COURSE PRICE: $33.00 This sale price expires May 31, 2015.
CONTACT HOURS: 10
Wild Iris Medical Education, Inc. is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center's Commission on Accreditation.
Wild Iris Medical Education, Inc. (CBRN Provider #12300) is approved as a provider of continuing education for RNs and LVNs by the California Board of Registered Nursing.
This program has been pre-approved by The Commission for Case Manager Certification to provide continuing education credit to CCM® board certified case managers.
Course Availability: Expires August 1, 2016. You must score 70% or better on the test and complete the course evaluation to earn a certificate of completion for this CE activity. 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. Medical Disclaimer Legal Disclaimer Disclosures
LIMITED TIME OFFER: 25% off! Pass this course and register for your certificate by May 31, 2015 to get this course for $33 instead of the regular price of $45.
Copyright © 2013 Wild Iris Medical Education, Inc. All Rights Reserved.
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.
Upon completion of this course, you will be able to:
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.
There are two major stroke classifications:
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:
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 micro-hemorrhages.)
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 24–48 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:
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:
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.
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).
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).
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.
Deaths from cardiovascular diseases, U.S., 2010. Stroke represents 16.4% of all cardiovascular deaths. (Source: NHLBI, 2013.)
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., 1999–2010. (Source: NHLBI, 2013.)
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.
PERCENTAGE OF PEOPLE WHO WERE EVER TOLD THEY HAD A STROKE, 2008
The heavy concentration of strokes in the southeast has given that region the nickname “the stroke belt.” (Source: CDC, 2010a.)
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).
Before discussing the assessment, treatment, and care of acute strokes, it is important to review the anatomy and physiology underlying the disease.
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:
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.)
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.
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.)
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).
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:
In addition, unusual symptoms such as alien-hand syndrome and callosal disconnection syndromes can occur with ACA strokes (Bartolo, 2011).
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:
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.
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.
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.
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:
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:
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:
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 presents additional problems for the hemorrhagic stroke patient, particularly in the acute phase and within the early recovery period.
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.
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 cascade of calcium-triggered processes, including the activation of catabolic enzymes, such as proteases, phospholipases, and endonucleases. In a short time, the neuron self-destructs and dies. The entire process is termed cortical spreading depression (Lauritzen et al., 2011; Sukhotinsky et al., 2010).
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).
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 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).
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).
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.
The reduction of the blood flow to a region of the brain leads to an ischemic stroke. Causes of such reductions include:
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.
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).
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.
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 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 been associated with Patent Foramen Ovale (PFO) Syndrome (Freeman & Aguilar, 2011; Thaler & Kent, 2010; Thaler et al., 2013).
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).
Hemorrhagic 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.
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).
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, 2010.
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 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).
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:
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:
In addition, daily aspirin is often recommended for adults who are at high risk for cardiovascular disease.
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).
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.
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:
Classic signs of a stroke. (Source: NINDS, 2013.)
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:
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.
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:
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).
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.
When a person calls 911, the operator can give additional guidance for any other necessary first aid (CDC, 2012; Go et al., 2013).
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 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:
In general, EMS telephone operators and dispatchers have these responsibilities:
There are additional responsibilities regarding potential stroke victims:
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.
Normally, the 911 operator asks these questions, using the same sequence:
A person may have had a stroke if any of the following problems have appeared in the course of a few hours or less:
When the caller’s description includes any of the preceding signs, the 911 operator asks three stroke questions:
911 dispatchers decide what type of response is appropriate for each emergency. They choose:
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 CO2 monitoring, and ECG monitoring. Ideally, there should be a minimum of two paramedics who are certified in AHA Advanced Cardiovascular Life Support (ACLS) and 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 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 to a stroke center.
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).
Written records of the information collected during the first contact with the patient can be critical for emergency department (ED) 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 screening questions, is then faxed or sent by computer to the ED that is receiving the patient.
Nurse educators are often responsible for teaching first response techniques for strokes to local emergency medical technicians (Cameron, 2013; Ireland et al., 2010). The basic information to be covered is found in the American Heart Association’s ACLS provider manual and online (AHA, 2010). Nurse educators place special emphasis on:
As an EMS instructor, a nurse needs to be able to tailor the emergency response protocols to the local region. First, the nurse must know which medical techniques can be performed by paramedics and emergency medical technicians under local regulations. Second, the nurse must learn which area hospitals are equipped and staffed for treating acute strokes.
A typical EMS team responds to only four to ten stroke patients per year, and it has been estimated that emergency personnel forget about one half of the stroke care instructions by 12 months after a training session. Moreover, the needs of a community, the availability of acute stroke care, and the recommended prehospital assessments and care protocols continue to be updated. Therefore, continuing education courses should ideally be held as frequently as twice each year (Jauch et al., 2013; Patel et al., 2011).
When they reach the victim, members of the EMS response team follow the standard protocol by assessing the situation and stabilizing the patient. In cases in which there is a question of stroke, paramedics then determine the likelihood of stroke and collect critical background information. Speed has a major impact on patient outcomes, requiring the EMS team to provide as much of the patient care as possible while en route to the hospital (Mears et al., 2010; Millin et al., 2007).
More components of the EMS responders’ protocol for likely stroke victims (modified from NHTSA, 2002) include:
Responders first state their name and tell the patient that they are part of the emergency team that has come to help.
Manage airway, breathing, and circulation. Ischemic strokes—the most common strokes—tend to leave the patient responsive and breathing autonomously. Hemorrhagic strokes, however, can worsen quickly and deteriorate into stupor or coma with respiratory depression or breathing irregularities. Therefore, even when a potential stroke victim appears to need no airway care, the EMS response team must be alert to the sudden appearance of breathing problems.
After stabilizing the patient, EMS responders assess the patient’s level of consciousness, document any signs of stroke, and collect critical background information. It is essential to use a standardized screening test for stroke, as studies have shown that a prescreening test is significantly useful in identifying stroke patients (Berglund et al., 2012). Therefore, first characterize the level of consciousness—A, V, P, or U:
Second, determine the likelihood that the patient has had a stroke using the Cincinnati Prehospital Stroke Scale.
One of the simplest and most widely used stroke assessment tools is the Cincinnati Prehospital Stroke Scale (CPSS), developed by Kothari et al. (1999). This is the recommended tool for EMS assessment (Bray et al., 2010; Govindarajan et al., 2012; Mingfeng et al., 2012).
In the CPSS, the patient is asked to perform three actions. An abnormal response to any of the three indicates that it is likely that the patient is having or has recently had a stroke. The actions and the range of stroke and nonstroke responses are:
A stroke that affects the motor system can cause weakness in the muscles of only one side of the face. The request to “please smile” is an attempt to gauge whether the facial muscles contract with equal strength on the right and left sides. In order to make this assessment, some health professionals ask potential stroke victims to try to smile. However, the normal smile of a healthy person is often asymmetric, and an asymmetric smile in a patient can be the result of habit rather than a sign of a stroke.
Instead of asking for a smile, neurologists ask potential stroke victims to “show me your teeth,” which is intended to demonstrate a grin that bares both sides of their upper teeth. This task requires the patient to strongly contract facial muscles on both the right and the left sides of the mouth. Weakness on one side produces a lopsided grin that reveals more upper teeth on the stronger side.
The public is often told to use “please smile” because its use requires less explanation, but “show me your teeth” is the preferred stroke test.
Regardless of the information already collected by the 911 dispatcher, paramedics should attempt to collect essential information about the patient (see the “Critical Background Information about Potential Stroke Victims” box above).
Because time is of the essence, responders should gather telephone numbers of relatives and witnesses. If knowledgeable acquaintances are available, they are asked to meet responders at the receiving hospital, or if necessary, to travel with responders. For emergency treatments, it will be helpful if next-of-kin are immediately available for consent.
Records are completed and then passed on to the medical team at the receiving hospital. Ideally, EMS teams will use developed checklists with the essential questions to capture all the critical information.
Marcella has just finished her training to become an EMS first responder. She performed well in all the training classes, but she is still quite nervous about her first call as a full-fledged EMS professional. Within the first half hour of her first shift, Marcella hears the call from the dispatcher about a likely stroke victim. Rushing to the scene, Marcella and her team are greeted at the door by the patient’s daughter, who is frantic with worry.
The patient is an 86-year-old African American woman sitting on the sofa. Marcella does an initial visual assessment and notices that the woman’s face appears to be sagging on the right side. While another team member is getting the woman’s vital signs, Marcella asks the woman to “Smile and show me your teeth.” The woman’s face clearly shows asymmetry. Then Marcella asks the woman to stretch out her arms as far apart as she can. The woman tries, but Marcella notices that her left arm is drifting down. More certain that the team is dealing with a stroke victim, Marcella asks the woman to repeat the sentence “The sky is blue in Cincinnati.” When the woman slurs her words, Marcella tells the other team members that they need to take the woman to the nearby primary stroke center. The team is able to quickly transport the woman, whose vital signs remain stable, in under 10 minutes to the stroke center.
Later that evening, while reflecting on her first day as an EMS professional, Marcella realizes the importance of her stroke training. Within 30 minutes of the onset of symptoms, the woman was examined by stroke specialists and now has a good prognosis for eventual recovery.
Maintaining airway, breathing, and circulation are the first priorities. For strokes, keeping the head flat (i.e., supine or 0-degrees elevation) usually offers better brain circulation than keeping the head elevated, when the flat position does not impair the ABCs.
After stabilizing the patient, time is paramount. As soon as possible, begin transporting the patient to the appropriate ED and continue the rest of the prehospital care en route. Each EMS unit should be provided with maps showing the nearest appropriate ED for stroke management in any area (Jauch et al., 2013).
As they manage the patient, members of the EMS team should make contact with the destination ED. Simply notifying the receiving hospital that a potential acute stroke patient will be arriving has been shown to shorten the eventual time between delivery to the hospital and receipt of treatment (Abdullah et al., 2008). Describing the patient’s condition, time of onset of symptoms, and medical history allows the mobilized physicians, nurses, imaging specialists, and pharmacists of the acute stroke team to begin planning.
Information is exchanged between the EMS team and the ED stroke team. The hospital stroke team can tell the paramedics about the size and placement of the IV access that will be needed, and hospital specialists can advise the paramedics about managing complications, such as severe hypertension, hyperglycemia, or cardiac dysfunction.
Oxygen. Strokes are crises of insufficient oxygen delivery to the brain, so it is important to keep the patient’s blood oxygen saturation at normal levels. Attach a pulse oximeter and treat hypoxemia (in this case, oxygen saturation <95%) with supplemental O2. Currently, there is no indication that supplemental oxygen will benefit a patient who already has normal levels of blood oxygen saturation.
IV access. When acute resuscitation is needed, insert an IV line immediately. Otherwise, consider starting an IV en route after consulting the destination ED. Some key brain imaging studies require large bore IV lines that must be inserted proximally (i.e., no more distal than the antecubital fossa). If the receiving hospital will need a specialized IV line, placing the appropriate line in advance can save time.
