Stroke: Comprehensive Acute Stroke Care

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1 COPYRIGHT 2013, WILD IRIS MEDICAL EDUCATION, INC. ALL RIGHTS RESERVED. Contact Hours: 10 INSTRUCTIONS This is a complimentary PDF copy of a healthcare continuing education (CE) course from Wild Iris Medical Education, Inc. To receive a certificate of completion, read and study the course at your convenience, then go to WildIrisMedicalEducation.com to take the test. After passing the test, you will complete a course evaluation and register your course completion in order to receive your certificate. ACCREDITATION (See last page) Wild Iris Medical Education, Inc. is an accredited/approved provider of continuing education for nurses, OTs, PTs, EMTs/paramedics, and other healthcare professionals. See the last page of this document, and our website, WildIrisMedicalEducation.com, for more information. DISCLOSURE Wild Iris Medical Education, Inc. provides educational activities that are free from bias. The information provided in this course is to be used for educational purposes only. It is not intended as a substitute for professional health care. Neither the planners of this course nor the author have conflicts of interest to disclose. (A conflict of interest exists when the planners and/or authors have financial relationship with providers of goods or services which could influence their objectivity in presenting educational content.) This course is not co-provided. Wild Iris Medical Education, Inc. has not received commercial support for this course. There is no off-label use of medications in this course. All doses and dose ranges are for adults, unless otherwise indicated. Trade names, when used, are intended as an example of a class of medication, not an endorsement of a specific medication or manufacturer by Wild Iris Medical Education, Inc. or ANCC. Product trade names or images, when used, are intended as an example of a class of product, not an endorsement of a specific product or manufacturer by Wild Iris Medical Education, Inc. or ANCC. accreditation does not imply endorsement by Wild Iris Medical Education, Inc. or ANCC of any commercial products or services mentioned in conjunction with this activity. ABOUT THIS COURSE This course will expire or be updated on or before August 1, You must score 70% or better on the test and complete the course evaluation to earn a certificate of completion for this CE activity.

2 2 BY Jassin M. Jouria, Jr., MD; Michael Jay Katz, MD, PhD COURSE OBJECTIVE: The purpose of this course is to present a current and evidence-based discussion of the anatomy, pathophysiology, diagnosis, evaluation, and treatment options for acute stroke, emphasizing immediate care and initial rehabilitation. LEARNING OBJECTIVES Upon completion of this course, you will be able to: Describe the anatomy of the brain and its vasculature. Identify the anatomical and physiological alterations associated with acute stroke. Discuss risk factors for acute stroke. Recognize the symptoms of the two types of acute stroke. Describe the neurological examination and imaging techniques used to locate and define the type of acute stroke. Discuss the guidelines for early treatment and management of patients with acute stroke. Describe the role of the acute care nursing staff both immediately post-stroke and during the initial post-stroke rehabilitation period. Identify the complications and associated interventions that may occur during the ICU care of acute stroke patients. Discuss the goals and methods of rehabilitation therapists who specialize in post-acute stroke rehabilitation. WHAT ARE STROKES AND HOW COMMON ARE THEY? Types of Stroke A stroke also called a cerebrovascular accident (CVA) or a brain attack is a reduction or an interruption of the flow of blood through an artery to one or more areas of the brain within the territory supplied by that artery. The end result is varying degrees of neurological and/or cognitive malfunction lasting longer than 24 hours. MAJOR STROKE CLASSIFICATIONS There are two major stroke classifications: Ischemic stroke, which may occur as a transient ischemic attack (TIA), occurs when a clot, either of local or distant origin, blocks a cerebral artery and causes oxygen deprivation with subsequent tissue damage. The term ischemic refers to an insufficient

3 3 blood supply. The most common extracranial source of emboli is the cervical bifurcation of the common carotid artery, while the most common sources of intracranial thrombi are the main trunk and branches of the middle cerebral artery. Hemorrhagic stroke occurs as a bleed within the brain, often causing tissue damage due to pressure-related changes. Most commonly, intracerebral hemorrhages are caused by rupture of vessels due to long-term atherosclerotic damage and arterial hypertension. Two types of stroke. (Source: CDC, 2010b.) In the United States, most strokes are ischemic and caused by the sudden blockage of a cerebral artery. Ischemic strokes may occur in two ways: Cerebral thromboses are due to clots that form in the cerebral arterial tree. This type of stroke may be called a thrombotic stroke. Cerebral emboli, causing embolic strokes, are due to clots that arise from outside the cerebral arterial tree and travel through the arterial system until they become lodged within smaller arteries. In contrast, hemorrhagic strokes occur from the rupture of cerebral blood vessels. Such ruptures may occur due to weakened vascular walls (aneurysms) or as a result of congenital arteriovenous malformations (AVMs), with subsequent bleeding into the brain or the subarachnoid space surrounding the brain. (AVMs are dilated, often tangled, blood vessels where the arterial blood flows directly into the venous system bypassing the usual capillary bed. Over time, local damage to the tissue occurs due to compression, insufficient blood flow, irritation, or microhemorrhages.)

