Approximately 400,000 people have an ischemic stroke in the United States each year (Hock, 1999). An ischemic stroke, cere-brovascular accident (CVA), or what is now being termed “brain attack” is a sudden loss of function resulting from disruption of the blood supply to a part of the brain. This event is usually the result of long-standing cerebrovascular disease. The term “brain attack” is being used to suggest to health care practitioners and the public that a stroke is an urgent health care issue similar to a heart attack. This change in terms also reflects a similar manage-ment strategy in both diseases. Early treatment results in fewer symptoms and less loss of function. Only 8% of ischemic strokes result in death within 30 days (American Heart Association, 2000).
The net lifetime stroke-related costs in patients over the age of 65 with a first ischemic stroke are estimated at $62,000 ($45,000 direct costs plus $17,000 indirect costs). The cost for younger patients (those less than 65 years) is even greater, at $198,000 per year ($65,000 direct costs plus $133,000 indirect costs). The approximate annual cost in the United States for ischemic stroke care is over $71.8 billion (Matchar & Samsa, 2000).
Ischemic strokes are subdivided into five different types ac-cording to their cause: large artery thrombosis (20%), small pen-etrating artery thrombosis (25%), cardiogenic embolic stroke (20%), cryptogenic (30%) and other (5%) (see Table 62-1).
Large artery thrombotic strokes are due to atherosclerotic plaques in the large blood vessels of the brain. Thrombus forma-tion and occlusion at the site of the atherosclerosis result in is-chemia and infarction.
Small penetrating artery thrombotic strokes affect one or more vessels and are the most common type of ischemic stroke. Small artery thrombotic strokes are also called lacunar strokes be-cause of the cavity that is created once the infarcted brain tissue disintegrates.
Cardiogenic embolic strokes are associated with cardiac dys-rhythmias, usually atrial fibrillation. Emboli originate from the heart and circulate to the cerebral vasculature, most commonly the left middle cerebral artery, resulting in a stroke. Embolic strokes may be prevented by the use of anticoagulation therapy in patients with atrial fibrillation.
The last two classifications of ischemic strokes are cryptogenic strokes, which have no known cause, and other strokes, from causes such as cocaine use, coagulopathies, migraine, and spon-taneous dissection of the carotid or vertebral arteries (Hock, 1999; Schievink, 2001).
In an ischemic brain attack, there is disruption of the cerebral blood flow due to obstruction of a blood vessel. This disruption in blood flow initiates a complex series of cellular metabolic events referred to as the ischemic cascade (Fig. 62-1).
The ischemic cascade begins when cerebral blood flow falls to less than 25 mL/100 g/min. At this point, neurons can no longer maintain aerobic respiration. The mitochondria must then switch to anaerobic respiration, which generates large amounts of lactic acid, causing a change in the pH level. This switch to the less efficient anaerobic respiration also renders the neuron inca-pable of producing sufficient quantities of adenosine triphosphate (ATP) to fuel the depolarization processes. Thus, the membrane pumps that maintain electrolyte balances begin to fail and the cells cease to function.
Early in the cascade, an area of low cerebral blood flow, re-ferred to as the penumbra region, exists around the area of in-farction. The penumbra region is ischemic brain tissue that can be salvaged with timely intervention. The ischemic cascade threatens cells in the penumbra because membrane depolariza-tion of the cell wall leads to an increase in intracellular calcium and the release of glutamate (Hock, 1999). The penumbra area can be revitalized by administration of tissue plasminogen acti-vator (t-PA), and the influx of calcium can be limited with the use of calcium channel blockers. The influx of calcium and the re-lease of glutamate, if continued, activate a number of damaging pathways that result in the destruction of the cell membrane, the release of more calcium and glutamate, vasoconstriction, and the generation of free radicals. These processes enlarge the area of in-farction into the penumbra, extending the stroke.
