Introduction

The first description of a carotid endarterectomy (CEA) for stroke was published in the Lancet in 1954.⁵ Since that time, more clinical trials have been completed for CEA than for any other surgical procedure, first addressing the question of surgery versus best medical practice (clearly answered in favor of surgery in most cases) and, most recently, addressing the question of surgery versus endovascular carotid intervention. (These latest trials currently also favor open surgery versus endovascular intervention.)

We can review current indications for surgical intervention for carotid stenosis as follows. The first large cooperative trials randomized surgical reconstruction versus best medical therapy. The North American Symptomatic Carotid Endarterectomy Trial (NASCET) established that symptomatic patients with internal carotid artery stenoses of 50% or more benefit from surgical resection of the offending lesion.^1,3 The Asymptomatic Carotid Atherosclerosis Study (ACAS) and the European Asymptomatic Carotid Surgery Trial (ACST) trial^6,7 provided compelling evidence that asymptomatic patients with 60% or more stenosis of the cervical internal carotid artery have a more favorable outcome with endarterectomy, provided that perioperative morbidity and mortality remain low (<3%),² and that the patient otherwise has a 5-year life expectancy (the time needed to achieve a surgical benefit).

Surgical reconstruction (CEA) has now been randomized against carotid stenting (CAS) in several trials. To date, none has shown an advantage of CAS in either safety or efficacy. The latest trials, EVA-3S and SPACE, continue to demonstrate that open surgery is the safest and best treatment in most cases.^28,29 The SAPPHIRE trial randomized “high-risk” asymptomatic and symptomatic carotid stenosis patients to CAS or CEA.³² Both techniques were effective, with statistically equal risk, in the treatment of symptomatic patients. For asymptomatic patients, there was a trend (p = NS) to lower risk with CAS. Questions have been raised, however, whether high-risk asymptomatic patients should be treated at all, since American Heart Association (AHA) guidelines have specified that surgical treatment is inappropriate for these patients.⁴ The only true answer to this question would be a study of CAS versus medical therapy in this group. No such study exists at present, although one large but non-randomized three-arm trial, the Japan Carotid Atherosclerosis Study (JCAS), will be forthcoming from Japan.

The National Institute of Neurological Disorders and Stroke (NINDS) and National Institute of Health (NIH)–funded Carotid Revascularization Endarterectomy versus Stenting Trial (CREST) completed enrollment of 2522 patients (53% symptomatic, 47% asymptomatic) on July 18, 2008 using the same criteria as NASCET and ACAS.^10,30 Final results of this trial have yet to be published. CREST and other similar trials in Europe (The International Carotid Stenting Study–Carotid and Vertebral Artery Transluminal Angioplasty Study [ICSS–CAVATAS 2]) and in Japan will hopefully provide level 1 evidence for therapeutic decision making. Curiously, the lead-in CREST data show that the risk of CAS, 30-day rates of stroke and death = 11.1%, is unacceptably high in elderly patients, aged >75, a group that was thought to represent excellent candidates for the procedure because of medical comorbidities.^8,10

Indications for surgery

Patients with neurological symptoms localizing to the side of their carotid stenosis are considered symptomatic. Neurological symptoms include ipsilateral monocular blindness, contralateral motor weakness with greater involvement of the arm and face compared to the leg, contralateral sensory deficits, and aphasias (if the dominant hemisphere is involved). Symptoms may take the form of transient ischemic attacks (TIAs), reversible ischemic neurological deficits (RINDs), or cerebrovascular accidents (CVAs), the duration of the deficit being the primary difference. Non-specific neurological complaints, such as dizziness, syncope, or ill-defined visual disturbances, do not meet the criteria for symptomatic carotid stenosis.

Most patients with symptomatic carotid artery stenoses of ≥50%, as measured by the NASCET method, are offered surgery at our institution. We offer endovascular counseling to these patients particularly if they have major medical comorbidities but we educate them that there is no level 1 evidence that stenting is equivalent to surgery in any but the highest-risk cases. The patients are counseled pre-operatively about surgical risks and benefits. There is good evidence that nondiabetic men with hemispheric symptoms have the greatest benefit from surgery; diabetes certainly increases the surgical risk, and amaurosis fugax appears to be a marker for lower stroke risk carotid lesions.²⁶

Asymptomatic patients with linear stenoses of 60% or more benefit from surgery, as determined by the ACAS and ACST trials. It is important to appreciate, however, that the patients should have an expected 5-year survival following surgery for the benefit to be realized; in addition, the benefit is not as great in women, and the combined surgical morbidity and mortality must remain below 3%. Asymptomatic patients with metastatic cancer, profound medical comorbidities, or other life expectancy-reducing conditions should generally not be offered treatment.

