compromise. An expanding hematoma should be evacuated emergently and the bleeding source

identified. Cranial nerve injuries are a common complication, however, the incidence varies greatly

with a range between 1% and 30%, more common experience showing an incidence of 0.5% to

4.7%.25,37 Cranial nerve injuries are shown in Table 89-4. Cerebral hyperperfusion is an uncommon

complication after CEA. The cause of hyperperfusion is disordered autoregulation of arteriolar cerebral

blood flow after return of flow after a tight stenosis. Symptoms start with a headache and progress to

seizures and intracerebral hemorrhage with a high mortality rate. Severe hypertension is a risk factor

and requires urgent lowering of the blood pressure and anticonvulsant therapy. Contralateral severe

internal carotid artery stenosis is another important risk factor for the development of cerebral

hyperperfusion syndrome. Restenosis can occur after CEA. If occurring within 2 years, it is likely related

to intimal hyperplasia and can improve. After 2 years, it is likely caused by atherosclerosis. Patch

infection and pseudoaneurysm formation are also other complications following CEA.

Carotid Stenting

Technique

CAS requires careful patient identification and examination of adequate preoperative imaging for

procedural success. Prior to intervention, axial imaging is highly recommended. This is most generally

an MRA or CTA with thin cuts. This should include imaging from the aortic arch all the way to beyond

the circle of Willis. Examination of the aortic arch will identify those with anatomy that would make

brachiocephalic vessel cannulation and the tracking of wires and catheters difficult. With excessive

manipulation, or not identifying arch pathology, a stroke could be possible. The angle of the aortic arch,

brachiocephalic ostial disease, tortuosity of brachiocephalic vessels, arch thrombus, or calcification must

all be identified for safe carotid stenting. Furthermore, there are specific lesion characteristics that can

make stenting more difficult or risky, such as, hypoechoic plaque, ulceration, lesion length,

circumferential calcification, or thrombus. A careful physical examination must be performed to identify

femoral and iliac artery anatomy that would make arterial access difficult. Although the transfemoral

approach is the most common, there are a variety of other approaches that are possible, including

transcervical or transradial.

Table 89-4 Cranial Nerve Injuries Associated with Carotid Endarterectomy

Prior to the carotid stenting procedure, the patient should be on dual antiplatelet therapy, typically

aspirin 325 mg for at least a week prior and have received around 450 mg of clopidogrel. The

procedure is either performed in an angiography suite or hybrid operating room. The patient requires

arterial line placement for blood pressure control and should stay awake during the procedure for

frequent neurologic checks. The patient is placed in the supine position and the groins are prepped.

Retrograde femoral access is gained and the patient is heparinized (100 units/kg). Thoracic angiogram

is rarely required because previous CTA or MRA can clearly define arch anatomy. Selected

catheterization is then performed. The anatomy dictates the combination of wire and catheter that will

work in a particular situation. Angiography after proximal carotid artery cannulation should be

performed to evaluate the stenosis for location and severity, contralateral circulation, vertebrobasilar

circulation, and intracerebral circulation. These can all influence the approach to the procedure. Balloon

occlusion, for instance, may not be a good option for embolic protection if preoperative imaging and

2555

angiography reveal an incomplete circle of Willis and inadequate collateral flow.

Once the decision is made to proceed with carotid stenting, selective catheterization of the ipsilateral

external carotid artery is accomplished, as long as the lesion does not involve its origin, and the catheter

advanced. Great care must be taken to avoid inadvertently manipulating the lesion and risk

embolization distally. Once the catheter is in the external carotid artery, a long stiff 0.035-in-wire is

exchanged and navigated through the arch. Significant tortuosity can often require subsequent

maneuvers for success, such as breath holds or the use of special guiding sheath and selective catheter

systems that can be advanced over each other seamlessly in difficult anatomy. At this point a 90-cm 6-Fr

sheath is advanced into the proximal common carotid artery, again insuring that the sheath is not

advanced past the beginning of the plaque. The stiff wire is removed and angiography is again

performed for mapping purposes, assisting in cannulation of the internal carotid artery (Fig. 89-11).