Each step in the ischemic cascade represents an opportunity for intervention to limit the extent of secondary brain damage caused by a stroke. Medications that protect the brain from sec-ondary injury are called neuroprotectants (Reed, 2000). A num-ber of clinical trials are focusing on calcium channel antagonists that block the calcium influx, glutamate antagonists, antioxidants, and other neuroprotectant strategies that will help prevent sec-ondary complications (NINDS, 1999; Reed, 2000).
An ischemic stroke can cause a wide variety of neurologic deficits, depending on the location of the lesion (which vessels are ob-structed), the size of the area of inadequate perfusion, and the amount of collateral (secondary or accessory) blood flow. The pa-tient may present with any of the following signs or symptoms:
· Numbness or weakness of the face, arm, or leg, especially on one side of the body
· Confusion or change in mental status
· Trouble speaking or understanding speech
· Visual disturbances
· Difficulty walking, dizziness, or loss of balance or coordi-nation
· Sudden severe headache
Motor, sensory, cranial nerve, cognitive, and other functions may be disrupted. Table 62-2 reviews the neurologic deficits fre-quently seen in patients with strokes. Table 62-3 compares the symptoms seen in right hemispheric stroke with those seen in left hemispheric stroke. Patients exhibit deficits in specific locations as well as different behavior.
A stroke is a lesion of the upper motor neurons and results in loss of voluntary control over motor movements. Because the upper motor neurons decussate (cross), a disturbance of voluntary motor control on one side of the body may reflect damage to the upper motor neurons on the opposite side of the brain. The most com-mon motor dysfunction is hemiplegia (paralysis of one side of the body) due to a lesion of the opposite side of the brain. Hemi-paresis, or weakness of one side of the body, is another sign.
In the early stage of stroke, the initial clinical features may be flaccid paralysis and loss of or decrease in the deep tendon re-flexes. When these deep reflexes reappear (usually by 48 hours), increased tone is observed along with spasticity (abnormal in-crease in muscle tone) of the extremities on the affected side.
Other brain functions affected by stroke are language and com-munication. In fact, stroke is the most common cause of aphasia. The following are dysfunctions of language and communication:
· Dysarthria (difficulty in speaking), caused by paralysis ofthe muscles responsible for producing speech
· Dysphasia or aphasia (defective speech or loss of speech), which can be expressive aphasia, receptive aphasia, or global (mixed) aphasia
· Apraxia (inability to perform a previously learned action),as may be seen when a patient picks up a fork and attempts to comb his hair with it
Perception is the ability to interpret sensation. Stroke can result in visual-perceptual dysfunctions, disturbances in visual-spatial relations, and sensory loss.
Visual-perceptual dysfunctions are due to disturbances of the primary sensory pathways between the eye and visual cortex. Homonymous hemianopsia (loss of half of the visual field) may occur from stroke and may be temporary or permanent. The af-fected side of vision corresponds to the paralyzed side of the body.
Disturbances in visual-spatial relations (perceiving the relation of two or more objects in spatial areas) are frequently seen in pa-tients with right hemispheric damage.
The sensory losses from stroke may take the form of slight im-pairment of touch or may be more severe, with loss of proprio-ception (ability to perceive the position and motion of body parts) as well as difficulty in interpreting visual, tactile, and audi-tory stimuli.
If damage has occurred to the frontal lobe, learning capacity, memory, or other higher cortical intellectual functions may be impaired. Such dysfunction may be reflected in a limited atten-tion span, difficulties in comprehension, forgetfulness, and a lack of motivation, which cause these patients to become frustrated in their rehabilitation program. Depression is common and may be exaggerated by the patient’s natural response to this catastrophic event. Other psychological problems are common and are man-ifested by emotional lability, hostility, frustration, resentment, and lack of cooperation.
Any patient with neurologic deficits needs a careful history and a complete physical and neurologic examination. Initial assessment will focus on airway patency, which may be compromised by loss of gag or cough reflexes and altered respiratory pattern; cardio-vascular status (including blood pressure, cardiac rhythm and rate, carotid bruit), and gross neurologic losses.