IV fluids. Treat shock or significant dehydration with balanced salt solutions (isotonic crystalloids, such as normal saline). Otherwise, saline lock the IV or set the IV to drip the minimum amount of balanced salt solution to keep the line open. In general, the goal is to add only a minimal amount of extra fluid, because overhydration can cause cerebral edema. Another concern is hyperglycemia, which can worsen the injury in a stroke. Therefore, do not use dextrose solutions unless you are correcting hypoglycemia.
Blood glucose level. Hypoglycemia produces symptoms that look like stroke, and persistent hypoglycemia will cause brain injury. Therefore, as soon as possible, check the patient’s capillary blood glucose level and treat hypoglycemia with glucose.
ECG. Attach a 3-lead ECG and monitor the patient’s heart continuously with two specific objectives:
Hypertension management. Hypertension is a common finding in acute stroke. However, blood pressure management is a delicate matter in the acute phase of strokes, and the choice of treatment depends on a detailed diagnosis that can only be made in a hospital. Therefore, current recommendations are that EMS and nursing personnel not attempt to treat high blood pressure en route to the hospital.
Recently trained as an EMS provider, John takes a call from the dispatcher about an 83-year-old female patient with a possible stroke. On arrival, after taking the patient’s vital signs, John notes that the patient has a blood pressure of 200/90 mm Hg, a respiration rate of 28 breaths/minute, and a blue tinge around her mouth. John’s supervisor instructs him to place an oxygen mask on the patient, start an IV line, and continue monitoring the patient’s blood pressure.
When John asks about the potential dangers of the patient’s high blood pressure, the supervisor tells him that during an acute stroke, the current recommendations are to avoid attempting to control blood pressure until the patient can be fully evaluated by medical personnel. John continues to monitor the patient’s blood pressure, which remains the same, and her other vital signs. After five minutes on oxygen, John notices the patient’s color and her respiration rate normalizing. Another five minutes later, the EMS team and the patient arrive at the hospital, where the stroke team takes over the patient’s care.
EMS teams ideally attempt to transport potential stroke victims to hospitals that have been designated as stroke centers. Stroke centers, by definition, have well-rehearsed protocols for dealing efficiently with stroke patients. However, not all regions are served by stroke centers, and even when stroke centers are accessible, approximately one half of all stroke patients coming to emergency departments do not use EMS transportation. For these reasons, all EDs need to have protocols in place for the following:
When a potential stroke patient enters any ED, staff must begin a protocol that can lead directly to the administration of a thrombolytic drug at the present hospital or at a stroke center.
Stroke centers have a permanent stroke team with two divisions. The code team—a neurologist (or ED stroke specialist) and a neurology nurse—is always available to respond to a page and institute emergency care. The larger support team is a task force that keeps the stroke program organized, efficient, and up-to-date. This support team includes an EMS director, an ED administrator, a neurologist, and others (Ballard et al., 2012; Hornik et al., 2013).
Source: Jauch et al., 2013; Shulkin et al., 2011.
Emergency department care begins with triage. The EMS team ideally will have identified any potential stroke victims that it is bringing, but approximately one half of all stroke patients will not use an EMS service for transportation to the ED. Therefore, the ED registration staff must be trained to look for signs of possible stroke (Jauch et al., 2013; Shulkin et al., 2011).
The front desk nurse should have a written stroke-recognition checklist. This will ensure that any triage nurse can quickly channel potential stroke victims into the ED’s stroke protocol.
For patients with an acute onset of neurological signs, triage nurses complete the following:
The time sheet then follows the patient to keep providers, nurses, and technicians on schedule.
Time-to-treatment is critical. Therefore, patients with suspected acute stroke are assigned the same high priority as patients with acute myocardial infarction or serious trauma, regardless of the severity of the neurological deficits.
The Emergency Nurses Association and the American College of Emergency Physicians recommend a 5-level Emergency Severity Index (ESI) as a preferred system for triage in a busy ED (Gilboy et al., 2011). This index stratifies patients into five levels (“1” being the most severe and “5” being the least) by determining acuity and resource needs. The system puts all stroke patients in the level 2 or “needs immediate assessment” category, the same as for an unstable trauma patient or a critical-care cardiac patient (Jauch et al., 2013).
A 5-level ESI triage algorithm. (Source: Adapted from Tanabe et al., 2004.)
This algorithm triages patients based on the severity of symptoms.
Resource determination. Resources include laboratory tests, imaging studies, medications needed (IV, IM, nebulized), consultations required, and whether simple or complex procedures are needed. Resources do not include needing a history and physical, saline or heplock, oral medications, immunizations, primary call provider, simple wound care, or items such as crutches, slings, or splints. If more than one resource is required but the patient’s vital signs are stable, the patient is considered Level 3. If at least one resource is required, the patient is considered Level 4. If no resources are required, the patient is considered Level 5.
The ESI Level-5 algorithm allows for rapid and non-overlapping sorting of patients. It is important to remember that it is not a full assessment but gathers the necessary information for a rapid response.
When a potential stroke patient has been identified, a stroke page is initiated from the incoming EMS vehicle or from the ED triage nurse. The stroke code team then reports to the ED, joins the ED receiving team, and begins the acute stroke protocol once the patient is medically stable.
The first parts of the stroke protocol include drawing blood and taking a medical history; these can be done immediately by the nurses, who should have standing orders. Next, the patient needs a selected physical examination and a complete neurological examination with a formal stroke assessment—the NIH Stroke Scale and, for patients with a reduced level of consciousness, a Glasgow Coma Scale Score. In this time-limited evaluation stage, a chest x-ray is warranted only when needed for immediate decisions about heart or lung problems. Finally, all suspected stroke patients need cranial imaging.
For speed and efficiency, the ED nurses should have standing written orders for as many steps in the acute stroke protocol as possible. These orders can be enacted while the code stroke team is reporting to the ED (Gilboy et al., 2011).
Eleanor, a 62-year-old African American female patient, arrives to the emergency department accompanied by her daughter. Eleanor presents with sudden onset of left eye blindness, beginning 30–45 minutes ago while she was at home reading a magazine. Her daughter called 911 for immediate transport. Eleanor says it was as if “someone had dropped a gray curtain over my left eye” but that her vision is improving.
The nurse in the ED, Joan, asks the patient if she has had a headache, weakness, dizziness, tingling, fatigue, or slurred speech in the past. Beyond occasional headaches, Eleanor denies any of these symptoms and adds that this blindness has never happened to her before. Eleanor’s health history reveals that she has well-controlled type 2 diabetes and hypertension, with untreated hyperlipidemia that was recently diagnosed. Eleanor’s medications include metformin (Glucophage), 1000 mg, twice daily; lisinopril (Zestril), 5 mg, daily; and hydrochlorothiazide (Esidrix), 25 mg, daily. Eleanor was also on estrogen replacement therapy for eight years post-hysterectomy. Her pertinent family history includes a mother who had a cerebrovascular event at age 82 years.
Based on Eleanor’s symptoms, medical history, and family history, the nurse immediately consults with the ED physician and alerts the stroke team. The nurse also reassures Eleanor and her daughter that they were right to call 911.
As the ED evaluation proceeds, the basic nursing plan includes:
IV access. Patients eligible for rtPA therapy will need a minimum of two IV sites—one for IV fluids and/or IV medications and one dedicated to rtPA administration.
Airway. Increased intracranial pressure can suppress the respiratory reflex and control mechanisms in a stroke victim, and intubation may be needed to ensure sufficient ventilation. Vomiting can be another consequence of increased intracranial pressure, and intubation can protect the lungs from aspiration.
Bed rest. Keep the neck straight and the airway patent. Head position is decided on an individual basis. In general, keeping the head flat will maximize blood flow to the brain. Elevating the head 25 to 30 degrees is suggested for:
Oxygen. For oxygen saturation <92%, give O2 via nasal cannula at 2–3 L/min
Vital signs and neurological check. Every 30 minutes in the ED
Cardiac monitoring. Continuous
Call physician if:
Source: Jauch et al., 2013; Shulkin et al., 2011.
For all potential stroke patients, a comprehensive metabolic panel, a CBC, coagulation studies, and urinalysis are appropriate. Oximeter readings of blood oxygen saturation can be taken immediately, and a finger stick for blood glucose level will rule out hypoglycemia.
For blood work of a potential stroke victim, the minimum stat tests are listed in the box below. For certain patients, hepatic function tests, lipid profile, toxicology screening, blood alcohol level, or pregnancy test will also be appropriate. In addition, in the case of an intracerebral hemorrhage, blood typing and cross matching should be done if fresh frozen plasma may be needed to reverse a coagulopathy. The ED’s stroke protocol should explain how to determine whether any of these extra tests are necessary.
Source: Kaltenbach et al., 2013; Dhillon, 2012; Jauch et al., 2013.
To get laboratory results quickly, blood tests are drawn early in the evaluation, before sending the patient for imaging. For speed and efficiency, ED nurses require standing written orders for the blood tests for patients who fit the ED stroke profile (Dhillon, 2012; Jauch et al., 2013).
The two most essential laboratory tests for acute stroke patients are blood sugar levels and coagulation studies because:
The importance of other tests depends on the situation. Young or middle-aged patients may need drug-screening tests. Women of childbearing age must be given pregnancy tests. If a stroke is suspected, however, treatment with rtPA should not be delayed even if laboratory results are incomplete (Dhillon, 2012; Jauch et al., 2013). Lumbar punctures are not usually indicated, though some specific exceptions are noted below.
If an acute subarachnoid hemorrhage (SAH) is a possibility but it cannot be identified in the imaging results, lumbar puncture is indicated. SAH leads to blood in the cerebrospinal fluid (CSF) in less than 30 minutes. With a small hemorrhage, there may only be several hundred red blood cells per cc of fluid; nonetheless, even a few hundred blood cells per cc will make the normally crystal-clear CSF appear cloudy.
A common confounding factor is blood that has leaked into the CSF sample from vessels injured by the lumbar puncture needle (a “traumatic tap”). One indication that the blood probably came directly from the CSF is the finding that the blood count does not decrease in consecutive collecting tubes. Another indication that the patient had a SAH is the finding that the initial (opening) pressure of the lumbar puncture is higher than about 200 mm H2O, which is the upper limit of normal in patients who are not obese (Ropper & Samuels, 2009).
While blood is being drawn, the patient needs a focused history and physical exam. Here, the goals are:
ED nurses can take the lead in getting a useful history from the patient, relatives, and any witnesses (Cameron, 2013; Tan & Christensen, 2012). The key information that is needed includes:
Recent medical events
Health problems, asking specifically about a history of stroke or TIA, diabetes, seizures, hypertension, cardiac problems, drug abuse/overdoses, and mental disorders.
Current medications, asking specifically about insulin, oral hypoglycemics, and anticoagulants (e.g., Coumadin/warfarin).
The time and sequence of the appearance of neurological deficits give important clues for distinguishing strokes from stroke mimics and also for identifying the stroke type. Open-ended questions do not bring out these details. Patients’ descriptions of the course of the symptoms are best elicited by specific questions, such as, “How did your ability to walk (talk, understand, use your hands, etc.) change after you first noticed a problem?” “Did you have any problems seeing things?” “What television show were you watching when the problems began?” (Cameron, 2013).
