Carotid Endarterectomy

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Chapter 33 Carotid Endarterectomy

Wesley S. Moore

Historical Background

The development of surgery for carotid artery disease required three important advances: (1) recognition of the relationship between atherosclerotic disease of the carotid bifurcation and stroke, (2) premorbid identification of carotid bifurcation disease, and (3) the vascular surgical techniques necessary to remove carotid bifurcation atherosclerotic plaque.

For many years, the relationship between carotid artery disease and stroke was overlooked because autopsy protocol did not include harvesting the cervical vessels. Therefore, the only pathology observed in hemispheric stroke was thrombus in the intracranial vessels, most commonly the middle cerebral artery (MCA).One of the earliest observations of the relationship of cervical carotid artery disease with stroke was made in 1856 by Savory, who described a patient with left monocular blindness, right hemiplegia, right dysesthesia, and an occluded left internal carotid artery (ICA) at the carotid bifurcation.¹ A similar observation was made by Gowers in 1875.² It was not until 1914 that Hunt described the relationship between carotid artery disease, transient ischemic attacks (TIAs), and stroke.³ The ability to identify carotid bifurcation disease prior to death awaited the work of Moniz, who in 1927 reported on the technique of carotid angiography. This, for the first time, provided the opportunity to identify carotid artery occlusive disease in the living patient.⁴ In spite of this, clinicians solely used cerebral angiography to evaluate the intracranial circulation. In 1951, Fisher reemphasized the importance of the cervical carotid artery, pointing out that prior to occlusion, a stenosis was present that might be amenable to surgical correction.⁵

The surgical phase for treating carotid artery disease began in 1951. Carrea et al. from Buenos Aires resected the diseased segment of an ICA and restored flow by anastomosing the external carotid artery (ECA) to the distal ICA. They waited until 1955 for sufficient follow-up before reporting the case.⁶ Probably the first successful carotid endarterectomy (CEA) was performed by DeBakey et al. in 1953, but it was not reported until 1959, with a long-term follow-up reported in 1975.⁷ The publication that led to rapid incorporation of carotid artery surgery into clinical practice was the operation reported by Eastcott et al. in 1954. They described a case of a woman who was experiencing hemispheric TIAs, with an associated stenosis of the bulb of the carotid artery. They resected the carotid artery bifurcation and restored flow by a direct anastomosis between the common and distal ICAs with a successful outcome and cessation of symptoms. This report led to an explosion of interest in the treatment of carotid bifurcation disease.⁸

Pathology of Carotid Bifurcation Disease

The most common lesion of the carotid artery bifurcation is an atherosclerotic plaque involving the bulb of the ICA. This localization of plaque is predictable and provides the opportunity for treatment with CEA. The plaque can be calcific, fibrous, or composed of atherosclerotic elements of mixed consistency. Plaques can expand slowly or, with intraplaque hemorrhage, rapidly. Other pathological lesions causing carotid artery stenosis include fibromuscular dysplasia (FMD), Takayasu’s arteritis (TA), radiation arteriopathy, and (rarely) aneurysms of the cervical ICA.

Pathogenetic Mechanisms of Stroke and Transient Ischemic Events

The pathogenetic mechanism for ischemic events is primarily thrombotic or atheroembolic (also see Chapter 30). If the occlusive plaque in the carotid bulb progresses to critical flow reduction, the ICA will proceed to thrombotic occlusion. The pace of the occlusive process is important. If this process occurs slowly, collateral circulation may develop from the contralateral carotid and vertebral arteries. In addition, the ipsilateral ECA can be a source of collateral blood flow by flow reversal through the ophthalmic artery to the siphon of the ICA. Under these circumstances, thrombosis of the ICA may be a silent event. On the other hand, if plaque expansion occurs rapidly or if collateral circulation is inadequate, there will be thrombotic propagation beyond the ophthalmic branch of the ICA into the middle cerebral artery, causing hemisphere infarction and neurological deficit.