Stroke patients may present to the acute care facility at any point along a continuum of neurologic involvement. A system that uses the time course to classify patients along this continuum may be used to guide treatment. Strokes using the time course are com-monly classified in the following manner: (1) transient ischemic attack (TIA); (2) reversible ischemic neurologic deficit; (3) stroke in evolution; and (4) completed stroke (Hock, 1999) (Chart 62-1).
The initial diagnostic test for a stroke is a noncontrast com-puted tomography (CT) scan performed emergently to deter-mine if the event is ischemic or hemorrhagic (which determines treatment). Further diagnostic workup for ischemic stroke in-volves attempting to identify the source of the thrombi or emboli. A 12-lead electrocardiogram and a carotid ultrasound are stan-dard tests. Other studies may include cerebral angiography, trans-cranial Doppler flow studies, transthoracic or transesophageal echocardiography, magnetic resonance imaging of the brain and/or neck, xenon CT, and single photon emission CT (Bonnono et al., 2000; Petty et al., 2000).
In a patient with a TIA, a bruit (abnormal sound heard on aus-cultation resulting from interference with normal blood flow) may be heard over the carotid artery. There are diminished or absent carotid pulsations in the neck.
Diagnostic tests for TIA may include carotid phonoangiography; this involves auscultation, di-rect visualization, and photographic recording of carotid bruits. Oculoplethysmography measures the pulsation of blood flow through the ophthalmic artery. Carotid angiography allows visu-alization of intracranial and cervical vessels. Digital subtraction angiography is used to define carotid artery obstruction and pro-vides information on patterns of cerebral blood flow.
Primary prevention of ischemic stroke is the best approach. Stroke risk screenings are an ideal opportunity to lower stroke risk by identifying high-risk individuals or groups and educating the pa-tients and the community about recognition and prevention of stroke (Lindsey, 2000; Manzella & Galante, 2000).
Advanced age, gender, and race are well-known non-modifiable risk factors for stroke (American Heart Association, 2000). Specifically, high-risk groups include people over the age of 55, because the incidence of stroke more than doubles in each suc-cessive decade, and men, who have a higher rate of stroke than women (due to the higher prevalence of women in the elderly population, however, the absolute numbers of men and women with stroke are similar). Another high-risk group is African Amer-icans: the incidence of first stroke in African Americans is almost twice that in Caucasians. African Americans also suffer more extensive physical impairments and are twice as likely to die from stroke than Caucasians. Hispanic, Native American Indian, Alaska native, and Asian/Pacific Islander ethnic groups also have a higher relative risk of stroke compared to Caucasians.
Modifiable risk factors for ischemic stroke include hyperten-sion, cardiovascular disease, high cholesterol, obesity, smoking, and diabetes (Chart 62-2). For people at high risk, interventions that alter modifiable factors, such as treating hypertension and hyperglycemia and stopping smoking, will reduce stroke risk. Many health promotion efforts involve encouraging a healthy lifestyle, including eating a low-fat, low-cholesterol diet and in-creasing exercise. Recent evidence suggests that eating fish two or more times per week reduces the risk of thrombotic stroke for women (Iso et al., 2001).
Several methods of preventing recurrent stroke have been identified for patients with TIAs or mild ischemic stroke. Patients with moderate to severe carotid stenosis are treated with carotid endarterectomy (Wolf et al., 1999). In patients with atrial fibril-lation, which increases the risk of emboli, administration of war-farin (Coumadin), an anticoagulant that inhibits clot formation, may prevent both thrombotic and embolic strokes.
Patients who have experienced a TIA or mild stroke from atrial fibrillation or from suspected embolic or thrombotic causes are candidates for nonsurgical medical management. Those with atrial fibrillation are treated with dose-adjusted warfarin sodium (Coumadin) unless contraindicated. The INR target is 2.5. When warfarin is contraindicated, aspirin is used in doses be-tween 50 and 325 mg/d (Wolf et al., 1999).