4 4 Both types of vascular damage clots and ruptured vessels may also occur in the spinal cord. These occurrences are referred to as spinal cord strokes. The simple term stroke, however, generally refers to vascular damage to the brain. Ischemic strokes typically give rise to specific (focal) and often painless neurological symptoms. Onset is abrupt and may progressively evolve over hours. More commonly, however, the patient presents with an acute completed stroke, and the focus can quickly shift to care and rehabilitation (Langhorne et al., 2011). Stroke symptoms depend on the area affected. The middle cerebral artery or one of its deep branches is most often affected. Symptoms can include: Numbness or weakness on one side of the body (usually contralateral hemiplegia) or face (e.g., ptosis, or drooping eyelid) Confusion, difficulty speaking or writing (expressive aphasia), or difficulty understanding (receptive aphasia) Difficulty seeing and/or visual field defects (e.g., homonymous hemianopsia) Gait deviations Severe headache with no known cause (NINDS, 2010) TRANSIENT ISCHEMIC ATTACK (TIA) The current definition of transient ischemic attack (TIA) endorsed by the American Heart Association is a brief episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction (Siket & Edlow, 2013). TIA is sometimes referred to as a warning stroke or a mini-stroke that results in no lasting damage (CDC, 2010b). TIA has in the past been defined as an episode of focal neurological dysfunction with abrupt onset and rapid resolution lasting less than 24 hours that is due to altered circulation to a limited region of the brain. However, in recent years it has become clear that symptoms of TIA can resolve well before the 24-hour time frame and that waiting can delay treatments for stroke prevention. In 60% of cases, the symptoms associated with TIAs are resolved within 60 minutes. In 71% of cases, the symptoms resolve within 2 hours. Because advances in diagnostic imaging techniques allow the rapid diagnosis of TIAs and because TIAs have been associated with an increased risk of acute stroke, it is currently recommended that all patients showing symptoms of TIA be treated as stroke patients. It is estimated that 15% of all strokes are preceded by an episode of TIA. TIAs often present as amaurosis fugax, a transient loss of vision in one eye (Panagos, 2012). A TIA can present with one or more of these symptoms: Sudden weakness, numbness, or paralysis in the face, arm, or leg (most often, this occurs on one side of the body)

5 5 Confused, muttered, slurred, or garbled speech Difficulty in understanding when someone else is speaking Sudden blindness in one or both eyes or double vision Dizziness, loss of balance, or loss of coordination Statistics about Stroke in the United States Stroke is a serious health hazard. On the average, someone in the United States has a stroke every 40 seconds (Go et al., 2013). One person dies of a stroke every four minutes, and it is estimated that 1 of 19 people die of stroke (Roger et al., 2012; Sidney et al., 2013). A recent study of Americans found that 25% of people who had a stroke died within a year and 8% had another stroke within one year.... [Altogether,] 50% died or had another stroke or a heart attack within four years (Feng, 2010). Stroke is also an economic drain. The American Heart Association estimated stroke costs of $74 billion in 2010, including the cost of healthcare services, drugs, and lost productivity (Lloyd- Jones et al., 2010). The morbidity, mortality, and cost of strokes are not spread equally among the population. Those at higher risk include the elderly, African Americans, those of lower socioeconomic status, and residents of the southeastern United States. Presented below are some relevant data compiled by the National Center for Health Statistics (NCHS) for stroke in the United States. INCIDENCE Each year, almost 800,000 Americans suffer a stroke. For more than 600,000 Americans, this will be their first stroke, but almost 200,000 of the yearly strokes are recurrences (Sidney et al., 2013). PREVALENCE In the United States, almost 3% of adults have had a stroke. For example, in 2005, 3.9 million American women and 2.6 million American men were survivors of a stroke. It is estimated that approximately 17% of these survivors have residual difficulty performing the basic functional activities of their daily lives (CDC, 2010a). MORTALITY AND MORBIDITY There are about 140,000 stroke deaths each year, and stroke is listed as a contributing factor to an additional 100,000 deaths. Thus, stroke is the third leading cause of death in this country, after heart disease and cancer (CDC, 2010a, b). From 1999 to 2009, however, the overall rate of death from stroke declined by 36.9% (Murphy et al., 2013). The most common reason cited for this decrease is the presence of regional stroke centers.

6 6 Deaths from cardiovascular diseases, U.S., Stroke represents 16.4% of all cardiovascular deaths. (Source: NHLBI, 2013.) POPULATION DIFFERENCES Different sectors of the population have been shown to have differing levels of risk of having a stroke. Increased stroke risk has been found to be associated with the following factors: Age. Most people who have a stroke are older than 65 years of age. Additionally, the chance of dying from a stroke increases with the patient s age (NCHS, 2012). Gender. Stroke is most common in people older than age 75, and because women live longer than men, overall about 1.5 times more women than men die of stroke in the United States each year. However, men younger than 75 have a higher incidence of stroke than women of the same age (CDC, 2010a, b). Racial Demographics. African Americans and Hispanic Americans are at higher risk of death from strokes. Native Americans or Alaska Natives have an even higher risk of stroke (NCHS, 2012). Age-adjusted death rates for stroke by race/ethnicity and sex, U.S., (Source: NHLBI, 2013.)

7 7 Socioeconomic Status (SES). Low SES is associated with an increased risk of stroke. A lower level of educational achievement is also associated with an increased risk of stroke (CDC, 2012). Geographic Location. In the United States, living in the Southeast carries with it the highest risk for stroke compared to the rest of the nation s population. The heavy concentration of strokes in the southeast has given that region the nickname the stroke belt. (Source: CDC, 2010a.) ECONOMIC BURDEN Stroke is a significant burden on the healthcare system. In 2010, the annual direct medical cost of strokes was $28.3 billion. By the year 2030, the direct medical cost of strokes is projected to be $95.6 billion, representing a 238% increase from 2010 (Heidenreich et al., 2011).