In addition to thrombotic occlusion of the ICA, the more common mechanism for ischemic events is rupture of the intimal cover of the atherosclerotic plaque, permitting the discharge of soft atherosclerotic debris into the blood flow stream. These fragments are carried distally to the intracranial branches, fostering either permanent branch occlusion and cerebral infarction or, with fragmentation and thrombolysis of the embolus, a temporary and reversible neurological deficit or TIA. Following plaque rupture and a primary wave of embolization, a defect is left in the plaque that on angiographic inspection resembles an ulcer. This ulcer or plaque defect can be the source of continual embolization, or it can be the nidus for platelet aggregate and thrombotic material to reside. Since there is no attachment of this material within the ulcer crater, pulsatile blood flow can dislodge the material residing with the ulcer crater, leading to a secondary wave of embolization.

Clinical Evaluation

Clinical evaluation of patients with cerebrovascular disease (carotid artery disease) is discussed in Chapter 30.

Preoperative Imaging

The noninvasive examination of choice for patients with suspected carotid artery disease is a carotid duplex ultrasound scan using modern equipment in a validated vascular laboratory (also see Chapter 12). This study identifies lesions in the carotid artery, classifies the severity of stenosis, and provides information regarding plaque consistency. The opportunity to examine flow velocity and pulse wave velocity analysis provides information about other portions of the circulation, including proximal lesions at the level of the aortic arch and distal intracranial lesions. In many centers, the duplex scan serves as the definitive preoperative study.⁹ Additional studies such as magnetic resonance imaging (MRI), magnetic resonance angiography (MRA), computed tomographic angiography (CTA), or catheter-based contrast angiography are reserved for special circumstances.⁹ Use of MRA or CTA in conjunction with duplex ultrasound of the carotid artery is considered when the results of duplex ultrasonography are difficult to interpret or inconsistent with the clinical presentation.

Magnetic resonance angiography is used frequently because it does not require ionizing radiation. When contrast is added, the images are often clear and resemble those obtained via catheter-based intraarterial angiography, providing a sensitivity and specificity of 88% and 84%, respectively, for diagnosing a 70% to 99% stenosis.⁹ Magnetic resonance angiography permits imaging of the intracranial vascular anatomy, and when combined with MRI, can identify areas of cerebral infarction or other intracranial pathology. The major limitation of MRA is that it tends to overestimate percent stenosis of lesions in the carotid bifurcation (also see Chapter 13). This phenomenon occurs because turbulent blood blow, such as occurs at carotid bulb stenosis, results in signal dropout and void, giving the impression of a high-grade carotid stenosis.

Computed tomography (CT) and CTA are also quite helpful in identifying intracranial lesions. Computed tomography angiography is accurate in identifying and quantifying intracranial and extracranial carotid stenosis (also see Chapter 14). The sensitivity and specificity of CTA for determination of carotid artery stenosis are 95% and 99%, respectively.¹⁰ The major drawbacks of CT scanning are exposure to ionizing radiation and the requirement for a large volume of iodinated contrast material, which can be nephrotoxic or cause allergic reaction in patients sensitive to iodine.

Intraarterial contrast angiography is considered the gold standard for identifying and quantifying arterial stenoses. Major disadvantages of this invasive procedure include arterial injury, occlusion, and embolization resulting in cerebral infarction. In the Asymptomatic Carotid Artery Study (ACAS), angiography was associated with a 1% stroke rate.¹¹ In addition, it requires ionizing radiation and iodinated contrast material. This technique is now rarely indicated prior to carotid endarterectomies. It does have a role for preprocedure imaging as a part of carotid angioplasty/stenting.

Techniques of Carotid Endarterectomy

An arterial canula is placed for continuous blood pressure monitoring and periodic sampling of blood gases. Carotid endarterectomy can be performed under either local or general anesthesia. General anesthesia is more comfortable for the patient. It affords a quiet operative field and allows the surgeon to concentrate without distraction by patient movement or discomfort. It also allows optimal airway control, ventilation, and oxygenation.