Platelet-inhibiting medications (aspirin, dipyridamole [Per-santine], clopidogrel [Plavix], and ticlopidine [Ticlid]) decrease the incidence of cerebral infarction in patients who have experi-enced TIAs from suspected embolic or thrombotic causes. Cur-rently the most cost-effective antiplatelet regimen is aspirin 50 mg/d and dipyridamole 400 mg/d (Sarasin et al., 2000).
Thrombolytic agents are used to treat ischemic stroke by dis-solving the blood clot that is blocking blood flow to the brain. Recombinant t-PA is a genetically engineered form of t-PA, a thrombolytic substance made naturally by the body. It works by binding to fibrin and converting plasminogen to plasmin, which stimulates fibrinolysis of the atherosclerotic lesion. Rapid diag-nosis of stroke and initiation of thrombolytic therapy (within 3 hours) in patients with ischemic stroke leads to a decrease in the size of the stroke and an overall improvement in functional out-come after 3 months (NINDS t-PA Stroke Study Group, 1995). To realize the full potential of thrombolytic therapy, community education directed at recognizing the symptoms of stroke and obtaining appropriate emergency care is necessary to ensure rapid transport to a hospital and initiation of therapy within the 3-hour time frame (Manzella & Galante, 2000). Delays make the patient ineligible for thrombolytic therapy because revascularization of necrotic tissue (which develops after 3 hours) increases the risk for cerebral edema and hemorrhage.
After being notified by emergencymedical service personnel, the emergency department calls the appropriate staff (neurologist, neuroradiologist, radiology de-partment, nursing staff, and electrocardiogram technician) and informs them of the patient’s imminent arrival at the hospital. Many institutions have brain attack teams that respond rapidly, ensuring that treatment occurs within the allotted time frame (Alberts et al., 2000; Bonnono et al., 2000).
Initial management requires the definitive diagnosis of an is-chemic stroke by CT scanning and determination of whether the patient meets all the criteria for t-PA therapy (Chart 62-3). Some of the contraindications for thrombolytic therapy include symp-tom onset greater than 3 hours prior to admission, a patient who is anticoagulated, a patient who has had a recent myocardial in-farction, or a patient who has had any type of intracranial pathol-ogy (eg, stroke, head injury, trauma). Once it is determined that the patient is a candidate for t-PA therapy, no anticoagulants are to be administered in the next 24 hours.
Before receiving t-PA, the patient should be assessed using the National Institutes of Health Stroke Scale (NIHSS), which con-tains 42 items evaluating neurologic deficits and is useful in dif-ferentiating between ischemic strokes and TIAs (Table 62-4). A patient with an NIHSS score of greater than 22 is not eligible to receive t-PA.
The patient is weighed to deter-mine the dose of t-PA. The minimum dose is 0.9 mg/kg; the maximum dose is 90 mg. The loading dose is 10% of the calcu-lated dose and is administered over 1 minute. The remaining dose is administered over 1 hour via an infusion pump. After the in-fusion is completed, the line is flushed with 20 mL of normal saline solution to ensure that all the medication is administered.
The patient is admitted to the intensive care unit, where con-tinuous cardiac monitoring is implemented. Vital signs are ob-tained every 15 minutes for the first 2 hours, every 30 minutes for the next 6 hours, then every hour for 16 hours. Blood pressure should be maintained with the systolic pressure less than 180 mm Hg and the diastolic pressure less than 100 mm Hg. Airway man-agement is instituted based on the patient’s clinical condition and arterial blood gas values.
Bleeding is the most common side effect of t-PA ad-ministration, and the patient should be closely monitored for any bleeding (intracranial, intravenous [IV] insertion sites, urinary catheter site, endotracheal tube, nasogastric tube, urine, stool, emesis, other secretions) (Scroggins, 2000). Intracranial bleeding is a major complication that occurs in approximately 6.5% of pa-tients (NINDS t-PA Stroke Study Group, 1995).