8 8 INTRACRANIAL ANATOMY AND THE PHYSIOLOGY OF STROKE Before discussing the assessment, treatment, and care of acute strokes, it is important to review the anatomy and physiology underlying the disease. Structural Anatomy of the Major Cerebral Arteries The brain comprises 2% of the body s mass, but it receives 17% of the heart s output and consumes 20% of the body s oxygen supply. The brain receives its blood through four main arteries: Two large arteries, the right and left internal carotid arteries, ascend from the chest in the anterior portion of the neck. Two smaller arteries, the right and left vertebral arteries, ascend via the posterior portion of the neck. The carotid arteries supply blood to about 80% of the brain, including most of the frontal, parietal, and temporal hemispheres and the basal ganglia. The vertebral arteries supply blood to the remaining 20% of the brain, including the brainstem, cerebellum, and most of the posterior cerebral hemispheres. Inferior view of the brain s blood supply. (Source: Fotolia.com.)

9 9 The carotid arteries supply 80% of the brain s blood supply. The common carotid artery leaves the aorta on the left and the brachiocephalic artery on the right. It bifurcates into the internal and external carotid arteries about halfway up each side of the neck. The internal carotid artery continues upward, passes through the foramen magnum, and joins the arterial Circle of Willis. (Source: NIH, 2009, with added labels.) The anterior circulation of the brain is formed by those cerebral blood vessels that are branches of the internal carotid arteries, while the posterior circulation of the brain is formed by those cerebral blood vessels that are branches of the vertebral arteries. The anterior and posterior circulations connect through a circular anastomosis of arteries called the Circle of Willis. Functional Anatomy of the Major Cerebral Arteries One characteristic of the brain is that many of its functions are not spread diffusely; instead, specific neurological functions are dependent upon specialized brain regions. Each artery primarily supplies a particular brain region. It is often stated that strokes cause focal neurological deficits. Simply put, because most regions of the brain are associated with characteristic neurological functions, damage to cerebral arteries tends to lead to corresponding losses of neurological function. In a stroke patient, it is easier to assess the external neurological problems than it is to see the internal arterial damage. On the other hand, knowing the typical layout of the cerebral arteries (i.e., the map of the functional brain regions fed by each artery), one can use the observed deficits to infer which particular arteries have been damaged. The functional anatomy of the cerebral arteries begins with a basic distinction between internal carotid artery (anterior circulation) strokes and vertebral artery/basilar artery (posterior circulation) strokes. In general, middle cerebral artery and internal carotid artery strokes cause contralateral motor and eye dysfunction with speech and sensory deficits, while vertebral/basilar artery strokes cause balance, vertigo, and cranial nerve dysfunction. (Dysfunction is possible in the cerebellar functions, cranial nerve functions, and spinal sensory and motor functions.)

10 10 The Circle of Willis is frequently found to have aneurysms or congenital malformations. Symptoms of a ruptured aneurysm in the Circle of Willis are similar to other hemorrhagic stroke symptoms and can include a sudden headache, nausea, vomiting, neck pain, fainting, light sensitivity, or a loss of consciousness and seizures. A cerebral aneurysm. (Source: NIH, 2011a.) Another useful functional distinction arises from the fact that the first branch of the internal carotid artery is the ophthalmic artery to the retina. Therefore, a blockage of the internal carotid circulation on one side of the brain will often produce a characteristic sudden and painless blindness in the eye on the side of the blockage, which would be termed an ipsilateral blindness. Beyond the ophthalmic arteries, the internal carotid artery circulation supplies the inferior, lateral, and medial surfaces of the cerebral hemispheres. These regions include the primary motor and sensory cortices; therefore, a blockage of the internal carotid artery circulation often produces unilateral motor weakness or sensory loss. In contrast, the vertebral arteries supply the brainstem, cerebellum, occipital cortices, and thalamus. Blockages of the vertebral circulation can produce problems of vegetative functions, such as consciousness and respiration, and problems of balance, hearing, motor coordination, and visual perception (Judd et al., 2013). Injuries to branches of these major cerebral arteries also produce specific and characteristic stroke syndromes, and these syndromes help to infer which brain areas have been damaged in a specific patient s stroke. Following, in brief, are the major stroke syndromes of the anterior, middle, and posterior cerebral arteries and the vertebral and basilar arteries (Beal, 2010; Jones et al., 2010).

11 11 INTERNAL CAROTID ARTERY STROKES Anterior Cerebral Artery (ACA) Stroke Syndromes Cutting off the blood supply to the entire field of one ACA will affect frontal regions on the medial surface of one half of the brain, much of the corpus callosum, part of the internal capsule, and regions of the basal ganglia. The resulting symptoms can include: Loss of discriminatory sensation and weakness or paralysis of the contralateral foot and leg, perhaps with some deficits in the contralateral (opposite side) shoulder and arm Occasionally, deviation of the head and eyes toward the side of the affected cerebral artery Occasionally, central motor problems, ranging from expressive aphasia to abulia (slowness and reduced spontaneity) to dyskinesia In addition, unusual symptoms such as alien-hand syndrome and callosal disconnection syndromes can occur with ACA strokes (Bartolo, 2011). Middle Cerebral Artery (MCA) Stroke Syndromes Cutting off the blood supply to the entire field of one MCA will affect the primary sensory and motor cortices on the lateral surface of the cerebral hemisphere, sections of the internal capsule, and parts of the inferior parietal and lateral temporal lobes. The resulting symptoms can include: Full sensory loss and weakness or paralysis of the face, arm, and leg on the opposite side of the body Blindness in the opposite visual field (contralateral homonymous hemianopia) Deviation of the head and eyes toward the side of the affected MCA If the dominant (usually left) MCA has been occluded, global (i.e., both expressive and receptive) aphasia If the nondominant (usually right) MCA has been occluded, contralateral neglect (hemineglect) or the patient s unawareness or denial of their neurological deficits (anosognosia) Cutting off the blood supply to only the superior branches of the MCA will lead to a subset of these deficits. For example, there is often less effect on the contralateral leg and foot, and the communication difficulties are typically limited to expressive (Broca s) aphasias.

