Lange Review Ultrasonography Examination, 4th Edition
Chapter 12. Cerebrovascular Sonography
George L. Berdejo, Joshua Cruz, Fernando Amador, and Evan C. Lipsitz
The systemic circulation begins with the left side of the heart.1–4 The aortic arch is the first segment of the aorta, which is the longest artery in the body. The aorta is divided into four main segments:
1. Ascending aorta or aortic trunk
2. Aortic arch
3. Descending or more commonly known as the thoracic aorta
4. Abdominal aorta
The great vessels include the aortic arch and its three major branches that include the following:
1. Innominate artery or brachiocephalic trunk
2. Left common carotid artery (CCA)
3. Left subclavian artery
The anatomy of the cerebrovascular circulation consists of both intracranial and extracranial vessels (Fig. 12–1). The extracranial cerebrovascular arteries can be further divided into the carotid artery circulation, which supplies blood to the anterior part of the brain, and the vertebrobasilar circulation, which supplies blood to the posterior part of the brain. The anterior and posterior portions of the brain are connected by the circle of Willis.
FIGURE 12–1. Diagram showing the relationship and anatomic locations of the intracranial and extracranial carotid vessels.
Except for the origin of the common carotid arteries, the right and left carotid artery circulation are identical. The right carotid artery circulation begins at the level of the right clavicle where the brachiocephalic trunk divides and becomes the right common carotid artery (CCA) and right subclavian artery. The left CCA and the left subclavian artery both originate directly from the aortic arch. Bilaterally, the CCA courses anteriorly to the superior level of the thyroid gland. Here, the CCA bifurcates into the internal carotid artery (ICA) and the external carotid artery (ECA).
The primary role of the ICA is to perfuse the ophthalmic artery, anterior portion of the brain, and the circle of Willis. The origin of the ICA is slightly dilated; hence, the term the carotid bulb or carotid sinus. The bulb may encompass the most distal segment of the CCA. This is an important anatomical site, as it is here where carotid artery disease is most likely to develop. The ICA continues to course anterolaterally until it enters the skull through the carotid canal. There are no branches of the ICA outside of the skull. Intracranial branches of the internal carotid include the anterior choroidal, posterior communicating, and ophthalmic arteries. The ophthalmic artery, which perfuses the eye, originates at the carotid siphon. The carotid siphon appears as an “S”-shaped curve. The termination of the ICA forms the lateral aspects of the circle of Willis (Fig. 12–2), and this is where the origins of the middle and anterior cerebral arteries are located.
FIGURE 12–2. The circle of Willis.
The external carotid artery courses superiorly and anteriorly and yields several branches, which primarily feed the thyroid, tongue, tonsils, and ears (Table 12–1). The ECA does not perfuse the brain and is, even when disease is present, not considered a source of transient ischemic attack or cerebrovascular accident.
TABLE 12–1 • External Carotid Artery Branches
1. Superior thyoid
2. Ascending pharyngeal
6. Posterior auricular
8. Superficial temporal
The ECA can become an important source of collateral blood flow in the presence of severe ipsilateral internal carotid artery disease.5, 6 In rare cases; ECA stenosis can result in symptoms in patients with ipsilateral ICA occlusion and, therefore, should be carefully evaluated in those patients.
The posterior circulation of the brain, also known as the vertebrobasilar system, includes the vertebral arteries that originate from the proximal subclavian arteries.7–9 Both the right and left vertebral arteries course on either side of the vertebral column and through openings in each of the transverse processes of the cervical vertebrae. As the vertebral arteries enter the base of the skull, they join to form the basilar artery. The basilar artery then terminates at the circle of Willis where the right and left posterior cerebral arteries originate.
The circle of Willis is a very small network of vessels that is about the size of a quarter and may serve as a collateral pathway in the presence of significant disease. The circle of Willis is formed by the (1) termination of the right and left ICAs, (2) right and left anterior cerebral arteries (ACA-A1), (3) anterior communicating artery (ACom), (4) right and left posterior communicating arteries (PCom), and (5) posterior cerebral arteries (PCAs). The middle cerebral artery (MCA) originates off the circle of Willis at the termination of the ICA and is not considered to be a part of the circle of Willis (Fig. 12–2).
Collateral pathways are abundant in the cerebrovasculature.5, 6 Other pathways include connections between the supraorbital and frontal arteries (branches of the ophthalmic artery), and the superficial temporal artery, a branch of the ECA. The occipital branch of the ECA communicates with the atlantic branch of the vertebral arteries.
In addition to collateral pathways, there is also a compensation factor to consider. Since the intracranial circulation is perfused by four main vessels, the bilateral flow of the ICA and vertebral arteries may increase in any of these vessels to compensate for the presence of hemodynamically significant disease in the others. Therefore, an understanding of all circulatory factors in the carotid system must be taken into consideration for a complete diagnostic picture.
PHYSIOLOGY AND HEMODYNAMICS
Peripheral resistance of a vascular bed is one factor that determines the amount of blood flow to a region of the body. The resistance is primarily controlled by the vasoconstriction and vasodilatation of the arterioles within that vascular bed. Vasodilatation decreases the peripheral resistance allowing blood to move in that direction. Vasoconstriction increases the resistance and blood tends to move in the direction of lower resistance. The resistance within a given system is reflected in the diastolic component of the Doppler spectral waveform.
The brain is a very low resistance vascular bed that allows for continuous blood supply throughout the cardiac cycle, so we should expect there to be continuous forward flow throughout diastole in all vessels that directly provide blood to the brain (Fig. 12–3).10 These include the ICA and vertebral arteries, which in general will yield very similar Doppler spectral waveforms. The ECA, however, perfuses the areas of the face and smaller structures of the head and generally will yield very little flow in diastole. Accordingly, there is a distinct difference in the Doppler waveforms that represent these vessels. It is extremely important for the examiner to recognize this difference so as to allow proper identification of the bifurcation vessels. Since the CCA is common to the ICA and ECA, it yields characteristics belonging to both vessels (Fig. 12–4).
FIGURE 12–3. Spectral waveform from the internal carotid artery. The diastolic flow component of the cardiac cycle is outlined by the dotted yellow lines. Note that there is continuous forward flow (flow above the baseline) throughout the cardiac cycle.
FIGURE 12–4. Ultrasound images with corresponding Doppler spectral waveforms from the common carotid (A), internal carotid (B), external carotid (C), and vertebral (D) arteries.
MECHANISMS OF DISEASE
Risk Factors for Stroke
Some stroke risk factors are hereditary, while others are a function of natural processes. Still others result from a person’s lifestyle. Non-modifiable risk factors include age, heredity and race, gender, and prior stroke, transient ischemic attack (TIA), or heart attack.11
Advancing age is a risk factor for stroke. The chance of having a stroke approximately doubles for each decade of life after age 55 years. While stroke is common among the elderly, many people younger than 65 years also suffer strokes.
