Eversion Carotid Endarterectomy

Eversion carotid endarterectomy (eCEA) involves oblique transection of the internal carotid artery (ICA) at its origin at the carotid bifurcation, followed by extirpation of the plaque by means of eversion and subsequent reimplantation of the ICA into the carotid bulb. It has been validated in randomized and nonrandomized prospective studies as a safe and effective surgical treatment for carotid stenosis. The efficacy of surgical treatment of atherosclerotic carotid stenosis in the prevention of stroke is well documented.

Worldwide, stroke is a leading cause of mortality; cerebrovascular disease accounted for approximately 7 million deaths in 2020.[1]  In the United States, the annual incidences of stroke and transient ischemic attacks (TIAs) are approximately 795,000 and 300,000 cases, respectively, and stroke was responsible for approximately 150,000 US deaths in 2019.[1]

Stroke is an important cause of long-term disability.[2]  Only 29% of patients with nonfatal stroke recover with normal neurologic function.[3] In the Framingham study, which prospectively followed 5184 men and women from the general population for 26 years, Sacco et al reported a very high incidence of recurrent cerebrovascular infarctions (9% per year) in patients who survived an initial stroke. In the same study, the cumulative 5-year recurrent stroke rate was 42% for men and 24% for women.[4]

In addition to high rates of death, recurrence, and long-term disability, management of stroke imposes a substantial economic burden on society. The annual health care expenditure directly and indirectly related to stroke in the United States is greater than $52 billion.[1]

In routine clinical practice, indications for the treatment of patients with carotid stenosis are based on the presence of symptoms and the degree of stenosis.[5]  In 2018, the European Society for Vascular Surgery (ESVS) issued guidelines for the management of atherosclerotic carotid and vertebral artery disease.[6]  In 2021, the Society for Vascular Surgery (SVS) issued updated evidence-based clinical practice recommendations for the management of carotid stenosis.[7]

The SVS guidelines recommended carotid endarterectomy (CEA) as the treatment of choice for low-risk symptomatic patients with carotid artery stenosis greater than 50% and low-risk asymptomatic patients with carotid artery stenosis greater than 70%.[7]  Generally, carotid surgery is performed if a patient’s perioperative stroke or mortality risk is less than 3% and the life expectancy is greater than 5 years.[8]

The reference standard for calculation of the degree of carotid artery stenosis is based on the North American Symptomatic Carotid Endarterectomy Trial (NASCET) criteria (see the image below). In this approach, the smallest residual lumen at the level of stenosis is compared with the normal distal ICA lumen by means of catheter-based arteriography.

An alternative (though one that is less frequently used during catheter-based arteriography) is to determine the degree of the carotid artery stenosis by using the European Carotid Surgery Trial (ECST) criteria. In the ECST approach, the smallest residual lumen at the level of stenosis is compared with the local estimated diameter of the carotid bulb.

A 70% carotid stenosis calculated according to the NASCET criteria corresponds to an 85% carotid stenosis calculated according to the ECST criteria. By the NASCET criteria, moderate stenosis is defined as 50-69% stenosis and severe stenosis as 70-99%. By the ECST criteria, the corresponding values are 75-84% for moderate stenosis and 85-99% for severe.

Duplex ultrasonography (US) is the imaging modality of choice for the diagnosis of carotid artery stenosis (see the image below); it is safe, quick, and reliable in experienced hands. However, the accuracy of duplex US is highly operator-dependent. In addition, factors that affect flow velocities, such as severe contralateral ICA stenosis or occlusion, can cause compensatory elevations of velocity and result in overestimation of the degree of stenosis.

Computed tomography (CT) and magnetic resonance angiography (MRA) can be used to identify plaque morphology and in cases where US is technically difficult (eg, heavily calcified or high lesions); this can be helpful in planning CEA or stenting (see the image below).[9, 10, 11]

The underlying etiology of carotid artery stenosis (see the image below) is the formation of atheromatous plaque at the bifurcation of the common carotid artery (CCA) and in the origins of the ICA or, less frequently, the external carotid artery (ECA).[12] The temporary or permanent clinical manifestations of carotid artery stenosis (TIA or stroke) result from cerebral hypoperfusion through the embolized artery in most cases, as well as stenosis due to plaque progression in situ.[13]

The reduction in the radius of carotid blood vessels has a significant negative effect on cerebral perfusion, in that blood flow through these vessels, as determined by Poiseuille’s law, is directly related to the fourth power of their radius.