12 12 Cutting off the blood supply to only the inferior branches of the MCA will lead to a subset of deficits, with little sensory or motor loss on the contralateral body side but with a full or partial contralateral homonymous hemianopia. In this case, the patient s communication difficulties are typically limited to receptive (Wernicke s) aphasias. VERTEBRAL ARTERY/BASILAR ARTERY STROKES Vertebral Artery Stroke Syndromes Cutting off the blood supply to the entire field of one vertebral artery will affect the medulla of the brainstem. Vertebral artery strokes can produce a wide variety of symptoms, including vertigo, nystagmus, vomiting, ipsilateral (same-sided) ataxia, and hypoglossal nerve dysfunction. Basilar Artery Stroke Syndromes Cutting off the blood supply to the entire field of the basilar artery will affect the long ascending and descending motor and sensory tracts, the vestibular and cochlear nerves and nuclei, and the reticular activating system (Acke et al., 2011; Mattle et al., 2011). The resulting symptoms can include: Bilateral neurological problems, such as bilateral sensory and motor deficits Combined cerebellar and cranial nerve problems When the stroke affects the medulla oblongata, stupor, coma, or a quadriplegic, mute, but conscious condition ( locked-in syndrome) (Kwon & Jang, 2012; Schjolberg & Sunnerhagen, 2012) Hemiparesis with contralateral cranial nerve dysfunction or with ipsilateral ataxia Posterior Cerebral Artery (PCA) Stroke Syndromes Cutting off the blood supply to the entire field of one PCA will affect the thalamus, hippocampus, underside of the temporal lobe, medial surface of the occipital lobe, and motor areas of the midbrain (Searls et al., 2012). PCA strokes can produce a wide variety of symptoms, including: Sensory loss on the entire contralateral body (all the way to the midline); here, when sensation gradually returns, it is frequently accompanied by pain Facial (VII) cranial nerve palsy, which may also be associated with hemiparesis, hemiplegia, ataxia, or decreased levels of consciousness Movement disorders on one side of the body, such as hemiballismus, hemichoreoathetosis, or hemiataxia

13 13 Visual loss, specifically, homonymous hemianopia Dyslexia Cell and Tissue Injuries Caused by Strokes For decisions about acute treatment, the particular stroke syndrome is usually less important than the type of vascular injury that has occurred. As discussed above, the two main classes of stroke injuries are ischemic and hemorrhagic: Ischemic strokes result from injuries that reduce blood flow to a region of the brain without initially causing significant cerebral bleeding; usually, the vascular damage is a blockage in an artery. Hemorrhagic strokes result from injuries that cause bleeding into the brain or the cerebrospinal fluid (CSF) from the outset; usually, the vascular damage is a tear in an artery or the rupture of an aneurysm. The term ischemia indicates oxygen and nutrient deprivation due to an insufficient supply of blood. Ischemic stroke is the name used for nonbleeding strokes due to clots, but both ischemic and hemorrhagic strokes cause ischemic damage. Beyond ischemic damage, hemorrhagic strokes cause additional physical damage due to the pressure that builds from the excess blood that has been released into the brain or the CSF. This increase in intracranial pressure (ICP) presents additional problems for the hemorrhagic stroke patient, particularly in the acute phase and within the early recovery period. ISCHEMIC DAMAGE When cerebral blood flow is reduced, the affected regions of the brain begin to stop functioning, and the patient begins to lose the ability to perform the tasks that are localized in those regions. Both ischemic strokes and hemorrhagic strokes cause ischemic damage. Complete Ischemia If the blood supply to a brain region is cut off entirely, as occurs during cardiac arrest, cell damage is widespread and neurons begin to die quickly. The brain uses energy at a high rate, but it can only store a small back-up supply of energy. Complete ischemia immediately decreases the available oxygen and glucose in the affected region of the brain, and without continual nourishment, local neurons will run low on their internal back-up stores of adenosine triphosphate (ATP) within seconds. Once a neuron s ATP is depleted, its membranes depolarize and extracellular ions stream in; this swells the cell with an accompanying inrush of water. The depolarization also sets off the release of unusually large amounts of extracellular excitatory neurotransmitters. These events cause the influx of calcium ions, which set off an unregulated intracellular