Heredity (family history) and race plays an important role. It is well known that stroke risk is greater if a parent, grandparent, sister, or brother has had a stroke. African Americans have a much higher risk of death from a stroke than Caucasians. This is partly because African Americans have higher risks of high blood pressure, diabetes, and obesity.
Stroke is more common in men than in women. In most age-groups, more men than women will have a stroke in a given year. However, more than one-half of total stroke deaths occur in women. At all ages, more women than men die of stroke. Use of birth control pills and pregnancy pose special stroke risks for women.
The risk of stroke for someone who has already had one is many times that of a person who has not. Episodes of TIA are “warning signs” that produce stroke-like symptoms but no permanent damage. This is discussed further in the text. TIAs are strong predictors of stroke and a person who has had one or more TIAs is almost ten times more likely to have a stroke than someone of the same age and sex who has not. Recognizing and treating TIAs can reduce the risk of a major stroke.
The modifiable risk factors for stroke include hypertension, diabetes, cigarette smoking, hyperlipidemia, carotid artery stenosis, atrial fibrillation, excessive alcohol consumption, and physical inactivity (Table 12–2).12
TABLE 12–2 • Risk Factors: Modifiable and Non-Modifiable
• Advanced age
• Atrial fibrillation
• Carotid artery stenosis
• Cigarette smoking
• Excessive alcohol consumption
• Family history of stroke
• Heart disorders
• History of transient ischemic attacks
• Physical inactivity
• Use of oral contraceptives
The most important controllable risk factor is hypertension, which increases the risk of stroke twofold to fourfold.13 This higher risk is seen in both systolic and diastolic hypertension, as well as in isolated systolic hypertension in the elderly. Blood pressure control significantly reduces the risk of stroke; it has been shown to prevent 30 strokes for every 1,000 patients treated. Many people believe the effective treatment of high blood pressure is a key reason for the accelerated decline in the death rates for stroke. According to the current recommendation of the Stroke Council of the American Heart Association (AHA), blood pressure should be maintained at <140/90 mm Hg.11
Diabetes mellitus is an independent risk factor for stroke. Diabetes increases stroke risk 1.8- to 6-fold. Many people with diabetes also have high blood pressure and blood cholesterol and are overweight. This increases their risk even more. While diabetes is treatable, the presence of the disease still increases the risk of stroke.
In recent years, studies have shown cigarette smoking to be an important risk factor for stroke. Approximately 27% of men and 22% of women in the United States smoke cigarettes. Smokers have a relative risk of stroke in the range of 1.8, and the estimated population attributable risk of stroke due to smoking is 18%. The nicotine and carbon monoxide in cigarette smoke damage the cardiovascular system in many ways. The use of oral contraceptives combined with cigarette smoking greatly increases stroke risk. Fortunately, this increased risk disappears within 5 years of smoking cessation.11, 12
Hyperlipidemia is a risk factor for a stroke. Lipid disorders have been shown to increase the risk of stroke by 1.8- to 2.6-fold. Most of the information regarding the effect of lowering cholesterol on stroke risk comes from secondary analyses of trials on the prevention of coronary disease, but it is prudent to use these guidelines when evaluating patients for stroke risk. Tighter control of hyperlipidemia is indicated for patients who have a history of stroke or cardiovascular disease.12
Carotid or other artery disease results in an increased risk for stroke, as the carotid arteries supply blood to the brain. A carotid artery narrowed by fatty deposits from atherosclerosis may become blocked by a blood clot. Carotid artery disease is also called carotid artery stenosis. Peripheral artery disease can result in the narrowing of blood vessels carrying blood to leg and arm muscles. People with peripheral artery disease have a higher risk of carotid artery disease, which raises their risk of stroke.
Atrial fibrillation is a heart rhythm disorder that raises the risk for stroke. The heart’s upper chambers do not beat effectively, which can let the blood pool and clot. If a clot breaks off, enters the bloodstream, and lodges in an artery leading to or in the brain, a stroke can result. People with coronary artery disease or heart failure have a higher risk of stroke than those with hearts that work normally. Dilated cardiomyopathy (an enlarged heart), heart valve disease, and some types of congenital heart defects also raise the risk of stroke.
Sickle cell disease is a genetic disorder that mainly affects African American and Hispanic children. “Sickled” red blood cells are less able to carry oxygen to the body’s tissues and organs. These cells also tend to stick to blood vessel walls, which can block arteries to the brain and cause a stroke. Stroke is the second leading killer of people younger than 20 years who suffer from sickle cell anemia.14
Physical inactivity and obesity can increase the risk of high blood pressure, high blood cholesterol, diabetes, heart disease, and stroke.
Atherosclerosis is a chronic systemic disease that affects the arterial system and occurs within the arterial wall, typically within or beneath the intima. There are various characteristics of the disease, among them location. Atherosclerosis is commonly seen at origins and bifurcations of vessels. Since flow divides and changes its laminar characteristics, a shearing force is created at the flow divider, which over time is responsible for the wear of the intima.15 For this reason the carotid bifurcation is a prime location for carotid artery disease. It is a chronic inflammatory response in the walls of arteries, in large part due to the accumulation of macrophage white blood cells and promoted by low-density (especially small particle) lipoproteins (plasma proteins that carry cholesterol and triglycerides) without adequate removal of fats and cholesterol from the macrophages by functional high-density lipoproteins (HDLs). It is commonly referred to as a “hardening” of the arteries.
Plaque formation may begin as simple layers of lipids called fatty streaks that are deposited in the wall. Over time, plaques on the walls may progress to a more fibrous component that includes the accumulation of lipids, collagen, and fibrin that is soft and gelatinous in texture appearing as a hypoechoic structure along the arterial wall. Over time, the plaque may proliferate further into the lumen causing narrowing, also known as stenosis. The walls may harden secondary to a more calcium and collagen component. Unstable plaques or plaques that have areas that are weak, compared to more firm or well-integrated plaque within the wall, potentially can be a source of embolic debris.15
Atherosclerosis is caused by the formation of multiple plaques within the arteries.15, 16 The atheromatous plaque is divided into three distinct components:
1. The atheroma, which is the nodular accumulation of a soft, flaky, yellowish material at the center of large plaques, composed of macrophages nearest the lumen of the artery
2. Underlying areas of cholesterol crystals
3. Calcification at the outer base of older/more advanced lesions.
Atherosclerosis typically begins in early adolescence and is usually found in most major arteries, yet is asymptomatic and not detected by most diagnostic methods during life. Autopsies of healthy young men that died during the Korean and Vietnam Wars showed evidence of the disease.17, 18 It most commonly becomes seriously symptomatic when interfering with the coronary circulation supplying the heart or cerebral circulation supplying the brain and is considered the most important underlying cause of strokes, heart attacks, various heart diseases including congestive heart failure, and most cardiovascular diseases, in general. Atheroma in arm or, more often, leg arteries, which results in decreased blood flow, is called peripheral artery occlusive disease.