Atheromatous plaque not only reduces cerebral blood flow but also represents an irregular surface within the lumen of the carotid artery that is prone to thrombus formation (see the image below). Ulceration and rupture of the plaque create a highly thrombogenic surface that promotes platelet aggregation and creates thromboembolic debris, which subsequently leads to distal arterial embolization.

Extracranial cerebrovascular atherosclerosis, which accounts for most carotid artery disease, is responsible for 15-52% of all ischemic strokes.[14, 15] Hypertension is another important cause of stroke. Other rare entities of carotid artery disease include fibromuscular dysplasia, arterial kinking secondary to elongation, extrinsic compression, carotid body tumors, traumatic occlusion, intimal dissection, and radiation.

The efficacy of surgical treatment of atherosclerotic carotid stenosis in the prevention of stroke has been well documented.[7, 1]  Level 1 data from several large multicenter clinical trials, as well as data from National Surgical Quality Improvement Program (NSQIP) database and large multicenter studies, have validated the efficiency and safety of CEA as the treatment of choice for reducing the risk of ipsilateral stroke in both asymptomatic and symptomatic patients with moderate-to-severe carotid artery stenosis.[16, 17]

In NASCET, the 5-year incidence of ipsilateral stroke was 15.7% in patients with moderate stenosis treated surgically, compared with 22.2% in patients with moderate stenosis who received optimal medical therapy.[16] NASCET also demonstrated a cumulative risk of ipsilateral stroke of 26% and 9% at 2-year follow-up in patients treated medically and those treated with CEA, respectively. This reduction in the incidence of stroke in the CEA group was demonstrated in patients with symptomatic, high-grade stenosis (ie, 70-99%).

Similarly, ECST data demonstrated that the 3-year risk of ipsilateral stroke was 2.8% in patients randomized to undergo CEA and 16.8% in those randomized to receive medical therapy alone.[17] The 3-year risk of disabling or fatal stroke or death was 6.0% and 11.0% for surgically and medically treated patients, respectively. Both patient cohorts were symptomatic and had high-grade carotid stenosis.

In the Asymptomatic Carotid Atherosclerosis Study (ACAS), a randomized clinical trial from North America comparing best medical therapy with surgery in 1622 asymptomatic patients with carotid artery stenosis, CEA significantly reduced the overall 5-year risk of ipsilateral stroke and any perioperative stroke or death from 11.0% to 5.1% in patients with asymptomatic carotid stenosis greater than 60%.[18] This corresponded to a relative risk reduction of 53% and an absolute risk reduction of approximately 1% per year.

Similarly, in the Asymptomatic Carotid Surgery Trial (ACST), a study carried out in Europe, the investigators demonstrated that CEA yielded a significant reduction in the 5-year risk of stroke or death, from 11.8% to 6.4%.[19]

Numerous randomized and nonrandomized prospective studies have validated eCEA as a safe and effective method for the surgical treatment of carotid stenosis and have shown it to be characterized by low restenosis rates.

Data from the Eversion Carotid Endarterectomy Versus Standard Trial (EVEREST), which included 1353 patients, demonstrated that eCEA and patch angioplasty had significantly lower restenosis rates when compared with primary closure CEA.[20]

A Cochrane review of the literature that included close to 2500 patients from five controlled clinical trials found that eCEA was associated with a lower risk of restenosis than patch angioplasty CEA.[21] Data from the same study showed no significant differences between the two groups with respect to the rate of perioperative stroke (1.7% for eCEA and 2.4% for patch angioplasty) and perioperative mortality (2.0% and 1.9%).

In 2014, Ballotta et al published results of a study that evaluated 2007 consecutive primary CEAs in 1773 patients over 12 years.[22] ACAS and NASCET recommendations were used as inclusion criteria for asymptomatic and symptomatic patients, respectively. Of the 2007 patients, 1446 (72.1%) were symptomatic at the time of surgery. All procedures were performed by the same surgeon in patients under general anesthesia. Intraoperative electroencephalography was used for the assessment of cerebral perfusion and need for the selective shunting.