Preoperative evaluation and preparation

Carotid stenosis is identified in many different ways. Some patients come for surgical evaluation following workup for a TIA or stroke, where carotid duplex scanning, CTA, or MRA reveals a significant carotid lesion. Other patients present with clinically silent carotid bruits. Regardless of the referral type, we prefer catheter angiography (arch, both carotids, cervical, and cranial) for all patients being considered for surgery. This allows both accurate measurement of the stenosis using NASCET methodology and appropriate preoperative planning. The NASCET equation, where N is the linear diameter at the region of greatest narrowing and D is the greatest diameter of the normal artery distal to the carotid bulb, follows:

Preoperative imaging should also include CT or MRI of the brain to exclude the possibility of a mass lesion mimicking cerebral ischemia. Patients should also undergo appropriate preoperative medical risk stratification and workup especially for cardiac risks factors, and their medical management of cardiac disease, hypertension, hyperlipidemia, and diabetes should be optimized.

Surgical technique

Positioning

The patient is placed in the supine position with the head extended and turned away from the side of the operation (Figure 19–1). Folded sheets or pillowcases are placed beneath the shoulder blades to aid in extension of the neck; the preoperative arteriogram is reviewed to visualize the relationship between the internal and external carotid arteries (ICA and ECA) to choose the appropriate degree of head turning. Normally, the carotid vessels are superimposed in the anteroposterior plane, and rotating the head away from the operative side improves intraoperative visualization of the ICA by forcing it into a more lateral position. When the ICA is medial to the ECA (perhaps 10% of cases), no amount of head rotation will bring the ICA lateral enough, and the surgeon should recognize this and be prepared to dissect posterior and inferior to the ECA to find the “hidden” ICA and mobilize it laterally into the surgical position.

Figure 19–1 Initial positioning. The patient is in the supine position with the head extended and turned away from the operation side. The degree of rotation will be dependent on the relationship of the ICA and ECA. Generally, rotation brings the ICA into a more lateral position. Note the marking for the linear incision along the medial border of the sternocleidomastoid muscle.

Operative technique

The cerebral angiogram is used to locate the height of carotid bifurcation, and the incision is planned accordingly. We prefer a linear incision along the medial border of the sternocleidomastoid muscle (see Figure 19–1), which may extend as high as the retroaural region and as low as the suprasternal notch, as needed. Following sterile prep (never a vigorous scrub) and drape, the skin and subcutaneous tissues are dissected sharply down through the platysma, unavoidably transecting the transverse cervical nerve. (For this reason, patients should be instructed preoperatively to expect numbness anterior to the incision, which usually resolves after 6 months.) Meticulous hemostasis is obtained using monopolar and bipolar cautery superficially, and bipolar alone once the dissection is deep to the sternomastoid muscle. The medial edge of the sternocleidomastoid muscle is located and kept in view by placing a superficial blunt-bladed self-retaining retractor and dissecting through the overlying fat (Figure 19–2). The medial retractor blade (of this and all retractors) remains superficial to prevent injury to the recurrent laryngeal nerve in the tracheo-esophageal groove, while the lateral blade may safely be placed more deeply, on or under the sternocleidomastoid muscle.

Figure 19–2 Initial dissection. After sharp and electrocautery dissection, the anterior edge of the sternocleidomastoid muscle is identified. Care is taken that the medial blunt retractor remains superficial, avoiding delicate structures below, particularly the recurrent laryngeal nerve in the tracheo-esophageal groove.

Attention is next focused on the middle of the incision where the dissection proceeds down the sternocleidomastoid muscle until the internal jugular vein is reached. When dissection is carried under the muscle, the surgeon must be careful not to injure the laterally-placed spinal accessory nerve by inadvertent transection or over-retraction. The jugular vein is a key landmark in the dissection, and it typically lies lateral, parallel, and slightly anterior to the ICA and common carotid artery (CCA). The medial jugular border is fully exposed, and the vein can be retracted as needed using blunt blades over a cottonoid pattie; it is crucial that the retractor blades are blunt to prevent vascular injury. In this portion of the dissection, the rather large common facial vein, and occasionally several smaller veins, are doubly ligated and divided. The common facial vein is a key landmark as it generally crosses the field at the level of the carotid bifurcation and carotid bulb (Figure 19–3).