According to U.S. data for the year 2004, for about 65% of men and 47% of women, the first symptom of atherosclerotic cardiovascular disease is heart attack or sudden cardiac death (death within one hour of onset of the symptom). Most artery flow-disrupting events occur at locations with less than 50% residual lumen.
An embolus can be a solid, liquid, or a gas that travels through the bloodstream. Embolic strokes are usually caused by a blood clot that forms elsewhere in the body or plaque debris and travels through the bloodstream to the brain. Embolic strokes often result from heart disease or heart surgery and occur rapidly and without any warning signs. About 15–50% of embolic strokes occur in people with atrial fibrillation; the rest are attributable to a variety of causes, including (1) left ventricular dysfunction secondary to acute myocardial infarction or severe congestive heart failure, (2) paradoxical emboli secondary to a patent foramen ovale, and (3) atheroemboli. These latter vessel-to-vessel emboli often arise from atherosclerotic lesions in the aortic arch, carotid arteries, and vertebral arteries. In paradoxical embolism, a deep vein thrombosis embolizes through an atrial or ventricular septal defect in the heart then into the brain.19 This phenomenon may manifests itself as symptoms of TIA or even cerebrovascular accident (CVA), more commonly known as a stroke. By identifying these lesions with duplex ultrasound, the risks associated with significant atherosclerotic disease can be prevented with appropriate treatment.
Subclavian Steal Syndrome
Subclavian steal syndrome refers to the reversal of flow in the ipsilateral vertebral artery to supply the distal subclavian artery in the presence of a proximal subclavian or innominate artery obstruction (Fig. 12–5). This phenomenon demonstrates the hemodynamic effects of severe stenosis and the compensatory nature of the circulatory system. Patients with this condition experience vertebrobasilar symptoms in response to exercise of the ipsilateral arm. It is more common on the left since the left subclavian is an isolated artery and does not communicate with the carotid artery. Therefore, the anatomy of the innominate artery is protective. Arm ischemia is rare in these patients, although a significant difference in blood pressure often exists between the two arms. A decreased radial artery pulse, combined with symptoms of vertebrobasilar insufficiency exacerbated by arm exercise, is pathognomonic. The diagnosis is confirmed angiographically by late films demonstrating filling of the distal subclavian by retrograde vertebral blood flow or by duplex ultrasound detection of reversed flow in the vertebral artery.20 A vertebral artery Doppler signal can also yield an alternating (toward and away) flow pattern (Fig. 12–6). This alternating pattern can transition to complete flow reversal with exercise of the ipsilateral upper extremity or after reactive hyperemia testing and can be demonstrated by observation of the vertebral artery Doppler signal after exercise or release of a blood pressure cuff that has been inflated to a suprasystolic blood pressure for approximately 3 minutes. A standard transcranial Doppler evaluation with particular attention to the blood flow direction and the velocities in the vertebral arteries and the basilar artery can also be useful. Blood flow is normally away from the transducer (suboccipital approach) in the vertebrobasilar system. If flow is toward the transducer at rest or with provocative maneuvers, there is evidence of a steal.21
FIGURE 12–5. This diagram depicts the anatomy and physiology of a subclavian steal. Flow in the right vertebral artery is antegrade (toward the brain) to the basilar. Flow then reverses in the contralateral vertebral to perfuse the left subclavian artery in the presence of a hemodynamically significant stenosis in the left subclavian artery proximal to the left vertebral artery origin.
FIGURE 12–6. Doppler waveforms of the vertebral artery in various degrees of subclavian artery stenosis. Top is a normal waveform. Middle is an altemating flow waveform, and bottom demonstrates complete reversal of flow.
Dissection is a nonatherosclerotic condition that is usually the result of trauma that causes a sudden tear in the intimal lining of the vessel. The intima then separates from the media and adventitia (Fig. 12–7). This separation creates a “false” lumen wherein blood may pulsate. The dissection may extend proximally or distally and may remain asymptomatic or may thrombose and cause neurological symptoms when it is flow limiting.
FIGURE 12–7. This is an ultrasound image of a common carotid artery dissection with two patent flow lumens.
An aneurysm is defined as a permanent focal dilation of an arterial segment greater than 50% of the diameter of the normal adjacent vessel. Aneurysms of the extracranial carotid artery are rare (Fig. 12–8); several decades ago, such aneurysms were often attributed to syphilitic arteritis and peritonsillar abscess. Currently, the most common causes are trauma, cystic medial necrosis, fibromuscular dysplasia, and atherosclerosis.22 Neurologic manifestations are varied and include (1) cranial nerve involvement, which may produce dysarthria (hypoglossal nerve), hoarseness (vagus nerve), dysphagia (glossopharyngeal nerve), or tinnitus and facial tics (facial nerve); (2) compression of the cervical sympathetic chain and Homer’s syndrome; and (3) ischemic syncopal attacks, resulting from embolism or interference with blood flow. Commonly, patients with an extracranial carotid aneurysm present to their physician with a cervical or parapharyngeal mass. Sometimes, an unsuspecting physician will perform a needle biopsy, which is followed by significant bleeding, hematoma formation, or strok.23 An aneurysm of the carotid artery must not be misdiagnosed as a large carotid bulb. Note that the carotid bulb presents in various sizes and locations (Fig. 12–9). In addition, a comparison to the contralateral side is helpful.
FIGURE 12–8. Patient with an internal carotid artery aneurysm. The top figure is a sagittal ultrasound image of an internal carotid artery aneurysm. The middle image is the confirmatory arteriogram, and the bottom image shows the intraoperative finding.
FIGURE 12–9. This cartoon illustrates the variable location of the carotid “bulb” outlined in aqua blue. Note that although the level of the bifurcation (dotted white line) is unchanged, the bulb may encompass any or all parts of the bifurcation, internal or external carotid arteries. Therefore, the level at which the common carotid artery divides into the internal and external carotid arteries should be referred to as the carotid bifurcation and not the carotid “bulb.”
Carotid Body Tumors
Haller introduced glomus tumors of the head and neck into the medical record in 1762 when he described a mass at the carotid bifurcation that had a glomus body-like structure. In 1950, Mulligan renamed this type of neoplasm a chemodectoma to reflect its origins from chemoreceptor cells. In 1974, Glenner and Grimley renamed the tumor paraganglioma on the basis of its anatomic and physiologic characteristics. They also created a classification method based on the location, innervation, and microscopic appearance of the tumors.
