INTRODUCTION

In the United States, the incidence of new and recurrent stroke is estimated at approximately 700,000 per year, with over 80% attributable to an ischemic etiology.¹ Surgery for the prevention of ischemic stroke from atherosclerotic extracranial vascular disease was first performed by Eastcott, Pickering and Rob in 1954. A carotid endarterectomy (CEA) was performed for symptomatic atheroembolic disease. The procedure fell into disfavor by many in the ensuing years until two prospective, randomized trials (North American Symptomatic Carotid Endarterectomy Trial [NASCET] and Asymptomatic Carotid Atherosclerosis Study [ACAS]) as well as numerous corollary trials demonstrated CEA to be effective for symptomatic and asymptomatic patients with appropriate degrees of stenosis.²^–⁵ CEA is a procedure heavily dependent on the experience and technique of the operating surgeon. The actual surgical technique that is the foundation of CEA has changed little, but patient selection, intraoperative care, and postprocedural follow-up have been greatly refined.

The CEA has long maintained a prominent position in stroke prevention, and its efficacy has been borne out in a number of landmark trials. Nationally, between 180,000 and 200,000 CEAs are performed each year.⁴ NASCET and the European Carotid Stenosis Trial (ECST) both demonstrated decreased stroke risk in symptomatic patients undergoing CEA. Symptomatic patients, in a medically treated cohort, with 70% or greater arterial stenosis were shown to have a cumulative 2-year risk of ipsilateral stroke of 26% versus 9% in those treated surgically; the absolute risk reduction was 17%.² In the ACAS, a lower risk of stroke and death was seen in patients managed with surgery over matched controls receiving medical management. The 5-year risk of stroke was 5.1% in patients treated with surgery versus 11% in those treated medically, with an absolute risk reduction of 5.9%.³ These findings accounted for a 53% relative risk reduction in the surgical cohort over the 5-year study period.³

Unlike therapy for coronary and most other peripheral vascular occlusive disease, the critical clinical aspect of extracranial cerebrovascular disease is not chronic ischemia and lack of blood flow, but embolic events. Although we continue to use the degree of stenosis as a primary factor in the evaluation of appropriate candidates for therapy, symptoms are the most predictive finding. Much remains to be done to determine the nature of plaque stability and to develop an understanding of the critical events that transform a “dormant” lesion into an “active” lesion with acute changes and embolic phenomena.

Open surgical exposure of the carotid bifurcation results in a small physiologic insult to the patient. Subcutaneous exposure of the carotid bifurcation can be done with the patient under either local or general anesthesia. The procedure requires a maximum amount of control through employing distal control of the internal carotid, reversal of flow in the internal carotid prior to restoring antegrade flow, visual inspection and débridement of the plaque site, and control of the proximal and distal endpoints of the endarterectomy. CEA is based on five fundamental principles:

1. Minimal physiologic insult—predictable location and subcutaneous exposure.

2. Arterial control—reliably achieved without additional manipulation.

3. Maintenance of cerebral perfusion.

4. Plaque removal—complete removal of embolic lesion.

5. Lumen enlargement—endarterectomized vessel greater than 100% of native vessel diameter, especially with patch angioplasty providing prevention of restenosis.

KEY DECISION POINTS

• Anesthesia: local/regional versus general

• Intraoperative shunting: selective versus routine

• Arterial closure: primary versus patch

INDICATIONS

• Symptomatic stenosis greater than 50%

• Asymptomatic stenosis greater than 60% to 80%

• Symptomatic ulcerated plaque type B/C

• Asymptomatic ulcerated plaque type C

OPERATIVE PROCEDURE

Patient Positioning

During CEA, the patient assumes a supine position with extension of the neck and contralateral rotation of the head toward the opposite side. The arms should be tucked to the sides and the table slightly flexed at the waist. Proper positioning affords maximal exposure of the carotid triangle. The geometry of the neck may also be enhanced by using a shoulder roll to optimize neck extension. Caution is exercised to avoid hyperextension because this may place excessive tension on the vessels of the neck. The patient should be prepared widely and draped in a manner that allows exposure of the anterior cervical triangle. The operative table may be rotated to provide the optimum visibility for the operator.

Improper Positioning

Skin Incision

The length of the skin incision is often governed by the morphology of the neck. A vertical skin incision extending from the mastoid process to just above the sternoclavicular junction coursing along the anteromedial margin of the sternocleidomastoid muscle represents the classic skin incision utilized during exposure of the cervical carotid artery (Fig. 58-1). Preprocedure duplex-assisted localization of the carotid bifurcation may be used in order to limit the length of the traditional skin incision to one that may be more esthetically pleasing.⁶ Alternatively, a transverse cervical incision made along Langer’s lines may be used to gain access to the carotid artery. There is no demonstrable difference in results when comparing the longitudinal and the transverse incisions with similar efficacy and incidence of cranial nerve deficits.⁷

Figure 58-1 Classic vertical skin incision.

Limited Exposure

• Repair

Additional exposure can be obtained by extension of the incision. Distal exposure is most commonly the problem. Care must be taken not to violate the substance of the parotid gland during this maneuver so as to avoid injury to the facial nerve or create a sialocutaneous fistula. Subluxation of the mandible can also aid in very high distal exposure.

• Prevention

Whereas preoperative duplex localization may facilitate identification of the carotid bifurcation prior to skin incision, these incisions may necessitate the use of excessive amounts of traction in order to adequately mobilize the distal internal carotid artery. Ideally, adequate exposure should include the diseased portion of the common and internal carotid arteries as well as a region on the normal-appearing distal internal carotid artery where vascular clamps may be applied. By compromising adequate exposure, the operator may experience difficulty securing an adequate dissection endpoint or may cause inadvertent neurovascular injury, leading to increased patient morbidity.

Dissection and Exposure of the Carotid Artery

The skin incision is deepened through to the platysma muscle, and the dissection is carried along the anteromedial border of the sternocleidomastoid muscle until the carotid sheath is reached. Division of the facial vein allows lateral retraction of the internal jugular vein and visualization of the carotid artery. The vagus nerve should be identified as it courses deep and posterolateral to the common and internal carotid arteries (Fig. 58-3). In a small subset of patients, the vagus nerve may assume an anterior position within the carotid sheath. This must be recognized and the nerve carefully retracted to complete the arterial exposure. During the arterial dissection, caution should be taken to avoid manipulation of the vessels by “dissecting the patient away form the artery.” Mobilization of the internal carotid artery should be extended distally just beyond the region of disease. Anticoagulation is administered prior to obtaining proximal and distal arterial control, beginning with the distal internal carotid artery, followed by the common and external carotid arteries.

Figure 58-3 Intraoperative dissection with vagus nerve (arrow).

Perturbation of the Carotid Baroreceptor

• Consequence

The carotid sinus region is an important baroreceptor area involved in blood pressure regulation.⁸ During dissection of the carotid artery, caution should be exercised to avoid disruption of the carotid sinus nerves (Fig. 58-4). Sinus bradycardia and hypotension may occur owing to baroreceptor stimulation with the possibility of a new setpoint established in the perioperative period.

Grade 1 complication