During the study,[22] there were nine (0.47%) asymptomatic late carotid restenoses (six moderate [50%-69%] and three severe [≥70%]) and one (0.05%) carotid occlusion. Data from Kaplan-Meyer analysis showed the rates of freedom from restenosis and/or occlusion to be 99.9 ± 0.1% at 1 year, 99.3 ± 0.2% at 5 years, 99.3 ± 0.2% at 10 years, and 99.3 ± 0.2% at 12 years. Data also showed a perioperative stroke rate of 0.4% and no intraoperative mortality. This study demonstrated that eCEA can be performed in both asymptomatic and symptomatic patients with extremely low perioperative morbidity and mortality, as well as low restenosis rates.

A study by Schneider et al, using data from the SVS Vascular Quality Initiative (SVS VQI) database for 2003-2013, found that  eCEA and conventional CEA were comparable in terms of freedom from neurologic morbidity, death, and reintervention; that eCEA was associated with significantly shorter procedure times; and that eCEA reduced certain expenses more commonly associated with conventional CEA.[23]  In a study of 1385 consecutive cases, Ben Ahmed et al found eCEA to be both safe and cost-effective.[24]

In 2018, Paraskevas et al published an updated systematic review and meta-analysis aimed determining whether eCEA confers significant benefit over conventional CEA.[25]  They found eCEA to be superior with respect to perioperative outcomes (stroke, death, death/stroke) and late restenosis but did not find a significant difference between it and patched CEA with regard to either early or late outcomes. Their data suggested  that early and late outcomes after conventional CEA are similar to those after eCEA, provided that the arteriotomy is patched.

In a meta-analysis that included 10 studies (N = 3568; 3672 operations) comparing eCEA (n = 1718) with CEA with patch plasty (n = 1954), Gavrilenko et al examined outcomes in the immediate and remote postoperative periods.[26]  They found eCEA to be associated with a shorter time of carotid artery cross-clamping, a lower frequency of intraoperative temporary bypass, and fewer cases of ischemic stroke in the immediate and remote postoperative periods, as well as fewer instances of restenosis in the long-term postoperative period.

In a multicenter clinical trial (N = 25,106) evaluating long-term (mean follow-up, 124.7 mo) outcomes of eCEA (n = 18,362) against those of conventional CCA (n = 6744), Belov et al found eCEA to be associated with lower frequencies of fatal outcome, cerebrovascular death, nonfatal ischemic stroke, and repeated revascularization because of restenosis greater than 60%.[27]

The choice of surgical technique for the treatment of carotid artery stenosis should depend on the clinical judgment, experience, and preference of the operating surgeon, in the context of a discussion of the options with the patient.

Anesthesia

Both local/regional anesthesia and general anesthesia have been used for eversion carotid endarterectomy (eCEA); which approach is preferable in this setting remains a matter of debate. Data from several randomized trials comparing regional and general anesthesia, including an international multicenter randomized trial of 3526 patients from 24 countries, have shown that the choice of anesthesia does not independently predict the outcome of the operative procedure.[28, 29, 30, 31]

Subsequent analysis of data from the same database showed that in patients for whom either anesthetic approach was clinically indicated, cost-effectiveness analysis favored local anesthesia.[32] Ultimately, the surgeon, in consultation with the anesthesiologist and the patient, must make the final decision regarding the best anesthetic management in each case.

If local or regional anesthesia is selected, mild sedation may be administered, but the patient must be alert enough to be evaluable for neurologic changes. Usually, two or three simple questions are agreed on with the patient in advance and then repeated during carotid cross-clamping. Drapes may be suspended above the patient’s head on a Mayo stand to create more space for the patient.

Generally, regional anesthesia is optimal in calm patients with slender and mobile necks; it may be less successful in patients who are claustrophobic or anxious, have high lesions or immobile necks, or have previously undergone carotid endarterectomy (CEA).

Positioning

The patient is placed in the supine position with the neck hyperextended (see the image below). Once the neck is hyperextended, the head is rotated 15-20º away from the side of the lesion to face the opposite side. This maneuver moves the mandible superiorly, exposes the mediolateral aspect of the neck, and opens up the angle of access to the anterior neck triangles on the side of the lesion. Folded sheets may be placed under the shoulders, or a tape may be placed across the patient’s forehead and secured at the edges of the table.

Proper positioning is important because excessive hyperextension of the neck can tighten the sternocleidomastoid muscle and restrict the mobility of the common carotid artery (CCA) and the carotid bifurcation, thereby making exposure of the lesion more difficult. Another reason for avoiding extensive hyperextension of the neck is to ensure that the internal jugular vein (IJV) remains lateral, rather than anterior, to the carotid artery.