Carotid body tumors, also called chemodectomas, are vascular tumors that arise from the paraganglionic cells in the outer layer of the carotid artery at the bifurcation level (Fig. 12–10).
FIGURE 12–10. Color-flow duplex image of a carotid body tumor. Note the typical splaying of the bifurcation vessels secondary to the location of the tumor between the ICA and ECA, which are indicated by the green arrows. Hypervascularity is evident by the color Doppler.
This disease, which may be hereditary, is more common in South America than in North America. Tumors can become sizable before causing symptoms, such as a painless, pulsating mass in the upper neck, and eventually can cause difficulty in swallowing. Ten percent of these tumors occur on both sides of the carotid artery. Although these can be noted on duplex ultrasonography,24, 25 they are definitively diagnosed using computed tomography (CT) or magnetic resonance imaging (MRI) scans, and sometimes angiography.26 These tumors are generally benign; only about 5–10% are malignant. Treatment includes surgery and occasionally radiation therapy.27
Fibromuscular Dysplasia (FMD) is a non-atherosclerotic disease that usually affects the media of the arterial wall due to abnormal cellular development that causes stenosis of the renal arteries, carotid arteries, and less commonly, other arteries of the abdomen and extremities. This disease can cause hypertension, strokes, and arterial aneurysm and dissection.
FMD is often diagnosed incidentally in the absence of any signs or symptoms during an imaging study. Angiography with contrast will show a characteristic “string of beads” morphology in a vessel affected by FMD (Fig. 12–11). This pattern is caused by multiple arterial dilations separated by concentric stenosis. FMD tends to occur in females between 14 and 50 years of age. However, it has been found in children younger than 14 years, both male and female. Up to 75% of all patients with FMD will have disease in the renal arteries.28 The second most common artery affected is the carotid artery. More than one artery may have evidence of FMD in 28% of people with this disease.29 All relevant arteries should be checked if found.
FIGURE 12–11. Angiographic presentation of fibromuscular dysplasia. Notice the classic “string of beads” appearance in the distal segment of the extracranial internal carotid artery (ICA). (ECA: external carotid artery; CCA: common carotid artery.)
In the carotid system, it predominantly occurs in the mid segment of the ICA, it is bilateral in approximately 65% of the cases, and it is usually found in females. Color Doppler imaging may reveal a turbulent flow pattern adjacent to the arterial wall, with absence of atherosclerotic plaque in the proximal and distal segments of the ICA.21, 24, 25
Neointimal hyperplasia accounts for most re-stenoses occurring within the first 2 years following vascular intervention. Development of the a neointimal hyperplastic lesion involves the migration of smooth muscle cells from the media to the neointima, their proliferation, and their matrix secretion and deposition. Thus, mechanisms of smooth muscle cell migration are key to the formation of neointima, early re-stenosis, vessel occlusion, and ultimate failure of vascular interventions. This is often a factor in patients who experience re-stenosis after carotid endarterectomy.30
SIGNS AND SYMPTOMS
Physical examination of the extracranial carotid circulation includes palpation of common carotid, internal carotid artery, and temporal artery pulses. Acquisition of the bilateral brachial artery blood pressures can be performed routinely or per a prescribed algorithm and can be useful in the evaluation of patients with suspected vertebrobasilar symptoms as mentioned earlier. Auscultation of the carotid arteries is also part of the physical examination. Patients with evidence of cerebrovascular disease may in fact be asymptomatic. An asymptomatic stenosis is defined as any pre-occlusive lesion in the CCA, carotid bifurcation artery, or ICA in a patient with no ipsilateral monocular or cerebral hemispheric symptoms.
Cervical or carotid bruit is often the only indication for screening in patients with suspected hemodynamically significant carotid artery disease. Information about the incidence of carotid bruit in asymptomatic patients is available from the Framingham study. This study found that 3.5% of men and women had carotid bruits at 44–54 years of age. This increased to 7.0% at 65–79 years.31
Auscultation is performed by placing a stethoscope over the carotid artery. The patient is asked to take a deep breath and hold while the examiner listens for bruits (Fig. 12–12). A bruit is the result of vibration in the tissue that is transmitted to the surface of the skin. Bruits in the neck can be the result of the turbulent blood flow that is seen distal to a hemodynamically significant stenosis. They can also be heard in patients with loops, coils, kinks, and tortuosity of the ICA, or they can be cardiac in origin. Not all patients with these findings however will present with a carotid bruit. Other causes may include external compression from thoracic outlet syndrome, arteriovenous malformations, and tumor.32, 33
FIGURE 12–12. A stethoscope is placed over the cervical carotid artery and the examiner listens while the patient takes a deep breath.
Auscultation for carotid artery bruit during routine examination has a low specificity that requires the support of ultrasound investigation. Due to the relatively low prevalence of carotid artery disease in the community; a national screening program is not cost-effective. However, patients in whom a bruit is heard should have further investigations in order to prevent the sequelae of carotid artery disease.34, 35
Acute neurological deficits are differentiated as TIAs or strokes, based on whether the deficit resolves within or persists longer than 24 hours. A TIA is any neurological dysfunction that lasts for less than 24 hours and completely resolves. Transient symptoms however are often a precursor to more serious complications. The neurological dysfunction may be described by the patient as some variation of a motor or sensory deficit (Table 12–3). TIAs typically last for just a few minutes or even seconds and result from deprivation of blood supply to a focal area in the anterior circulation of the brain. This may be caused by emboli or severe stenosis in the carotid circulation, either intracranial or extracranial. Patients may suffer from repeated symptoms that are similar in nature but worsen or occur with increased frequency. These are referred to as crescendo TIA and is important to identify, as this may be a sign of impending stroke.
TABLE 12–3 • Common Signs and Symptoms of Cerebrovascular Disease (Transient Ischemic Attacks and Strokes)
Other temporary symptoms involve the vertebrobasilar system (posterior circulation). Symptoms include vertigo, syncope, ataxia, drop attacks, and any other symptom that is bilateral in nature. Although these types of symptoms are indications for cerebrovascular evaluation, they typically will not be caused by carotid disease, as there are many other differential diagnoses.36
CVA, commonly referred to as stroke, is defined as any motor or sensory deficit that lasts longer than 24 hours and does not completely resolve. Seventy-five percent of patients with stroke have experienced a previous TIA. CVA is essentially a result of necrosis or death of brain tissue. Major CVA can be debilitating, resulting in permanent paralysis and potentially death. In addition, it is quite possible for patients to have had a stroke and never have suffered any symptoms. Most of these are found incidentally on a CT scan of the head that is usually performed for some other reason.