A complete neurological exam is vital. (See “Assessment of Neurological Problems” under “Acute Care of a Stroke Patient” below for a checklist that can be used as a guide.) Other parts of the physical exam can be briefer, but certain features deserve special attention.
GI. Vomiting is common in hemorrhagic strokes but rare in ischemic strokes.
Skin. Jaundice, ecchymoses, purpura, or petechiae may be signs of coagulation problems.
Limbs. Asymmetric or diminished peripheral pulses can be signs of atherosclerotic artery disease or aortic dissection.
A heart exam is integral to stroke evaluations. Patients with stroke, especially an ischemic stroke, often have cardiac problems, and some of these problems (e.g., atrial fibrillation or atrial or ventricular enlargement) will predispose a person to emboli formation and are well-recognized stroke risks. Remember, however, an existing cardiac problem will not necessarily be the cause of a patient’s stroke; ischemic stroke victims tend to be elderly, and they may have cardiovascular problems independent of their stroke.
Besides causing a stroke, cardiac problems, such as myocardial ischemia, can also be caused by strokes. Therefore, cardiac monitoring with an ECG is part of the standard care protocol for stroke patients during the first 24 hours (Go et al., 2013; Jauch et al., 2013; Sidney et al., 2013).
Identifying concurrent cardiovascular disease is also important for later steps in the treatment of a stroke, because treatment includes the prevention of additional strokes. In people with known cardiac disease or with an undiscovered etiology for their current ischemic stroke, the prevention of future strokes requires a full cardiac exam and transthoracic and transesophageal echocardiographic studies of the heart and the aorta (Lahr et al., 2012; Pezzotti & Freuler, 2012; Siket & Edlow, 2012).
The evaluation of a patient with acute neurological dysfunction uses algorithms designed to develop a rational treatment plan. The appropriate treatment depends on the type of neurological injury, and an early decision point requires distinguishing between structural causes (e.g., ischemic stroke, hemorrhagic stroke, and brain parenchymal injury from head trauma) and metabolic causes (e.g., organ failure, hypoglycemia, drug overdose, and systemic hypoxia). Either class of insult—structural or metabolic—can reduce a patient’s level of consciousness and cause neurologic dysfunction.
As the stroke team learns details of the medical history and physical state of a patient, they formulate a hypothesis as to the class of insult.
If these values do not point to a particular metabolic cause and if there is little evidence for structural causes, the metabolic testing should continue with serum and urine toxicology screens, and possibly a lumbar puncture, if there is no evidence of increased intracranial pressure. Electroencephalogram (EEG) can also be useful, because it can show the generalized slowing caused by metabolic encephalopathy or the presence of clinically unapparent seizures. It is also useful to remember that encephalopathies can also be caused by hepatic failure, renal failure, sepsis, electrolyte disarray, certain anti-seizure medications (e.g., valproic acid/Depakene) and Wernicke’s encephalopathy (Frontera, 2012).
Stroke patients need a complete neurological exam; a sample checklist is shown in “Assessment of Neurological Problems” under “Acute Care of a Stroke Patient” below. In addition, the American Heart Association/American Stroke Association guidelines (Go et al., 2013a; Sidney et al., 2013) recommend all potential stroke victims be assessed using the NIH Stroke Scale. This is a measure of the severity of neurological deficits and can be used to objectively monitor the improvement or deterioration of the stroke.
Standardized stroke assessment tools do not replace a neurological exam. Instead, the stroke scale is an efficient way to objectively determine the extent of neurological damage. The initial stroke score is an aid when choosing between available treatments, while subsequent scores can be used to quantify the amount of neurologic change. It is important to remember that the NIHSS scale is a valid evidence-based tool but that a low score does not necessarily indicate that the patient has not had a stroke (Leira et al., 2012).
The NIHSS rates thirteen neurological characteristics of a patient (Leira et al., 2012; Saposnik, et al., 2013):
A booklet and sample scoring form with an explanation can be downloaded from the NIH website. Testing takes 5–8 minutes and requires no special equipment. A course can be accessed at the National Institute of Neurologic Diseases and Stroke (NINDS) website. (See “Resources” at the end of this course.)
In the NIHSS, points are assigned for neurological deficits, and the final scores range from 0 to 42, with higher scores indicating more severe deficits. The chances of a good recovery fall off dramatically in patients with scores greater than 10. A score >22 is labeled a major stroke.
|Predicted outcome after a year|
|<10||60%–70% chance the outcome will be considered good to excellent|
|>20||4%–16% chance the outcome will be considered good to excellent|
|Predicted need for long-term nursing care|
|<6||Most patients will be discharged home|
|6–13||Most patients will need short-term hospital care|
|>13||Most patients will need long-term nursing care|
|Predicted location of occlusion (for ischemic strokes) (Fischer et al., 2005)|
|>10||>96% chance a cerebral vessel is occluded and the occlusion will be identifiable with arteriography|
|>12||>91% chance the occluded vessel is the internal carotid, the basilar, or the middle cerebral artery|
For hemorrhagic strokes, another neurological assessment tool, the Glasgow Coma Scale, is an important guide for predicting outcomes (Mink & Miller, 2011; Oh & Seo, 2010). Like the NIHSS, the GCS is not a diagnostic tool, and it does not replace the neurological exam.
The Glasgow Coma Scale has been a part of neurologic practice for 35 years and has proven to be an objective and reproducible way to describe a patient’s level of consciousness and arousal. Administering the scale takes 3–5 minutes and requires no special equipment. External stimuli are given to a patient, and the tester rates three neurological aspects of the patient’s response: eye opening, limb movement, and vocalization.
On the Glasgow Coma Scale, points are given for higher levels of response and consciousness. Final scores can range from 3 to 15, with lower scores indicating more severe neurological deficiency. (Note that this is the reverse of the NIHSS, in which higher scores indicate more severe deficits.)
|>12||Minor brain injury|
|9–12||Moderate brain injury|
|3–8||Severe brain injury (coma)|
|>11||>85% chance of recovery with no worse than moderate disability|
|<5||>85% chance of dying in first 24 hours|
A comprehensive resource for stroke assessment scales can be found on the Internet Stroke Center website (ISC, 2013).
As information accumulates, the stroke team builds evidence for the diagnosis of stroke or nonstroke. For likely strokes, the team will also be weighing the evidence for and against intracranial bleeding.
Other disorders can look like stroke; these should be considered in the differential diagnosis. In addition to ischemic stroke, other causes of focal neurological defects include:
In addition to hemorrhagic stroke, other intracranial causes of severe headache and vomiting include:
In addition to hemorrhagic stroke, other causes of impaired consciousness include:
It is also important to remember that acute systemic illnesses can unmask or reactivate focal neurological deficits from previous strokes or TIAs. In some patients with previous stroke damage, the onset of a new nonstroke illness can make it appear as if the patient has suffered another stroke (Chen et al., 2011; Magauran & Nitka, 2012).
Effective screening methods to rule out the various differential diagnoses are blood tests, medical history, pattern of symptom onset, and electroencephalography.
Each type of stroke requires a rapid response, but each type of stroke also requires different treatment. If treated early enough, many ischemic stroke patients will benefit from thrombolytic therapy. On the other hand, hemorrhagic strokes will worsen if given a thrombolytic drug. Therefore, it is important to distinguish ischemic from hemorrhagic stroke patients early in the medical evaluation.
Computed tomography (CT) or MRI head imaging is the key to evaluating stroke type. In neurology, as is the case throughout medicine, diagnoses are often made from indirect evidence, and a robust diagnosis depends on compiling consistent evidence from many different perspectives. Sometimes, the CT or MRI images can definitively identify the type of stroke in a particular patient. Often, the images are suggestive of or at least consistent with a specific diagnosis. In all cases, however, the results of brain imaging need to be put into a clinical context (Schellinger et al., 2010). Therefore, before reviewing the imaging techniques used for stroke diagnoses, we will briefly review the additional types of clinical evidence that can be used to decide the type of a particular patient’s stroke.
Ischemic stroke. Recall that most ischemic strokes are caused by thrombi or emboli that result from atherosclerosis. On its own, atherosclerosis develops slowly, and otherwise healthy people younger than 40 years do not often have an ischemic stroke unless they have a strong family history of stroke at a young age. On the other hand, atherosclerosis is accelerated by diabetes, hypertension, hyperlipidemia, and smoking, and people with any of these conditions need not be elderly to have an ischemic stroke.
The obstructive strokes are divided into those generated by clots originating within the cerebral vasculature (i.e., thrombotic strokes) and those generated by clots originating elsewhere (i.e., embolic strokes). Pure motor strokes tend to be thrombotic, and a stroke is more likely to be thrombotic if it has been preceded by TIAs that produced similar signs and symptoms. Initially, thrombotic strokes often produce progressive symptoms that may fluctuate, worsening and then improving, but most ischemic strokes do not worsen after the second day.
Embolic strokes usually occur in patients with atherosclerosis or cardiac disease; coronary artery disease, myocardial infarction, atrial fibrillation, atrial or ventricular enlargement, or endocarditis all increase a patient’s risk of embolic stroke. An ischemic stroke is more likely to be embolic than thrombotic if two different arterial territories are obstructed or if the obstructed artery is large, emphasizing the importance of imaging studies. Embolic strokes often produce symptoms that are maximal at the beginning followed by improvement, which can sometimes be rapid.
Not all ischemic strokes are caused by obstructions of individual arteries. Occasionally, ischemic strokes are caused by systemic hypoperfusion, such as cardiac arrest or hypovolemia via traumatic blood loss.
Hemorrhagic stroke. In contrast to most ischemic strokes, hemorrhagic strokes often begin with a severe headache and vomiting, and they tend to present with acutely elevated blood pressure. Compared to ischemic strokes, hemorrhagic stroke is more common in young people, it is more likely to be triggered by trauma or physical activity, and it is more common in people taking anticoagulants (Grise & Adeoye, 2012; Oh & Seo, 2010).
Hemorrhagic strokes are characterized as those caused by bleeding inside the brain tissue (intracerebral hemorrhages) and those caused by bleeding directly into the cerebrospinal fluid (subarachnoid hemorrhages).
Symptoms from an intracerebral hemorrhage typically begin with a severe headache and vomiting, and the neurologic problems worsen during the first hour or hours. Often, the patient remains alert and has little or no neck stiffness. Most intracerebral hemorrhages lead to focal neurologic deficits. After the bleeding stops, blood from an intracerebral hemorrhage is absorbed slowly; therefore, the neurological problems do not disappear quickly but diminish gradually, over months.
Symptoms from a subarachnoid hemorrhage typically come on instantaneously with a severe headache and vomiting and with the maximum level of neurologic problems, especially when the cause is a ruptured aneurysm. The patient may remain awake but often has a decreased level of consciousness. A stiff neck is common. Focal neurologic defects, such as hemiparesis, are not typical of subarachnoid hemorrhages (ATACH, 2010; Koga et al., 2012).
Clinical signs can be suggestive, but early in a stroke investigation, an intracranial radiographic evaluation is needed. Imaging studies can often distinguish ischemia from hemorrhage stroke. They can also detect certain stroke mimics (e.g., tumors). Often, they can also identify the specific vessel(s) injured in the stroke.