Figure 19–3 Dissection. Identification of the common facial vein is an important step in the dissection. The common facial vein often marks the level of the carotid bifurcation. We always ligate and divide the common facial vein to gain adequate carotid exposure.

The CCA is typically encountered first, and at first visualization we instruct the anesthesiologist to administer 5000 units of intravenous heparin, which we do not reverse with protamine sulfate at the end of the procedure. The carotid is lifted and separated from surrounding structures upon opening of the carotid sheath with the aid of four sutures (4-0 silk) tied to more superficial tissue (Figure 19–4). The individual vessels (CCA, ICA, and ECA) are then dissected and encircled with 0 silk ties passed with a right-angle clamp. The carotid sinus is injected with 2 to 3 cc of 1% Xylocaine using a 25-gauge needle only if the anesthesiologist notes significant vital sign changes during vessel dissection in the region of the bifurcation. (We find this is very rarely necessary.) The CCA and ECA are not dissected free of the underlying tissue, in order to prevent postoperative kinking of these vessels; but they must, of course, be dissected circumferentially in the area where the silk ties or clamps are placed around them. The ICA is freed more extensively posteriorly, to facilitate full control of the vessel, and also where tacking sutures may later be placed.

Figure 19–4 Carotid sheath stitches. Four 4-0 silk stitches (shown here pointed out by vascular pickups) between the carotid sheath and superficial soft tissue are used to lift and separate the carotid from surrounding structures. The author finds this maneuver extremely helpful.

A Rummel tourniquet is created by passing the CCA encircling silk tie through a wire loop that is then pulled through a rubber sleeve; this allows constriction of the vessel around an intraluminal shunt, should one become necessary. Mosquito clamps on the ends are used to secure the ECA and ICA ties, and to hang them over the retractor handles. The superior thyroid artery is dissected out of the surrounding connective tissue, and a double-loop 00 silk ligature is placed around the vessel; this occlusive Pott’s tie is kept taut with a hanging mosquito clamp. If multiple proximal ECA branches are found, they must each be dealt with in order to prevent back-bleeding of these vessels during the procedure. Back-bleeding can also occur during the arteriotomy and repair if the ECA silk tie and subsequent cross-clamp are not placed proximal to any major external branches.

Cross-clamping of the carotid tree should not occur until the ICA is exposed and dissected well beyond the distal extent of the plaque. To obtain the critical high exposure, the plane between the lateral carotid wall and the medial jugular border is followed, allowing recognition of the hypoglossal nerve as it travels medial to the jugular and crosses toward the midline over the ICA. The nerve is mobilized along its lateral wall adjacent to the jugular and gently retracted from the field using a vessel loop, so that its position can be easily assessed at all times. Injury to the nerve is more likely when it is blindly retracted or inadvertently coagulated because its location is not clearly known. A small ECA arterial branch to the sternocleidomastoid muscle occasionally requires ligation and transection to facilitate adequate mobilization of the hypoglossal nerve.

Avoidance of nerve injury is essential, and the carotid surgeon must understand and anticipate cervical nerve anatomy. The position of the recurrent laryngeal, hypoglossal, and spinal accessory nerves has already been discussed. Deep to the carotid, within the carotid sheath, lies the vagus nerve, which can be involuntarily cross-clamped if not properly identified. Horner’s syndrome can result from injury to the sympathetic chain near the carotid, although this is extremely rare in our experience. The superior laryngeal nerve lies deep to the distal ICA and should not be inadvertently damaged with dissection, cautery, or vascular clamps.

We stress again that adequate control and exposure of the ICA distal to the plaque is imperative. A moistened finger can often feel the distal end of the hard plaque; another cue is that the vessel color returns to pinkish-blue pink distal to the hard, yellow plaque. If high exposure is necessary, the posterior belly of the digastric muscle can be divided partially with no clinical consequence.