Most practitioners use embolic protection devices (EPDs) to reduce the risk of CVA during the

procedure during wire manipulation, balloon angioplasty, and stent placement. There is a choice of

distal filters, distal balloon occlusion, and flow stasis or reversal (Fig. 89-12). Flow stasis or reversal

creates a situation where there is no antegrade flow in the internal carotid artery so embolization is

unlikely to occur. After completion of any case, suction can be performed to remove any free floating

debris. The benefit of flow reversal is the avoidance of having to cross the lesion unprotected. Filter

protection requires wire cannulation past the lesion and placement of a filter in the distal internal

carotid artery for embolic protection. The filter is removed at the completion of the case. Significant

vasospasm in the distal internal carotid artery may occur when a filter is used.

The EPD is carefully advanced over a 0.014-in wire into the distal internal carotid artery and

deployed. All remaining parts of the procedure occur over the EPD wire via a rapid exchange platform.

Predilatation of the lesion is typically accomplished with a 4- to 5-mm balloon, but should be used

sparingly as it can increase the risk of stroke. There are a variety of stents available, generally either

open or closed cell. This is in regard to the structure of the stent. The stents are self-expanding and their

flexibility is determined by the number of connections between the cells of the stent. The more

connection, the stiffer the stent (closed cell). Decisions regarding the type of stent depend on the lesion

characteristics, tortuosity, and symptomatic status. Most practitioners prefer closed-cell stents for use in

symptomatic patients to lessen embolization or extrusion of the plaque through the stent (Fig. 89-13).

Figure 89-11. Carotid angiography shows a high-grade stenosis with “string sign” in the internal carotid artery with underfilling of

the distal artery.

The size of the stent typically depends on the size of the internal and common carotid artery and

comes in straight and tapered configurations. Once the stent is deployed, often postdilatation is

necessary (Fig. 89-14). Care must be taken with balloon dilatation near the bulb as severe bradycardia

can occur secondary to stimulation of the glossopharyngeal nerve. Atropine should be immediately

2556

available and good communication with nursing and anesthesia is important. The EPD is removed and

completion angiography is performed. The sheath is then removed and the puncture site closed with a

closure device or manual compression. As heparinization is not typically reversed, it is common to use a

closure device, which allows early mobilization and hemodynamic stability. Throughout the procedure

the patient is assessed from a neurologic standpoint. Postprocedure the patient is monitored similar to a

CEA. The patient continues clopidogrel for 1 month and aspirin for life.

Complications

The most important and serious complication after carotid stenting is neurologic events. As the vast

majority of patients are awake, MI is much less frequent. The risk of MI after carotid stenting is lower

than CEA: 0.4 to 1.1 versus 0.6 to 2.3.24,25,38 The EPD can cause distal ICA vasospasm, dissection, or

occlusion if full of debris. A full filter should be removed slowly, a dissection treated with stenting, and

nitroglycerin injection used for severe vasospasm. Acute thrombosis of the stent can cause a profound

neurologic defect and usually requires immediate explantation and endarterectomy. An embolus

identified on angiography can be managed with neurorescue. Options include aspiration thrombectomy,

catheter-directed thrombolysis, or snare removal. Intracerebral hemorrhage is a rare complication.

Other complications include access site complications, such as bleeding and pseudoaneurysms.

Figure 89-12. Different type of embolic protection devices. A: RX Accunet embolic protection system (Abbott Vascular, Redwood

City, Calif.) B: Emboshield NAV6 embolic protection system (Abbott Vascular, Redwood City, Calif.). C: Mo Ma proximal cerebral

protection device with balloon occlusion (Medtronic, Minneapolis, Minn.). D: Gore flow reversal system (W. L. Gore and

Associates, Flagstaff, Ariz.).