14 14 cascade of calcium-triggered processes, including the activation of catabolic enzymes, such as proteases, phospholipases, and endonucleases. In a short time, the neuron selfdestructs and dies. The entire process is termed cortical spreading depression (Lauritzen et al., 2011; Sukhotinsky et al., 2010). Incomplete Ischemia Most strokes do not produce complete ischemia. Many ischemic strokes leave arteries only partially blocked. Even when an artery is entirely occluded, the cerebral circulation has some collateral coverage with overlap and interconnections, and some blood usually gets to the affected brain regions via other routes. The perfusion that remains will vary throughout the ischemic region. A common pattern is severely reduced perfusion in the core of an ischemic region, with gradually increasing perfusion toward the edges. Neurons become functionally silent when their arterial perfusion drops by a small amount. In a stroke, as soon as cerebral blood flow is reduced, electrical activity stops in the affected region of the brain and neurological deficits appear. For a time, the silent neurons remain alive, but they no longer have the energy to generate membrane potentials that are sufficient to respond to stimuli or to transmit signals. However, to remain alive, the silent neurons still need some arterial perfusion. If cerebral blood flow drops below approximately one third of normal in part of the affected region, the silent neurons begin to die (Lauritzen et al., 2011; Sukhotinsky et al., 2010). In most strokes, patients lose neurologic functions early, before all the neurons in the affected area are irreversibly damaged. Typically, strokes leave enough arterial perfusion that many neurons can maintain a low level of energy production sufficient to slow the onset of their deaths (Oechmichen & Meissner, 2006). In fact, treatment of hypertension in early stroke patients is somewhat controversial. Some studies have shown that delaying treatment with hypotensive agents may improve outcomes because the higher blood pressure maintains brain perfusion via collateral blood supply, and the artery often is incompletely blocked, thus allowing some blood flow (Dhillon, 2012; Shulkin et al., 2011). Strokes Leave an Early Therapeutic Window After an ischemic stroke, the amount of irreversible damage increases steadily as long as regions remain without sufficient blood supply. In those parts of the affected region that have no blood flow, neurons begin to die in less than 10 minutes. In those areas with <30% of the normal blood flow, neurons begin to die within an hour. In those areas with 30% 40% of the normal blood flow, some neurons begin to die within an hour, but others can be revived for many hours. Empirically, it has been found that collateral and residual blood flow can preserve neurons in the penumbral and border areas for as long as six hours after an ischemic

15 15 stroke. Within this six-hour window, certain treatments can reduce the amount of brain damage that is irreversible. One treatment the intravenous administration of the clot-dissolving (popularly known as clot-busting ) fibrinolytic drug rtpa has been confirmed to be clinically useful. The administration of rtpa has produced an eightfold improvement in the outcomes of ischemic strokes when the drug was given within the first three hours after symptoms appeared. The drug continues to be helpful for 4.5 hours and even up to 24 hours after the onset of an ischemic stroke, though shorter periods of delay have been linked to more favorable outcomes (Lahr et al., 2012; Yeo et al., 2013). MECHANICAL DAMAGE Hemorrhagic strokes release blood into the brain parenchyma or into the cerebrospinal fluid (CSF) and produce damage by three mechanisms: ischemia, physical destruction, and increased pressure. Intracranial bleeds produce ischemia by diverting blood from cerebral arteries. Ischemia is also produced when pressure from a hematoma or from brain edema constricts cerebral arteries. Likewise, bleeding into the CSF raises intracranial pressure, and this too will reduce cerebral blood flow. Besides ischemic damage, hemorrhagic strokes produce mechanical damage. The force of blood flowing extracellularly in the brain parenchyma pushes cells apart, dissects brain tissue, destroys connections, and injures brain cells. On a larger scale, the excess pressure can also be quite physically damaging. An expanding hematoma, in combination with cerebral edema, can push portions of the brain through intracranial narrow spaces, such as the dural openings or the foramen magnum. The result is brain herniation. Herniation can irreversibly damage brain regions, and when vegetative brain centers, such as the reticular activating system or the respiratory control nuclei, are compressed, the result can be coma or death. Moreover, the global compression caused by increased intracranial pressure (ICP) from a hemorrhagic stroke can cause the cardiovascular system to malfunction, and significant increases in ICP lead to reduced consciousness, global brain ischemia, and death (Arima et al., 2012; Grise & Adeoye, 2012; Merenda & DeGeorgia, 2010; Shah & Christensen, 2012). The Causes of Strokes Acute treatments attempt to reverse ischemia and to reduce local force and intracranial pressure. The long-term treatments for stroke focus on preventing recurrences and maximizing motor and functional capabilities. To plan long-term treatment, physicians must determine the location of the primary vascular injury and its underlying or predisposing causes.

16 16 CAUSES OF ISCHEMIC STROKES The reduction of the blood flow to a region of the brain leads to an ischemic stroke. Causes of such reductions include: Most commonly, an arterial blockage, initiated by local processes (thrombi) or as a result of clots from afar (emboli) Occasionally, a systemic cardiovascular problem, such as shock or cardiac arrest (atherosclerosis can also predispose to thrombi and/or emboli) Arterial Blockage Thrombi. Many ischemic strokes result from clots that form within the cerebral arteries. It is helpful to divide the conditions leading to such locally generated obstructions into large vessel pathologies and small vessel pathologies. Large vessel pathologies. Atherosclerosis is the most common cause of large vessel occlusive disease. Atherosclerotic thrombi are usually formed along plaque that has become ulcerated or disrupted, and such plaque disruptions tend to occur at places where the blood flow is turbulent (e.g., at arterial branch points). Atherosclerotic thrombi can enlarge in situ and reduce distal blood flow, or they can break off and occlude smaller arteries upstream. Besides atherosclerosis, other occlusive conditions of large cerebral vessels include vasoconstriction (as in migraine disease) and arterial dissections. Small vessel pathologies. Small vessel damage usually results from lipohyalinosis, which thickens the media in the walls of small arteries and eventually leads to small artery occlusions and stroke. Lipohyalinosis, which is produced by hypertension combined with atherosclerosis, is especially destructive to those branches of the middle cerebral, vertebral, basilar, and Circle of Willis arteries that come off at right angles to the parent artery and that dive into the brain parenchyma. Obstruction of these penetrating arteries produces small, deep, noncortical infarcts called lacunae, and the clinical results are called lacunar strokes (Go et al., 2013; NCHS, 2012). Emboli. Other ischemic strokes are caused by emboli (debris and clots that arise elsewhere and are subsequently swept into the cerebral circulation). Extracranial stroke emboli are formed by large vessel pathologies and by other conditions that foster the formation of blood clots that can crumble or be dislodged. One common source of stroke emboli is the left atrium of the heart, where thrombi can form during atrial fibrillation. Another source of stroke emboli is the carotid artery, from which atherosclerotic plaque and clots detach and are then carried deeper into the cerebral vasculature (CDC, 2012; Judd et al., 2013; NCHS, 2012).