The patient is positioned supine on the operating table. A cushion is placed under the shoulders to allow for mild neck extension, and the head is rotated away from the side of incision.

When the carotid artery is clamped for the endarterectomy procedure, the surgeon has several choices regarding the assurance of adequate blood flow to the ipsilateral cerebral hemisphere. About 90% of patients tolerate temporary clamping of the carotid artery because adequate collateral circulation is provided through the circle of Willis. For patients with inadequate collateral circulation, a temporary shunt is required to maintain adequate cerebral perfusion during endarterectomy to avoid periprocedural cerebral infarction. These observations have led to two forms of practice: routine shunting of all patients or selective shunting based upon intraoperative monitoring. The argument for routine shunting is that special monitoring is not required. The argument in favor of selective shunting is that there are complications unique to the use of an internal shunt. These include intimal damage with shunt placement and embolization of air or atheromatous debris through the shunt to the intracranial circulation, resulting in a cerebral infarction. In addition, when a shunt is in place, it is difficult to see the end of the endarterectomized segment, thus opening the possibility of leaving a residual intimal flap that can lead to thromboembolism and possibly postoperative carotid occlusion. Therefore, since only 10% of patients undergoing CEA require a shunt, there is little reason to expose the majority 90% who do not require a shunt to its potential complications.

There are several acceptable methods for monitoring the adequacy of cerebral perfusion. The first method that was described was measurement of ICA backpressure in patients undergoing CEA under local anesthesia. With clamping of the common carotid artery (CCA) and ECA, the residual pressure in the carotid artery determines the perfusion in the middle cerebral artery. One study found that the conscious response to clamping correlated with the ICA backpressure.¹² The minimum pressure associated with no neurological deficit was 25 mmHg. This observation was subsequently validated in patients undergoing operation with general anesthesia.^13,¹⁴ The next method, and one that is most commonly used today, is continuous electroencephalographic (EEG) monitoring. This method is sensitive, easy to use, and has the advantage of providing continuous monitoring rather than a single observation. Other methods used to monitor cerebral perfusion include assessment of the somatosensory evoked response and transcranial Doppler (TCD) interrogation.

There are two possible incisions that can be used. Some surgeons use an oblique incision in a skin crease, with the thought that the resulting scar will be more cosmetic in appearance. More proximal or distal exposure, when required, is quite difficult to obtain with this incision. The alternative is an incision placed along a line connecting the suprasternal notch with the mastoid process. The surgeon can begin with a relatively short incision over the carotid bifurcation and extend it proximally or distally if necessary. The incision is deepened through the platysma layer. The sternocleidomastoid muscle is mobilized until the jugular vein is identified. The common facial vein and any accessory facial veins are divided between ligatures. The vein is allowed to retract laterally, and the carotid artery will be found immediately below the vein. Care must be taken to identify the vagus nerve because its relationship within the carotid sheath can be quite variable. The CCA is circumferentially mobilized within the perivascular plane of Leriche. Mobilization is continued distally until the carotid bifurcation, ICA, and ECA are fully mobilized. The ICA should be exposed far enough so that circumferentially normal artery is encountered. If additional exposure is required, the nerve to the carotid sinus can be divided. This will allow the carotid bifurcation to drop inferiorly and permit more distal mobilization of the ICA. In the case of a high carotid bifurcation or long extension of the plaque in the ICA, more extensive exposure of the ICA can be obtained by mobilizing or, if necessary, dividing the posterior belly of the digastric muscle. Finally, exposure of the ICA to the base of the skull can be obtained by dividing the styloid process. This is very rarely required.

Once the arteries are sufficiently mobilized, intravenous (IV) heparin is administered. The dose varies from 2500 units to 5000 units depending upon the size of the patient and the nature of preoperative antiplatelet agents administered. The internal, external, and common carotid arteries are then clamped. A longitudinal arteriotomy is made in the CCA and extended through the plaque distal to normal ICA. During this time, the EEG monitor is observed. If no EEG changes indicative of brain ischemia appear with clamping, the surgeon proceeds with the endarterectomy procedure. If there are EEG changes with clamping, an internal shunt is placed. The exception for selective shunting occurs in patients who have had a prior stroke on the side of operation; shunt placement can lessen the risk of stroke in the ischemic penumbra that surrounds the area of infarction.