TESTING FOR CEREBROVASCULAR DISEASE
Duplex Ultrasound Technique37, 38
The examination is explained and a history (risk factors, symptoms) is obtained from the patient. Arm pressures are recorded bilaterally (<20 mm Hg difference is within normal limits) and the presence of cervical bruits if present is documented.
Suggested instrument setups for carotid duplex imaging are as follows: (1) use a high-frequency (5-10 MHz) linear array transducer, (2) image orientation: head to the left of the monitor, (3) color assignment: although color is based on the direction of blood flow (toward or away) in relation to the transducer, red is usually assigned to arteries and blue to venous blood flow, (4) the color scale (pulse repetition frequency [PRF]) should be adjusted throughout the examination to evaluate the changing velocity patterns, (5) the wall filter is set low, (6) the color box width affects frame rates (number of image frames per second), so the color display should be kept as small as possible, and (7) the color gain should be adjusted throughout the examination as the signal strength changes.
Duplex evaluation is primarily done in the long axis since the assessment of the carotid system requires Doppler insonation throughout the CCA, ICA, and origin of the ECA. The vertebral arteries also are included, especially in the presence of vertebrobasilar symptoms. The examination is performed with the patient in the supine position (Fig. 12–13). Anything that restricts access to the entirety of the extracranial carotid system from the base of the neck to the angle of the mandible is removed (Fig. 12–14). Pillows may be used to support the neck; however, the patient’s head should be positioned such that the chin is pointed up and the head slightly turned away from the side being examined.
FIGURE 12–13. the examination is performed in the supine position while the examiner is either (A) at the head of the patient or (B) standing or sitting beside the patient.
FIGURE 12–14. All restrictive garments such as turtleneck shirts and jewelry are removed to allow easy access to the neck, and the patient’s head is turned slightly away from the side that is examined.
The examination begins with a transverse sweep of the carotid system examining the vessels of interest from the origin of the common carotid artery to its bifurcation where the origins of the internal and external carotid artery are identified. This allows for a preview of all the vessels and surrounding structures (Fig. 12–15). Any abnormalities including extracarotid pathology and thyroid masses are noted. The sonographic appearance and size of these structures are included in a final report. Location of plaque, plaque characteristics, and location of the bifurcation are assessed as well.
FIGURE 12–15. Transverse ultrasound image of the common carotid artery and surrounding structures.
Sagittal to the long axis of the vessel, follow the course of the CCA from its origin (or as proximal as can be obtained) to the bifurcation. The origin of the right CCA almost always can be imaged since its origin is from the innominate artery (Fig. 12–16). In contrast, because access is limited secondary to depth and adjacent bony and muscular structures, the left CCA may be very difficult to visualize. Imaging with a sector transducer is an alternative and should be used when a significant stenosis is suspected at the origin of the left CCA. Using color-flow Doppler imaging as a guide, interrogate the length of the CCA with pulsed Doppler, noting peak systolic and end diastolic velocities. The CCA bifurcation is a common place for atherosclerotic plaque and is also the site of what is commonly referred to as the carotid bulb, although the location of the bulb itself may be variable (see Fig. 12–9). This area should be assessed from multiple views. At this point the ICA and ECA are followed individually, and it is important to distinguish the ICA from the ECA. Although the spectral waveform pattern is the primary determinant, other parameters are useful (Table 12–4).
FIGURE 12–16. Ultrasound image of the right common carotid artery off the innominate.
FIGURE 12–19. Long-axis view of the vertebral artery. Note that the bony structures indicated by the green arrows result in acoustic shadowing.
TABLE 12–4 • Differentiating the ICA from the ECA*
Follow the course of the ICA from its origin at the CCA bifurcation as far distal as possible. Using color-flow Doppler as a guide, interrogate the length of the vessel with pulsed Doppler and measure the peak systolic and end-diastolic velocities. Imaging from a posterolateral or lateral approach usually provides the best image. Where significant plaque is visualized, multiple views and Doppler assessment are imperative to ensure the data obtained is accurate and reproducible. Typically atherosclerotic disease occurs within the first few centimeters of the ICA, and elevated velocities at this segment in the presence of disease will be categorized based primarily on the spectral Doppler velocities. The distal ICA may be difficult to image secondary to depth and tortuosity. The clinical implication of tortuosity has yet to be proven as a significant finding; however, it should be noted that normal flow disturbances occur and elevated velocities may be recorded as a result of rapid changes in Doppler angles between the insonation beam and the acute changes in geometry of the blood vessel (Fig. 12–17).39 Consideration is, therefore, recommended before interpreting high velocities as indicative of hemodynamically significant disease. Look for other visual evidence of disease on the B-mode image and for the presence of post-stenotic turbulence.
FIGURE 12–17. Color duplex image of a tortuous internal carotid artery (ICA). Notice the changes in the color-flow pattern that indicate rapid changes in the Doppler angle and not necessarily elevated velocities associated with stenosis.
A Doppler waveform is obtained at the origin of the ECA. This is done to document patency and to help distinguish this vessel from the ICA (Fig. 12–18).
FIGURE 12–18. Color duplex illustrating branches of the external carotid artery. This is helpful for identification of the internal carotid artery versus the external carotid artery.
The vertebral artery lies deeper than the CCA and can be located by angling the transducer slightly laterally from a longitudinal view of the mid/proximal CCA. To reliably identify the vertebral artery, it should be followed distally, and periodic shadowing should be visualized from the transverse processes of the vertebrae (Fig. 12–19). The vertebral artery is accompanied by the vertebral vein and proper identification of the artery is made by evaluation of the Doppler signal. Once the vertebral artery has been correctly identified, it should be followed as far proximally as possible. The use of color Doppler will greatly assist in locating the vertebral artery and its origin, as well as in evaluating the direction of blood flow.
Doppler interrogation of the carotid system is performed in the longitudinal plane using a 60° angle between the ultrasound beam and the vessel walls, as well as the angle cursor parallel to the vessel wall (placement of the Doppler sample volume parallel to the color jet has not undergone extensive validation criteria). Using a constant Doppler angle permits comparison of repeated studies in the same individual. Insonation angles >60° should never be used for data acquisition and analysis, as significant measurement error is introduced in even small changes in the Doppler angle of insonation when it is >60°. The Doppler sample volume is moved slowly through the artery searching for the highest velocity. The color Doppler display will help guide the proper placement of the sample volume and is useful in locating sites of disease as evidenced by the presence of aliasing of the color-flow image.