We like to use a sterile marking pen to draw out the proposed arteriotomy (Figure 19–5), lessening the risk of a jagged or curving suture line. We then ensure that the small spring-loaded Loftus shunt clamp will fit snugly around the ICA (Figure 19–6). Next, we notify the electroencephalograph (EEG) and SSEP technicians of the impending cross-clamp.^12–21 For the past several years we have been monitoring with both modalities simultaneously and are currently acquiring data to determine which modality is most sensitive in detecting ischemia. Following baseline EEG/SSEP acquisition, the ICA is occluded first with a small low closing force bulldog clamp. (Occluding the ICA first protects the brain from any debris released by clamp application elsewhere.) The CCA is then occluded with a large soft-shoe Fogarty vascular clamp and the ECA is closed with a second, larger and stronger, straight bulldog clamp. The arteriotomy is begun in the CCA with a no. 11 scalpel blade, and Potts angled scissors are used to extend the incision once the lumen is fully visualized. One needs to take care not to insert the no. 11 scalpel blade too deeply to avoid injury to the back wall of the carotid (Figures 19–7 and 19–8). The blue-marked arteriotomy line is followed from the CCA up to the bifurcation, and then up the ICA until normal vessel is encountered. In severely stenotic vessels, identification of the lumen is not always straightforward, and great care must be taken not to cut the back wall of the carotid. The possibility of a false lumen should be excluded prior to shunt placement.

Figure 19–5 Arteriotomy. Left-sided carotid exposure. A marking pen is used to draw the proposed arteriotomy. Note in this view the double-loop ligature around the superior thyroid artery and the single loop around the ECA. A blue vessel loop is seen around the hypoglossal nerve.

Figure 19–6 Shunt clamps. A selection of Loftus shunt clamps is displayed. This unobtrusive encircling pinch clamp is used to secure the shunt in the internal carotid artery and prevent displacement or back-bleeding.

Figure 19–7 Inadvertent injury to the back wall of the carotid. This stab wound injury (indicated by the suction tip) was identified upon inspection of the back wall of the carotid for adherent plaque. The plaque in this case was very firm and this injury was likely caused by excessive downward pressure with the no. 11 scalpel blade during the first step of the arteriotomy.

Figure 19–8 Repair of carotid back wall. The injury was repaired with a double-armed 6-0 Prolene suture with knots tied on the outside of the vessel.

In our practice, EEG/SSEP changes in any form lead to placement of an intraluminal shunt (Figure 19–9). Our preference is the Loftus Carotid Endarterectomy Shunt (Integra LifeSciences, Plainsboro, NJ), which is a 15-cm straight silicone tube with a black marker band in the center, allowing for easy identification and correction of shunt migration; the shunt is tapered at the ends for easy insertion, and the proximal end has a bulb that facilitates anchoring by the Rummel tourniquet.^15,24,25

Figure 19–9 Placement of a shunt. Right-sided carotid exposure. A Loftus Carotid Endarterectomy Shunt (Integra Lifesciences, Plainsboro, NJ) is pictured in situ. The black band marks the middle of the shunt. Having the black band allows the surgeon to return the shunt to appropriate position after sliding the shunt cranially/caudally to test for proper placement.

The CCA is cannulated first, and the shunt is secured by pulling up on the silk ties; a mosquito clamp is used to hold the rubber sleeve in place. The shunt tubing is held shut by a pair of heavy vascular forceps grasping the region of the black marker band. The tubing is cleared of air and debris by briefly releasing the vascular forceps, filling the shunt with fresh blood, and allowing confirmation of blood flow as well. The lumen of the ICA is visualized, and the distal end of the shunt is placed at the ICA orifice; the shunt is bled into the ICA to blow apart the vessel walls. The bulldog clamp on the ICA is then released and the shunt is advanced up the ICA until the black marker band lies in the center of the arteriotomy (see Figure 19–9). The shunt should slide up and down the ICA easily; no unnecessary force should be used, to avoid intimal damage and possible dissection. Our small Scanlan-Loftus custom clamp (Figure 19–6), or a Javid clamp, is then placed to secure the shunt in the distal ICA. A hand-held Doppler probe is used to confirm blood flow in the shunt.

A Scanlan plaque dissector, or a Freer elevator, is used to dissect the plaque away from the arterial wall (Figure 19–10). The wall of the vessel is held with a fine vascular pickup while the instrument is moved from side to side, first developing a plane in the lateral wall of the arteriotomy. We go approximately halfway around the wall from the lateral side when the plaque comes easily, and then repeat the dissection on the medial side of the CCA. The plaque is then transected proximally with Potts scissors, leaving a smooth transition zone, since a clean feathering away of the plaque is almost never possible in the CCA. The proximal end may create a flap despite the direction of blood flow; hence, care should be taken to ensure that the CCA endpoint is not free-floating.

Figure 19–10 Dissection of plaque. Right-sided carotid exposure. The plaque is gently dissected from the arterial wall with a Scanlan plaque dissector or a Freer elevator. The assistant everts the borders of the arteriotomy. Note the abnormal yellow appearance of the plaque, and the deep ulceration with fresh thrombus at the carotid bulb.