Noncontrast or nonenhanced computed tomography (NECT) of the head is still the recommended initial diagnostic imaging tool for acute stroke. CT is rapid, effective for recognizing intracranial hemorrhage, and more widely available than magnetic resonance imaging (MRI) in most U.S. EDs.
Conventional MRI is an acceptable alternative to NECT. MRI, however, cannot be used on some patients due to contraindications, including any electronic or metal implants. Other contraindications for MRIs are respiratory or hemodynamic instability, vomiting, agitation, impaired consciousness, or patient claustrophobia (Dani et al., 2012; Rasalkar & Chu, 2012).
Image of a transverse (axial) noncontrast CT scan of a patient with a hemorrhagic stroke. Blood is seen as light areas along the left cerebral ventricle (arrows). (The front of the head is at the top of the image.) (Source: Internet Stroke Center.)
Because time is of primary importance, there should be a standing order for a cranial scan for all potential stroke patients. There should also be a plan for getting the scan read quickly. Cranial imaging should be completed within 25 minutes of the patient’s arrival at the ED, and the interpretation by the radiologist on call should be available within 20 minutes of the scan’s completion.
CT RADIATION EXPOSURE
To reduce radiation exposure, which can be significant with CT scans, some stroke centers have replaced CTs with MRIs as the imaging technology of choice, assuming no contraindications to an MRI (Sorensen & Heiss, 2010).
Imaging techniques are constantly improving beyond discriminating between an ischemic and a hemorrhagic stroke. Current advances in imaging techniques focus on one of three areas:
There are a number of CT techniques currently in use, including enhanced and dynamic CTs capable of providing important information. MRIs can be weighted in various ways as well to provide important clinical data. Recent advances in vascular imaging can provide even greater detail, particularly for hemorrhagic strokes.
Until recently, the medical arsenal contained few actual treatments for stroke. As Gerber (2003) wrote in her review of the history of stroke therapies:
The only treatment option available to stroke patients during the first half of the twentieth century was rehabilitation. Rehabilitation as a treatment option was a great place to start; however the patient first had to survive the initial injury and somehow avoid all secondary injuries to even be a candidate for stroke treatment.
Between the 1960s and 1980s, the technique of endarterectomy for unblocking carotid arteries was improved and used widely, but this surgery was done as a preventative treatment rather than as a stroke therapy. Another key innovation in the medical management of stroke was the development of computed tomography (CT), which became available throughout the United States in the 1970s and 1980s. CT scanning proved an excellent imaging technique for distinguishing between ischemic and hemorrhagic strokes.
The impetus for high-priority emergency stroke treatment began in 1996 when the FDA approved the use of a thrombolytic agent for stroke. For some patients, this drug—recombinant tissue plasminogen activator (rtPA)—can reverse the neurological effects of an acute ischemic stroke.
In the years when stroke treatment had revolved around rehabilitation, the watchwords for therapy were “supportive care” and “caution.” Some physicians waited 12–24 hours to commit to a diagnosis of stroke, because transient ischemic attacks (TIA) and minor strokes were thought to clear autonomously within 24 hours. The introduction of thrombolytic treatment changed the cautious approach of stroke management. Currently, rtPA should be administered as soon as possible after a stroke occurs, and the new paradigm considers all stroke symptoms to be potential emergencies in the class of acute myocardial infarctions. Now, the slogan is “time lost is brain lost.” Within three hours of initial appearance of symptoms is considered the standard of care, but treatment within 4.5 hours is still significantly beneficial (Alberts et al., 2011; Jauch et al., 2013; Mink & Miller, 2011).
Thrombolytic treatment for the most common strokes (i.e., ischemic strokes) is time dependent. Although there has not yet been the same dramatic innovation for treatment of hemorrhagic strokes, which are less common than ischemic strokes, they too require emergency care. Hemorrhagic strokes often deteriorate rapidly, producing severe neurological deficits and a high rate of death and disability.
Current management of all acute strokes stresses early identification and quick, efficient treatment using blood pressure control, lytic agents, both surgical and catheter procedures, and anticoagulation. The new protocols require that EMS personnel; emergency department physicians and nurses; and surgical, neurological, and radiological specialists all be prepared to work on stroke victims quickly and efficiently (Jauch et al., 2013).
Today, there is still no effective “in-the-field” treatment for a stroke. Stroke patients must be taken to a hospital. Moreover, they must be taken quickly, because the clock is ticking for acute stroke victims: secondary damage from strokes increases as time passes, and early intervention can save critical brain tissue.
The rapid diagnosis of an acute stroke and the determination of its type allow a stroke team the widest range of direct treatment options. Thrombolytic treatment (“clot-busting”) of ischemic strokes is recommended within a limited time window (currently, 4.5 hours after the initial stroke symptoms). Time is such a critical element that a written time sheet is maintained for each stroke patient. Timekeeping is one of the important tasks for the ED and stroke team nurses; nurses are the team members who keep stroke care on schedule (Jauch et al., 2013).
The time of 45 minutes is set as the first milestone in the ED stroke protocol. Within the first 45 minutes of a patient’s evaluation, they should be channeled into one of two treatment pathways:
By 45 minutes, the stroke team should have distinguished ischemic from hemorrhagic strokes.
An ischemic stroke is usually represented as a gradient of decreasing brain perfusion. The central area—the core area—that is fed by the blocked artery receives the least oxygenated blood. At the same time, the periphery of the area fed by the blocked artery can still be receiving sufficient blood flow to keep brain tissue alive; these peripheral areas are called the penumbra of the stroke.
Neurons are exquisitely sensitive to decreases in oxygen and glucose, and even small decrements in local blood flow will affect function. For this reason, the entire field of the blocked artery in an ischemic stroke will become ischemic.
The core of the stroke area infarcts rapidly because any brain tissue that is receiving little or no blood flow begins to die in <10 minutes. The penumbra, however, can still be receiving sufficient blood flow to keep its neurons from dying, although the reduced blood flow has stopped their ability to signal. Many of these penumbral neurons can be revived if blood flow is restored early enough.
Therefore, current treatments for ischemic stroke attempt to reperfuse the penumbral regions of the brain. The main reperfusion technique is thrombolysis, i.e., dissolving the arterial obstruction with a clot-lysing drug such as rtPA (alteplase, Activase, Cathflo) (Baldwin et al., 2010; Dhillon, 2012; Lukovits & Goddeau, 2011).
Your patient, Eleanor, is diagnosed as suffering an ischemic stroke. Recall that she is on lisinopril (Zestril) and hydrochlorothiazide (Esidrix) to control her hypertension and that she has been diagnosed with type 2 diabetes and is currently on metformin (Glucophage) to control her blood sugar. She was treated with an infusion of rtPA at two hours, according to her charted timeline. She is currently resting in the ED, eight hours after she was initially seen.
As your team meets to discuss her case, it is determined that Eleanor will be admitted for a full cardiac and neurological examination as soon as possible. The neurologist also recommends that aspirin be added to Eleanor’s daily medication regimen to minimize the risk of a new clot forming. During the night, you continually check Eleanor’s vital signs and laboratory results while she awaits transport to the floor. Eleanor has a restless few hours but stays symptom free and appears stable.
You later learn that Eleanor’s echocardiogram is normal but that her left carotid artery is 90% occluded and that she had a second episode of transient blindness in her left eye. Eleanor is scheduled for a carotid endarterectomy by the neurosurgeon for the next day.
Hemostatic approaches to hemorrhagic strokes can include correcting coagulopathies with protamine sulfate or vitamin K. Clotting factor replacement using fresh-frozen plasma (FFP) or prothrombin complex concentrate (PCC) can also be beneficial. These are generally most useful in hemorrhagic strokes apparently caused by anticoagulant therapies. However, in a spontaneous hemorrhagic stroke, the use of hemostatics is more controversial because thromboembolic events have been associated with its use.
Management after a hemorrhagic stroke is most often decided on a case-by-case basis, though antithrombotics, including antiplatelet and anticoagulant agents, should be discontinued after an acute intracranial hemorrhage. Blood pressure management is more controversial. Excessively high BP increases the risk of bleeding, and low BP increases the risk of cerebral hypoperfusion (Lukovits & Goddeau, 2011). While blood pressure is monitored for all hemorrhagic stroke patients, control of blood pressure, which is an active area of research, is determined by each patient’s clinical parameters. If implemented, nicardipine (Cardene) is the current antihypertensive agent of choice.
Attempts to control intracranial pressure (ICP) are usually decided on an individual basis and are often based on the immediate clinical status of the patient. Hyperosmolar agents have been used to attempt to reduce ICP but have not been proven to be of benefit for most patients. Alternatively, diuretics have been used (Owens, 2011).
Finally, surgical or endovascular techniques may be considered if the hemorrhage is subarachnoid (Lukovits & Goddeau, 2011).
To carry out these acute treatment protocols, medical care providers need both specialized knowledge and practical experience. However, the facilities, equipment, and personnel for acute stroke management are expensive and are not available at most hospitals. It is not economical for every emergency department to be a high-tech stroke treatment center because only 0.6% of ED patients need stroke care (Ballard et al., 2012; Hornik et al., 2013).
High-quality stroke management improves the health of a community, but the healthcare system cannot afford to outfit every hospital with full-service stroke care. Therefore, the public health goal is to develop regional centers responsible for maintaining the complement of people and technologies needed to treat acute strokes. These hospitals are called primary stroke centers (Alberts et al., 2011; Ballard et al., 2012; Hornik et al., 2013).
Emergency departments vary in their abilities to manage acute strokes, so there is currently a push to develop a core of high-quality primary stroke centers throughout the United States. To standardize the requirements for an excellent primary stroke center, the Joint Commission has developed a program to certify particular EDs as designated primary stroke centers. As of October 2009, there were more than 600 certified primary stroke centers in 49 states. The eventual goal is to have a specialized stroke center within 100 miles of all cities across the nation (Hornik et al., 2013; Shulkin et al., 2011).
To be certified as a primary stroke center, an emergency department (or its hospital) must meet these criteria:
A primary stroke center must have written protocols for the diagnosis and treatment of a full range of strokes, and the protocols must be compatible with the most current American Heart Association/American Stroke Association recommendations. In addition, a primary stroke center must keep standardized records of its patients, their treatments, and the outcomes; these records are used to monitor the performance of the center (JCAHO, 2010).
Healthcare directors and hospital administrators who would like to transform their hospitals into primary stroke centers can begin with the detailed practical guide “Building the Case for a Primary Stroke Center: A Resource Guide,” available from the National Stroke Association’s website.
A primary stroke center has the ability to efficiently diagnose and categorize strokes and to quickly administer certain acute therapies, most notably intravenous rtPA. Ischemic strokes with major complications and hemorrhagic strokes can require an even higher level of care, needing dedicated neurological ICUs and experienced neurosurgeons, endovascular surgeons, and neuroradiologists. Hospitals with these advanced stroke facilities are called comprehensive stroke centers (Hornik et al., 2013; Shulkin et al., 2011).
