Patients with diagnosed cerebrovascular disease typically have a history of transient ischemic attacks (TIAs) or stroke. Patients with TIAs undergoing surgery for other indications have an increased risk of perioperative stroke. Asymptomatic carotid bruits occur in up to 4% of patients older than age 40 years, but do not necessarily indicate signifi-cant carotid artery obstruction. Fewer than 10% of patients with completely asymptomatic bruits have hemodynamically significant carotid artery lesions. An asymptomatic carotid bruit may not increase the risk of stroke following surgery, but increases the likelihood of coexisting coronary artery disease. Moreover, the absence of a bruit does not exclude significant carotid obstruction.
The risk of perioperative stroke increases with patient age and varies with the type of surgery. The overall risk of stroke associated with surgery is low, but is greater in patients undergoing cardiovascu-lar surgery. Rates of stroke after general anesthe-sia and surgery range from 0.08% to 0.4%. Even in patients with known cerebrovascular disease, the risk is only 0.4% to 3.3%. Patients at greatest risk of postoperative stroke are those undergoing open heart procedures for valvular disease, coro-nary artery disease with ascending aortic athero-sclerosis, and diseases of the thoracic aorta. Stroke following open heart surgery is usually due to embolism of air, clots, or atheromatous debris. Inone study, 6.1% of patients experienced an adverse neurological outcome following cardiac surgery. Stroke following thoracic aortic surgery may be due to emboli or ischemia secondary to prolonged circulatory arrest or a clamp placed close to the ori-gin of the carotid artery.
The pathophysiology of postoperative strokes following noncardiovascular surgery is less clear, but may involve severe sustained hypotension or hypertension. Hypotension with severe hypo-perfusion can result in so-called “watershed” zone infarctions or thrombosis of cerebral arter-ies, whereas hypertension can result in intracere-bral hemorrhage (hemorrhagic stroke). Sustained hypertension can disrupt the blood–brain barrier and promote cerebral edema. Widened pulse pres-sure (>80 mm Hg) can produce endothelial vessel injury, potentially resulting in cerebral hypoperfu-sion or embolism. Perioperative atrial fibrillation can likewise lead to atrial clot formation and cere-bral embolism. The period of time during which anesthesia and surgery should best be avoided following a stroke has not been determined. Abnormalities in regional blood flow and metabolic rate usually resolve after 2 weeks, whereas altera-tions in CO 2 responsiveness and the blood–brain barrier may require more than 4 weeks. However, urgent surgery is performed for acute intracranial hemorrhage, symptomatic carotid disease, and car-diac sources of emboli.
Patients with TIAs have a history of tran-sient (<24 h) impairment, and, by definition, no residual neurologic impairment. These attacks are thought to result from emboli of fibrin-platelet aggregates or atheromatous debris from plaques in extracranial vessels. Unilateral visual impairment, numbness or weakness of an extremity, or aphasia is suggestive of carotid disease, whereas bilateral visual impairment, dizziness, ataxia, dysarthria, bilateral weakness, or amnesia is suggestive of vertebral–basilar disease. Patients with TIAs have a 30% to 40% chance of developing a frank stroke within 5 years; 50% of these strokes occur within the first year. Patients with TIAs should not undergo any elective surgical procedure with-out an adequate medical evaluation that generally includes at least noninvasive (Doppler) flow and imaging studies. The presence of an ulcerative plaque of greater than 60% occlusion is generally an indication for carotid endarterectomy or endo-vascular intervention.
Preoperative assessment requires neurologic and cardiovascular evaluations. The type of stroke, the presence of neurologic deficits, and the extent of residual impairment should be determined. Thromboembolic strokes usually occur in patients with generalized atherosclerosis. Most patients are elderly and have comorbid conditions, such as hyper-tension, hyperlipidemia, and diabetes. Coexisting coronary artery disease and renal impairment are common. Following nonhemorrhagic strokes or TIAs, many patients are placed on long-term war-farin and/or antiplatelet therapy. Management of antiplatelet therapy and antithrombotic therapy should be reviewed by the anesthesia, primary care, and surgical teams to determine the risk/benefit of the discontinuation or maintenance of such ther-apy perioperatively. Other systemic diseases, such as diabetes, hypertension, coronary artery disease, heart failure, and chronic obstructive lung disease frequently manifest in the patient with cerebrovas-cular disease.
Patients may present for surgery following embolic, thrombotic, and hemorrhagic strokes.
Management of the patient following acute embolic stroke is directed toward the embolic source. Cardiac surgery is performed to remove atrial myxomas. Systemic emboli can also be pro-duced from endocarditic vegetations, as well as from degenerated heart valves and intracardiac thrombus.
Patients with acute strokes secondary to carotid occlusive disease present for carotid end-arterectomy and endovascular procedures. When an awake carotid endarterectomy is undertaken, the patient serves as a monitor of the adequacy of cerebral blood flow during application of vessel clamps to facilitate the surgical repair. When gen-eral anesthesia is used electroencephalography, evoked potentials, carotid stump pressure, cerebral infrared spectroscopy, transcranial Doppler, and surgeon subjective sense of collateral back flow are all used to estimate the adequacy of cerebral oxy-gen delivery during cross clamp. When monitors or lack of appropriate patient response indicate hypo-perfusion, the surgeon places a shunt to deliver blood to the brain around the cross-clamped ves-sel. Even with adequate cerebral blood flow, peri-operative stroke can occur during carotid surgery secondary to emboli.
Management of patients following thrombotic or hemorrhagic stroke for nonneurological surgery must be individualized. Cerebral autoregulation of blood flow may fail, leaving flow directly dependent upon cerebral perfusion pressure (Figure28–1). The penumbra of potentially salvageable neurologic tis-sue may therefore be very sensitive to injury from the effects of both hypotension and hypertension (Figure28–2).
Patients taken to surgery following administra-tion of thrombolytic therapy are at risk of cerebral hemorrhage, and tighter blood pressure control may be indicated to mitigate the possibility of cerebral bleeding.Patients with intracerebral hemorrhage or traumatic brain injury undergo evacuation of
hematoma and decompressive craniectomy. These patients usually require invasive arterial pressure monitoring to facilitate blood pressure manage-ment in settings where cerebral autoregulation is likely deranged (Figure 28–1). Hypertension is fre-quently treated with intravenous vasodilators and β-blockers.
Patients with intracranial mass lesions present to surgery with both malignant and nonmalignant lesions. Such patients frequently present to their pri-mary care physicians with complaints of headache, vision disturbance, or seizures. Radiologic studies confirm the presence of a lesion, and initial treat-ment is aimed at decreasing cerebral edema with dexamethasone. Electrolytes should be reviewed perioperatively in all patients undergoing cranial surgery, as both hyponatremia and hypernatre-mia can develop secondary to cerebral salt wast-ing, inappropriate antidiuretic hormone secretion, or central diabetes insipidus ( Table28–1). Patients with altered mentation preoperatively may likewise be dehydrated. Hyperglycemia secondary to steroid use is frequently seen.
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