For select patients with ischemic strokes, early intervention with fibrinolytic therapy (“clot-busting drug”) is the standard of practice to improve blood flow to or through the brain. The success of fibrinolytic therapy from a stroke depends on the interval between the time the patient was last seen normal (LSN) and available treatment. It also depends on where the treatment is given. Hospitals with stroke centers or specialized stroke teams who care for numerous stroke patients have lower mortality rates than those hospitals that care for fewer of these patients (Bederson et al., 2009).

Intravenous (systemic) fibrinolytic therapy (also called thrombolytic therapy) for an acute ischemic stroke (AIS) dissolves the cerebral artery occlusion to re-establish blood flow and prevent cerebral infarction. Recombinant tissue plasminogen activator (rtPA [Retavase]) is the only drug approved at this point for the treatment of acute ischemic stroke. Thrombolytics activate plasminogen, which degrades the thrombus by breaking down fibrin. The most important factor in whether or not to give rtPA is the time LSN. The standard window for eligibility is 3 hours from time LSN. However, in 2009, the American Stroke Association recommended an expanded time interval from 3 to 4.5 hours for patients unless they fall into the following categories:

Fibrinolytic therapy is explained to the patient and/or family member, and informed consent is obtained. The dosage of the drug is based on the patient’s actual weight. Each hospital has strict protocols for mixing and administering rtPA and for monitoring the patient before and after rtPA administration.

Endovascular procedures include intra-arterial thrombolysis using drug therapy and mechanical embolectomy (clot removal). Intra-arterial thrombolysis has the advantage of delivering the fibrinolytic agent directly into the thrombus within 6 hours of the stroke’s onset. It is particularly beneficial for some patients who have an occlusion of the middle cerebral artery or those who arrive in the ED after the window for rtPA. If the patient arrives in less than 8 hours, the interventional neuroradiologist may perform mechanical embolectomy using special instrumentation systems that can remove the clot by suction or other method (Mink & Miller, 2011a). Patients having either fibrinolytic therapy or endovascular interventions are admitted to the critical care setting for intensive collaborative monitoring.

Some patients may have worsening of their neurologic status starting within 24 to 48 hours after their stroke. A major complication is increased intracranial pressure (ICP) (Chart 47-6). Reassess patients every 1 to 4 hours (depending on severity of the condition) using the approved assessment tools.

Keep the head of the bed (HOB) elevated to between 25 and 30 degrees to prevent a decreased blood flow to the brain. The best HOB positioning has not yet been determined, and more studies are needed to determine best practice. Provide oxygen therapy to prevent hypoxia for patients with oxygen saturation less than 92% or those with a decreased LOC (Summers et al., 2009). Maintain the head in a midline, neutral position to help promote venous drainage from the brain. When severe hemiparesis is present, position the patient on his or her side to prevent aspiration and promote comfort.

In collaboration with other team members, avoid patient care activities that may increase ICP, especially if the patient has indications of cerebral edema. Avoid positioning the patient in extreme hip and neck flexion. Extreme hip flexion may increase intrathoracic pressure, which may make ICP more difficult to control. Extreme neck flexion interferes with venous drainage from the brain, also affecting ICP control.

Additional nursing considerations include avoiding the clustering of nursing procedures (e.g., giving a bath followed immediately by changing the bed linen) within a short time. This action is needed because the effect on ICP elevation is more dramatic when multiple activities are clustered within a narrow time period. Hyperoxygenating the patient before suctioning may also be appropriate to avoid even transient hypoxemia and resultant ICP elevation from dilation of cerebral arteries. Assess the necessity of suctioning because it increases ICP.

A quiet environment is particularly important for the patient experiencing a headache, which is common with an aneurysm or increased ICP. The patient may have photophobia (sensitivity to light). Therefore keep the room lights very low.

Monitor vital signs closely, at least every 1 to 2 hours. Notify the health care provider if the blood pressure exceeds acceptable levels. Generally, the health care provider allows the patient with acute ischemic stroke to be slightly hypertensive (a systolic blood pressure [SBP] between 140 and 150 mm Hg) to promote cerebral tissue perfusion. A higher blood pressure (above 180 mm Hg systolic and/or 110 mm Hg diastolic) could lead to a hemorrhagic stroke or rebleeding of an aneurysm (if present).

Evidence-based guidelines are not available for managing blood pressure in patients with hemorrhagic strokes, but for many patients, severe hypertension is the cause of their stroke (Mink & Miller, 2011b).

