considered the gold standard for the surgical treatment

of occlusive carotid artery stenosis. Since the Food and Drug Administration (FDA) approved CAS in

2004, there was a proliferation of the technology and use for the treatment of symptomatic and

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asymptomatic carotid disease. High-risk patients from an anatomic or medical reason, as well as elderly

patients were thought to benefit from CAS over CEA. The Stenting and Angioplasty with Protection in

Patients at High Risk for Endarterectomy (SAPPHIRE) trial examined CAS versus CEA for high-risk

patients (medical comorbidities and anatomical features), and CAS was associated with a lower risk of

major events at 1 year, with a greater advantage in asymptomatic patients.23 The Endarterectomy

Versus Angioplasty in Patients with Symptomatic Severe Carotid Stenosis Trial (EVA-3S) trial was a

European trial for symptomatic patients with >60% stenosis that was stopped prematurely due to

higher 30-day stroke risk with CAS. However, embolic protection device was optional and its use was

associated with similar results to CEA.24 The Stent-Supported Percutaneous Angioplasty of the Carotid

Artery versus Endarterectomy trial (SPACE) trial examined patients with ≥70% symptomatic stenosis

failing to prove noninferiority of CAS to CEA.38 Most recently, the Carotid Revascularization

Endarterectomy versus Stenting Trial (CREST) examined CAS versus CEA in standard-risk patients for

both symptomatic and asymptomatic patients. Overall, there was no difference between CAS and CEA

long-term, but this was likely due to a higher rate of MI with CEA, and a higher rate of periprocedural

CVA with CAS. Despite the similar rate of complications overall, stroke-related complications portended

a worse long-term survival.25 Currently, the Centers for Medicare and Medicaid Services (CMS) limits

reimbursement for CAS to high-risk symptomatic patients with carotid stenosis >70%.

5 6 Despite some uncertainty regarding CAS versus CEA, there are some subpopulations that do

better than others with a particular treatment option. Contrary to initial belief regarding advanced age

as a benefit for carotid stenting, age ≥68 was associated with a significantly higher risk of stroke and

death for carotid stenting.25,26 Symptomatic patients undergoing CAS appear to have a higher risk of

stroke or death if performed in <7 days after the symptomatic event.27 There are no sufficient data to

support CAS for asymptomatic patients outside high risk for CEA by anatomical factors (stoma, previous

neck radiation, contralateral vocal cord paralysis, or high lesion) or severe medical comorbidities

(coronary or pulmonary disease) (Table 89-2). Furthermore, patients with significant anatomical factors

that put them at risk for CAS should undergo CEA (Table 89-3). Currently, ongoing clinical trials seek to

determine more understanding of the patients that will benefit best from each therapy as well as the

assessment of new stent designs, such as mesh-covered stents.

Table 89-2 Criteria for High-Risk Carotid Endarterectomy

CAROTID ENDARTERECTOMY

Technique

There are many decisions a surgeon has to consider for a CEA. First, there is the choice of anesthetic:

local, regional, or general. Depending on the choice of anesthetic, there is a choice of cerebral

monitoring. If the patient has the procedure under local anesthesia, their ability to respond to

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commands dictates the adequacy of collateral flow during clamping. If the patient is under general

anesthesia, there is the choice of electroencephalogram (EEG), TCD, stump pressure measurement, or

somatosensory evoked potentials (SSEPs) that guide the use of a shunt for cerebral protection. EEG is

the most widely used technique of cerebral monitoring. It requires the addition of 8 to 16 leads and

monitors brain activity. The use of a shunt is based on a positive test, which is a drop of fast

background activity of 50%. EEG, however, is likely overly sensitive, overestimating the number of

people that require a shunt.28,29 TCD works in a similar manner, evaluating the middle cerebral artery

(MCA) for changes in flow with clamping. Measuring a stump pressure requires clamping the common

and external carotid artery while maintaining the internal carotid artery open and using a transducer to

check the back pressure. A minimum mean pressure of 40 mm Hg has been most widely adopted for the

threshold for shunting. Stump pressure measurement does, however, have a small risk of embolization.

Others opt for routine shunting, allowing a consistent endarterectomy technique without anxiety.

Shunting completely relieves intracerebral ischemia, but requires a safe technique with shunt placement

above the superior aspect of the plaque. Routine shunting has been met with excellent results.30,31

Table 89-3 Contraindications to Carotid Artery Stenting

Correct patient positioning is paramount for a successful endarterectomy, especially for a high lesion.