More hospitals have the staff and facilities to become primary stroke centers than to become comprehensive stroke centers. It is estimated that there are currently at least 200 comprehensive stroke center hospitals in the United States, but there is still no national accreditation plan for these centers. Experts hope that, throughout the country, primary stroke centers in a region will eventually become satellites of a centrally located comprehensive stroke center. In such regions, EMS teams would transport acute stroke patients to the nearest primary stroke center, where eligible patients could be quickly treated with rtPA. Patients with complex strokes, hemorrhagic strokes, and complications from rtPA treatments would be rapidly transferred to the affiliated comprehensive stroke center.
Samantha, an RN who plans to return to full-time nursing, has experience working in an emergency department. Samantha decides to attend a local job fair to see what is available in her area. At the job fair, she gets into a conversation with two recruiters, one from a primary stroke center and the other from the regional comprehensive stroke center. Samantha has experience caring for stroke patients but is not clear as to what the differences are between the two stroke centers.
In her conversation with the recruiters, Samantha learns that there are different levels of stroke care hospitals. The first is a local “stroke-ready” facility, where tPA therapy may be initiated and providers may also contact stroke specialists remotely or by using video Telestroke evaluations. If the evaluation determines a patient needs more intensive or specialized care, the patient may be transported to a primary stroke center (the next level), or if the patient is determined to require the highest level of care, the patient will be treated at a comprehensive stroke center.
A primary stroke center is fully capable of delivering acute stroke treatment, including rtPA and extensive evaluation, detailed management of the patient, and rehabilitation services. A comprehensive stroke center is staffed with stroke specialists who have the experience and training to “intervene” with the stroke event by using specialized techniques to remove a clot or stop an active cranial bleed.
The recruiter also tells Samantha that other advantages of a comprehensive stroke center include their rehabilitative services and follow-up care. Comprehensive stroke centers are especially involved with monitoring patient outcomes and following patients for three months after their stroke. Samantha is excited about the prospects of working so closely with patients and having the ability to follow their recovery process. She promptly completes an application to work for the comprehensive stroke center.
Stroke centers are dedicated to quick, efficient care. The recommended time targets for key steps in the management of acute stroke are as follows:
Specialists must also be easily accessible in a primary stroke center, with a neurologist available within 15 minutes and a neurosurgeon (possibly at another hospital) within two hours.
At stroke centers, stroke teams and ancillary services, such as imaging and pharmacy, must be able to operate effectively day and night, including weekends. This is especially true for the treatment of intracerebral hemorrhages, for which weekend admissions have been shown to lead to higher mortality rates in many locations (Williams & Rudd, 2010).
Just as in the general accreditation process for hospitals, nurses are central players in getting a stroke center certified. The head nurse in a hospital’s stroke team is the key organizational figure. The head nurse ensures that there is a written protocol for guiding stroke victims through the steps leading to a treatment decision. The head nurse is also responsible for organizing and training a team of nurses and technicians who understand strokes and who are sufficiently experienced to keep the stroke protocol moving while watching over the patient’s often-fragile health (Cameron, 2013; Catangui & Slark, 2012; Gocan & Fisher, 2008; Kerr, 2012; Roots et al., 2011).
It is recommended to treat stroke patients with the fibrinolytic drug rtPA. This is a time-limited treatment:
Certain patients to whom IV rtPA cannot be given may be eligible instead for catheter-administered intra-arterial rtPA. Other treatments for ischemic stroke are being tested, but none is yet recommended for widespread use later than 4.5 hours after the stroke symptoms appeared.
A variety of interventional stroke treatments are actively being pursued, but the only interventional treatment recommended for general use for acute ischemic stroke is the thrombolytic drug rtPA. For eligible stroke patients, IV rtPA can significantly improve outcomes (Jauch et al., 2013; Yeo et al., 2013). If treated within 3 hours of the onset of their symptoms, 80% of eligible patients will survive at least 3 months and 38% will have a complete or nearly complete recovery (vs. 21% when treated with placebo). Of the survivors, 60% will be independent in their activities of daily living, 20% will remain moderately dependent on caregivers, and 20% will be completely dependent on others (Dhillon, 2012).
Trials on the use of ultrasound enhancement of fibrinolysis are currently underway, as are the use of combinations of fibrinolytic agents with anticoagulants and/or antiplatelet agents (Jauch et al., 2013).
TPA is the abbreviation for tissue plasminogen activator, a naturally occurring human enzyme. rtPA is tPA that has been made in the lab using recombinant DNA technology.
Tissue plasminogen activator is a protease that turns plasminogen into plasmin, which is a molecule that cuts apart the fibrin strands holding blood clots together.
The generic name for rtPA is alteplase and the brand name is Activase. The drug is a white powder that is reconstituted in sterile water. Besides being used to treat acute ischemic stroke, rtPA is used to treat acute myocardial infarction.
rtPA is used to treat an acute ischemic stroke, not a hemorrhagic stroke. Eligible patients should not have any risk factors for significant bleeding events: they cannot have had recent major surgery, myocardial infarction, stroke, or other internal injuries, and they must have normal clotting functions and a sufficient number of platelets. Additionally, the patient should not have significant hypertension (Baldwin et al., 2010; Dhillon, 2012).
There is also a time window for the most effective use of rtPA. The best prognosis is if the drug has been administered within 90 minutes of the onset of stroke symptoms. The value of using rtPA is reduced but beneficial within 180 minutes, and the benefits still outweigh the risks at 270 minutes. Currently, there is controversy regarding the use of rtPA after 4.5 hours (Dhillon, 2012).
* The currently available research demonstrating the value of using rtPA between 3 and 4.5 hours after the onset of stroke symptoms is from a study with a more limited set of patients than the study of rtPA administration <3 hours after stroke onset. The study at the later time period only followed patients <80 years, with an NIHSS >25, without the combination of previous stroke and diabetes, and not taking anticoagulants, regardless of their current INR value (del Zoppo et al., 2009).
** A patient with a seizure at the time of onset of the stroke might still be eligible for treatment provided the clinician is convinced that the residual impairments are due to a stroke and not to the seizure.
Blood Vessel Status
*** If greater than these levels, the patient can be given 1 or 2 doses of labetalol or a similar drug and then treated if the blood pressure decreases to the indicated range, providing that the other eligibility criteria are met.
Understanding of Risks/Benefits
Source: Dhillon, 2012.
The protocol for administering rtPA should be written, and the involved members of the stroke team should review it in advance.
Before giving rtPA. Treating an ischemic stroke with rtPA must be done promptly. Therefore, stroke EDs need electronic standing orders for the drug and an established procedure for quickly dispensing the drug from the pharmacy at any hour.
When possible, informed consent is obtained from the patient or from a surrogate. Verbal consent is adequate. rtPA is an FDA-approved treatment for acute stroke, and if appropriate consent cannot be obtained, the drug can still be administered in an emergency (Dhillon, 2012).
Following is a suggested text for informing patients of the risks and benefits of rtPA:
There is a treatment for your stroke called alteplase that must be given within 4.5 hours after the stroke started. It is a “clot-buster” drug. Overall, it is estimated that alteplase treatment is 10 times more likely to help than to harm eligible patients when given within three hours of stroke onset. The likelihood of benefit decreases with time, but treatment is still more likely to help than harm up to 4.5 hours after the stroke begins. Thus, the potential benefits of this treatment outweigh the risks.
However, this treatment has a major risk, since it can cause severe bleeding in the brain in about 1 of every 15 patients. If bleeding occurs in the brain, it can be fatal. When used to treat large numbers of stroke patients, on average the potential benefits of this treatment outweigh the risks; however, in any individual patient it is a very personal decision (Oliveira-Filho & Samuels, 2009).
Malpractice suits have been brought for failure to offer or to administer rtPA to eligible patients. When it is consistent with the best clinical practice, thrombolytic therapy can be administered even if the patient is unable to authorize it and when a legally authorized representative is not available.
However, the “best clinical practice” has not yet been firmly established across the United States. The FDA guidelines are not precise, and the American Heart Association/American Stroke Association recommendations emphasize that neurologists must use their own clinical judgment. Therefore, as a legal safeguard, physicians (or providers) should discuss treatment options (including getting a second opinion and transferring the patient to another institution) with patients and family when there is sufficient time. Doctors should then document the discussions or the need for immediate treatment without these discussions (Bruce et al., 2011).
Before giving the drug, all procedures that might induce bleeding, such as inserting Foley catheters or nasogastric tubes, should be completed. At least two large-bore IV lines must be in place.
Usually, a nurse administers rtPA. The nurse begins by rechecking the eligibility of the patient, including the verification of adequate coagulation functions, sufficient platelets, a head scan showing no hemorrhage, and that time remains in the 4.5-hour window after the onset of stroke symptoms.
While giving rtPA. rtPA is given intravenously. The total dose is 0.9 mg/kg up to a maximum of 90 mg (i.e., all patients weighing >100 kg [220 lbs.] receive a total of 90 mg of drug). If all of the drug in the bottle will not be needed, the excess is removed in advance and discarded to prevent accidental overdose. The first 10% of the dose is given as a bolus, and the remainder is delivered as a 60-minute infusion (Baldwin et al., 2010; Dhillon, 2012). Verifying doses, infusion settings, and the amount of any discard with a second nurse is key to avoiding errors.
During the infusion and in the succeeding 24 hours, acute hypertension, severe headache, nausea, or vomiting can be signs of intracranial bleeding. If any of these arise, the infusion must be stopped and an emergency CT obtained. Immediate blood work is also done to check the patient’s platelet count and coagulation functions. In addition, emergency neurosurgical and hematologic consults are called to advise on the immediate treatment plan.
In the hands of experienced neurologists following recommended guidelines, symptomatic intracerebral hemorrhages will be caused in about 6% of rtPA treatments. No characteristics of the patients or their strokes have yet been found that can reliably predict who will suffer a symptomatic intracerebral hemorrhage when treated with rtPA (Baldwin et al., 2010; Dhillon, 2012).
After giving rtPA. After giving the drug, the patient must be monitored closely in an intensive care unit for at least 24 hours. Vital signs are checked every 15 minutes for 2 hours, every 30 minutes for the next 6 hours, and once every hour for the following 16 hours. A neurological assessment is done each time the vital signs are taken.
During the first 24 hours, blood pressure is maintained at <180/105 mm Hg if judged clinically necessary, no antiplatelet or anticoagulant drugs are given, and no arterial punctures are done. Likewise, intra-arterial catheters, nasogastric tubes, and indwelling bladder catheters are not inserted during the first 24 hours.
The main risk factors for developing ICH after alteplase is infused are:
The overall rate of ICH after treatment is 1.8% (Mazya et al., 2012).
Intra-arterial fibrinolysis with rtPA. Normally, rtPA is given intravenously. A higher concentration can be delivered to the clot by injecting rtPA through an intra-arterial catheter placed near the clot. Intra-arterial thrombolysis has been used to treat large clots in the middle cerebral artery, life-threatening basilar artery clots, and in certain other cases when patients are not eligible for IV rtPA. When administered intra-arterially, the total dose of rtPA is about one third of that used intravenously. Ongoing studies are also testing the efficacy of combining intravenous and intra-arterial thrombolysis in serious strokes (Gounis & Wakhloo, 2010).