Doppler signals are recorded from the proximal, mid, and distal CCA; the origin of the ECA; the proximal, mid, and distal ICA; the origin of the vertebral artery; and the subclavian artery bilaterally. In a normal vessel, the Doppler sample volume placement should be at the center of the lumen. The pulsed Doppler sample volume placement width is set at 1-2 mm to detect discrete changes in blood flow and minimize artifactual spectral broadening. When a stenosis is identified, a thorough interrogation of the stenotic area is performed. In the presence of disease, color-flow Doppler imaging should be used as a guide to aid in the optimal placement of the pulsed Doppler sample volume where the highest velocity may be obtained. Be sure to profile the lesion by moving the sample volume back and forth through the lesion to elicit the highest velocity within the stenosis. A Doppler waveform is obtained at the site of stenosis, where highest velocity is suspected (Figs. 12–20 and 12–21), and a second Doppler waveform obtained distal to the lesion for documentation of post-stenotic turbulence that almost always accompanies a hemodynamically significant stenosis. It is important to evaluate all Doppler signals bilaterally to correctly perform a carotid duplex imaging examination.
FIGURE 12–20. Internal carotid artery stenosis evident by the significant elevation of the velocity.
FIGURE 12–21. Spectral Doppler waveform that demonstrates post-stenotic turbulence as evident by flow above and below the baseline; spectral broadening; and irregular picket-fence configuration of the envelope of the spectral waveform throughout the cardiac cycle.
The location of any plaque, as well as its surface characteristics (smooth versus irregular) and echogenicity (homogeneous, heterogeneous, or calcified), visualized during the examination should be described (Fig. 12–22).
FIGURE 12–22. (A) Calcific plaque that creates an acoustic shadow indicated by the arrows. (B) A smooth plaque that is heterogeneous in texture with a calcific component that causes an acoustic shadow indicated by the dotted arrow. (C) A plaque with an irregular border and heterogeneous in texture. (D) A smooth and predominantly homogeneous plaque. (CCA: common carotid artery; ECA: external carotid artery; ICA: internal carotid artery.)
Interpretation and Diagnostic Criteria
The accurate interpretation of a carotid duplex imaging examination depends on the quality and the completeness of the evaluation. Often the patient’s body habitus will affect the quality of the image and the sonographer’s ability to search the entire carotid system with Doppler. The sonographer must know when and be prepared to switch transducers when necessary to complete the carotid examination and have a complete understanding of the equipment controls to optimize the duplex imaging system. In addition to the peak systolic velocity, end-diastolic velocity, direction of blood flow, and the shape of the Doppler spectral waveform should be compared at the same level bilaterally. Abnormal waveform shape (increased or decreased pulsatility) may be an indicator of more proximal (innominate, subclavian) or distal (intracranial) disease (Fig. 12–23).
FIGURE 12–23. This is a comparison of the spectral Doppler waveforms obtained at the level of the common carotid artery (CCA) bilaterally in a patient with a left internal carotid artery (ICA) occlusion. (A) Normal spectral Doppler waveform of the right CCA. (B) On the contralateral side, a high-resistance spectral Doppler waveform with no diastolic flow suggestive of the distal ICA occlusion on the ipsilateral side.
To determine the degree of stenosis present, a complete Doppler evaluation of the artery is necessary. There should be an elevated velocity through the narrowed segment and post-stenotic disturbances distal to the stenosis. The highest velocity obtained from a stenosis is used to classify the degree of narrowing. Doppler signals obtained distal to the area of post-stenotic flow disturbance may be normal or diminished, and the upstroke of the distal Doppler spectral waveform may be slowed.
University of Washington criteria were traditionally used to categorize disease from the origin of the internal carotid artery (Table 12–5). However, because the carotid endarterectomy trials [North American Symptomatic Carotid Endarterectomy Trial (NASCET),40 Asymptomatic Carotid Atherosclerosis Study (ACAS)41, European Carotid Surgery Trial (ECST)] used specific thresholds for surgical treatment, ultrasound criteria for ICA stenosis more than 70% and more than 60% were needed to classify patients. Investigators have found that an ICA/CCA peak systolic velocity (PSV) ratio is useful in grading ICA stenosis more than 70%43 and more than 60%, respectively44(Table 12–6). The ratios are calculated using the highest PSV from the origin of the ICA divided by the highest PSV from the CCA (approximately 2-3 cm proximal to the bifurcation).
TABLE 12–5 • Strandness Criteria for Grading ICA Stenosis
TABLE 12–6 • NASCET and ACAS Criteria for Grading ICA Stenosis
In the presence of a contralateral ICA occlusion, the velocity from the ipsilateral ICA may be elevated. This may lead to overestimating the extent of ipsilateral ICA disease.45, 46 To avoid overestimation of the ICA stenosis, new velocity criteria have been suggested. A PSV of more than 140 cm/s is used for a stenosis >50% diameter reduction and an end-diastolic velocity of >155 cm/s for a stenosis greater than 80% diameter reduction of the lumen.46
Anatomic features, such as a high carotid bifurcation (<1.5 cm from the angle of the mandible), excessive distal extent of plaque (>2.0 cm above the carotid bifurcation), or a small distal ICA diameter (≤0.5 cm), or a redundant or kinked ICA can complicate carotid endarterectomy. In the past, arteriography was the only preoperative study capable of imaging these features. Accordingly, in the presence of ICA stenosis, other important information to include in the evaluation and interpretation of a carotid duplex imaging examination is (1) the location of the bifurcation relevant to the angle of the mandible (or some other external landmark), (2) the distal extent of the plaque beyond the ICA origin, (3) patency and diameter of the distal ICA, (4) the presence of tortuosity or kinking of the vessels, and (5) plaque characteristics (e.g., smooth versus irregular surface, calcification). This information is particularly relevant in patients undergoing carotid endarterectomy based on the duplex scan findings alone.47
Diagnosis of ICA Occlusion
Atherosclerosis is by far the most common cause of occlusion of the extracranial carotid arteries; however, fibromuscular dysplasia and dissection are additional causes. Most occlusions occur in the ICA48. ICA occlusion is not amenable to surgical intervention and a false-positive diagnosis will preclude the potential for treatment in this patient population. It is, therefore, important for patient management to differentiate between high-grade stenosis versus occlusion of the ICA. Differentiation of these two clinical entities was a major concern in ultrasound in the era before color-flow Doppler. However, with the advent of and technological advances in the 2D image and in color and power Doppler imaging, ICA occlusion can now very accurately be distinguished from high-grade stenosis.48–50
In the presence of a suspected ICA occlusion, the artery should be evaluated with spectral Doppler, color Doppler, and power Doppler to rule out the presence of trickle flow. Secondary ultrasound characteristics of an ICA occlusion include echogenic material filling the lumen, lack of arterial pulsations, reversed color blood flow near the origin of the occlusion, and the loss of diastolic blood flow in the ipsilateral CCA (Figs. 12–23A and B and 12–24).