Next, the plaque is dissected away from the ICA in the same manner. However, the plaque usually feathers down much more smoothly at the ICA endpoint (Figure 19–11). Occasionally, a shelf of normal tissue protrudes and must be tacked down with suture.

Figure 19–11 Dissection of plaque. Left-sided carotid exposure, plaque removed in toto. The plaque has been dissected along the ICA as well. Loose fragments must be avoided. The surgeon has the option of using tack-down sutures at the ICA endpoint. In this case there is a clean and smooth transition zone that will not require tacking sutures.

The ECA attachment is now the remaining point of plaque fixation. We grasp across the entire plaque at the ECA opening; traction on the plaque everts the ECA, allowing dissection a few centimeters up into the ECA. In addition, the distal ECA can be pushed (milked) proximally with the clamp or forceps. The clamp often tethers plaque to the ECA, so it is sprung while the lumen is held closed with heavy forceps to minimize bleeding, and the plaque is avulsed from the distal ECA. Quick reapplication of the clamp is tempting to stop annoying back-bleeding, but a complete plaque removal is essential. A thrombus can form and can propagate back into the carotid bulb (disastrous) if ECA plaque removal is inadequate, so if there is any question we do not hesitate to extend the arteriotomy up the ECA on an as-needed basis to ensure adequate plaque removal, and then close it with a separate suture line.

All loose fragments should be sought and removed following gross plaque removal. We use a Kittner “peanut” sponge to gently stroke areas that appear loose; the fragments should be removed in a circumferential fashion, elevating them the complete vessel width until they come free at the arteriotomy edge. (The micro-ring tip forceps in the Scanlan-Loftus set are useful for this step.) No attempt should be made to dissect firmly attached fragments that have no danger of elevating or embolizing.

Occasionally, removal of a stony hard plaque, the most difficult type, results in areas of thinning of the posterior arterial wall where only the adventitial layer remains. One or two double-armed, interrupted stitches of 6-0 prolene are used to primarily plicate the thin spot, similar to a tacking suture (from the inside out, with the knot extraluminal). Following declamping, if the arterial wall has a transparent or overly thin appearance, an encircling piece of vascular Hemashield can be used to reinforce the vessel (this is rare). The Hemashield surrounds the artery and is sewn together at the top (Figure 19–12), taking care not to pull it too snug.

Figure 19–12 Reinforcement option. Left-sided carotid exposure. In some cases, such as heavily calcified carotid plaques, the residual arterial arterial wall appears thin, and a buttressing encircling Hemashield sling may be applied at the conclusion of the repair, taking care to ensure that no stenosis is created by pulling the sutures too tight!

While some surgeons prefer to use the microscope to perform the arteriotomy closure, we prefer to continue working under 3.5x loupe magnification. If tacking sutures in the distal ICA are required, two such sutures may be placed, at the four and eight oElsevier Masson SASapos;clock positions. The patch material is then fashioned by placing it over the arteriotomy, cutting it to the length of the opening, and tapering the patch ends. Double-armed 6-0 prolene suture is then used to attach each of the patch ends to the arteriotomy, and rubber-shod clamps are used to secure the needles (Figure 19–13). A running, non-locking stitch is used to close the medial wall suture line from the ICA anchor to the CCA anchor; the anchors are tied together. The suture line is then inspected, and the lateral wall is closed to the level of the carotid bulb with the remaining limb of the ICA anchor stitch. The CCA anchor stitch is then used to close the lateral CCA wall up to the ICA limb. Care must be taken to include all arterial layers and to advance the stitch in small enough intervals so that leaking will not be problematic; no stray adventitial tags or suture ends are sewn into the lumen (Figure 19–14).

Figure 19–13 Anchoring the graft. Left-sided carotid exposure. A Hemashield patch is cut to size and sutured in position at each end with double-armed 6-0 prolene suture.

Figure 19–14 Suturing the graft. The Hemashield patch is secured on both sides with running non-locking stitches. Leaks after declamping are treated with either individual sutures or digital pressure.

If a shunt has been placed, a small opening is temporarily left on the lateral CCA wall where the shunt can be removed. After the EEG technician is notified, the shunt is double-clamped with two parallel, straight mosquito clamps and then cut between the clamps, being sure that the suture material is not entangled in the clamps. Each end of the transected shunt is then removed separately, and the vascular clamps are reapplied.

