Mortality & Morbidity Statistics
Types of Stroke
Initial Patient Management
Treatment Options
References
Glossary
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Medical Imaging of Cerebrovascular Disease by Ken McCormick, M.Ed., R.T.(R)(CV) |
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Mortality & Morbidity Statistics
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Cerebrovascular disease may be defined as "any process that is caused by an abnormality of the blood vessels or blood supply to the brain."1 Cerebrovascular disease, most commonly known as stroke, is the third leading cause of death in the U.S.2, and is the second leading cause of neurologic disability, after Alzheimer's disease.8 In 1996 there were 160,431 fatalities from cerebrovascular disease4 (Appendix A). Each year approximately 600,000 people suffer from stroke. While about 100,000 of these are recurrent or subsequent strokes, around 500,000 are new. There are about 4,400,000 stroke survivors alive today.2 Factors that indicate overall risk for stroke include advancing age (the risk doubles for each decade after age 55), male sex (a 19% greater risk than females for all types of stroke), family history, previous stroke or TIA, cigarette smoking (risk also greatly increases if smoking is combined with oral contraceptives), hypertension, diabetes mellitus, heart disease, and high red blood cell count (hypercoagulation).5 Geographically, death rates from stroke are much higher in the southeastern states, the so-called "stroke belt" states, for reasons that yet unclear.5,6 |
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There are two basic mechanisms of cerebrovascular disease, which are ischemic disease and hemorrhagic disease. There are two components of ischemic disease. These are cerebral thrombosis (clot formation within an intracerebral artery) and cerebral embolus (clot or other embolic material originating from outside the cerebrovascular system). Ischemic stroke accounts for 70-80% of all strokes, with cerebral thrombosis the most common type.7 However, cerebrovascular disease resulting from infection, trauma, neoplasm, or other condition that produces similar cerebrovascular effects will not be considered in the discussion of stroke.3 Cerebral Thrombosis With advancing age, vessels in the brain can become arteriosclerotic. This condition, long referred to as "hardening of the arteries", is characterized by the thickening and loss of elasticity of the arteral walls. This provides a favorable environment for the development of thrombus on the inner walls of the arteries. When blood flow slows down inside an artery with an existing accumulation of thrombus, occlusion can occur. Hence, strokes of this type usually occur during sleep or upon rising. The onset of symptoms is relatively gradual, with neurological deficits such as hemiplegia, aphasia, or paresthesia increasing in severity over a few hours or days. Cerebral thrombosis may be preceded by one or more transient ischemic attacks (TIA's)7, and is more likely in the hypercoagulable patient. A transient ischemic attack, or TIA, is a temporary onset of stroke-like symptoms, a sort of "mini-stroke", and is a warning of impending major stroke. Most TIA's are caused by small emboli from ulcerated atherosclerotic plaques, usually in the carotid or vertebral arteries, or from clots in the heart. Symptoms rarely last longer than 1 to 2 hours before resolving, but are identical to symptoms of a full stroke, only transient. TIA's may occur several times a day, or a few times over years.8 Cerebral Embolus 5 to 14% of all strokes result from cerebral embolus.7 Recent cardiac surgery, valve replacement, left atrial fibrillation and infective endocarditis are heart conditions that can allow the build up of thrombus on the walls of the cardiac chambers. Particles of these thrombi can dislodge, becoming thromboemboli, and travel into the cerebral circulation. Atherosclerotic disease of the common carotid artery bifurcation is also a major contributor to cerebral embolus. The stenotic lesion can produce emboli in the form of small fragments of plaque that may break loose in circulation or blood clots that are likely to form on or near the lesion. The carotid bifurcation is the most common site of plaque formation.8 Large lesions may produce flow disturbances audible to auscultation, called a bruit or thrill. Carotid artery disease (CAD) is often discovered in this way. Cerebral emboli can lodge anywhere in the cerebral circulation, but the most common site of occlusion is the middle cerebral artery or one of its branches. This vessel supplies extensive portions of the frontal, parietal, and temporal lobes, and occlusion here causes hemiplegia, hemianesthesia, hemianopia of the opposite side of the body, and possible aphasia or apraxia.8 TIA's are also common precursers to embolic stroke. There are also two components of hemorrhagic disease, which are intracerebral hemorrhage, accounting for about 10% of all strokes, and subarachnoid hemorrhage (SAH), accounting for about 7%. Intracerebral hemorrhage is most often caused by the rupture of a degenerative arteriosclerotic vessel due to chronic hypertension, but may also be the result of a ruptured