FIGURE 12–24. Color duplex image of a carotid artery occlusion.
To reach this level of accuracy, it is important to employ several technical strategies:51 (1) The ultrasound instrument must be adjusted to allow for the detection of very low flow velocities. The operator must take care to ensure the appropriate pulse repetition frequency (PRF); this is referred to as the scale on some instruments. The wall filter must be adjusted so it does not exclude low-frequency signals. (2) The operator must make sure to obtain the best possible image of the vessel in question and inspect the lumen for any evidence (2D or Doppler) of active blood flow. This may require multiple angle views and approaches so that both the 2D and Doppler analysis have been optimized. (3) The operator must interrogate all visualized segments of the ICA with spectral Doppler. If flow is detected, be careful to ensure the correct flow direction so as to not mistake an adjacent vein for a patent ICA. (4) The operator must use both the sagittal and transverse planes to evaluate the suspected occlusion for any potential flow channels. (5) If possible, the operator should image the very distal ICA. In the presence of a suspected occlusion, the presence of antegrade flow distally is likely to mean that a patent lumen proximally has been overlooked.
CCA occlusion/stenosis occurs much less often than ICA occlusion and it can be accompanied by stroke or other neurologic events or it can be asymptomatic. Often these patients present after radiation therapy to the neck region and atherosclerosis is a less likely cause.
Pitfalls in the diagnosis of ICA occlusion include calcific plaques (Fig. 12–25). These will cause acoustic shadowing that limits or prevents visualization of the vessel of interest. Other pitfalls include high bifurcations and deep vessels that can limit the investigation and a pulsatile jugular vein that can be mistaken for a patent ICA.
FIGURE 12–25. Color duplex image of a calcific plaque that in many cases limits and sometimes prohibits adequate visualization of the carotid bifurcation. These plaques must be imaged from multiple approaches to achieve an adequate evaluation.
Transcranial Doppler and Imaging
Routine transcranial Doppler (TCD) ultrasound examination of the intracranial arteries was demonstrated to be possible in 1982.52 TCD, and more recently, transcranial color Doppler and power imaging, gives detailed information about the flow velocity in brain arteries and veins (Fig. 12–26). This hemodynamic information is routinely used in the diagnosis of cerebrovascular disease. Used to help in the diagnosis of emboli, stenosis, vasospasm from a subarachnoid hemorrhage (bleeding from a ruptured aneurysm), and other problems, this relatively quick and inexpensive test is growing in popularity in the United States.53, 54 It is often used in conjunction with other tests such as MRI, magnetic resonance angiography, carotid duplex ultrasound, and CT scans.
FIGURE 12–26. Power Doppler image of a portion of the circle of Willis.
One fact to keep in mind when utilizing TCD is that the value obtained for a particular artery is the velocity of blood flowing through the vessel, and unless the diameter of that vessel is established by some other means, it is not possible to determine the actual blood flow. Thus, TCD is primarily a technique for measuring relative changes in flow. The utility of the technique is now well established for a number of different disease processes.54–64
Two methods of recording may be used for this procedure. The first uses the B-mode image in combination with the Doppler information. Once the desired blood vessel is found, blood flow velocities may be measured with a pulsed Doppler, which records velocities over time. This is referred to as transcranial Doppler imaging (TCDI) and is performed using the duplex scanner. The second method of recording uses only the Doppler probe function, relying instead on the training and experience of the clinician in finding the correct vessels. This is referred to subsequently as TCD.
The operator must be aware that the Doppler spectral waveforms obtained during a TCDI examination are based on hemodynamics, and that the waveforms obtained do not provide anatomic information. TCDI is an advancement of intracranial ultrasound techniques since it combines the hemodynamic information with anatomic landmarks, enabling the accurate identification of the intracranial arteries. Increases in intracranial arterial velocity may be due to but not limited to increased volume flow without a lumen diameter change, a decrease in lumen diameter (stenosis) without a change in volume flow, or by a combination of an increase in volume flow and a decrease in lumen diameter.
The accurate interpretation of a patient’s TCDI examination may be difficult without knowledge of the location and the extent of atherosclerotic disease present in the extracranial vasculature.
The TCD technique was introduced as a method to detect cerebral arterial vasospasm following subarachnoid hemorrhage. During the past 20 years, the list of clinical applications for transcranial Doppler has grown (Table 12–7) and the addition of new areas of research will permit better understanding of intracranial cerebrovascular hemodynamics.
TABLE 12–7 • Transcranial Doppler Applicati
1. Diagnosis of intracranial vascular disease
2. Monitoring vasospasm in subarachnoid hemorrhage
3. Screening of children with sickle cell disease
4. Assessment of intracranial collateral pathways
5. Evaluation of the hemodynamic effects of extracranial occlusive disease on intracranial blood flow
6. Intraoperative monitoring
7. Detection of cerebral emboli
8. Monitoring evolution of cerebral circulatory arrest
9. Documentation of subclavian steal
10. Evaluation of the vertebrobasilar system
11. Detection of feeders of arteriovenous malformations
12. Monitoring anticoagulation regimens or thrombolytic therapy
13. Monitoring during neuroradiologic interventions
14. Testing of functional reserve
15. Monitoring after head trauma
Examination Protocols and Techniques
Transcranial Doppler Imaging (TCDI).65-67 The quality of the intracranial image depends on proper adjustment of many instrument controls. Increasing the power setting and the color gain to the appropriate level during a TCDI study are probably the most important instrument control adjustments. Adjusting the focal zone in the range of 6-8 cm will improve the image and color resolution. Maintaining a small image sector width and color box width will keep the highest possible frame rates. Checking for the appropriate color PRF, sensitivity, and persistence settings are also very important to obtain good quality color Doppler intracranial images.
The color display is important because it assists in the proper placement of the Doppler sample volume. The interpretation of the TCDI examination is made from the Doppler spectral waveform information. Therefore, Doppler signals are obtained from various depths along the artery’s path (Table 12–8). The color Doppler display helps guide the operator, as the Doppler sample volume is “swept” through the intracranial arteries to obtain the Doppler spectral waveforms. At each depth setting, it is important to adjust the position of the sample volume on the color display and angle the transducer to optimize the Doppler signal.
