Symptoms of extracranial carotid disease are most often caused by embolization. Arterial emboli account for approximately one-quarter of strokes in Europe and North America, and 80% of these originate from atherosclerotic lesions in a surgically accessible artery in the neck. The most common lesion is at the bifurcation of the carotid artery. Transcranial Doppler studies have shown that emboli are seen in approximately 20% of patients with moderate (> 50% stenosis) lesions at the carotid bifurcation and even higher rates with more than 70% stenoses. The incidence and frequency of emboli are increased in recently symptomatic patients.
The neurologic dysfunction associated with microemboli may appear as sudden or transient, neurologic symptoms that may include unilateral motor and sensory loss, aphasia (difficulty finding words), or dysarthria (difficulty speaking due to motor dysfunction). These are termed Transient Ischemic Attack (TIA). Most TIAs are brief (minutes). By convention, 24 hours is the arbitrary limit of a TIA. If the symptoms persist, it is a stroke, or cerebrovascular accident (CVA). An embolus to the ophthalmic artery, the first branch of the internal carotid artery, produces a temporary monocular loss of vision called amaurosis fugax or permanent blindness.
Lesions of atherosclerosis in the internal carotid artery occur along the wall of the carotid bulb opposite to the external carotid artery origin. The enlargement of the bulb just distal to this major branch point creates an area of low wall shear stress, flow separation, and loss of unidirectional flow. Presumably, this allows greater interaction of atherogenic particles and the vessel walls at this site and accounts for the localized plaque at the carotid bifurcation.
The accessibility of this localized atheroma allows effective removal of the plaque and a dramatic reduction in stroke risk. Without treatment, 26% of patient with TIAs and more than 70% with carotid artery stenosis will develop permanent neurological impairment (CVA) from continued embolization at two years. The risk of CVA can be reduced to 9% with plaque removal and is usually lower for a patient presenting with amaurosis fugax.
Asymptomatic carotid stenosis > 60% by angiography or 70% by duplex ultrasound.
Symptomatic carotid stenosis (cerebrovascular accident, transient ischemic attack, or amaurosis fugax) > 50%.
Carotid endarterectomy can be performed safely under regional anesthesia in patients with a severe chronic obstructive pulmonary disease, coronary artery disease (CAD), and other comorbidities.
Carotid stenting can be considered in patients with a history of neck irradiation, modified radical neck dissection, or reoperative carotid endarterectomy.
Only patients with concurrent symptomatic carotid stenosis and symptomatic CAD should be considered for combined carotid endarterectomy and coronary artery bypass grafting.
There are no absolute contraindications other than distal internal artery occlusion.
Duplex ultrasound is highly sensitive and specific and is the only preoperative imaging required in most cases.
Arteriography (conventional or CT) is reserved for cases involving restenosis, a history of radiation or prior neck dissection, or atypical findings on duplex ultrasonography.
The patient should be in a semi-seated position with a small roll across the shoulder blades. This allows for gentle extension and external rotation of the head to the contralateral side.
The ipsilateral arm is tucked, padding the elbow and wrist.
Care should be taken not to over-rotate or extend the head to avoid kinking of the vertebral arteries or contralateral carotid artery.
Landmarks such as the ear lobe, angle of the mandible, mastoid process, sternal notch, and clavicle must be included in the prepared area.
Carotid endarterectomy can be performed under regional anesthesia, general anesthesia with routine shunting, or general anesthesia with selective shunting based on adjuncts such as intraoperative EEG monitoring or stump pressures.
The main purpose of CEA is to prevent stroke. The benefit of CEA depends on low morbidity and mortality rates of the procedure. It is indicated for symptomatic high-grade stenosis, symptomatic moderate stenosis as well as the asymptomatic high-grade stenosis of the internal carotid artery.
In 1991, the results of the randomized North American Symptomatic Carotid Endarterectomy Trial (NASCET) of medical treatment for carotid endarterectomy were reported. All patients had either hemispheric retinal TIAs or nondisabling strokes within 120 days of entry into the trial and 70% to 99% stenosis in the symptomatic carotid artery. The actuarial risk of any ipsilateral stroke at two years was significantly lower at 9% in the 328 surgical patients versus 26% in the 331 medical patients. The data-safety monitoring committee halted further randomization given the widely disparate 18-month follow-up data. For major or fatal ipsilateral strokes, the risk was 2.5% for surgical patients versus 13.1% for medical patients (p < .001). When all strokes and deaths were included, carotid endarterectomy still was better than medical treatment. Subsequent follow-up studies from this trial indicated that the benefit of carotid endarterectomy in symptomatic patients extended to those with even moderate (50% to 69%) carotid artery lesions.
The Veterans Affairs Cooperative Study of symptomatic carotid stenosis reported in 1991 results of randomizing 189 men with stenoses greater than 50% to medical or surgical treatment. After one year, there was a significant reduction in stroke or TIAs in the patients having carotid endarterectomy (7.7%) compared with medically treated patients (19.4%), with even more divergent results with carotid stenosis greater than 70%.
The European Carotid Surgery Trial randomized 2518 patients with nondisabling stroke, TIA, or retinal infarction in conjunction with ipsilateral carotid stenosis to medical or surgical treatment. For the 778 patients with stenoses of 70% to 99%, the cumulative risk of stroke at carotid endarterectomy of 7.5%, plus an additional late stroke rate at three years of 2.8%, was less than the 16.8% rate for medically treated patients. At three years the cumulative risk of operative death, operative stroke, ipsilateral ischemic stroke, and any other stroke was 12.3% for the surgical cohort versus 21.9% for the medical group (p < .01). Finally, the risk of fatal or disabling ipsilateral stroke at 3 years was 6.0% for the carotid endarterectomy patients versus 11.0% for the medical control patients (p < .05).
Although the benefit of endarterectomy in these studies was due in part to the high risk of stroke in medically treated patients, the results were significant even in an era when the 30-day combined stroke and death risk of endarterectomy were about 7.5%. Although the combined stroke and death risk of carotid endarterectomy are higher in symptomatic versus asymptomatic patients, the current combined risk is about 2% to 4%.