Once the decision is made concerning the shunt, the surgeon proceeds with endarterectomy. Endarterectomy of the external carotid is blind. There should be a feathered endpoint in the ICA. The endarterectomy is carried to the clamp, which serves as the endpoint. The plaque should be cleared in the common carotid artery, and the proximal endpoint may require sharp division. Once the plaque is removed, the carotid artery is irrigated with heparinized saline, and any loose bits of medial debris are carefully removed. The segment between the ICA endarterectomy and normal intima is carefully inspected to ensure that the intima is adherent to the media at that level. If an intimal flap is present, it is carefully removed back to a point of adherence.

The arteriotomy is closed with a patch (typically Dacron) to prevent stenosis and accommodate any restriction from intimal hyperplasia that might occur with primary closure. Patch closure is associated with a lower incidence of postoperative thromboembolic complication and recurrent carotid stenosis.¹⁵ Before the arteriotomy is completely closed, the vessels should be “backbled” and flushed to remove any debris. Upon completion of closure, flow is restored first to the ECA and then the ICA. At this time, it is important to verify the quality of the endarterectomy by intraoperative duplex ultrasound scanning or a completion angiogram. The latter permits accurate visualization of the carotid artery bifurcation and the intracranial portion of the repaired ICA to detect any anatomical problems or residual stenosis. If an intimal flap is seen in the ICA, the patch is removed and the arteriotomy extended beyond the flap, thereby reducing the risk of postoperative thromboembolism. A new patch is used to close the arteriotomy. More commonly, an endpoint problem is found in the ECA, which can lead to postoperative thrombosis of the ECA and then in retrograde propagation of thrombus to the ICA, embolism, and stroke.¹⁶ When a problem is identified, the ECA is clamped both at its origin and distally. A transverse arteriotomy is made just distal to the residual lesion, and the remaining plaque is removed. The transverse arteriotomy is closed with interrupted polypropylene sutures, and flow is restored. The neck incision is then closed. Closure consists of a running absorbable suture in the platysma layer and a running absorbable subcuticular suture for cosmetic skin closure.

Postoperative Management

A brief postoperative neurological assessment is performed in the operating room following extubation. If no neurological deficits are noted, the patient is transferred to the recovery room for monitoring. Once the patient is fully awake, the blood pressure controlled, and the neck free of hematoma, the patient is transferred to a regular hospital room for overnight observation. Postoperative blood pressure monitoring and treatment is important. Patients often become hypertensive after awakening from anesthesia. Regulation of blood flow is impaired on the side of endarterectomy for approximately 3 to 6 weeks, so the ipsilateral cerebral hemisphere is vulnerable to elevated postoperative blood pressure. Uncontrolled hypertension can result in excessive perfusion pressure, the consequences of which range from headache to seizures and lead to intracerebral bleeding resulting in major stroke or death. Hypotension and bradycardia occur from baroreceptor activation caused by stimulation of the nerve to the carotid sinus. This can easily be treated by injecting the nerve with 1% lidocaine. Following recovery from anesthesia, hypotension is a rare occurrence.

If the patient is stable overnight and does not have a new neurological complication, he or she can be discharged the following morning. The patient is instructed to resume usual medications, including an antiplatelet agent.

The first postoperative visit should occur in approximately 3 weeks, at which time a carotid duplex ultrasound scan is performed to assess the result of endarterectomy and establish a new baseline for further follow-up. Additional carotid ultrasound examinations are recommended at 6 months and then 1 year from the time of operation.

