Carotid Endarterectomy

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Chapter 33 Carotid Endarterectomy

Historical Background

The development of surgery for carotid artery disease required three important advances: (1) recognition of the relationship between atherosclerotic disease of the carotid bifurcation and stroke, (2) premorbid identification of carotid bifurcation disease, and (3) the vascular surgical techniques necessary to remove carotid bifurcation atherosclerotic plaque.

For many years, the relationship between carotid artery disease and stroke was overlooked because autopsy protocol did not include harvesting the cervical vessels. Therefore, the only pathology observed in hemispheric stroke was thrombus in the intracranial vessels, most commonly the middle cerebral artery (MCA).One of the earliest observations of the relationship of cervical carotid artery disease with stroke was made in 1856 by Savory, who described a patient with left monocular blindness, right hemiplegia, right dysesthesia, and an occluded left internal carotid artery (ICA) at the carotid bifurcation.1 A similar observation was made by Gowers in 1875.2 It was not until 1914 that Hunt described the relationship between carotid artery disease, transient ischemic attacks (TIAs), and stroke.3 The ability to identify carotid bifurcation disease prior to death awaited the work of Moniz, who in 1927 reported on the technique of carotid angiography. This, for the first time, provided the opportunity to identify carotid artery occlusive disease in the living patient.4 In spite of this, clinicians solely used cerebral angiography to evaluate the intracranial circulation. In 1951, Fisher reemphasized the importance of the cervical carotid artery, pointing out that prior to occlusion, a stenosis was present that might be amenable to surgical correction.5

The surgical phase for treating carotid artery disease began in 1951. Carrea et al. from Buenos Aires resected the diseased segment of an ICA and restored flow by anastomosing the external carotid artery (ECA) to the distal ICA. They waited until 1955 for sufficient follow-up before reporting the case.6 Probably the first successful carotid endarterectomy (CEA) was performed by DeBakey et al. in 1953, but it was not reported until 1959, with a long-term follow-up reported in 1975.7 The publication that led to rapid incorporation of carotid artery surgery into clinical practice was the operation reported by Eastcott et al. in 1954. They described a case of a woman who was experiencing hemispheric TIAs, with an associated stenosis of the bulb of the carotid artery. They resected the carotid artery bifurcation and restored flow by a direct anastomosis between the common and distal ICAs with a successful outcome and cessation of symptoms. This report led to an explosion of interest in the treatment of carotid bifurcation disease.8

Pathology of Carotid Bifurcation Disease

The most common lesion of the carotid artery bifurcation is an atherosclerotic plaque involving the bulb of the ICA. This localization of plaque is predictable and provides the opportunity for treatment with CEA. The plaque can be calcific, fibrous, or composed of atherosclerotic elements of mixed consistency. Plaques can expand slowly or, with intraplaque hemorrhage, rapidly. Other pathological lesions causing carotid artery stenosis include fibromuscular dysplasia (FMD), Takayasu’s arteritis (TA), radiation arteriopathy, and (rarely) aneurysms of the cervical ICA.

Pathogenetic Mechanisms of Stroke and Transient Ischemic Events

The pathogenetic mechanism for ischemic events is primarily thrombotic or atheroembolic (also see Chapter 30). If the occlusive plaque in the carotid bulb progresses to critical flow reduction, the ICA will proceed to thrombotic occlusion. The pace of the occlusive process is important. If this process occurs slowly, collateral circulation may develop from the contralateral carotid and vertebral arteries. In addition, the ipsilateral ECA can be a source of collateral blood flow by flow reversal through the ophthalmic artery to the siphon of the ICA. Under these circumstances, thrombosis of the ICA may be a silent event. On the other hand, if plaque expansion occurs rapidly or if collateral circulation is inadequate, there will be thrombotic propagation beyond the ophthalmic branch of the ICA into the middle cerebral artery, causing hemisphere infarction and neurological deficit.

In addition to thrombotic occlusion of the ICA, the more common mechanism for ischemic events is rupture of the intimal cover of the atherosclerotic plaque, permitting the discharge of soft atherosclerotic debris into the blood flow stream. These fragments are carried distally to the intracranial branches, fostering either permanent branch occlusion and cerebral infarction or, with fragmentation and thrombolysis of the embolus, a temporary and reversible neurological deficit or TIA. Following plaque rupture and a primary wave of embolization, a defect is left in the plaque that on angiographic inspection resembles an ulcer. This ulcer or plaque defect can be the source of continual embolization, or it can be the nidus for platelet aggregate and thrombotic material to reside. Since there is no attachment of this material within the ulcer crater, pulsatile blood flow can dislodge the material residing with the ulcer crater, leading to a secondary wave of embolization.