2557

Figure 89-13. Different carotid artery stents. A: Xact carotid artery stent (Closed cell) (Abbott Vascular, Redwood City, Calif.) B: RX

Acculink carotid artery stent (Open cell) (Abbott Vascular, Redwood City, Calif.)

Figure 89-14. Carotid angiography after stent placement with resolution of the stenosis and improved filling in the distal artery.

Nonatherosclerotic Disease of the Carotid Artery

Carotid Coiling and Kinking. The internal carotid artery typically takes a straight path into the skull.

At times there can be excessive elongation and tortuosity that makes a coil (Fig. 89-15). This can occur

congenitally and is seen in children, or it occurs in adults with elongation over time due to elasticity and

excessive angulation. This results in a C or S shape of the vessel. A kink is elongation with angulation

that exceeds 90 degrees. Kinks can cause cerebral hypoperfusion, and rarely can embolize. Head

position with rotation and either flexion or extension can exacerbate the symptoms. Treatment is

indicated for ipsilateral cerebral symptoms, and other nonspecific symptoms, such as dizziness, syncope

if no other causes are found. Options for treatment include transposition to a more proximal area in the

common carotid artery, or segmental resection.

Fibromuscular Dysplasia

FMD is a nonatherosclerotic disorder that can affect a variety of vascular beds within the body. Most

commonly found in the renal and iliac arteries, FMD is also found in the carotid and vertebral artery

2558

systems with an incidence of 0.42%.39 Carotid FMD is associated with cerebral aneurysms. The exact

etiology of FMD is unknown. There are four types of FMD, most commonly the medial fibroplasia, with

the classic appearance of a “string of beads.” This angiographic appearance is seen in the majority of

cases and is caused by segmental encroachment of the arterial lumen and poststenotic dilatation and can

be a nidus for hypoperfusion and embolization. The internal carotid artery is usually involved and the

lesion avoids the bifurcation. FMD can however be associated with vertebral and renal FMD, cerebral

aneurysms, and carotid aneurysms/dissection. Up to 50% of patients with internal carotid FMD have

associated cerebral aneurysms.40

Duplex ultrasound can be used for diagnosis; however, can miss the typical appearance or identify

elevated velocities. CTA has replaced a need for angiography, although angiography does remain the

“gold standard.” CTA or MRA is useful for the identification of intracerebral aneurysms.

The natural history of FMD is not well established. If FMD is associated with symptoms, repair is

indicated. Asymptomatic patients can be treated with antiplatelet agents, however, do progress over

time.40 With concomitant atherosclerosis, identification of the cause of symptoms must be identified.

Surgical treatment focuses on breaking the webs associated with FMD. This can be performed via open

or endovascular means. In open repair, dilators are introduced through a common carotid arteriotomy

with progressively increasing sizes. Although the technique allows for backbleeding, the risk of stroke

remains from debris caused by rupturing the webs.

Figure 89-15. Duplex ultrasonography with color shows an extremely tortuous internal carotid artery.

CAROTID ARTERY DISSECTION

Dissection of the carotid artery can either be spontaneous or secondary to a precipitating event, such as

trauma. Although carotid artery dissections account for a small number of overall strokes, they account

for up to 20% of strokes in younger patients.41 Spontaneous dissection is common in the carotid and

vertebral arteries due to their mobility and proximity to bony structures. Chiropractic manipulation is a

major cause of spontaneous dissection. There is usually no atherosclerosis present in patients who

develop carotid dissection. The classic triad in carotid dissection is neck or head pain, Horner syndrome,

and cerebral ischemia; however, it is rare to have all three. Headache is the most common symptom,

typically ipsilateral frontotemporal in location. Patients can also develop TIA, CVA, nausea, amaurosis

fugax, and cranial nerve palsies. CTA, MRA, and DUS are all utilized for diagnosis, and angiography

remains the gold standard. The treatment options for carotid artery dissection typically begin with

anticoagulation or antiplatelet therapy. There are no head-to-head trials comparing the two; however,

most patients are treated for a minimum of 3 months with intravenous heparin and transition to oral

anticoagulation. The indications for surgical treatment include the inability to anticoagulate, worsening

symptoms on anticoagulation, aneurysm formation, or severe neurologic symptoms with severe flow

limitation. Options for surgical repair include surgical bypass, patch angioplasty, or carotid ligation

(thought to be safe if the stump pressure is >70 mm Hg).42 Results of endovascular stenting are

promising for the treatment of carotid dissection.