Carefully monitor the patient’s temperature because fever may cause increased ICP. Hypothermia may cause decreased cerebral perfusion. A complete discussion of the management of increased ICP, including drug therapy, is on p. 1027 under Interventions in the Traumatic Brain Injury section.

Patients admitted to a critical care unit are connected to a cardiac monitor and observed for dysrhythmias. The nurse performs a cardiac assessment, with particular attention directed toward auscultation of heart sounds to identify the presence of cardiac murmurs or atrial fibrillation (AF). Murmurs or AF may place the patient at increased risk for emboli. Close physical assessment for indications of hemodynamic stability is indicated. Invasive hemodynamic monitoring is often needed to monitor and evaluate physiologic stability and response to therapy.

Although previously widely used, anticoagulants are controversial and are not considered current best practice by the American Stroke Association for acute ischemic strokes or for preventing future strokes (Adams et al., 2007). Sodium heparin and other anticoagulants, such as warfarin (Coumadin, Warfilone ), are high-alert drugs that can cause bleeding, including intracerebral hemorrhage.

However, an initial dose of 325 mg of enteric-coated or other form of aspirin (Ecotrin, Ancasal ) is recommended within 24 to 48 hours after stroke onset. Aspirin should not be given within 24 hours of rtPA administration. These drugs are antiplatelet drugs and prevent blood clotting by reducing platelet adhesiveness (clumping). They can cause bruising, hemorrhage, and liver disease over a long-term period. Teach the patient to report any unusual bruising or bleeding to the health care provider. The 2007 best practice guidelines for the treatment of acute ischemic stroke recommend against the use of clopidogrel (Plavix) alone or in combination with aspirin (Adams et al., 2007). However, many health care providers still prescribe them.

To treat seizures, lorazepam (Ativan), a benzodiazepine, may be administered with close neurologic and cardiopulmonary monitoring. For long-term antiseizure therapy, the health care provider may also prescribe antiepileptic drugs (AEDs), such as phenytoin (Dilantin), gabapentin (Neurontin), or topiramate (Topamax). Neuroprotective drugs such as calcium channel blockers (e.g., nimodipine [Nimotop]) may be given to treat or prevent cerebral vasospasm after a subarachnoid hemorrhage. Vasospasm, which usually occurs between 4 and 14 days after the stroke, slows blood flow to the area and worsens ischemia. Calcium channel blockers work by relaxing the smooth muscles of the vessel wall and reducing the incidence and severity of the spasm. Neurologic functioning may improve, and further deterioration from ischemia is then prevented. In addition, these drugs dilate collateral vessels to ischemic areas of the brain. Although these neuroprotective and vasodilating drugs are sometimes used, the American Stroke Association does not recommend them (Adams et al., 2007). Stool softeners, analgesics for pain, and antianxiety drugs may also be prescribed as needed for symptom management. Stool softeners also prevent the Valsalva maneuver during defecation to prevent increased ICP.

A technique using a distal/embolic protection device has made this procedure very safe. The device is placed beyond the stenosis through a catheter inserted into the femoral artery (groin). The device catches any clot debris that breaks off during the CAS procedure. Placement of a carotid stent is performed to open a blockage in the carotid artery typically at the division of the common carotid artery into the internal and external carotid arteries. Throughout the procedure, the patient’s neurologic and cardiovascular status are assessed. CAS is less invasive, causes less blood loss, requires shorter hospital stays (overnight) and recovery time, and has fewer complications than a carotid endarterectomy. Postprocedure care is the same as that provided for a carotid endarterectomy (see Surgical Management on p. 1016).

A rare postprocedure complication, hyperperfusion syndrome, has a very high morbidity and mortality rate. This syndrome is thought to be the result of an impaired autoregulation of cerebral blood flow, which results from longstanding decreased cerebral perfusion pressure that occurs with carotid artery disease. The signs and symptoms include severe temporal headache, hypertension, seizures, and focal neurologic deficits. This syndrome may be associated with intracranial hemorrhage and may occur within 1 hour postprocedure up to 24 hours or even 1 week later (Oran & Oran, 2010).

The usual treatment of an arteriovenous malformation (AVM) uses interventional therapy to block abnormal arteries or veins and prevent bleeding from the vascular lesion. The same procedure may be performed to occlude the vessels surrounding an aneurysm. Under fluoroscopic guidance, the physician inserts a microcatheter into the carotid artery, typically using a femoral artery approach, and threads it to the vessel to be embolized. The physician then injects an embolic liquid agent to embolize the involved arteries (Fig. 47-4). When the liquid makes contact with the blood, it immediately hardens. Embolization is usually done before gamma knife or conventional surgery. (See later discussions of these procedures in this chapter.)

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