In sequential fashion, the ICA, ECA, and CCA are opened and closed to ensure that back-bleeding is present. The ICA is then opened and closed again to be certain that no debris or air has re-entered the blind sac there. A heparinized saline syringe with a blunt tip is inserted into the arterial lumen while the two stitches are held tight; the vessel is filled with heparinized saline while a surgeon’s knot is thrown and laid down, and the syringe is then withdrawn, preventing air from entering the vessel. Ten more throws are placed into this final stitch. Declamping is performed in a specific, sequential manner: first the ECA, then the CCA, and after at least a 10-second pause, the ICA. This ensures that any remaining debris or small bubbles are flushed into the ECA circulation. The suture line is then inspected for leaks. Digital pressure and patience will achieve hemostasis within a few minutes; occasionally, a single throw of 6-0 prolene is needed to secure a persistent arterial bleeding point, but rarely (almost never) is reapplication of the vessel clamps necessary if the arteriotomy has been closed properly. Surgicel gauze is then used to line the repair, and all three vessels are checked for patency by a hand-held Doppler probe.

The retractors are removed and wound hemostasis is ensured by direct inspection. Carotid patency is once again confirmed with the hand-held Doppler. To protect against infection, the carotid sheath is closed, and a Hemovac drain is left inside; the platysma is closed as a separate layer for a good cosmetic appearance. The skin edges are approximated using subcuticular stitches, interrupted or running, followed by a tissue adhesive to the skin. A dry, sterile dressing is applied. We do not give protamine.

Postoperative care

Patients are continued on aspirin after surgery. The Hemovac drain is removed the first postoperative day, and patients are generally discharged on the second postoperative day. Any postoperative neurological deficit, including TIA, mandates immediate evaluation of the adequacy of the repair. High-quality, color duplex ultrasonography, CTA, or angiography should be used to check for partial or complete occlusion of the arteries (we do not find MRA to be as helpful here). If there is evidence of a postoperative occlusion the patient is returned to surgery for immediate re-exploration and repair. (This has never happened again once we began the use of routine patch grafting for CEA, which clearly reduces the frequency of this complication.)

Complications

As we have said, low perioperative morbidity and mortality results, commensurate with the results of the cooperative trials, are necessary to justify a recommendation of CEA over medical management. For a skilled experienced surgeon, with proper attention to patient selection and technique, these excellent results should be achievable and reproducible, and technical errors are rare. The majority of complications will be cardiac or pulmonary, and a systematic team approach to the overall care of every patent is essential to minimize this.

Complications such as wound infections or significant postoperative hematomas are rare. Wound infections should be treated with antibiotics and, as needed, exploration with washout; if the deep tissues are involved, an angiogram or CTA should be considered to exclude the possibility of an infectious false aneurysm. Small superficial hematomas usually resolve without intervention, but should be investigated with duplex, CTA, or angiography to be certain that there is no arterial disruption or leak source. In actual fact, we have never seen this happen in our practice of 25 years.

Special situations

Recurrent Stenosis

Recurrent stenosis following primary CEA does occur. The only risk factor repeatedly shown to play a role is continued smoking, but other factors such as hypertension and diabetes mellitus may also contribute. The operation for recurrent stenosis is much more technically demanding and, even as performed by experienced surgeons, is clearly associated with higher risks (Figure 19–15). Our approach is mostly conservative for moderate-grade asymptomatic recurrent stenosis, where we offer the patient either observation for progression or a primary endovascular strategy. For symptomatic recurrent stenosis, or for rapidly progressing (to high-grade) asymptomatic recurrent disease, we are more aggressive, especially with medical therapy failure patients, and we do not hesitate to operate in such cases if the patient clearly understands the attendant risks.

Figure 19–15 Recurrent stenosis. Right-sided reoperation carotid. Dissection and exposure of a redo carotid endarterectomy presents a challenge to any carotid surgeon. In this particular case note the presence of scar tissue, the inability to clearly identify the internal jugular vein, and loss of freely dissectible anatomic planes.

Conclusion

Randomized clinical trial study data confirm the superiority of surgical management, by qualified surgeons, for both symptomatic (>50%) and asymptomatic (>60%) carotid artery lesions. At present, cooperative trial data shows that the best option remains surgery in most cases, despite the intrinsic appeal of less invasive endovascular procedures. Surgical correction of significant carotid artery disease by an experienced surgeon affords excellent outcomes and improves patients’ quality of life.

While every patient is different, and every patient’s anatomy has the potential for being more or less challenging, a standardized approach to CEA repair benefits both the surgeon and the patient. We have described the approach that works best for us and trust that this will prove helpful to surgeons at every level of expertise.