Complications of Carotid Endarterectomy

The mortality rate reported in large surgical trials of CEA is approximately 1% and is usually cardiovascular in nature.¹⁷ This mortality rate is similar to that observed in a general vascular surgical practice.¹⁸ The risk of stroke is approximately 2.6%.¹⁹ The principal etiology of postoperative stroke is embolism of thrombus or atheromatous debris.²⁰

Cranial nerve injury occurs in up to 7% of patients, although permanent nerve palsy is noted in 1%.²¹ Several cranial nerves lie within the operative field, including the vagus (X), hypoglossal (XII), and (less commonly) glossopharyngeal (IX). The mandibular branch of the facial nerve (VII) may be at risk if the surgical incision is made anterior to the ear instead of on a line connecting the mastoid process and the suprasternal notch.

Despite achieving hemostasis prior to wound closure, hematomas may develop. These are usually evident within the first 4 hours following operation. Patients with expanding hematomas should return to the operating room for evacuation and restitution of hemostasis. A bleeding source after hematoma evacuation usually is not found. Judicious use of heparin, particularly if the patient is on more than one antiplatelet agent, is important. Heparin reversal with protamine is associated with risk of anaphylaxis. Prevention may be the best strategy. Irrigating the wound with a dilute antibiotic solution and observing for bleeding sites (to be controlled with ligature or electrocoagulation) may be the best strategy.

Wound infection is rare because patients undergoing CEA receive prophylactic antibiotics. If a wound infection occurs, the patient should be hospitalized and treated with an IV antibiotic therapy regimen. A deep wound infection may affect a prosthetic patch and threaten the integrity of the carotid artery.

Clinical Trials of Carotid Endarterectomy

Prospective randomized trials comparing CEA to medical management involve either symptomatic or asymptomatic patients. They serve as the basis for current CEA recommendations in appropriately selected patients.²¹

Symptomatic Carotid Endarterectomy Trials

The North American Symptomatic Carotid Endarterectomy Trial (NASCET) was a multicenter prospective randomized trial carried out in the United States and Canada. The trial was divided into two cohorts; one involved patients with carotid artery stenosis of 70% to 99%, and the other involved patients with stenosis of 50% to 69%. The high-grade (70%-99%) stenosis component of the study was stopped after only 18 months because stroke morbidity and mortality for CEA was 9%, compared with 26% for best medical management.²² The second part of the study, for patients with moderate stenosis, went to completion. It demonstrated a 5-year event rate after CEA of 15.7%, vs. 22.2% for medical management.²³ The European Carotid Endarterectomy Trial (ECST) was conducted during the same time as NASCET. It recruited a population similar to the high-grade stenosis portion of NASCET, with similar findings. Stroke morbidity and mortality after CEA was 10.3%, vs. 16.8% for medical management.²⁴ The Veterans Administration Symptomatic Trial was started after the other two trials were ongoing. It was stopped after 189 patients were entered as the results of the North American and European trials were reported. Despite the small number of patients, the rate of stroke and crescendo TIA after only 12 months’ follow-up was 7.7% for surgery and 19.4% for medical management.²⁵ Based on these trials, CEA is recommended for symptomatic patients with greater than 50% stenosis.²¹

Asymptomatic Carotid Endarterectomy Trials

The Veterans Affairs Asymptomatic Carotid Endarterectomy Trial enrolled 444 asymptomatic men with carotid artery stenoses greater than 50% as documented by angiography. These were randomized to CEA plus best medical management, or best medical management alone. At the end of 5 years, the primary event rate of TIA, stroke, and death was 8% for surgery, vs. 20.6% for medical management.²⁶ The ACAS trial was a multicenter prospective randomized trial that compared CEA plus best medical management to best medical management alone. At the end of 5 years, the primary event rate of stroke or death was 5.1% for CEA and 11% for medical management.¹¹ The Asymptomatic Carotid Stenosis Trial (ACST) randomized 1560 patients to immediate CEA and 1560 patients to medical management. At the end of 5 years, the primary event rate for immediate CEA was 6.4%, compared with 11.8% in patients randomized to medical management.¹⁹ The American College of Cardiology/American Heart Association (ACC/AHA) guidelines give a class IIa recommendation for CEA for asymptomatic patients with carotid artery stenosis greater than 70%.