Because cervical arthritis is prevalent in the age group for which eCEA is most commonly indicated, the neck must be carefully manipulated and slowly hyperextended at the craniocervical joint. Introducing some degree (10-20°) of reverse Trendelenburg is useful for maximizing exposure, reducing venous pressure and congestion, and minimizing bleeding.

After proper positioning, a topical antiseptic agent is carefully applied to the neck with minimal pressure (to avoid dislodging emboli from the carotid plaque). The operating area is cordoned off with four sterile drapes (see the image below). Incorporating the ear lobe and mastoid process (superiorly) and the neck midline (medially) and the sternoclavicular joint (inferiorly) into the surgical field is essential. A single weight-based dose of an intravenous antibiotic (cefazolin) is administered within 1 hour of making the incision.

If the patient is afebrile, neurologically intact, and hemodynamically stable, he or she may safely be discharged on postoperative day 1. Before discharge, the neck is examined and the Blake drain removed. The patient is instructed to return if any problems develop and given detailed discharge instructions. A routine follow-up visit is scheduled 4 weeks after the operation; this visit should include carotid duplex evaluation.

The 2018 guidelines from the Society for Vascular Surgery (SVS) recommended that after CEA, surveillance with duplex ultrasonography (US) should be carried out at baseline and every 6 months for 2 years and annually thereafter until the patient is stable.[33] ​ 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.

Two techniques are commonly used for carotid endarterectomy (CEA): patch angioplasty and eversion CEA (eCEA). In the former, a longitudinal arteriotomy is made and then carried beyond the plaque both proximally and distally. This is typically followed by the use of a patch angioplasty closure; several randomized trials demonstrated that clinically relevant outcome measures favored patch closure over primary closure.[34, 35, 36, 37, 38]

In eCEA, the internal carotid artery (ICA) is obliquely transected at its origin at the carotid bifurcation, and the plaque is then extirpated through eversion and reimplantation of the ICA into the carotid bulb. Although eCEA was first described by DeBakey in the 1950s, it was not until the 1990s that it gained widespread use as a technique that shortens operating time, avoids use of prosthetic material, facilitates reconstruction of a kinked or coiled ICA, and lowers restenosis rates.

To minimize skin-edge bleeding, 0.5% bupivacaine mixed with epinephrine may be preoperatively infiltrated into the skin and subcutaneous tissue. Constant attention to hemostasis is critical throughout the procedure.

A vertical incision is most effective for exposure of the carotid sheath and the carotid vessels (from the distal common carotid artery [CCA] to the disease-free portion of the ICA and the proximal external carotid artery [ECA]) during eCEA. In addition, a vertical incision allows additional exposure of the carotid vasculature if necessary because it can readily be extended superiorly, toward the posterior belly of the digastric muscle.

The incision is created over the anterior border of the sternocleidomastoid muscle, along the line connecting the sternocleidoclavicular junction with the processus mastoideus (see the image below), and carried down to the carotid sheath. The great auricular nerve must be preserved superiorly; injury to this nerve leads to paresthesia of the ear.

The incision should be slightly curved posteriorly, toward the processus mastoideus, to avoid injury to the marginal mandibular branch of the facial nerve. Marginal mandibular nerve palsy leads to a cosmetic deficit (drooping at the corner of the mouth) as well as a functional deficit (drooling).

Mobilization of sternocleidomastoid and dissection of carotid sheath

The skin incision is deepened through the subcutaneous fat and the platysma. The platysma is divided longitudinally. This yields access to the investing layer of deep cervical fascia, which is then incised along the anterior border of the sternocleidomastoid muscle (see the image below).

After the fascial incision, the medial border of the sternocleidomastoid muscle is mobilized along the entire length of the incision to expose the underlying carotid sheath (see the first image below). Dissection of the carotid sheath is carried low on the neck, along the medial aspect of the internal jugular vein (IJV). The initial incision of the carotid sheath should be performed carefully to avoid injury to the vagus nerve, which is located anterior to the carotid artery 10% of the time (see the second image below).

In most patients, the vagus nerve occupies the most posterior part of the carotid sheath. Although this nerve contains somatovisceral afferent and efferent neurons, the most important neurologic deficit associated with vagus nerve injury at the level of CEA is recurrent laryngeal nerve palsy. This deficit leads to ipsilateral vocal cord paralysis characterized by hoarseness, impaired phonation, and ineffective cough.