TABLE 12–8 • Mean Velocities Using Various Doppler US Approachs
Conventional color orientation for TCDI examinations is set for shades of red indicating blood flow toward the transducer and shades of blue indicating blood flow away from the transducer. By keeping this color assignment constant, intracranial blood flow direction in the arteries can be readily recognized. The appearance of intracranial arterial blood flow is dependent on many instrument controls that can affect its presentation. Therefore, estimations of arterial size are not accurate from the color Doppler display
The Doppler evaluation of the intracranial arteries is performed with a low-frequency (2-3 MHz) phased-array imaging transducer. A large sample volume is used to obtain a good signal-to-noise ratio. With TCDI, a smaller gate (i.e., 5-10 mm) can be placed on a specific arterial segment that is readily identified from a color-flow image. Intracranial arterial velocities acquired with TCDI are acquired assuming a zero-degree angle.
Additionally, with the use of TCDI, many investigators are reporting results using peak systolic and end-diastolic velocities instead of the traditionally accepted mean velocities (time average peak velocities). Each institution will have to decide which velocity value to report and adjust the diagnostic criteria accordingly.
Transcranial Doppler (TCD) is a “blind” technique that encompasses many of the concepts described above but employs a Doppler probe, only without the image component to analyze the intracranial vasculature.66, 67 Using various windows (Fig. 12–27) and depths, mean velocities are acquired and a diagnosis can be rendered (see Table 12–8).
FIGURE 12–27. Transcranial Doppler is accomplished using the following approaches: (A) transtemporal, (B) suboccipital, (C) transorbital.
Large observational studies and atherosclerosis regression trials of lipid-modifying pharmacotherapy have established that intima-media thickness (IMT) of the carotid and femoral arteries, as measured noninvasively by B-mode ultrasound, is a valid surrogate marker for the progression of atherosclerotic disease.68 IMT is a measurement that can be obtained at the level of the carotid bifurcation (Fig. 12–28). Although automated software is required to ensure accurate and reproducible data to assess a patient’s risks for such events, we can comment on the integrity of the vessel wall and look for variations of wall thickness along its length. Measuring the IMT is simply a screening tool and is mentioned here as an attempt to increase awareness of it and its utilization.69
FIGURE 12–28. Carotid intima-media thickness (CIMT) measurement using proprietary software (Prowin).
Other tests used in the diagnosis and management of patients with known or suspected cerebrovascular diseases include contrast arteriography, magnetic resonance angiography (MRA) and computed tomography (CTA).
Arteriography is the gold standard for the preoperative assessment of patients considered for carotid interventions, although the reported complications of stroke and death range between 0.2% and 0.7%. Noninvasive modalities such as MRA, combined duplex ultrasound and TCD, and duplex ultrasound alone are attractive because they avoid the contrast and catheter-related complications associated with arteriography. In many institutions, duplex ultrasound has emerged as the sole preoperative imaging study prior to carotid and other arterial and venous interventions.46, 70
Arteriography is a catheter-based technique that may include assessment of the aortic arch as well as selected injections of individual subclavian and carotid arteries with anteroposterior, lateral, and oblique views to evaluate the intracranial and extracranial vessels (Fig. 12–29).20, 71
FIGURE 12–29. Angiographic diagnosis of an internal carotid artery stenosis.
CT of the head is useful in identifying silent infarcts, determining the timing of surgery, evaluating the risk of surgery, and ruling out other causes of disease or symptoms. CT provides radiographic images of the body from many angles. A computer combines the pictures into two- and three-dimensional images. This test can also be performed with the administration of contrast dye to highlight the cerebrovasculature.19
MRA is increasingly being used as a noninvasive method for analyzing the carotid bifurcation. Many studies comparing duplex, MRA, and angiography have now been performed. While initial reports on MRA suggest it to be accurate for identifying carotid occlusion, MRA appears less reliable than duplex for categorizing stenosis in areas of moderate to severe narrowing where flow is turbulent, and it tends to overestimate disease. MRA remains an adjunct to duplex or angiography72–75.
The management options for patients with carotid artery stenosis include the following on their own or in combination: (1) conservative management (risk factor modification), (2) carotid endarterectomy (CEA), or (3) balloon angioplasty and stenting (CAS).13
The standard surgical procedure is CEA, while the newer minimally invasive endovascular intervention is called carotid artery angioplasty with stenting. Common indications for these procedures include transient ischemic attacks (TIAs) or cerebrovascular accidents (CVAs, strokes), although CEA can also be performed in asymptomatic patients with carotid stenosis. CAS is typically reserved for more high risk patients.13
CEA is the removal of plaque on the inside of an artery. The internal, common, and external carotid arteries are clamped, the lumen of the ICA is opened, and the atheromatous plaque substance removed. The artery is closed, hemostasis achieved, and the overlying layers closed. Many surgeons use a temporary shunt to provide blood supply to the brain during the procedure. The procedure may be performed under general or local anesthesia. The latter allows for direct monitoring of neurological status by intraoperative verbal contact and testing of grip strength. With general anesthesia, indirect methods of assessing cerebral perfusion must be used, such as electroencephalography (EEG), TCD analysis, and carotid artery stump pressure monitoring. At present, there is no good evidence to show any major difference in outcome between local and general anesthesia.
Angioplasty and stenting of the carotid artery is undergoing investigation as alternatives to CEA (Fig. 12–30). CAS is a less invasive procedure that can be performed via a percutaneous approach or through a small incision for intra-arterial access. A catheter is advanced into the carotid artery to the area of stenosis. This catheter has a balloon at its tip, which may vary in size. When the balloon is advanced over the lesion, the balloon is inflated. Inflation of the balloon compresses the plaque in the artery and makes a larger opening inside the artery to restore the lumen for improved blood flow. A stent (a tiny, expandable metal coil) is often deployed at the site to help keep the artery from narrowing or closing again (recoil).
FIGURE 12–30. Ultrasound image of a carotid stent. Notice the plaque that has been pushed against the wall as a result of balloon angioplasty.
Because of the potential for emboli to the brain that may cause stroke, embolic prevention devices (EPDs) should be used during CAS. One type of EPD has a filter-like basket attached to a catheter that is positioned in the artery in order to “catch” any clots or small debris that might break loose from the plaque during the procedure. This technique may help reduce the incidence of stroke during CAS.76
Intraoperative Carotid Duplex Imaging
The assessment of the CEA site by duplex imaging for technical adequacy has been shown to be an effective method to improve the results of the operation. Intraoperative duplex imaging identifies disturbed blood flow and anatomic abnormalities such as residual plaque, thrombus, and platelet aggregation. The detection of peak systolic velocities >150 cm/s with the presence of an anatomic defect warrants correction because of its potential to progress. Investigators have reported that the use of intraoperative carotid duplex imaging has had a favorable impact on the stroke rate and incidence of restenosis of the carotid artery; however, it is recommended that each institution should establish its own diagnostic criteria whether for use in the operating room or for diagnosis of atherosclerotic lesions.77–79
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