aneurysm. SAH is most commonly associated with a ruptured intracranial aneurysm. These are the most lethal types of stroke, with an initial mortality rate of over 50%7. Either type of hemorrhage may also be caused by arteriovenous malformation.1 Intracerebral Hemorrhage This type of stroke occurs due to the effect of chronic hypertension on degenerative atreriosclerotic vessels, resulting in rupture of the vessel and subsequent hemorrhage into the brain parenchyma. Although more than 50% of patients suffering from large intracerebral hemorrhage die within the first few days, those who survive have a good chance of reasonable functional recovery.8 In many patients, as the hematoma is resorbed, a surprising amount of lost function gradually returns, although some deficit usually remains.8 Subarachnoid Hemorrhage Subarachnoid hemorrhage is most commonly the result of the rupture of a congenital "berry" aneurysm. This type of aneurysm is a sac-like dilatation of a portion of an artery due to a congenital weakness in the vessel wall. The origin of the aneurysm sac is a relatively narrow "neck" through which blood enters from the normal vessel. If the sac is larger than 25 mm in diameter it is classified as a "giant" aneurysm12. There are approximately 28,000 cases of ruptured cerebral aneurysm each year in the U.S and Canada, with a greater than 50% rate of morbidity and mortality.12* They occur most often in patients from 50-60 years of age, and are 1.5 to 3 times more likely in females than males.12 A history that indicates hemorrhagic aneurysmal disease includes hypertension, arteriosclerosis, possibly a series of previous minor headaches (warning leaks), and onset of symptoms during exertion. Signs usually include severe headache, often followed by loss of consciousness, coma or stupor, nausea, vomiting and delirium, or seizures. CSF will be bloody and under increased pressure, although lumbar puncture should be considered carefully, as there is a risk of brain stem herniation with increased intracranial pressure due to the hemorrhage. Symptoms may arise from a number of mechanisms. Bleeding into the subarachnoid space can cause severe headache due to the increase in intracranial pressure. Headache can also result from the pressure of an expanding aneurysm encroaching on adjacent structures (mass effect). This may also cause other neurological signs according to the location of the aneurysm. Vasospasm is a serious side effect which may occur in neighboring vessels resulting in ischemia or even occlusion. Vasospasm may be treated with nimodipine, a calcium channel blocker. Bleeding into the subarachnoid space can also result in communicating hydrocephalus, which may require the surgical placement of a ventricular shunt.8 Arteriovenous Malformation An additional mechanism of cerebrovascular disease which has a different etiology from the other types of stroke, but produces similar neurological effects, is the arteriovenous malformation. An arteriovenous malformation (AVM) is a tortuously dilated collection of abnormal vessels characterized by multiple enlarged feeder arteries and dilated venous outflow resulting in rapid flow through the vessels. This accelerated blood flow causes shunting of blood away from normal brain tissue, increases the risk of hemorrhage, and may cause neurological deficits from the mass effect of the growing lesion. Symptoms and signs of AVM's include all those associated with stroke, but are more likely to cause seizures. AVM's will be discussed in further detail in Unit 3. |
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Depending on the specific type, signs and symptoms of stroke can include sudden onset of one or more the following: hemiparesis, aphasia, visual disturbances or blindness, dizziness or loss of balance or coordination, or severe headache with no known cause.9 Initial management of stroke patients depends on the severity of their condition. A patient may be stable, presenting with only a severe headache, or presenting with varying degrees of neurological deficit.8 The National Institute of Health Stroke Scale (Appendix B) is a tool used to help assess the patient's condition and prognosis. The scale consists of 11 items that test a patient's ability to perform a series of simple physical maneuvers and cognitive tasks. The patient is given a score according to each response. A score of 0-4 indicates a minor stroke. A score of 5-22 indicates that improvement is possible without thrombolytic therapy, while a score of 23 or above indicates a profound stroke. The acute phase of stroke is from 48-72 hours after onset10. Primary goals for the seriously ill, unconscious or comatose patient during this period include maintaining the patient's airway and ventilation, including oxygen support, to prevent cerebral hypoxia or respiratory arrest. Portable chest radiographs are periodically ordered to help in evaluating potential pulmonary complications (such as atelectasis or pneumonia) or cardiac complications (such as cardiomegaly, arrhythmias, or congestive heart failure [CHF]). Mechanical ventilation is often necessary for this patient. The patient's head is usually elevated slightly to lower cerebral venous pressure. Diuretics may be prescribed to help reduce cerebral edema, which peaks from 3 to 5 days after onset.10 |