Identification and mobilization of carotid vessels

Once the carotid sheath is entered, the medial aspect of the IJV is exposed until the common facial vein is visualized. The common facial vein is a landmark for the carotid bifurcation in the vast majority of patients; it courses across the CCA and drains into the IJV. The facial vein is mobilized, suture-ligated, and divided (see the first image below). Once this has been done, the IJV is retracted laterally to yield clear exposure of the underlying CCA and ICA (see the second image below).

Next, the CCA is mobilized circumferentially and encircled with vessel loops. Circumferential exposure of the CCA is required only for the arterial segment where vessel loops are to be placed; great care must be taken posteriorly, where the vagus nerve is expected to be found in most patients (see the image below). To avoid injury to the vagus nerve, gaining and maintaining the dissection plane immediately external to the adventitia of the artery is critical.

To expose the carotid bifurcation, periarterial dissection of the surrounding tissues is continued superiorly. During the exposure of the carotid bifurcation and the carotid sinus, bradycardia may occur. Recognizing any significant alterations in heart rate and rhythm at this point in the procedure is critical because many patients with carotid artery stenosis have coexisting coronary artery disease.

If sinus bradycardia occurs, 1-2 mL of 1% lidocaine may be administered topically between the ICA and the ECA to block nerve conduction to the carotid sinus. Some surgeons routinely administer lidocaine at the time of bifurcation exposure to prevent sinus bradycardia.

The ECA lies superficial to the ICA and can easily be identified by its proximal branches (the superior thyroid artery and the ascending pharyngeal artery). The ECA is dissected free of surrounding tissue and encircled with a colored vessel loop (see the image below), as is the proximal superior thyroid artery. The ICA lies posterolaterally in the carotid sheath and is exposed superior to the carotid bifurcation.

Before mobilization of the ICA, the hypoglossal nerve should be identified and preserved (see the image below). This can be facilitated by dividing the ansa cervicalis. The fibers of the ansa cervicalis diverge from the hypoglossal nerve as it crosses the ICA and descend superficial to the CCA and ICA to innervate the strap muscles. Division of the inferior or superior roots of the ansa cervicalis does not result in neurologic defects.

A suture tie placed on the divided ansa cervicalis serves as a retractor and allows the hypoglossal nerve to be moved or elevated without being injured. The hypoglossal nerve courses obliquely, just superior to the carotid bulb, and is tucked under the posterior belly of the digastric muscle. It runs in immediate proximity to the sternocleidomastoid branch of the occipital artery.

If the extent of the plaque and the course of the bifurcation necessitate additional distal exposure of the ICA, dissection of the sternocleidomastoid arterial branch of the occipital artery allows mobilization of the hypoglossal nerve superomedially for better rostral exposure. Injury to the hypoglossal nerve causes ipsilateral deviation of the tongue when the patient attempts to extrude the tongue, as well as difficulty with initiation of swallowing.

In very high dissections of the ICA, the glossopharyngeal nerve may be encountered as it parallels the course of the hypoglossal nerve superiorly. This nerve, located between the IJV and the ICA, passes superficial to the ICA and courses between the ICA and the ECA to enter the base of the tongue. It supplies sensation to the pharynx and innervates muscles that elevate the pharynx and larynx during swallowing. Injury to the glossopharyngeal nerve leads to impairment of swallowing.

The spinal accessory nerve runs lateral to the carotid sheath and innervates the trapezius and the sternocleidomastoid muscle. This nerve may be injured by excessive lateral retraction. Dysfunction of the accessory nerve is characterized by shoulder pain, winging of the scapula, and inability to shrug the shoulder.

Once the abovementioned nerves are identified and preserved, the ICA is mobilized well distal to the palpable atheromatous lesion, which can be visualized as a yellowish discoloration of the artery that feels firm and is less compressible than a healthy artery. Adequate mobilization can be confirmed by carefully palpating the normal arterial segment of the ICA above the lesion with a finger.

The same is done for the ECA to ensure that the superior thyroid artery branch is not injured. The superior laryngeal nerve is medial to the carotid sheath, and its external branch comes into proximity with the superior thyroid artery. Thus, dissection of the ECA and ligation of its proximal branches should stay close to the artery so as not to cause injury to the superior laryngeal nerve, which can lead to voice fatigue and alteration in sound quality with loss of high tones.