17 17 Atrial fibrillation can lead to stasis of blood in the left atrium. The sluggish pools of blood tend to form clots, which can then be carried through the left ventricle, into the aorta, and then into the carotid arteries (Palka et al., 2010; Pezzotti & Freuler, 2012). (Source: NIH, 2011b.) When a stroke is embolic, acute stroke treatments only work on the immediate problem, rather than the cause. For long-term treatment, both the site of the extracranial arterial pathology and the source of the emboli must be discovered and treated if future strokes are to be prevented. Systemic Cardiovascular Problems Widespread cerebral hypoperfusion can produce global brain ischemia. The causes of cerebral hypoperfusion range from arrhythmias to cardiac arrest and from respiratory failure to bleeding or shock. The symptoms of a global reduction of blood flow to the brain are diffuse, bilateral, and nonfocal, and they include the signs of circulatory compromise pallor, sweating, tachycardia, and hypotension. There have also been reports of impaired executive function and migraines associated with hypoperfusion (Appelman et al., 2010; Hansen et al., 2011). Cryptogenic Strokes Cryptogenic strokes are ischemic strokes in which a comprehensive evaluation cannot define the cause. Most cryptogenic strokes produce symptoms similar to those of strokes known to be caused by emboli; nonetheless, the strokes are labeled cryptogenic if available tests cannot document the specific cause, though many cryptogenic strokes have

18 18 been associated with Patent Foramen Ovale (PFO) Syndrome (Freeman & Aguilar, 2011; Thaler & Kent, 2010; Thaler et al., 2013). Transient Ischemic Attacks (TIAs) The definition of a TIA is an episode of reversible neurologic deficit caused by temporary focal central nervous system hypoperfusion. Risks for TIAs include hypertension, atherosclerosis, heart disease, atrial fibrillation, type 2 diabetes, and polycythemia. Approximately one third of patients experiencing TIAs can progress to a full stroke (Béjot & Giroud, 2009; Siket & Edlow, 2013). CAUSES OF HEMORRHAGIC STROKES Hemorrhage strokes are caused by bleeds from ruptured aneurysms or torn arteries. When the injured arteries are inside the brain tissue, the strokes are called intracerebral hemorrhages. When the injured arteries are outside the brain (where they run in the subarachnoid space), the strokes are called subarachnoid hemorrhages. Intracranial bleeds and subsequent hemorrhagic strokes can be produced by trauma. However, spontaneous hemorrhagic strokes occur, too. Spontaneous hemorrhagic strokes typically happen in people with hypertension, and they can be precipitated by tumors, drugs (e.g., anticoagulants or cocaine), the weakening of preexisting aneurysms, or physical activity. Intracerebral Hemorrhage (ICH) ICH is usually caused by bleeding from smaller arteries or arterioles. The most common concomitant problems are hypertension, trauma, amyloid angiopathy, bleeding diatheses (including anticoagulant or thrombolytic drugs), cocaine or amphetamine use, and ruptured vascular malformations or aneurysms (Hays, 2011). CEREBRAL AMYLOID ANGIOPATHY In older people, one common cause of ICH is a metabolic dysfunction called cerebral amyloid angiopathy. In this disorder, beta-amyloid, a 42-amino-acid proteolytic product of amyloid precursor protein (APP), accumulates in the walls of small and medium-sized arteries, leading to a progressive weakening and erosion of the vascular wall. Beta-amyloid appears to be the same compound that accumulates in Alzheimer s disease, and 80% 90% of people with Alzheimer s disease also have cerebral amyloid angiopathy. Source: Menon, ICH, which accounts for approximately 20% of strokes worldwide, is most commonly found in the basal ganglia (specifically, the putamen) and the adjacent internal capsule. The other common sites are axonal tracts (central white matter) of the temporal, parietal, or frontal lobes; the thalamus; the cerebellar hemispheres; and the pons. The specific