Not all patients are candidates for t-PA therapy. Other treatments include anticoagulant administration (IV heparin or low-molecular-weight heparin) for ischemic strokes and careful maintenance of cerebral hemodynamics to maintain cerebral perfusion. Increased intracranial pressure (ICP) and its associated complications may occur following a large ischemic stroke. Interventions during this period include methods to reduce ICP, such as administer-ing an osmotic diuretic (eg, mannitol), maintaining PaCO2 within the range of 30 to 35 mm Hg, and positioning to avoid hy-poxia. Other treatment measures include the following:
· Elevation of the head of the bed to promote venous drainage and to lower increased ICP
· Intubation with an endotracheal tube to establish a patent airway, if necessary
· Continuous hemodynamic monitoring. Systolic pressure should be maintained at less than 180 mm Hg, diastolic pressure at less than 100 mm Hg. Maintaining the blood pressure within this range reduces the potential for addi-tional bleeding or further ischemic damage.Neurologic assessment to determine whether the stroke is evolving or whether other acute complications are develop-ing, such as bleeding from anticoagulation or medication-induced bradycardia, which can result in hypotension and subsequent decreases in cardiac output and cerebral perfu-sion pressure.
See the acute ischemic stroke clinical guidelines in Appendix A.
Adequate cerebral blood flow is essential for cerebral oxygenation. If cerebral blood flow is inadequate, the amount of oxygen sup-plied to the brain will decrease and tissue ischemia will result. Therefore, maintaining cardiac output within the normal range of 4 to 8 L/min, or sometimes greater, can improve the cerebral blood flow and oxygen delivery. Adequate oxygenation begins with pulmonary care, maintenance of a patent airway, and ad-ministration of supplemental oxygen as needed. The importance of adequate gas exchange cannot be overemphasized in these pa-tients, many of whom are elderly and more prone to developing pneumonia, which can interfere with gas exchange.
The main surgical procedure for managing TIAs and small stroke is carotid endarterectomy, currently the most frequently per-formed peripheral vascular procedure in the United States (Krenzer, 1999). A carotid endarterectomy is the removal of an atherosclerotic plaque or thrombus from the carotid artery to pre-vent stroke in patients with occlusive disease of the extracranial cerebral arteries (Fig. 62-2). This surgery is indicated for patients with symptoms of TIA or mild stroke found to be due to severe (70% to 99%) carotid artery stenosis or moderate (50% to 69%) stenosis with other significant risk factors (Wolf et al., 1999).
The primary complications of carotid en-darterectomy are stroke, cranial nerve injuries, infection or hematoma at the incision, and carotid artery disruption. It is im-portant to maintain adequate blood pressure levels in the imme-diate postoperative period. Hypotension is avoided to prevent cerebral ischemia and thrombosis. Uncontrolled hypertension may precipitate cerebral hemorrhage, edema, hemorrhage at the surgical incision, or disruption of the arterial reconstruction. Sodium nitroprusside is commonly used to reduce the blood pres-sure to previous levels. Close cardiac monitoring is necessary be-cause these patients have a high incidence of coronary artery disease.
A neurologic flow sheet is used to monitor and document all body systems, with particular attention to neurologic status, fol-lowing carotid endarterectomy. The neurosurgeon is notified immediately if a neurologic deficit develops. Formation of a thrombus at the site of the endarterectomy is suspected if there is a sudden increase in neurologic deficits, such as weakness on one side of the body. The patient should be prepared for repeat endarterectomy.
Difficulty in swallowing, hoarseness, or other signs of cranial nerve dysfunction must be assessed. The nurse should focus on assessment of cranial nerves VI, X, XI, and XII (Krenzer, 1999). Some swelling in the neck after surgery is expected; if large enough, however, swelling and hematoma formation can obstruct the airway. Emergency airway supplies, including those needed for a tracheostomy, must be available. Table 62-5 provides more information about potential complications of carotid surgery.
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