Atherosclerosis accounts for approximately 90% of extracranial cerebrovascular disease, with the remaining 10% being attributed to such disease processes as fibromuscular dysplasia, traumatic or spontaneous dissection, aneurysms, and arteritis, including Takayasu arteritis.

Atherosclerotic plaques occur preferentially at areas of vessel bifurcations, and the process is similar to that seen with coronary artery disease (CAD). It often begins in the bulbous portion of the ICA on its posterior lateral wall. These plaques can enlarge in several ways; they may continue to slowly enlarge from accumulation of cholesterol and fibroblasts. Aternately, central necrosis of the plaque and rupture of the intimal lining of the vessel will lead to discharge of atheromatous debris into the lumen of the vessel as an embolus. The atherosclerotic plaque can also become a nidus for platelet deposition and thrombosis and/or further embolization to the brain. Accumulation of the arteriosclerotic plaque may result in progressive stenosis or total occlusion of the carotid artery with subsequent thrombosis of the ICA distal to the lesion. Another mechanism by which there may be sudden plaque enlargement is intraplaque hemorrhage. If the intima overlying the site of plaque hemorrhage ulcerates, the necrotic contents of the atheroma escape into the lumen and cause cerebral embolization with transient ischemic attacks (TIAs) or cerebral infarcts. The CCA bifurcation and the proximal ICA account for 50% of atherosclerotic extracranial cerebrovascular lesions. Vertebral artery lesions account for 20%, left subclavian arterial lesions account for 10% to 15%, and lesions of the innominate and right subclavian arteries account for 15%.

The most common cause of symptomatic cerebral ischemic events is an embolus. The majority are arterial in origin (carotid) with cardiac sources a distant but still significant second. If the embolism breaks up quickly
from mechanical forces or from the effect of arterial prostacycline, the symptoms will be transient, i.e., TIAs. If the embolic fragment persists, however, it can lead to focal infarction. An ICA thrombosis usually produces a column of thrombus that stops at the ophthalmic artery and remains stable if there is sufficient collateral circulation via the circle of Willis. In this instance, the thrombotic event may be entirely asymptomatic. However, if small thrombi rather than a thrombotic column form and are subsequently carried to the intracranial vessels by continuous blood flow, then the patient will experience cerebral symptoms that can vary from transient amaurosis fugax or hemispheric events to a profound fixed hemiplegia. If the collateral circulation to the circle of Willis is inadequate, the sudden loss of blood flow through a diseased ICA may induce a sudden drop in flow to the cerebral hemisphere, resulting in ischemic infarction.

Identification of disease in the carotid system uses both qualitative and quantitative data. Careful attention to unusual echoes on the image serves as a qualitative guide to the presence of disease at sites where careful scrutiny with a Doppler component should be performed. The changes in spectra obtained from the common, internal, and external carotid arteries provide quantitative information for the determination of the severity of disease in these locations. Multiple clinical studies have reported an overall accuracy of 80% to 97% in diagnosing carotid artery stenosis.

Duplex ultrasound is likely to remain the initial screening method of the carotid bifurcation in most centers. However, MRA may be used as a screening method in two situations:

In many centers, angiographic carotid evaluation is no longer routine. The risk of stroke during angiography is about 1% and the cost of angiography is $5,000 to $6,000. There is a theoretical potential to miss significant lesions in the carotid siphon or an intracranial aneurysm or tumor as the cause of symptoms. However, it is unlikely that carotid siphon disease will produce significant symptoms. Intracranial aneurysms occur in approximately 1% to 2% of patients undergoing arteriography, but most are small and unlikely to be affected by CEA. With the advances in imaging techniques, the concern for occult brain tumors has become less relevant.

Overall, CEA can safely be performed without arteriography when the following criteria are met:

Most of our patients undergoing CEA receive general anesthesia with intra-arterial pressure monitoring, routine shunting, and preferential patching with or without intraoperative imaging. Although some surgeons prefer local or cervical block anesthesia, general anesthesia has the advantage of reducing several metabolic demands and increasing cerebral blood flow. Endotracheal intubation also provides good airway control and reduces patient and physician anxiety. Nasotracheal intubation can be used to facilitate exposure of the distal cervical segment of the ICA in patients who are known to have high carotid stenosis or in patients undergoing reoperation. Aspirin therapy is generally continued throughout the peri-operative period. The liberal use of vasopressors or nitroprussides to maintain blood pressure in the patient’s optimal physiologic range is critical.