Not all acute stroke patients are eligible for rtPA therapy. In some of these patients, other anti-thrombotic drugs have been tried acutely. Currently, aspirin is the only antiplatelet drug recommended for treating some acute ischemic stroke patients. Studies show that when begun within 48 hours of the onset of stroke symptoms, aspirin (160–300 mg/day) reduces the incidence of stroke recurrence and improves overall outcome compared to no treatment, but may not reduce overall mortality (Rist et al., 2013; Wang et al., 2012).
For acute ischemic stroke patients who are not receiving rtPA, IV heparin, or oral anticoagulants, daily aspirin (325 mg on the first day followed by 150–325 mg/day thereafter) is recommended, beginning within the first 48 hours. Aspirin is not a substitute for other stroke treatments but has shown some benefit in reducing recurrence (Geeganage et al., 2012).
Studies of anticoagulation with heparin or low molecular-weight heparin have not demonstrated significant benefits for most acute ischemic stroke patients. Anticoagulation cannot be used in patients with hemorrhagic stroke; and stroke patients with large infarctions, uncontrolled hypertension, or bleeding conditions should not be given full-dose anticoagulation treatment. On the other hand, neurologists sometimes use anticoagulation in selected stroke patients with any of the following conditions:
Researchers are also exploring the use of mechanical devices to physically open cerebral artery blockages. These devices range from clot removers or retrievers to angioplasty catheters to deployers of self-expanding stents. One goal of the development of physical clot disruption devices is to provide acute stroke treatments that can be used when thrombolytic drugs would endanger the patient, such as after recent cardiac surgery. Although they can be used alone, physical clot disruption techniques are typically used along with catheters delivering intra-arterial rtPA. Many endovascular devices show promise; none is yet recommended for widespread community hospital use (Hassan et al., 2012; Mokin et al., 2012).
Acute ischemic strokes usually present with elevated blood pressure, but this is not always an indication for aggressive treatment of the hypertension. After a stroke, some degree of hypertension may be needed to maintain adequate perfusion of the brain, although very high blood pressure (systolic pressure >200 mm Hg) has been linked to higher mortality rates after stroke (Grise & Adeoye, 2012).
Currently, it is recommended that mild or moderate hypertension not be initially treated in an acute ischemic stroke. With this general rule comes a list of situations in which hypertension should usually be reduced:
When lowering blood pressure in an acute ischemic stroke, IV labetalol (Trandate) is commonly used, and the goal is a cautious reduction in blood pressure of about 15% during the first 24 hours.
A different blood pressure goal is used for patients who are eligible for treatment with rtPA:
The time-dependent stroke treatments, such as intravenous rtPA, are only recommended for use in hospitals with experienced staff and well-equipped facilities. Ideally, the treatment of all acute strokes would be done in primary stroke centers, but many areas of the country are far from primary stroke centers. One way to extend the range of acute stroke treatment, especially the administration of thrombolytic agents, into areas far from stroke specialists is by using video teleconsultation or Telestroke.
Telestroke is a two-way videoconference between distant stroke-care specialists and local bedside-care providers. Telestroke works exactly like a direct onsite consultation, and as with onsite consultations, patients or their families are kept involved and asked to grant permission. Telestroke is not considered therapy: it is a consultation to advise the local physicians who are directly treating the patients. At the moment, medical licensing liability laws may limit the use of out-of-state Telestroke consultations.
Telestroke, which is endorsed by the American Heart Association (Schwamm et al., 2009), has proved effective and cost-efficient. The following telestroke case history was reported by a group of neurologists at the primary stroke center of the Medical College of Georgia (Hess et al., 2006). It is a good example of how telestroke can extend time-dependent stroke therapy into communities far from primary stroke centers (Müller-Barna et al., 2012; Rafter & Kelly, 2011; Silva et al., 2012).
A 62-year-old woman with a history of paroxysmal atrial fibrillation suddenly develops weakness of her left arm and left leg and falls when getting out of her car on her way to an exercise class. During the fall, she sustains trauma to her left orbit. She is taken to the local 56-bed rural hospital in Washington, Georgia, and arrives in the emergency department within 30 minutes. The emergency room physician activates a REACH (remote evaluation of acute ischemic stroke) Telestroke consultation with the Medical College of Georgia, 61 miles away in Augusta, Georgia.
During examination over remote video, the patient shows severe neglect and a dense left hemiparesis. Her National Institute of Health Stroke Score (NIHSS) is 16. She has swelling over the left eye, making it difficult for her to open her eyelid. The CT scan of brain—viewed remotely by a personal access communications system built into REACH—is normal without any evidence of hemorrhage or early infarct signs. The consultant advises alteplase, and the REACH system calculates a weight-based dose. Recommendations, including dose of alteplase, are printed out at the local rural hospital. Ninety mg of alteplase is started intravenously at 1 hour and 50 minutes from the time of symptom onset. The patient is transferred by helicopter to the Medical College of Georgia.
On arrival, the patient still has neglect and left-arm weakness, but she is now moving her left leg against gravity and her NIHSS is 13. Transcranial Doppler shows absence of flow in the right middle cerebral artery. After examination of her left orbit by the ophthalmology department, she is taken to the neurointerventional suite, where the angiogram shows occlusions in the proximal superior and a few branches of the inferior division of the right middle cerebral artery. She receives a total of 7 mg of intra-arterial alteplase with complete recanalisation at 7.5 hours after symptom onset. She slowly improves and is discharged to a rehabilitation hospital 9 days later on warfarin with an NIHSS of 8. After three months she is able to take care of most of her daily activities but has residual mild left arm weakness. (Hess et al., 2006; © 2006, Elsevier Ltd.)
The treatment paths for a stroke victim diverge dramatically at the point in the stroke evaluation where the physician answers the question, “Are there any signs of intracranial hemorrhage?” Strokes with bleeding cannot be treated using fibrinolytic drugs because these drugs will make the patient’s condition worse. Cranial imaging is the best way to identify intracranial hemorrhaging, and CT or MRI studies must be done early in a patient’s evaluation so that subsequent treatment can be started quickly.
For ICH, treatments attempt to stop or decrease the bleeding, remove extravascular blood, and maintain the patient in a well-oxygenated nonhypertensive state; the specific treatment steps are decided on a case-by-case basis. For subarachnoid hemorrhages, the goals are similar, the treatments are also individually tailored, and there is the additional possibility of physically stabilizing ruptured aneurysms (Vergouwen et al., 2012).
As treatment plans are formulated for a patient with an intracranial hemorrhage, it is important to check the patient’s current medications. Existing anticoagulation, such as warfarin (Coumadin) therapy, is a common cause of cerebral bleeds. In such patients, the anticoagulant drug must be stopped and its effects reversed. Usually, this requires IV vitamin K, prothrombin-complex concentrates, fresh frozen plasma, or recombinant human clotting factor VIIa (Grise & Adeoye, 2012; Lukovits & Goddeau, 2011).
Approximately 10% of all strokes are intracerebral hemorrhages (ICH), i.e., bleeds into the substance of the brain. ICH has a high mortality rate, and most of the deaths occur within the first 48 hours. Larger hemorrhages have poorer prognoses, especially when the stroke has led to coma (Grise & Adeoye, 2012; Nijboer & ten Duis, 2010; Oh & Seo, 2010; Steiner & Bosel, 2010).
Currently, basic medical management appears to be more beneficial than any surgical interventions for most ICH. Patient treatment must be individualized, but some general goals include addressing the following concerns:
Bed rest. The patient needs constant hemodynamic monitoring in an ICU.
Ventilation. Adequate ventilation and oxygenation should be ensured.
Fever. For any increase in body temperature, antipyretic medicines are administered to lower the body temperature to normal.
Hyperglycemia. Insulin is used to lower blood glucose levels to <140 mg/dL.
Hydration. Hypovolemia should be corrected using IV normal saline.
Increased intracranial pressure (ICP). If increased ICP is suspected, the head of the bed should be elevated to 20 to 30 degrees. Analgesia (morphine or alfentanil) and sedation (propofol, etomidate, or midazolam) can often help to reduce ICP. Dehydrating agents such as mannitol are sometimes administered, with the goal of making the blood plasma hyperosmolar (300 to 310 mOsm/L). Treatments for increased ICP are best monitored by continuous direct measurement of the ICP. (See “Acute Complications” below for more details.)
Hypertension. Most patients with an intracerebral hemorrhage are hypertensive immediately after the stroke, and some degree of hypertension may be necessary to maintain sufficient perfusion throughout the brain. However, severe hypertension can worsen the stroke, so high blood pressure is usually treated with an IV antihypertensive (e.g., labetalol [Trandate]). Nurses and physical therapists can monitor blood pressure readings, as can some occupational therapists, depending on state licensure laws (AOTA, 2012; Frese et al., 2011).
Treatment recommendations for hypertension in acute ICH are:
Infusion of hemostatic agents. Studies are ongoing, but the prothrombotic agents tested to date have not proved beneficial.
Surgical evacuation of hematoma. In general, surgical interventions have given no better results than medical management. Surgery can be critical, however, for reversing brainstem compression or for relieving hydrocephalus (e.g., from an expanding cerebellar hemorrhage) (Merenda & DeGeorgia, 2010, Liu et al., 2011; Tan et al., 2011).
Approximately 3% of all strokes are subarachnoid hemorrhages (SAH), most of which result from ruptured aneurysms. Like ICH, SAH has a high mortality rate; for SAH, mortality is almost 50% within the first month. Large hemorrhages and hemorrhages producing coma or stupor have the poorest prognoses. In a recent Finnish study, SAH survivors had nearly twice the risk of death as their age-matched cohorts (Korja et al., 2013; Lauritzen et al., 2011; Shah & Christensen, 2012).
Currently, medical management is the basis of treatment for SAH, with percutaneous or surgical obliteration of the remnants of the aneurysm when possible (Aburto-Murrieta et al., 2012; Liu et al., 2012; Muroi et al., 2012; Olkowski et al., 2013). Patient treatment must be individualized, but some general goals include addressing the following concerns.
Bed rest. Patients have constant hemodynamic monitoring in an ICU. A set of baseline Transcranial Doppler (TCD) ultrasonography measurements is taken; repeat TCDs are then used to monitor for vasospasms, especially in the middle cerebral and basilar arteries. Prophylaxis is instituted against deep venous thrombosis by applying compression stockings or mechanical pneumatic compression devices.
Ventilation. Adequate ventilation and oxygenation should be ensured.
Fever. For any increase in body temperature, antipyretic medicines are administered to lower the body temperature to normal.
Hyperglycemia. Insulin is used to lower blood glucose levels to <140 mg/dL.
Hydration. In the majority of patients, intravascular volume becomes depleted in the days after a subarachnoid hemorrhage, and this greatly increases the chances of an ischemic infarction from vasospasm. Therefore, fluids are given to maintain an above-normal circulating blood volume and central venous pressure.
pH. Metabolic acidosis is a potential complication to monitor and correct.
Pain. Analgesia is given for headache.
Increased intracranial pressure (ICP). Intracranial pressure can increase, so when possible, some stroke centers place a ventriculostomy to directly monitor ICP.
