37: Intracranial and Cerebrovascular Disease

Published on 06/02/2015 by admin

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Last modified 22/04/2025

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CHAPTER 37 Intracranial and Cerebrovascular Disease

19 What are the common postoperative complications of carotid endarterectomy?

22 Describe the management of intracranial aneurysms following spontaneous subarachnoid hemorrhage

Early surgical intervention (aneurysm clipping) within the first 72 hours of the initial bleed improves neurologic outcome, but early treatment may be technically difficult secondary to cerebral edema and unstable concomitant medical conditions. Surgery is often delayed until the risk of maximal vasospasm has decreased. Initial treatment includes close hemodynamic monitoring and stabilization, stool softeners to prevent straining, bed rest, and analgesia. Anticoagulation, if present, should be reversed. If a patient does not have any neurologic deficits, is alert and appropriate, and has appropriate cerebral perfusion pressure (CPP), antihypertensive therapy may be used; but most hypertensive patients are left untreated so as to maintain CPP.

When blood pressure control is necessary, usually nitroprusside or nitroglycerin is avoided because it increases cerebral blood flow; labetalol is an acceptable alternative. The use of fibrinolytics is controversial and discouraged. Glucocorticoids confer neither a benefit nor a risk. If the patient is stuporous, has decerebrate posturing, or is in a coma, interventional radiologic procedures, ventriculostomy, or burr holes may be indicated. Patients chosen for aneurysmal coiling often have a number of uncontrolled comorbidities. Interventional radiologic procedures have become the treatment of choice for selected patient groups after cerebral aneurysm rupture.

25 Describe the treatment options if vasospasm is suspected following an spontaneous subarachnoid hemorrhage

Traditionally vasospasm has been treated with hypertensive, hypervolemic, hemodilution (HHH). Hypervolemia is achieved with colloid administration, with a goal of central venous pressure of 8 to12 mm Hg or pulmonary artery wedge pressure of 18 to 20 mm Hg. The desired level is a hematocrit of 27 to 30, thereby reducing viscosity and improving microcirculation. If the aneurysm is clipped, vasopressors (dopamine, phenylephrine) can be used to induce hypertension, with the goal being a mean arterial pressure approximately 20 to 30 mm Hg greater than baseline systolic pressure. Increased perfusion pressure will attenuate any cerebral ischemia and promote blood flow to transitional areas of injury (known as the penumbra). Calcium channel blockers (CCBs) are usually started empirically following SAH. CCBs have not been found to be consistent in decreasing the incidence of vasospasm (either angiographically or clinically). The CCB nimodipine has been shown to improve outcomes in SAH and should be used with appropriate monitoring. The overall mechanism of action in this setting is unknown, but decreased platelet aggregation, dilation of small arterioles, and reduction of calcium-mediated excitotoxicity are considered possible etiologies. Angioplasty can be performed, and papaverine infused if segmental vasospasm is present on angiogram.