19 19 location of ICH has genetic linkages with lobar ICH associated with APOE-epsilon2 or - epsilon4 genotype, while non-lobar ICH is associated with hypertension (Martini et al., 2012). Subarachnoid Hemorrhages (SAH) Many subarachnoid hemorrhages are due to trauma, but spontaneous ruptures of a cerebral aneurysm are also common. Most of these aneurysms are on or near the anterior portions of the Circle of Willis (Sunderrajan et al., 2013). The causes of aneurysm formation and rupture are still debated. Some relevant observations include: Two percent of the population have unruptured cerebral aneurysms >3 mm in diameter. Cerebral aneurysms develop gradually and most are not fully formed at birth. Rupture of a cerebral aneurysm is most often a condition of middle age, peaking in people aged years. Most ruptured cerebral aneurysms occur in people with normal blood pressure. The larger aneurysms are the ones most likely to rupture. The average cerebral aneurysm is 7.5 mm in diameter, but ruptured aneurysms tend to have been larger than 10 mm in diameter. The Basics of Stroke Prevention It has been estimated that 80% of all strokes can be prevented (NSA, 2009). The risk of having a stroke can be reduced in the same way that all cardiovascular disease risks can be reduced. The main controllable interventions are: Smoking cessation Treatment of: o Dyslipidemia o Hypertension o Diabetes o Abdominal obesity Improved nutrition, including a high-vegetable, low-fat/high-fiber diet Regular aerobic exercise In addition, daily aspirin is often recommended for adults who are at high risk for cardiovascular disease.

20 20 Any of these interventions is beneficial, but the more of these interventions and lifestyle adjustments that a person makes, the lower will be their risk for cardiovascular disease (Go et al., 2013; CDC, 2011; Sidney et al., 2013). MEDICAL EVALUATION OF A STROKE Strokes produce the sudden loss of neurocognitive function, including motor and sensory dysfunction. Many things can be done to reverse or to temper the effects of a stroke, but successful medical therapy depends on immediate medical attention. Therefore, patients having a stroke need to be taken immediately to an emergency department that has the personnel and equipment to provide comprehensive acute stroke treatment, preferably at a primary stroke center. (The Joint Commission is responsible for certifying primary stroke centers in the United States.) The Role of Patients and Bystanders RECOGNIZING A POTENTIAL STROKE Recognizing that a stroke may be taking place is the first step in caring for the patient, so public education and information is required in order to increase the recognition of potential strokes. Health professionals cannot assume that their patients know how to recognize potential strokes. Even people who have suffered one or more strokes need education: a survey by the American Heart Association (2010) found that only 55% of patients who had had a stroke could identify even one stroke warning sign. Therefore, all patients at risk for a stroke should be told its signs and symptoms, which include these sudden occurrences: Loss of sensation on one side of the body Weakness or paralysis on one side of the body Problems walking Problems speaking Problems understanding Problems with vision A severe headache (NLM, 2010) Classic signs of a stroke. (Source: NINDS, 2013.)

21 21 Patients should be told that if they are having any of these symptoms, they should call 911 or get someone else to call 911. However, even people who have been taught the warning signs may not realize that they are having a stroke. Some factors contributing to this problem are: Stroke can change a person s level of consciousness. Stroke can make a person confused. Stroke victims can misunderstand the seriousness of their bodies signals; for instance, pain is a major symptom of illness, but most strokes are painless. Stroke victims with damage to their nondominant parietal lobe can lose the ability to recognize that they are ill. The person may be in denial. For these reasons, it is often the family or a bystander who first realizes that a medical problem is occurring. The public should understand that if there is the possibility that someone is having a stroke, they should not hesitate they should call 911 immediately. STROKE TEST: A 3 PART TEST FOR RECOGNIZING POTENTIAL STROKES The signs of a stroke are being publicized through a number of different campaigns (e.g., the American Heart Association and the Stroke Awareness Foundation). A modified form of the Cincinnati Prehospital Stroke Scale (CPSS) (see EMS Stroke Assessment: The Cincinnati Prehospital Stroke Scale below) has been presented as a simple STRoke test, with the first three letters of stroke standing for: Smile. Ask the person to smile. Does their face look uneven? Talk. Ask the person to repeat a phrase. Does their speech sound strange? Raise your arms. Ask the person to raise both arms. Does one arm drift down? The sudden appearance of any one of these three symptoms indicates a possible stroke, and members of public are advised to immediately call 911 (Jones et al., 2010). FIRST AID FOR A STROKE = CALL 911 People often wonder what first aid to give to a stroke victim. The best first aid is professional transport to a hospital, and getting an ambulance is the most important thing that a bystander can do for a stroke victim. In addition, the one critical medical step that the public should know is how to control external bleeding. First aid providers should be taught to press on a bleeding area until the bleeding stops or an emergency medical services (EMS) team arrives.

22 22 When a person calls 911, the operator can give additional guidance for any other necessary first aid (CDC, 2012; Go et al., 2013). CALL 911 OR GO DIRECTLY TO THE HOSPITAL? In an emergency, people often feel that time is being lost by waiting for an EMS team to arrive, and family members or bystanders often hurriedly drive patients to the hospital. In fact, however, patients usually get to the appropriate hospital faster if they use the EMS system by calling 911. EMS teams are trained to choose the most appropriate hospital in the region, and this is not necessarily the closest hospital. In addition, the care and assessment that an EMS team gives a stroke victim shortens the time lag between the onset of stroke symptoms and the evaluation and treatment of the stroke. EMS teams should advocate for widely available 911 capabilities in their region. All landlines and wireless phones should be able to reach local 911 operators. It is also important that the caller s number and location be displayed automatically for dispatchers. At the moment, two telephone systems do not always give 911 operators the detailed locations of callers: Multiline Telephone Systems (MLTS), which are used by many large organizations, and Voice over Internet Protocol (VoIP) services. The Role of Emergency Response The medical care of stroke victims begins with the receipt of a 911 call. Strokes account for about 2% of all 911 calls, but those calls should set off a well-planned and speedy treatment protocol. Thrombolytic treatment of ischemic strokes ideally begins within a 4.5-hour window after the onset of symptoms, and strokes should be given the same priority of treatment as acute myocardial infarctions and trauma (Alspach, 2013; Berglund et al., 2012; Tan & Christensen, 2012). Besides stabilizing patients, dispatchers and EMS technicians make the first triage of potential stroke victims, collect critical background information, and expedite transport to the nearest hospital equipped to handle strokes. To plan for an effective response, directors of EMS units should: Have a stroke protocol written for their team. (For help and guidance, see Developing a Primary Stroke Center Guidelines in the resource section at the end of this course.) Divide the EMS unit s region into districts according to the nearest emergency department capable of treating acute strokes. Schedule regular training sessions that include such activities as having dispatchers and technicians practice using a standard screening test to determine the likelihood that a patient has had a stroke (Mears et al., 2010; Millin et al., 2007).