Hypertension. Some degree of hypertension may be needed to maintain sufficient perfusion throughout the brain. If ICP measurements are available, they can be used to calculate the cerebral perfusion pressure (CPP) using the mean arterial pressure (MAP), because CPP equals MAP minus ICP. Therefore, when ICP values are known, blood pressure can be titrated to maintain the CPP between 61 and 80 mm Hg. When ICP measurements are not known, the systolic blood pressure in conscious patients can usually be reduced to <140 mm Hg. In patients with impaired consciousness, hypertension is usually not treated. Labetalol (Trandate) is the commonly used antihypertensive drug.
Prevention of stroke from vasospasm. Repeat TCD measurements are used to monitor for vasospasm. Small studies suggest that by initiating statin treatment within 48 hours of an aneurysmal SAH or by continuing a preexisting statin, the incidence of vasospasms and the subsequent mortality rates are reduced.
Mobilization. A recent study concluded that early mobilization of SAH patients was safe and feasible and could provide significant benefits to patients; at the end of the 30-day study period, none of the patients in the study had died and all showed clinical improvement (Olkowski et al., 2013). Another study indicated that patients involved in early mobilization programs that included group therapy and solo exercise techniques spent less time in their rooms and in their beds (van de Port et al., 2012).
Infusion of hemostatic or antifibrinolytic agents. Studies are ongoing, but the prothrombotic agents tested to date have not proven beneficial.
Nimodipine therapy. By an unclear mechanism, nimodipine (a calcium channel blocker) has been shown to significantly improve the outcome of patients with an acute SAH. The standard therapy is oral administration of nimodipine, 60 mg, every 4 hours, beginning within 96 hours of the stroke’s onset. When giving nimodipine, the patient must be monitored for hypotension. Contraindications to therapy include hypotension, a history of MI, and unstable angina. Adverse effects include hypotension, flushing and sweating, edema of the extremities, and gastrointestinal distress (Aburto-Murrieta et al., 2012; Choi et al., 2012).
Surgical and percutaneous obliteration of the aneurysm. The risk of rupture of an aneurysm and some of the secondary problems that arise because of blood in the subarachnoid space can be reduced by early obliteration of the aneurysm. Surgically, aneurysms are occluded with external clips, typically made of titanium. Percutaneously, some aneurysms can be occluded by injecting them with a platinum coil; the coil then becomes coated with thrombus, which fills (and obliterates) the space in the aneurysmal sac (Dumont et al., 2010; Nguyen et al., 2010; Wess et al., 2010).
“[Current results suggest] that in the long run, clips and coils are equivalent therapies for the treatment of ruptured intracranial aneurysms. Each has strengths and weaknesses. Clipping is slightly more durable in terms of the risk of rebleeding, but even more importantly does not require the long-term serial angiography that most interventionists perform in patients they have coiled. The advantage to coils is that the procedure is less invasive and appears to be associated with less short-term procedural morbidity” (Mayer & Schwab, 2010).
Neurons retain a degree of plasticity, or physiological adaptation. This may be especially important in rehabilitation medicine as well as in the investigation of new treatment modalities (Hermann & Chopp, 2012; Ma et al., 2012; Nudo, 2011; Vogel, 2012; Wolpaw, 2012). To heal, injured brain cells must reestablish their transmembrane ionic gradients, repair torn membranes, and reassemble disrupted cytoskeletal elements. For neuronal plasticity to come to full fruition, cells need energy and oxygen (Johansson, 2011). Recovering cells also need their environments to be continuously washed of wastes, toxins, and other disruptive molecules.
Blood perfusion can deliver the required oxygen, nutrients, and extracellular detoxification that damaged brain cells need to repair themselves. Strokes, however, not only injure brain cells, they reduce or stop the blood supply to the injured tissue. Therefore, until fresh blood flow is reestablished, many brain cells cannot heal after a stroke; instead, the cells degenerate and die.
Even with reperfusion therapies, there is a delay in getting fresh arterial blood to injured brain cells. Neuroprotective techniques are attempts to slow the degeneration of injured brain cells until sufficient arterial perfusion can be reestablished. Still experimental, the neuroprotective agents include:
In addition to acute treatment for ischemic strokes and intracerebral and subarachnoid hemorrhages, efforts are necessary to prevent and manage specific complications that can arise in the ICU after the acute treatment phase. Besides neurological deterioration, non-neurological problems are frequent, and the stroke patient may face myocardial infarction, heart failure, aspiration pneumonia, and pulmonary embolism. Watchful monitoring and quick reaction to developing complications are the bases of effective acute care for stroke patients (Lukovits & Goddeau, 2011).
Within the first 24 hours of the onset of symptoms, many acute stroke patients will need intensive care in a unit staffed by ICU nurses who are also trained to recognize and manage intracranial complications.
Careful monitoring is the key to optimal stroke management. A significant number of stroke patients will deteriorate within the first 24 hours post-stroke (Lukovits & Goddeau, 2011). Because strokes also often leave victims in a medically unstable condition, acute stroke patients are monitored during their first 24 hours in an ICU with a nurse to patient ratio of 1:2. Even stroke patients with minor symptoms, but with no radiological evidence of a stroke, are typically monitored in a stroke ICU (or an ED observation unit) for 6, 12, or 23 hours, depending on the patient’s condition.
Stroke patients who may be eligible for fibrinolytic treatment are first channeled into the rtPA treatment protocol, while stroke patients with symptoms suggesting the need for neurosurgical intervention are first channeled into the neurosurgical evaluation protocol. However, the end station for both protocols is typically the stroke ICU.
Besides monitoring the patient’s neurological functioning, ICU care aims to keep the patient’s physiology stable and to prevent or treat additional medical complications. Meanwhile, during the ICU monitoring, the stroke team physicians work to establish the specific cause of the stroke and begin to plan a strategy to avoid reoccurrences.
Nurses take the lead in ICU care by writing a clinical pathway—a clinical plan or care map—for each patient. The clinical pathway is a specific care schedule. It is an individualized version of the ICU’s preexisting stroke protocol, and it lists a chronology of the tasks for physicians, nurses, rehabilitation specialists, and social workers.
Unlike the overall stroke protocol, a clinical pathway is an evolving document. It is shared with and modified by all members of the stroke team, and it is revised as the patient’s condition changes. The clinical pathway is the individualized plan that gives the timeline and steps needed for the effective care of a particular patient (Summers et al., 2009).
In their “Recommendations for Comprehensive Stroke Centers,” the Brain Attack Coalition offers these guidelines for staffing a stroke unit:
[H]igh-quality nursing care is a key factor in determining patient outcomes after a stroke. The majority of nurses caring for stroke patients in an ICU, stroke unit, or ward should be registered nurses. The nurses in a CSC should be familiar with standard neurologic assessments and scales, stroke protocols, care maps, ongoing research projects, and new patient-care techniques related to stroke. Nurses who care primarily for stroke patients should attend training sessions sponsored by the CSC (i.e., in-services, seminars, specialized lectures) three times per year. Such nurses should participate in 10 hours of continuing education units or other educational programs annually that are related to or focused on cerebrovascular disease. Each nurse should have a file that documents his/her participation in the above activities. It is suggested that each CSC nurse (stroke unit or ICU) attend one national or regional meeting every other year that focuses on some aspect of cerebrovascular disease.
An advanced practice nurse (APN) is a vital team member involved in several important aspects of a CSC, such as patient care, care maps, research activities, stroke registries, educational programs, and quality assurance. The designation of APN could include a nurse practitioner, master’s-prepared clinical nurse specialist, or American Board of Neuroscience Nurses–certified nurse. It is recommended that a CSC have one APN (or similar personnel) to implement and coordinate [care under the various stroke protocols] (Alberts et al., 2011).
The key to managing complications in the stroke ICU is recognizing them quickly. The deterioration in a patient’s neurological status is always a signal to search quickly for a complication.
Stroke ICU nurses are characterized by their experience in performing neurological function assessments. During the first 24 hours, acute stroke patients need a neurological assessment at least every 4 hours. Stroke assessments are usually made along with the check of vital signs (pulse, blood pressure, temperature, oxygen saturation, blood glucose, and respiratory pattern).
A sample checklist for a full assessment of neurological problems is provided below.
|A. MENTAL STATUS|
[ ] Not spontaneously, only to voice
[ ] Only to pain
[ ] Not at all
[ ] Agitated
[ ] Combative
[ ] Inappropriate
[ ] Restless
[ ] Doesn’t follow commands
[ ] Localizing to pain
[ ] Flexion to pain
[ ] Extension to pain
[ ] No response to pain
Has trach: [ ]
[ ] Inappropriate words
[ ] Sounds, not words
[ ] No speech
[ ] Slurred
[ ] Unintelligible
[ ] Expressive
[ ] Receptive
|Naming Objects: [ ] Inaccuracies|
|Orientation||Is Disoriented to:
[ ] Time
[ ] Place
[ ] Person
[ ] Short-term
[ ] Long-term
|B. CRANIAL NERVE DEFICITS|
|I||Odors: [ ] Cannot smell odors [ ] Not tested|
[ ] Decreased acuity
[ ] Field deficit
[ ] No vision
[ ] Decreased acuity
[ ] Field deficit
[ ] No vision
|III, IV, VI||EOM: Reports diplopia: [ ]|
|R eye does not move:
[ ] Down
[ ] Up
[ ] Out
[ ] In
[ ] Down+In
|L eye does not move:
[ ] Down
[ ] Up
[ ] Out
[ ] In
[ ] Down+In
Ptosis: [ ] R [ ] L Nystagmus: [ ] R [ ] L
[ ] Sluggish
[ ] Nonreactive
[ ] Nonreactive pinpoint
[ ] Nonreactive Dilated
[ ] No consensual reaction
[ ] Hippus
[ ] Right size > Left size
[ ] Sluggish
[ ] Nonreactive
[ ] Nonreactive pinpoint
[ ] Nonreactive Dilated
[ ] No consensual reaction
[ ] Hippus
[ ] Left size > Right size
|V||Touch sensation on face decreased: [ ] R [ ] L|
|For R face, pt reports:
[ ] Pain
[ ] Numbness
[ ] Tingling
|For L face, pt reports:
[ ] Pain
[ ] Numbness
[ ] Tingling
|Lack of corneal reflex on:|
[ ] Ipsilaterally
[ ] Via consensual pathway
[ ] Ipsilaterally
[ ] Via consensual pathway
|Chewing: [ ] Impaired [ ] Cannot chew|
|VII||Weak eye closure: [ ] R [ ] L|
|Facial droop: [ ] R [ ] L|
|VIII||Hearing impairment: [ ] R [ ] L|
|IX/X||Swallowing: [ ] Impaired|
|Gag reflex: [ ] Reduced|
|XI||Weak shoulder shrug: [ ] R [ ] L|
|XII||Tongue deviates to: [ ] R [ ] L|
(upper limbs, lower limbs)
[ ] RU [ ] LU [ ] RL [ ] LL
|Decreased discrimination of sharp from dull:
[ ] RU [ ] LU [ ] RL [ ] LL
|Decreased position sense:
[ ] RU [ ] LU [ ] RL [ ] LL
|Pt reports numbness:
[ ] RU [ ] LU [ ] RL [ ] LL
|Pt reports tingling:
[ ] RU [ ] LU [ ] RL [ ] LL
3=weak against gravity
2=weak even without gravity
|RU||[ ] 5 [ ] 4 [ ] 3 [ ] 2 [ ] 1 [ ] 0|
|LU||[ ] 5 [ ] 4 [ ] 3 [ ] 2 [ ] 1 [ ] 0|
|RL||[ ] 5 [ ] 4 [ ] 3 [ ] 2 [ ] 1 [ ] 0|
|LL||[ ] 5 [ ] 4 [ ] 3 [ ] 2 [ ] 1 [ ] 0|
|Drift:||[ ] RU [ ] LU|
|Specific Weakness:||Hand grasp:
[ ] R
[ ] L
Upper arm push: [ ] R [ ] L
Upper arm pull: [ ] R [ ] L
Foot dorsiflex: [ ] R [ ] L
Foot plantarflex: [ ] R [ ] L
|Coordination:||Impaired fine motor coordination:
[ ] R hand
[ ] L hand
Impaired rapid alternating movements: [ ] R hand [ ] L hand
Ataxia: [ ] RU [ ] LU [ ] RL [ ] LL
Gait: [ ] Impaired [ ] Not tested
[ ] RU
[ ] LU
[ ] RL
[ ] LL
Abnormal movements: [ ] RU [ ] LU [ ] RL [ ] LL
When first admitting an acute-care stroke patient to the ICU, the nurse conducts a full neurological assessment and determines the patient’s baseline NIHSS and Glasgow Coma Scale scores (see “Neurological Assessments” above). Thereafter, stroke protocols often recommend only a brief neurological examination unless some neurological deterioration is detected. Deterioration of neurological functioning has been defined as an increase of one point on the NIHSS (Saposnik et al., 2013).