In patients who have a high carotid bifurcation or a lesion that extends relatively distally within the ICA, additional exposure can be obtained by carefully dissecting the periarterial tissues at the confluence of the ICA and the ECA. As noted (see above), the ascending pharyngeal artery can be located in this position.

This dissection enables further mobilization of the ICA because the tissue acts as a suspensory ligament for the carotid bifurcation. If necessary, additional distal exposure of the ICA can be obtained by mobilizing and dividing the posterior belly of the digastric muscle distally, the omohyoid muscle proximally, or both.

Particular care must be taken during exposure and manipulation of the carotid bifurcation and the bulb of the ICA because this is the location of the atheromatous lesion. Careful dissection of periarterial tissue and manipulation of the CCA, the ECA, and the ICA are vital for preventing plaque dislodgment with subsequent cerebral embolization; the lesion may be friable and contain atheromatous debris.

Once the vessels have been exposed as described, a decision must be made regarding cerebral tolerance of carotid cross-clamping and, if necessary, the method of preserving adequate cerebral perfusion during carotid occlusion.

During periods of vulnerability to cerebral ischemia, including intraoperative arterial cross-clamping, collateral flow is critical for cerebral blood flow. The major pathways of collateral flow are the circle of Willis, the extracranial arterial anastomotic channels (eg, the contralateral ECA), and the leptomeningeal communications bridging watershed areas between major arteries.

Depending on the type of anesthesia used, several different modalities are available for assessing collateral cerebral circulation and the adequacy of cerebral perfusion. If the operation is performed under local anesthesia, trial occlusion is commonly used to determine the safety of temporary carotid clamping.

During the occlusion of the carotid arteries, the patient is continuously monitored for speech, cognitive, and motor function. The patient is asked to talk, answer questions, and move extremities on the side of the body contralateral to the lesion. Any alteration in speech or in cognitive or motor function is an absolute indication for shunt placement. It is estimated that adequate collateral circulation is present in 85-90% of patients; in the remaining 10-15%, an internal shunt is used.

If the operation is performed under general anesthesia, several methods can be used to assess the adequacy of collateral cerebral circulation.[39]

Intraoperative electroencephalographic (EEG) monitoring has been also used to assess cerebral perfusion; it is highly sensitive to changes in blood flow and can detect flow reductions of approximately 10-18 mL/g/min.[40]  Although intraoperative EEG monitoring has been used at several centers with excellent results, it can be cumbersome because of the need to place electrodes preoperatively, the effect of general anesthesia on EEG tracing, and the expertise needed to interpret EEG results.[41]

Transcranial Doppler (TCD) ultrasonography (US) is used as well because it determines the middle cerebral artery velocity and pulsatility throughout the operation and is highly sensitive for microembolic signals suggestive of an active embolism.[42]  Like EEG monitoring, TCD US also requires additional instrumentation that is placed before positioning, as well as additional personnel (to monitor the TCD results); consequently, it can be impractical and expensive.

Measurement of ICA stump pressure is the most widely accepted and commonly used method of evaluating collateral cerebral blood flow. After exposure of the carotid bifurcation and institution of weight-based heparinization (heparin 100 U/kg intravenously [IV]), a 22-gauge needle is connected to a pressure transducer via rigid pressure tubing. The ICA is occluded first, followed by the ECA and the CCA. The needle is inserted in the CCA and oriented axial to the artery, and the ICA is released.

The ICA stump pressure is then recorded. Because no antegrade pulsatile flow exists in the ICA, the pressures on the two sides of the carotid stenosis are equalized and are essentially equal to the pressure in the middle cerebral artery (MCA). Hence, this pressure is an indirect measurement of the perfusion pressure that is present on the ipsilateral side of the circle of Willis.

If the stump pressure is lower than 40 mm Hg, placement of an internal shunt is indicated.[43] The proper shunt and the appropriate instruments should be immediately available and should be promptly inserted to minimize cerebral hypoperfusion between carotid cross-clamping and shunt placement.

At the authors' institution, selective shunting is preferred to routine shunting for the following reasons:

• Shunts are indicated in only 10-15% of patients
• Shunts can cause intimal damage and secondary thromboembolism
• Shunts can prolong procedural times
• Shunts may interfere with access to the diseased arterial segments

In addition, Krul et al demonstrated that only 20% of intraoperative strokes are caused by hemodynamic failure and that most intraoperative cerebrovascular insults are caused by distal thromboembolic events.[44] On the other hand, proponents of routine shunting argue that routine delayed shunting is safe and effective,[45] that it allows unhurried operative performance, and that familiarity with shunt insertion makes it easier to operate around the shunt.

