A 60-year-old man with a history of hypertension and hyperlipidemia presents to the emergency department 24 hours after the onset of right-sided face, arm, and leg weakness. At the time of presentation, the patient believes his symptoms are significantly improved since onset. His physical examination is notable for a mild right facial droop and a right arm pronator drift. A noncontrast head computed tomography (CT) scan is performed that shows a subtle focus of hypodensity within the left frontal lobe and no evidence of hemorrhage (Figure 25-1).
Brain magnetic resonance imaging (MRI) as well as head and neck MR angiography (MRA) was performed in the emergency department. A left frontal lobe infarct was confirmed on the MRI and MRA and demonstrated high-grade stenosis at the origin of the left internal carotid artery (ICA) (Figure 25-2). The patient was started on aspirin 325 mg once per day and admitted to the neurology stroke/step-down unit equipped with cardiac and blood pressure monitoring. Electrolytes, troponin levels, chest X-ray, electrocardiogram, and transesophageal echocardiogram were ordered. A carotid Doppler ultrasound was obtained confirming origin of 60% to 79% stenosis in the left internal carotid artery.
Extracranial, large-vessel stenosis should be evaluated by at least two of the following three noninvasive modalities to determine the extent and degree of stenosis: MRA, CT angiography (CTA), or Doppler ultrasound. Carotid Doppler ultrasound is quick, inexpensive, and portable and thus is performed easily at the bedside; however, it is highly operator dependent. MRA has the advantage of not exposing patients to radiation and has demonstrated greater discriminatory power than ultrasound in assessing high-grade stenosis.1 CTA compares favorably with catheter angiography for the evaluation of carotid stenosis; however, radiation exposure and calcium artifact can be disadvantageous.2
Carotid endarterectomy (CEA) remains the gold standard intervention for the treatment of high-grade atherosclerotic carotid artery disease. In select patient groups, carotid angioplasty and stenting (CAS) should also be considered. The evidence from randomized clinical trials comparing CEA with best medical management in both symptomatic and asymptomatic patients is substantial. The North American Symptomatic Carotid Endarterectomy Trial (NASCET) found that CEA significantly reduced the risk of any ipsilateral stroke (17% absolute risk reduction) and major or fatal ipsilateral stroke (10.6% absolute risk reduction) for patients with ICA stenosis of 70% to 99%.3 Further analysis showed a less robust but still significant benefit for symptomatic patients with > 50% ICA stenosis. The Asymptomatic Carotid Artery Stenosis (ACAS) Trial found that patients with > 60% stenosis had a 6% reduction in the risk of stroke or death at 5 years.4
The Carotid Revascularization Endarterectomy versus Stenting Trial (CREST) was a randomized study comparing CEA to CAS in both symptomatic and asymptomatic patients.5 Although the composite primary outcome of stroke, myocardial infarction (MI), or death did not differ among the two groups, differences were noted for the individual outcomes. Higher rates of perioperative stroke were noted in the CAS group (4.1% vs 2.3%), while higher rates of MI were noted in the CEA group (2.3% vs 1.1%). It is notable that perioperative stroke but not MI was associated with worse health status as judged by quality of life assessment. Thus, although the decision to proceed with CEA is complex and must weigh many competing factors, we generally favor CEA for the treatment of symptomatic high-grade atherosclerotic carotid artery stenosis. CAS may be more appropriate for patients with unacceptably high surgical risk due to the presence of medical comorbidities, unfavorable surgical anatomy with a very high common carotid artery bifurcation (above C2), contralateral ICA occlusion or laryngeal palsy, radiation induced stenosis, restenosis after prior CEA, or prior neck dissection.
This patient is taken to the operating room where a left CEA was performed uneventfully (Figure 25-3). The patient is given a bolus of 5000 U IV heparin in preparation for carotid cross-clamping with ACT measurement to ensure at least doubling. No changes in EEG signals are noted during carotid cross-clamping with the blood pressure elevated 20% above baseline. The blood pressure returns to baseline levels prior to the resumption of ICA flow. Doppler ultrasound is used to confirm adequate flow within the common, internal, and external carotid arteries prior to skin closure, and heparin is not reversed.
Figure 25-3.
(A) The patient is positioned supine with the head turned contralateral to the operative side of the CEA. (B) The sternocleidomastoid muscle and jugular vein are retraced laterally and the internal (ICA), external (ECA), and common carotid arteries (CCA) are exposed after dissection within the carotid sheath. (C) The ulcerated atheromatous plaque is dissected on a side table after removal. Thrombogenic, fibrinous platelet debris is discovered upon inspection.
Management during the postoperative period after endarterectomy should focus on blood pressure control and early detection and management of complications. Table 25-1 lists rates of complications after CEA. In the postoperative period after CEA, blood pressure may be especially labile owing to changes in flow patterns and pressure at the carotid sinus. Such variation in blood pressure can result in undesirable stress on the myocardium, especially in patients with underlying coronary artery disease. Continuous cardiac monitoring and blood pressure monitoring with an arterial line should be continued for 24 hours postoperatively. We typically maintain the systolic blood pressure within the patient’s preoperative range with the use of phenylephrine or nicardipine infusions as appropriate.
| Type of Complication | Frequency (%) | Pathophysiology |
|---|---|---|
| Acute coronary syndrome | 0.5-2.33,5,7 | Hemodynamic disturbances in the setting of preexisting coronary atherosclerotic disease |
| Ischemic stroke | 2.1-5.53,5,7 | Thromboembolism, carotid occlusion, hemodynamic disturbances |
| Seizure | 0.88 | Hyperperfusion syndrome, emboli, hemorrhage |
| Intracerebral hemorrhage | 0.1-0.89,10 | Hyperperfusion syndrome |
| Nerve injury | 5.1 (0.5 at 4-month follow-up)11 | Compression from retraction or direct injury; hypoglossal nerve injury the most common (1.6%) followed by marginal mandibular (1.0%) and recurrent laryngeal (1.0%) |
| Neck hematoma | 1.7-1.9 requiring surgical intervention12,13 | Postoperative bleeding |
Aspirin therapy, usually 325 mg/d, should be continued uninterrupted.6,14 Alternative or additional antiplatelet agents such as clopidogrel or dipyridamole15 may be restarted at the discretion of the treating surgeon. High-dose statin therapy should also be started as tolerated by the patient.
The patient is a 58-year-old, right-handed man with a past history of hypertension and hyperlipidemia who presents after several episodes of left-sided weakness that completely resolve after several minutes. Doppler ultrasound of the carotid arteries reveals 80% stenosis of the right ICA just distal to the bifurcation and 30% stenosis of the left ICA at the level of the bifurcation. MRA confirms 70% to 80% stenosis of the right ICA. The patient is subsequently medically cleared for CEA. The surgery is uneventful without obvious intraoperative electroencephalographic (EEG) changes, and patency of the arteriotomy site was confirmed by Doppler ultrasound. Prior to extubation he is noted to have a dense hemiplegia on the left side.
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