The patient’s neck is slightly hyperextended and turned away, with a roll under the shoulder to open the

neck (Fig. 89-6). A longitudinal incision is made along the anterior border of the sternocleidomastoid

muscle (SCM). The use of ultrasound intraoperatively can help guide the surgeon to perform a limited

incision over the bifurcation. The platysma is divided. Care must be taken to avoid the anterior jugular

vein and carefully divide any venous tributaries. By retracting the SCM laterally the internal jugular

vein is identified in the carotid sheath. The facial vein is an important landmark for identification of the

bifurcation and is divided, however, frequently the hypoglossal nerve can traverse at this site and care

must be taken to avoid it. Often the superior belly of the omohyoid muscle is divided for exposure.

Inferior and medial to the internal jugular vein is the common carotid artery which is carefully exposed.

Care must be taken to avoid injuring the vagus nerve that is typically posterior to the artery, but can

travel anteriorly in some cases. After the common carotid artery is dissected out, the external carotid

and superior thyroid arteries are controlled. Often, dissection at the carotid bifurcation can cause

reactive bradycardia because of stimulation of the carotid body. This can be improved with

administration of 1% lidocaine directly into the carotid body. Care must be taken in dissecting out the

internal carotid artery to avoid excessive manipulation to prevent embolization and avoid the more

common location of the hypoglossal nerve that traverses the proximal artery. For high lesions,

extension of the incision posteriorly in a periauricular fashion and division of the posterior belly of the

digastric muscle can aid in distal exposure. If a lesion is felt to be very high, preoperative nasotracheal

intubation and mandibular subluxation with temporary fixation can assist in exposure of the distal ICA.

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Figure 89-6. The patient’s neck is slightly hyperextended and turned to the contralateral side. An incision is made along the

anterior border of the sternocleidomastoid centered over the carotid bifurcation.

Once all vessels are controlled, intravenous heparin is administered (100 units/kg) prior to clamping

(Fig. 89-7). As discussed previously, the choice of cerebral monitoring or routine shunting dictates how

the surgeon proceeds. Typically, the internal carotid artery is clamped first to avoid embolization after

ensuring the clamp site is in a normal segment of artery distal to the palpable plaque. The external and

common carotid arteries are then clamped. A longitudinal arteriotomy is created from the distal

common carotid artery into the internal carotid artery past the plaque. Often the ansa cervicalis limits

exposure as it traverses the carotid artery, which requires its ligation once it is indeed identified as the

ansa cervicalis. If necessary, a shunt can be placed from the common carotid artery to the internal

carotid artery to maintain antegrade flow (Fig. 89-8). An endarterectomy can be performed to remove

the plaque. Typically, a layer is teased out in the media, and the entire plaque is removed after either

cutting the plaque from the proximal and distal artery or carefully pulling free trying to avoid a flap.

The plaque extending into the external carotid artery is most easily dealt with by way of an eversion

technique. The entire endarterectomized surface must be examined to remove flaps or debris. This is of

most importance at the distal aspect in the internal carotid artery. If needed, tacking sutures with 7-0

prolene can be used to keep down a concerning endpoint to avoid a flap once flow resumes (Fig. 89-9).

At this point, closure of the arteriotomy is accomplished. Primary repair is not typically

recommended due to improved short- and long-term outcomes with patch closure, and CMS uses patch

closure as a quality metric during endarterectomy.32 The choices of patch include synthetic material,

such as Dacron or polytetrafluoroethylene, a biologic material, such as bovine pericardium, or an

autogenous vein (Fig. 89-10). Prior to closure, the shunt is removed and careful sequential flushing of

each of the vessels is performed to remove air of debris. Additionally, after closure, the internal carotid

artery clamp remains on for a few seconds to allow flushing through the external carotid artery to

ensure any remaining debris of thrombus does not proceed into the cerebral circulation. The heparin is

typically reversed with protamine sulfate. Once hemostasis is accomplished, closure is performed by

approximating the sternocleidomastoid back, closing the platysma and skin. A full neurologic

examination is performed prior to extubation or exit from the operating room if performed under local

anesthesia.

