Cerebrovascular accidents, or strokes, are the third leading cause of death in the United States and account for a yearly cost of $14 billion in medical expenses and lost productivity. Most strokes are caused by cerebral ischemia. In carotid atherosclerotic disease, subintimal fatty plaques can increase in size over time and incrementally occlude the vascular lumen, which results in decreased cerebral blood flow (CBF). The plaque may rupture and release fibrin, calcium, cholesterol, and inflammatory cells. This phenomenon can lead to abrupt occlusion of the lumen from thrombosis from platelet activation, or an embolus may form and decrease CBF distal to the carotid artery. In each scenario, an abrupt decrease in CBF leads to transient ischemic attacks (TIAs) or strokes.
More than half of all strokes are preceded by a TIA. The Framingham study reported that the risk of a stroke was 30% 2 years after a TIA and approximately 55% 12 years after a TIA had occurred. It is this increased risk of stroke associated with TIA that provides the rationale for use of carotid endarterectomy (CEA), the surgical procedure in which the internal carotid artery is incised, the carotid arterial lumen is opened, and the plaque within the lumen is removed to improve CBF.
The initial indication for CEA is symptomatic stenosis but not complete occlusive carotid disease. This presentation occurs in most patients who undergo carotid surgery. Some centers have extended the indications to include evolved (nondense), nonhemorrhagic strokes and asymptomatic severe stenosis or lesser stenosis associated with contralateral occlusive disease.
The surgical outcomes reported for CEA remain inconclusive because of differences in patient populations and varying degrees of surgical expertise. Other variables that cannot be stratified in studies but that may affect outcome include the state of collateral flow through the circle of Willis, the presence of concurrent atherosclerotic disease in the cerebral vasculature, the size and morphology of the offending plaque, the specific presenting symptoms, and the presence of concurrent cardiovascular disease. The perioperative mortality rate for CEA is approximately 0.5% to 2.5%, and the long-term postoperative stroke incidence ranges from 1% to 3% per year.
Criteria for the best candidates for carotid artery surgery remain unclear. The risks associated with having surgery and the possibility of a stroke should be measured against the risks associated with not having surgery and undergoing medical management. Several conditions that can increase the risk of perioperative complications include severe preoperative hypertension, CEA performed in preparation for coronary artery bypass, angina, internal carotid artery stenosis near the carotid siphon, age older than 75 years, and diabetes mellitus. Because CEA is performed prophylactically, it would seem prudent that patient selection be based on the risks associated with the neurologic and myocardial ischemia of surgery as opposed to the risks associated with the neurologic sequelae of nonsurgical management.
The neurologic symptoms of cerebrovascular dysfunction (e.g., TIAs and strokes) are most frequently related to a decrease in CBF. Asymptomatic carotid bruits may be a sign of the possibility of carotid artery disease. Amaurosis fugax or monocular blindness occurs in 25% of patients with high-grade carotid artery stenosis. This syndrome is believed to be caused by microthrombi that travel into the internal carotid artery and that decrease the blood supply of the optic nerve via the ophthalmic artery. Duplex ultrasonography, a noninvasive diagnostic modality that combines ultrasonography and Doppler analysis, is currently one of the most sensitive noninvasive techniques capable of evaluating extracranial occlusive disease. Arteriography may be performed if surgery is being contemplated and can provide anatomic details of arterial vessels. CT scan or MRI may be useful in patients with a neurologic deficit, in whom an alternative diagnosis may be discovered.
6. Preoperative assessment
a) The presence of concurrent CAD and carotid stenosis is well documented. Although stroke is a devastating consequence of CEA, MI contributes more frequently to poor surgical outcomes than stroke. Although coronary angiography may not be justified in all patients undergoing CEA, a systematic approach to the identification of CAD and its subsequent risks should be performed before elective surgery.
b) Patients with no significant medical history, normal physical examination, and normal ECG should proceed directly to surgery because these patients have low surgical risks.
c) When abnormal cardiac information is obtained, further evaluation should be performed. Radionuclide imaging is highly sensitive in diagnosing CAD. Redistribution demonstrated on dipyridamole-thallium imaging is very suggestive of increased risk of adverse cardiac events. In these patients, coronary angiography is suggested as a means of quantifying CAD and selecting an appropriate therapeutic intervention.
d) The progression of surgical intervention when CAD is present with carotid artery disease is controversial. Most agree that in cases of mild CAD, patients may undergo CEA with a low degree of risk. However, in cases of moderate to severe CAD, the direction of surgical intervention is unclear. One option is the simultaneous performance of CEA and coronary revascularization. Decisions should be guided by the patient’s symptoms, the associated risk factors, and the center’s experience.
7. Perioperative considerations
a) Cerebral physiology
(1) CBF can remain relatively constant at different cerebral perfusion pressures as a result of cerebrovascular autoregulation. Cerebral perfusion pressure can be expressed as the difference between MAP and intracranial pressure (ICP). During CEA, ICP is usually not elevated; therefore, MAP plays the predominant role in determining cerebral perfusion pressure.
(2) When MAP is maintained between 60 and 160 mmHg, CBF remains constant. However, the adverse effects of chronic systemic hypertension shift the patient’s cerebral autoregulatory curve to the right, and therefore a higher than normal MAP may be required to ensure adequate cerebral perfusion. CBF is also influenced by arterial carbon dioxide and oxygen levels as well as by inhalation agents.
(3) Carotid occlusive disease jeopardizes the cerebral perfusion pressure in the ipsilateral artery. Ischemia leads to the disruption of autoregulation and compensatory vasodilation, and thus blood flow becomes pressure dependent. During CEA, the anesthetic goals should focus on improvement and protection of CBF and diligent monitoring of brain function.
b) Cerebral monitoring
(1) In addition to standard monitoring, direct intraarterial pressure is continuously assessed to evaluate near–real-time values. During the administration of anesthetic agents, blood pressure fluctuation commonly occurs in patients who have a history of hypertension.
(2) Because of the high incidence of CAD and neurovascular disease in this patient population, prompt treatment of blood pressure values below 20% of the preoperative MAP value is imperative.
(3) Pulmonary artery catheterization is not warranted in most individuals unless the presence of concurrent cardiac disease justifies its use.
(4) Carbon dioxide has a potent effect on cerebrovascular tone. Both hypocapnia and hypercapnia directly affect CBF; therefore, maintenance of normocapnia is paramount.
(6) Various monitoring techniques have been proposed for the assessment of the adequacy of CBF during this maneuver.
(7) A summary of cerebral monitoring techniques is listed below. Each of these monitoring modalities has limitations, and the most sensitive and specific measure of adequate CBF is an awake patient.
(8) Electroencephalographic (EEG) monitoring constitutes the gold standard in the identification of neurologic deficits related to carotid artery cross-clamping. EEG has demonstrated reliability in the monitoring of cortical electrical function. Loss of β-wave activity, loss of amplitude, and emergence of slow-wave activity all are indicative of neurologic dysfunction.
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