23 23 EMS DISPATCHERS In general, EMS telephone operators and dispatchers have these responsibilities: Choose, notify, and send the team of responders that is appropriate for each emergency. Advise the callers on possible first aid for the victim. Get critical background information about the victim. There are additional responsibilities regarding potential stroke victims: Identify Potential Stroke Calls When assigning response teams, EMS dispatchers need to assess the type and severity of the emergency. To make decisions for stroke victims, 911 operators should be taught how to identify likely stroke symptoms. When a dispatcher is able to flag a possible stroke victim, the EMS team can be given time to review and plan during their outbound trip and to notify the nearest stroke center. Studies have indicated that notifying a primary stroke center significantly improves outcomes (Patel et al., 2011). Since strokes account for only 2% of all 911 calls, this translates to only four to ten stroke patients each year for the typical EMS team. The infrequency of stroke calls means that EMS operators may not have stroke-appropriate questions committed to memory, so a written set of screening questions should be on each operator s desk. 911 OPERATOR QUESTIONS Normally, the 911 operator asks these questions, using the same sequence: Is she/he completely awake (alert)? Is she/he breathing normally? Is she/he able to talk normally? Tell me why you think it is a stroke. o Movement problems? o Speech problems? o Numbness or tingling? When did this start (happen)? (Buck et al., 2009) A person may have had a stroke if any of the following problems have appeared in the course of a few hours or less: Loss of consciousness Change in level of consciousness Change in behavior Confusion or disorientation

24 24 Dizziness, weakness, or vertigo Difficulty moving Difficulty using hands, arms, or legs Difficulty talking Difficulty understanding Difficulty seeing Severe headache When the caller s description includes any of the preceding signs, the 911 operator asks three stroke questions: Does the patient have a new weakness of one side of the body? Does one side of the patient s face droop more than before? Is the patient s speech more slurred than before? Assign Potential Strokes High Priority 911 dispatchers decide what type of response is appropriate for each emergency. They choose: The skill level and equipment of the EMS response team: basic life support (BLS) or advanced life support (ALS) The type of vehicle to send The initial speed requirement (e.g., sirens, flashing lights, etc.) Acute strokes require the same level of emergency treatment as heart attacks and trauma. The current American Heart Association/American Stroke Association guidelines recommend that potential strokes be given the highest level of priority and that EMS dispatchers send the highest level of emergency care available (Jauch et al., 2013). When available, an ALS team is sent, fully equipped with ventilation and oxygenation capabilities, including the ability to provide advanced airway maintenance, endotracheal tube checks, end-tidal CO 2 monitoring, and ECG monitoring. Ideally, there should be a minimum of two paramedics who are certified in AHA Advanced Cardiovascular Life Support (ACLS) and are prepared to administer all ACLS Class I and Class II interventions on each stroke response (Acker et al., 2007). If a choice has to be made, however, speed of transport to a stroke center is the first consideration. Therefore, if an ALS team is not immediately available, a BLS team should be dispatched. When patients having a stroke are more than one hour s travel time by ambulance from a hospital that is equipped to treat acute strokes, then air transport should be considered. Helicopters or other aircraft can be used to take the EMS team to the patient and then to

25 25 transport the patient and the EMS team to a stroke center. Helicopters can also be used for secondary transport of patients from a remote receiving emergency department (ED) to a stroke center. Collect Critical Information When an EMS operator suspects that a call concerns a stroke victim, the operator begins collecting critical background information. For strokes, dispatchers should make a special effort to get an estimate of the time since any potential stroke symptoms first appeared (Berglund et al., 2012; Patel et al., 2011). CRITICAL BACKGROUND INFORMATION ABOUT POTENTIAL STROKE VICTIMS 1. Obtain the patient s medical history, inquiring specifically about: Past strokes TIAs Hypertension Diabetes Myocardial infarction and other heart problems Atherosclerosis and peripheral artery disease Bleeding disorders Recent surgeries Liver disease 2. Record the patient s current medications, inquiring specifically about: Aspirin, anticoagulants, and antiplatelet agents Insulin Antihypertensives Cocaine, amphetamine, and other street drugs Alcohol intake 3. Note the time when the symptoms first appeared and the last time that the patient did not have the symptoms. 4. Ask about any recent injury, inquiring specifically about head trauma. Forward a Written Record to the Emergency Department Written records of the information collected during the first contact with the patient can be critical for emergency department providers when they are making decisions about treatment. EMS operators should have a blank checklist that can be filled in with essential background information. This document, along with the results of stroke