An eversion endarterectomy is another technique for CEA and has the benefit of not requiring

prosthetic material for a patch. In the eversion technique, exposure of the vessels is similar to the

standard CEA. However, with the eversion technique, the internal carotid artery is transected at the

bulb. The edges of the vessel are peeled back in a plane removing the plaque as it proceeds distally. A

downside of the eversion technique is the inability to easily use distal tacking sutures. Closure is

primarily accomplished at the bifurcation and doesn’t compromise the internal carotid artery lumen.

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Figure 89-7. A: During carotid endarterectomy, vascular clamps are applied to the common carotid, external carotid, and internal

carotid arteries. Carotid plaque is elevated from the carotid lumen. B: Carotid plaque is removed and the arteriotomy is closed

either primarily or with a patch angioplasty.

COMPLETION STUDIES

Avoidance of a perioperative stroke is the primary objective during and after the endarterectomy. To

minimize that risk, typically caused by a technical error such as a flap, thromboembolism, or carotid

artery thrombosis, completion studies should be considered. At the completion of arterial closure,

continuous wave Doppler analysis can be used to check the patency of the vessels by identifying normal

Doppler flow or an area of stenosis. This is unlikely to pick up a small intimal flap or subtle stenosis.

DUS is an excellent modality for examination of blood flow waveforms and B-mode imaging to identify

small flaps or intimal defects. Angiography is considered the “gold standard” with contrast either

injected directly into the common carotid artery or via a transfemoral approach. However, these studies

have shown mixed results in the identification of defects, or can be overly sensitive and pick up defects

that might not cause problems while repair increases the morbidity and mortality.33,34

Figure 89-8. A temporary carotid shunt is inserted from the common carotid artery (long arrow) to the internal carotid artery (short

arrow) during carotid endarterectomy to provide continuous antegrade cerebral blood flow.

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Figure 89-9. The distal transition line (left side of the figure) in the internal carotid artery where the plaque had been removed

must be examined carefully and should be smooth. Tacking sutures (arrows) are placed when an intimal flap remains in this

transition to ensure no obstruction to flow.

Figure 89-10. A: An autologous or synthetic patch can be used to close the carotid arteriotomy incision, which maintains the

luminal patency. B: A completion closure of carotid endarterectomy incision using a synthetic patch.

Complications

The majority of patients tolerate the endarterectomy well and are discharged home after 24 hours.

Complications can range from mild to life threatening. Postoperative blood pressure control often

requires pharmacologic assistance due to carotid sinus manipulation during the procedure, but rarely

persists after 24 hours. An acute ipsilateral stroke is the most dreaded complication after a CEA,

especially if performed for asymptomatic disease. Cerebral ischemia can occur due to hypoperfusion or

embolization during the procedure. Hypoperfusion is related to the collateral flow through the

contralateral carotid artery and posterior circulation, and often relies on the status of the circle of

Willis. Embolization can occur from shunt placement, the clamp site, thrombus formed during the

procedure, or inadequate flushing prior to arteriotomy closure. Less frequently, the carotid artery can

occlude causing a stroke. This can be related to an intimal flap, platelet adhesion from the patch,

dissection, or anastomotic stricture. The importance of neurologic evaluation prior to leaving the

operative suite is the quick identification of a problem, and usually requires immediate reexploration.

Alternatively, if there was a normal postoperative duplex, angiography can be performed for the

identification of the etiology of the stroke. The perioperative risk after CEA differs depending on the

indication for the intervention. In symptomatic patients, the 30-day risk of stroke is 3.2% to 5.4%, MI

1.8% to 2.6%, and death around 1.1%.14,24,25,38 For asymptomatic patients, the 30-day risk of stroke is

1.4% to 5.4%, MI is 2%, and death is 1.1%.14,24,25,38 In CREST, the 30-day stroke and death rate after

CEA was 3.2% in symptomatic and 1.2% in asymptomatic patients. Additionally, when identifying

symptomatic patients treated by vascular surgeons, the 30-day risk of stroke and death was 1.3%, which

increased to 3.9% when combined with MI. Overall with endarterectomy, CREST showed a

periprocedural risk of death at 0.3%, CVA of 2.3%, and MI of 2.3%.25

Cardiac complications are common after CEA, and are a major cause of perioperative death.35,36 This

risk is due to the high number of patients with concomitant coronary artery disease, upward of 50% of

patients. Postoperative bleeding can cause a significant hematoma that can cause respiratory

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