The patient is positioned supine with the head turned away from the side of the operation. The neck is moderately extended on the shoulders. Proper lighting is essential and loupe magnification routine. The cervical incision is made parallel and somewhat anterior to the sternocleidomastoid muscle and centered over the carotid bifurcation (Fig. 27-1A). This incision can be extended proximally to the sternal notch for more proximal CCA lesions, and distally to the mastoid process for higher exposure. The upper end of the incision should be angled posterior to the earlobe to avoid the parotid gland. The incision is carried down through the platysma and the stenocleidomastoid muscle laterally. Self-retaining retractors are then placed. An alternative incision placed obliquely in the skin crease over the carotid bifurcation can be used (Fig. 27-1B). After the incision is deepened through the platysma, the subplatysmal space between the sternocleidomastoid and the trachea is mobilized. This incision has the advantage of producing a more cosmetically acceptable scar than the vertical incision. However, it does have the following disadvantages:

With either incision, subsequent steps are identical. The internal jugular vein is visualized, and the carotid sheath is opened along the anterior border of the vein. The internal jugular vein is retracted laterally, and the common facial vein is ligated (Fig. 27-1C, 27-1D, and Fig. 27-1E). Dissection is continued anterior to the CCA to avoid injury to the vagus nerve. The vagus nerve usually lies in the posterior lateral position within the carotid sheath but occasionally may spiral anteriorly, particularly in the lower end of the incision. Attention should be paid to various cranial nerves, including IX, X XI, and XIII, the marginal mandibular branch of VII, and the rare nonrecurrent laryngeal nerve that comes directly off the vagus on the way to innervate the vocal cord (Fig. 27-1E and Fig. 27-2A). This nerve can cross anterior to the carotid artery and be mistaken for a part of the ansa hypoglossi, resulting in cord paralysis. This anomaly is most often noted on the
right side of the neck (Fig. 27-2B). The vagus nerve may be closely adherent to the carotid bulb, and it becomes nearly confluent with the hypoglossal nerve near the styloid process. The CCA is generally mobilized for a sufficient length proximal to the carotid lesion. It may be necessary to inject a local anesthetic in the area of the carotid bifurcation to block the nerve to the carotid body to prevent reflex bradycardia. Dissection is continued upward to isolate the ECA. The ICA is mobilized to a point where the vessel is completely normal. The hypoglossal nerve is often surrounded by small veins that should be ligated carefully. The hypoglossal nerve may be injured by retraction; therefore, the structures that tether it in place, such as the artery and vein to the sternocleidomastoid muscle, the descending hypoglossal branch of the ansa cervicalis, and the occipital artery may require division to mobilize the nerve for distal ICA exposure. Careful attention should also be given to the superior laryngeal nerve, which is usually located medial to the ICA. The superior laryngeal nerve divides into external and internal branches that pass posterior to the superior thyroid artery, and it may be harmed while controlling either of these two vessels. The glossopharyngeal nerve crosses the ICA near the base of the skull and is best protected by maintaining dissection very close to the anterior surface of the ICA. Excessive or prolonged retraction of the upper aspect of the incision may cause temporary compression injuries laterally to the greater auricular nerve or medially to the marginal mandibular branch of the facial nerve.

In patients with a high carotid bifurcation or an extensive lesion, mobilizing the ICA distally can be achieved by several maneuvers. The skin incision can be extended all the way up to the mastoid process, with complete mobilization of the sternocleidomastoid muscle toward its tendinous insertion on the mastoid process. It is important to avoid injury to the spinal accessory nerve, which enters the substance of the sternocleidomastoid muscle at that level.
The digastric muscle can be mobilized anteriorly, or if necessary, divided, given additional exposure (Fig. 27-1D). If further exposure is needed, the styloid process can be transected, and then the mandible can be displaced anteriorly. Some authorities have described dividing the ramus of the mandible to gain additional exposure.