Chapter 58 Carotid Endarterectomy
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
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:
OPERATIVE PROCEDURE
Patient Positioning
Improper Positioning
• Consequence
• Consequence
• Prevention
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
Limited Exposure
• Consequence
• Repair
• Prevention
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.
Perturbation of the Carotid Baroreceptor
• Consequence
• Prevention
Cranial Nerve Injury
Most nerve injuries that occur during CEA are associated with retraction and are usually self-limiting. In order to minimize the risk of permanent injury, a thorough understanding of the neurovascular anatomy in the vicinity of the carotid artery is mandatory. In the NASCET and ACAS trials, the incidence of cranial nerve injury was 8.6%2 and 4.9%,3 respectively. Both studies showed complete resolution of symptoms in the overwhelming majority of their respective participants.
Vagus Nerve Injury
• Consequence
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