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The first step in treating the acute stroke patient is to correctly identify the type of stroke as either ischemic or hemorrhagic. Anticoagulants, such as heparin, or antiplatelet medications, such as aspririn, may be ordered in cases of ischemic stroke, but would be contraindicated in patients with hemorrhagic stroke. Heparin can help to protect the patient from further embolism or thrombosis, especially in patients with cardiac blood clots associated with atrial fibrillation. However, heparin carries the risk of hemorrhage. Advanced treatment options that will be further discussed are surgical carotid endarterectomy, and thrombolytic therapy with recombinant tissue plasminogen activator (rt-PA). Patients suffering from acute cerebral thrombosis are usually not candidates for surgery. These patients are generally treated with anticoagulant, antiplatelet, and diuretic drugs, and other supportive measures. However, in 1996, the FDA approved recombinant tissue plasminogen activator (rt-PA) for use in certain cases of non-hemorrhagic stroke.8 (See Appendix C for exclusion criteria for use of rt-PA in stroke.) t-PA was first described in 1947 as a naturally occuring enzyme in human tissues that acts to activate the conversion of plasminogen, a normal component of plasma, into plasmin, a potent proteolytic (protein destroying) enzyme. Plasminogen has a strong tendency to bind with fibrin, a protein that is the basic component of blood clots. Thus, in the presence of t-PA, the plasminogen that is bound to the fibrin in a thrombus converts to plasmin which lyses the fibrin, thereby dissolving the clot.12,14 Treatment with rt-PA must begin within 3 hours of the onset of symptoms. The most dangerous potential complication from the use of rt-PA, as with any thrombolytic agent, is hemorrhage. rt-PA is therefore contraindicated if there is any hemorrhagic component of the stroke. From the results of numerous comparative studies in which half the patients were given rt-PA and the other half placebo, it is largely accepted that patients receiving rt-PA within 3 hours of onset have more favorable recovery, although they also have a higher incidence of cerebral hemorrhage. Mortality rates are not significantly different for the two groups. Carotid endarterectomy is a procedure in which atherosclerotic plaque at the common carotid artery bifurcation (a primary source of cerebral thromboembolus) is surgically removed from within the vessel lumen, as this area is easily accessible to the surgeon. (CEA) is firmly established as beneficial for patients with significant carotid stenosis. The North American Symptomatic Carotid Endarterectomy Trial (NASCET) studied patients with 70-99% stenosis of one vessel by dividing them into two groups, those who underwent the surgery and those who were treated medically. The surgical group exhibited a 9% rate of stroke within two years, compared to a 26% rate in the medical group. A similar study, the Asymptomatic Carotid Atherosclerosis Study (ACAS) demonstrated a 55% reduction in stroke rates over 5 years in patient with carotid stenosis of 60% or greater.11 CEA is usually limited to use as a preventative measure, before the stroke has occurred. If embolism or infarction has taken place, surgery is indicated only if there is risk of loss of healthy brain tissue from further emboli.8 Surgery is rarely indicated for patients suffering from intracerebral hemorrhage, due to high surgical mortality or profound disability. A better prognosis is achieved if the patient is allowed to recover without the trauma of brain surgery, since hemorrhage is less destructive to brain tissue that infarction.8 Only in cases where large hemorrhages are immediately life threatening may surgical evacuation of the hematoma be justified.8 Surgery is effective, however, in preventing the often fatal subsequent hemorrhage of ruptured intracranial aneurysms. Left untreated, the rate of rebleeding in the first six months may reach 50%, with the greatest risk of rebleeding within the first 24 hours.13 The main focus in preventing rebleeding is to isolate the lumen of the aneurysmal sac from the normal vessel, thereby reducing the blood pressure within the aneurysm, and creating thrombosis which will fill the sac with blood clot, permanently removing it from the circulation. This is most commonly accomplished by surgically placing a stainless steel clip at the neck of the aneurysm. Although the rate of rebleeding after surgical clipping is extremely low, the procedure itself carries a 7% rate of major stroke or other complication leading to death.13 Other techniques include proximal vessel ligation and wrapping the aneurysm with plastic, gauze, or muscle. Surgery may also be required to place a ventricular shunt if hydrocephalus has occurred secondary to subarachnoid hemorrhage.8 |
References
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1. Eisenberg, R., and Dennis, C., Comprehensive Radiographic Pathology, C.V. Mosby, 1990 |
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Images and text copyright Ken McCormick, April 1999. All rights reserved.