Preoperative Imaging

The noninvasive examination of choice for patients with suspected carotid artery disease is a carotid duplex ultrasound scan using modern equipment in a validated vascular laboratory (also see Chapter 12). This study identifies lesions in the carotid artery, classifies the severity of stenosis, and provides information regarding plaque consistency. The opportunity to examine flow velocity and pulse wave velocity analysis provides information about other portions of the circulation, including proximal lesions at the level of the aortic arch and distal intracranial lesions. In many centers, the duplex scan serves as the definitive preoperative study.9 Additional studies such as magnetic resonance imaging (MRI), magnetic resonance angiography (MRA), computed tomographic angiography (CTA), or catheter-based contrast angiography are reserved for special circumstances.9 Use of MRA or CTA in conjunction with duplex ultrasound of the carotid artery is considered when the results of duplex ultrasonography are difficult to interpret or inconsistent with the clinical presentation.

Magnetic resonance angiography is used frequently because it does not require ionizing radiation. When contrast is added, the images are often clear and resemble those obtained via catheter-based intraarterial angiography, providing a sensitivity and specificity of 88% and 84%, respectively, for diagnosing a 70% to 99% stenosis.9 Magnetic resonance angiography permits imaging of the intracranial vascular anatomy, and when combined with MRI, can identify areas of cerebral infarction or other intracranial pathology. The major limitation of MRA is that it tends to overestimate percent stenosis of lesions in the carotid bifurcation (also see Chapter 13). This phenomenon occurs because turbulent blood blow, such as occurs at carotid bulb stenosis, results in signal dropout and void, giving the impression of a high-grade carotid stenosis.

Computed tomography (CT) and CTA are also quite helpful in identifying intracranial lesions. Computed tomography angiography is accurate in identifying and quantifying intracranial and extracranial carotid stenosis (also see Chapter 14). The sensitivity and specificity of CTA for determination of carotid artery stenosis are 95% and 99%, respectively.10 The major drawbacks of CT scanning are exposure to ionizing radiation and the requirement for a large volume of iodinated contrast material, which can be nephrotoxic or cause allergic reaction in patients sensitive to iodine.

Intraarterial contrast angiography is considered the gold standard for identifying and quantifying arterial stenoses. Major disadvantages of this invasive procedure include arterial injury, occlusion, and embolization resulting in cerebral infarction. In the Asymptomatic Carotid Artery Study (ACAS), angiography was associated with a 1% stroke rate.11 In addition, it requires ionizing radiation and iodinated contrast material. This technique is now rarely indicated prior to carotid endarterectomies. It does have a role for preprocedure imaging as a part of carotid angioplasty/stenting.

Techniques of Carotid Endarterectomy

An arterial canula is placed for continuous blood pressure monitoring and periodic sampling of blood gases. Carotid endarterectomy can be performed under either local or general anesthesia. General anesthesia is more comfortable for the patient. It affords a quiet operative field and allows the surgeon to concentrate without distraction by patient movement or discomfort. It also allows optimal airway control, ventilation, and oxygenation.

The patient is positioned supine on the operating table. A cushion is placed under the shoulders to allow for mild neck extension, and the head is rotated away from the side of incision.

When the carotid artery is clamped for the endarterectomy procedure, the surgeon has several choices regarding the assurance of adequate blood flow to the ipsilateral cerebral hemisphere. About 90% of patients tolerate temporary clamping of the carotid artery because adequate collateral circulation is provided through the circle of Willis. For patients with inadequate collateral circulation, a temporary shunt is required to maintain adequate cerebral perfusion during endarterectomy to avoid periprocedural cerebral infarction. These observations have led to two forms of practice: routine shunting of all patients or selective shunting based upon intraoperative monitoring. The argument for routine shunting is that special monitoring is not required. The argument in favor of selective shunting is that there are complications unique to the use of an internal shunt. These include intimal damage with shunt placement and embolization of air or atheromatous debris through the shunt to the intracranial circulation, resulting in a cerebral infarction. In addition, when a shunt is in place, it is difficult to see the end of the endarterectomized segment, thus opening the possibility of leaving a residual intimal flap that can lead to thromboembolism and possibly postoperative carotid occlusion. Therefore, since only 10% of patients undergoing CEA require a shunt, there is little reason to expose the majority 90% who do not require a shunt to its potential complications.

There are several acceptable methods for monitoring the adequacy of cerebral perfusion. The first method that was described was measurement of ICA backpressure in patients undergoing CEA under local anesthesia. With clamping of the common carotid artery (CCA) and ECA, the residual pressure in the carotid artery determines the perfusion in the middle cerebral artery. One study found that the conscious response to clamping correlated with the ICA backpressure.12 The minimum pressure associated with no neurological deficit was 25 mmHg. This observation was subsequently validated in patients undergoing operation with general anesthesia.13,14

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