CAROTID ARTERY ANEURYSMS

Carotid artery aneurysms are uncommon at about 1%; however, pseudoaneurysms after endarterectomy

2559

can occur more frequently. True aneurysms are most frequently caused by degeneration or

atherosclerosis and are typically at the carotid bifurcation or proximal internal carotid artery (Fig. 89-

16). Other causes include penetrating or blunt trauma, and dissection. A pulsatile mass is the most

frequent presenting symptom. Other patients can suffer from hemispheric neurologic symptoms, such as

a TIA or stroke, or cranial nerve dysfunction, such as Horner syndrome. Rupture is exceedingly rare.

Given the rarity of this disease entity, little is known regarding conservative management, and most

undergo surgical repair with bypass, and less frequently patch repair. A balloon occlusion test is helpful

prior to surgical intervention for large or distal aneurysms, and provides the possibility to bail out with

ligation of the carotid artery.

Figure 89-16. Duplex ultrasonography shows an extracranial carotid artery aneurysm in the proximal internal carotid artery.

CAROTID BODY TUMORS

Carotid body tumors arise from neural crest tissue from the third branchial arch. These masses usually

arise in the adventitial tissue at the carotid bifurcation. There are multiple neural crest tumors,

including carotid body tumors, paragangliomas, and glomus tumors. Paragangliomas can secrete

catecholamines and have systemic effects much like pheochromocytomas. These tumors are very rare.

They occur more often in situations of hypoxemia, like altitude, smoking, and chronic obstructive

pulmonary disease (COPD). Malignancy is rare, approximately 5%, and can metastasize to the lymph

nodes, liver, and skin. There is a hereditary pattern in carotid body tumors and can account for as much

as 35% of all cases. These masses arise at the carotid bifurcation and can envelope the internal and

external carotid arteries and the surrounding cranial nerves. DUS is useful for diagnosis with a

characteristic splaying of the internal and external carotid arteries. Needle biopsy is not recommended

for diagnosis as they are extremely hypervascular with blood flow arising from the external carotid

artery. Treatment involves resection, and large masses can benefit from preoperative embolization.

Surgical treatment involves similar exposure to a CEA and is carefully peeled off the underlying

arteries; however, can be injured and require bypass (Fig. 89-17). There is a high risk of cranial nerve

injuries with repair at approximately 10%.43

CAROTID TRAUMA

The extracranial carotid artery can be affected by blunt or penetrating trauma. Injury can be intimal

disruption, dissection, thrombosis, pseudoaneurysm formation, or transection. Penetrating cervical

trauma with concern for major arterial injury should undergo evaluation and treatment based on

location. Historically, zone 2 injuries undergo surgical evaluation due to the ease of surgical exposure.

Zone 1 and 3 injuries require workup for identification of an injury. Zone 1 injuries will require a

median sternotomy for control, whereas zone 3 will require maneuvers similar to high exposure for an

endarterectomy or the use of endovascular coil embolization or coverage with a stent graft. CTA is the

modality of choice for diagnosis in carotid injury. However, angiography remains the “gold standard”

for diagnosis. Medical management of a dissection includes either antiplatelet or anticoagulation.

However, if a dissection degenerates into a pseudoaneurysm, intervention is required by either open or

endovascular stent placement. Acute carotid thrombosis is treated with anticoagulation if the patient is

asymptomatic. Revascularization is required for patients with cerebral ischemia.

2560