Data from a Cochrane overview of the relevant randomized trials did not demonstrate that either strategy is more efficient than the other.[46] Accordingly, the choice between selective and routine shunting may be left to the surgeon’s discretion.[47]

Once proximal and distal control has been achieved, the ICA is obliquely detached from the CCA. Transection of the ICA is performed with a pair of Stephens scissors. The crook of the scissors is placed at the carotid bifurcation with the blades oriented inferolaterally so as to encircle the artery (see the first image below). The ICA is transected with a sharp, oblique and complete cut. This will yield exposure of the atheromatous plaque within the ICA (see the second image below).

The proximal part of the arteriotomy is “fish-mouthed.” Under direct vision, the plaque is reached with a DeBakey forceps. With gentle and constant downward traction on the plaque, the outer arterial layer of the ICA is peeled back to deliver the plaque (see the image below). Eversion is maintained, with forceps holding the edges of the transected artery, until the distal endpoints of the plaque are fully visualized within the ICA. This facilitates manipulation of the transected arterial end and subsequent anastomosis of the proximal ICA with the CCA.

After extraction of the atheromatous plaque (see the first image below), the everted edges, as well as the lumen of the proximal ICA, are carefully inspected for residual debris and well irrigated with the heparinized saline (see the second image below).

After the plaque has been removed from the ICA, attention is directed to the CCA. The optimal plane of dissection lies between the intima and the circular fibers of the media. This endarterectomy plane allows a smooth distal tapering of the endpoint. Once the proper endarterectomy plane of the CCA is established (see the image below), dissection is continued circumferentially about the artery.

To complete the circumferential mobilization of the plaque, a spatula is passed behind the plaque to isolate it from the adventitial plane on the opposite side of the artery (see the image below). The distal end of the plaque is transected with scissors placed perpendicular to the direction of the artery. Gentle traction is placed on the plaque with a forceps, and the plaque is removed from the CCA with a spatula in an upward direction (ie, toward the bifurcation).

After removal of plaque from the ICA and the CCA, attention is directed to the ECA. The plaque is separated from around the orifice of the ECA and held with forceps. With the clamp or a forceps, careful traction is applied to the plaque in the direction of the bifurcation. The distal ECA is gently pushed toward the orifice, and plaque is removed to a good distal endpoint. The lumen and edges of the CCA and ECA are thoroughly inspected for residual atheromatous plaques and debris and irrigated with heparinized normal saline (see the image below).

A double-armed continuous 6-0 polypropylene suture is used for the anastomosis (see the first image below). Creation of the end-to-side anastomosis begins with the stitch at the distal end of the artery, with one arm placed through the transected ICA and the other through the bifurcation (see the second image below). This is anchor-tied.

The front wall of the anastomosis is completed in the same manner as the back wall (see the first image below)—that is, from the distal end to the proximal end (see the second image below).

The suture should pass through all layers of the arterial wall, with particular care taken to include the intima so as to avoid creation and development of an intimal flap.[48] The suture must be carefully pulled and held taut continuously to prevent suture-line bleeding and facilitate adequate closure. The end-to-side anastomosis makes narrowing the arterial lumen at the suture line very difficult, and this lowers the restenosis rate.

Before the arterial closure is completed, the clamps are released one by one to flush out any residual debris (see the image below). To minimize the possibility of cerebral embolization with residual debris, the ECA circulation is restored first. The clamp on the ICA is removed last.

Finally, intraoperative duplex US is performed to verify the technical results of the procedure and to assess the patency of the carotid vasculature with the newly created anastomosis (see the image below).

Before closure is begun, a No. 19 Blake drain is placed through a separate stab incision, and the wound is well irrigated with normal saline (see the image below). After hemostasis is secured, the wound is closed in two layers with a continuous absorbable suture.

The only deep layer that is approximated is the platysma, closure of which is accomplished with 2-0 monofilament absorbable suture (see the first image below). For closure of the skin, a subcuticular technique with 4-0 monofilament absorbable suture is used because it provides skin closure with excellent cosmetic results (see the second image below).