A stroke ICU has plans in place for the most common medical complications. Members of the ICU staff will always have different levels of expertise, but written protocols and standardized stroke orders ensure that the best care can always be given without delay and with few mistakes.
The best care practices for stroke are evolving quickly, and ICU protocols should evolve, too. The stroke response team and the stroke ICU staff should regularly review their protocols and standing orders. Stroke care is complex, and frontline stroke ICUs are always learning and improving.
Intracranial problems are the most common causes of neurological deterioration after an acute stroke. Brain edema, additional ischemia, and bleeding are the main culprits: more than 33% of the deteriorations are caused by swelling of ischemic brain tissue, while approximately 20% of deteriorations are caused by an additional occurrence of cerebral ischemia or by new or continued intracerebral hemorrhaging. Seizures are an additional, although less common, intracranial cause of neurological deterioration (Magauran & Nitka, 2012; Westover et al., 2013).
Injured brain tissue swells from edema, and sufficient swelling will push the brain against the skull or nondispensable edges of the dura. In these situations, the brainstem is often squeezed, and the patient will show signs of cerebral herniation. Cerebral herniation should be suspected when new neurological signs include both cranial nerve problems (especially loss or reduction of pupillary responses) and peripheral motor deficits. Brain herniation is a life-threatening emergency.
Unfortunately, the clinical signs of herniation or of increased intracranial pressure are clearest late in the process (Merenda & DeGeorgia, 2010), and early stages of brain swelling cannot easily be recognized clinically in acute stroke patients, although serial head images can give suggestive clues. Therefore, protection against herniation and the other serious consequences of brain swelling depends on the stroke team already being on the alert for the possibility of edema.
Edema is an occasional consequence of any ischemic stroke, but brain edema is most likely when ischemic strokes involve occlusions of the MCA or multilobar and cerebellar infarcts. Excluding patients with cerebellar infarction, serious episodes of brain edema typically occur 3 to 5 days after an acute ischemic stroke rather than in the first 24 hours (Lutsep, 2013).
Besides these particular ischemic strokes, other factors that put a patient on the watch list for serious brain swelling include:
Source: Cruz-Flores et al., 2012; Lutsep, 2013.
If brain edema is suspected, steps to reduce the swelling include:
Hydrocephalus or posterior fossa swelling is treated with suboccipital craniotomy, and for any significant brain edema, a craniotomy can be done and necrotic tissue removed. Mannitol has been used for temporary reduction of brain swelling until surgery can be performed. In addition, hypothermia (to 33 °C to 34 °C) is sometimes tried. Nonetheless, even with timely therapy, significant brain swelling has a high mortality rate (Cruz-Flores et al., 2012).
In adults, normal intracranial pressure (ICP) is ≤15 mm Hg. Neurological problems will develop if the intracranial pressure increases to ≥20 mm Hg.
Both ischemic and hemorrhagic strokes sometimes increase intracranial pressure indirectly as a result of brain edema. Hemorrhagic strokes can also increase intracranial pressure directly by adding extravascular blood to the restricted intracranial space.
During a stroke, an increase in intracranial pressure further reduces cerebral perfusion, which can cause global neurological dysfunction and additional ischemia. Increased intracranial pressure can also cause lethal brainstem compression.
Clinically, elevated ICP presents as headache, vomiting, and a decreased level of consciousness. Papilledema can be seen in a funduscopic exam, and sometimes there is periorbital bruising. The appearance of Cushing’s triad—bradycardia, respiratory depression, and hypertension—is an especially ominous sign.
To keep increasing ICP from becoming life threatening, it should be monitored using direct intracranial measurements; typically, direct measurement is via an intraventricular catheter (a ventriculostomy) (Smith & Amin-Hanjani, 2009). Minimally, ICP measurements should be monitored in stroke patients who have coma (i.e., a Glasgow Coma Scale value of 3–8).
Treatments for increased ICP include positioning the head of the bed at a 20- to 30-degree angle, controlling pain (e.g., with morphine or alfentanil), aggressively treating fever with acetaminophen and mechanical cooling, and avoiding techniques and situations that increase intrathoracic pressure. (Moving some stroke patients to an upright posture will worsen their neurological status, so position changes must be done cautiously.)
Other measures to lower ICP include reducing the extravascular fluid volume with intravenous mannitol, inducing respiratory alkalosis with forced hyperventilation, sedation (e.g., barbiturates or propofol), avoiding hypotension, directly draining some CSF, or performing a craniotomy to mechanically decompress the intracranial space (Eide et al., 2011; Koennecke et al., 2011; Owens, 2011). Hydrocephalus, which is often seen after subarachnoid hemorrhage, can be relieved by a shunt or ventricular drain (Eide et al., 2011).
Another cause of deteriorating neurological functioning in the stroke ICU is additional intracerebral bleeding. This problem can be recognized using brain imaging, usually by CT scan.
After a stroke, seizure activity has been seen in as many as 25% of all patients, although some studies have reported seizures in as few as 3% of stroke patients. Most seizures are partial or nonconvulsive. In the ICU, seizures are usually treated with an IV antiepileptic (Magauran & Nitka, 2012; Westover et al., 2013).
An acute stroke patient commonly has periods of abnormal breathing, especially when the patient has decreased consciousness or a large or serious stroke. Tachypneic (fast breathing) patterns can be a problem if it lowers blood levels of carbon dioxide (CO2), thereby reducing cerebral perfusion. Other more common abnormal respiratory patterns, however, do not signal impending neurological deterioration. Nonetheless, any change in respiration should alert the nurses to check airway patency, vital signs, and neurological functioning (Cruz-Flores et al., 2012).
The most common abnormal breathing pattern in ICU stroke patients is periodic breathing.
Self-regulated breathing can be a problem for stroke victims, especially patients with hemorrhagic stroke or damage to the brainstem. Patients with breathing dysfunction usually have impaired consciousness or impaired airway reflexes, and an endotracheal tube is inserted if the patient’s protective airway mechanisms have been compromised.
Patients who develop aspiration pneumonia, pulmonary edema, stupor with reduced respiratory reflexes, or seizures are likely to require mechanical ventilation. The need for endotracheal intubation is a poor sign—approximately 50% of the acute stroke patients who are intubated will die within 30 days.
It can be difficult to wean stroke patients after extended periods of mechanical ventilation. Daily trials of autonomous breathing are recommended to exercise the respiratory muscles and to slow the inevitable muscular atrophy from disuse (Mayer & Schwab, 2010).
Ischemia from poor oxygenation of brain tissue is a major cause of the neurological deficits of a stroke, and longer periods of oxygen deprivation produce more extensive and irreversible damage. Therefore, to save brain tissue, it is critical to maintain normal blood oxygen saturation. Currently, there is no evidence that either supplemental or hyperbaric oxygen is helpful for stroke patients who already have normal blood oxygen saturation levels.
In the ICU, oxygen saturation is monitored continuously. Hypoxemia ≤92% is treated with supplemental oxygen at 2–4 L/min. Continuous pulse oximetry is required, because patients can be hypoxemic without showing clinical symptoms (Lukovits & Goddeau, 2011).
The appearance of hypoxemia should also alert the nurse to check:
If hypoxemia persists on supplemental oxygen, then blood gases and a chest film should be obtained.
Strokes and heart problems are frequent companions. Hypertension and atherosclerosis are shared precursors of a range of cardiovascular diseases, including stroke; thus, stroke patients often present with existing cardiac problems. Strokes can also be the cause of such heart problems as arrhythmias and myocardial infarctions. In a stroke patient, one must actively search for these problems, because myocardial infarctions concurrent with a stroke are often silent. Therefore, the initial evaluation of acute stroke patients includes a cardiac exam, an ECG, and blood tests for cardiac markers. Later, in the ICU, acute stroke patients need continuous cardiac monitoring (Feng et al., 2010; Grise & Adeoye, 2012; Lukovits & Goddeau, 2011).
Ninety percent of acute stroke patients have ECG abnormalities, 60% to 70% of acute stroke patients have significant cardiac disturbances, and 20% of all stroke victims will have a myocardial infarction within 10 years. By itself, having a stroke gives a patient the same risk for developing an arrhythmia or an acute coronary syndrome as having an established diagnosis of coronary artery disease (Jauch et al., 2013; Mink & Miller, 2011).
Seventy-three percent of stroke patients have a history of hypertension, and hypertension is the single most common risk factor for stroke. Thus, patients with acute stroke often present with high blood pressure; between 40% and 80% of acute ischemic stroke patients have hypertension in the first 24 hours. Significant hypertension makes a poor outcome likely after an acute stroke, and ICU stroke patients must have their blood pressures monitored frequently (Cha, 2012; Einhorn et al., 2010).
Ideally, ischemic stroke patients will have their blood pressures maintained at a systolic pressure of about 180 mm Hg and a diastolic pressure of 105–110 mm Hg during the first 24 hours. Higher blood pressures are treated cautiously. The temptation to immediately reduce high blood pressure should be tempered by two observations:
It has been suggested that markedly high blood pressures (>220 mm Hg systolic pressure or >110–120 mm Hg diastolic pressure) be lowered, but the reduction should be made gradually. A recommended course of action is to reduce hypertension only about 15% during the first 24 hours after an ischemic stroke.
Patients with intracerebral hemorrhages are usually treated for hypertension more aggressively than patients with ischemic strokes in an attempt to decrease the blood pressure’s contribution to increased intracranial pressure. As with ischemic strokes, the goal is to maintain the patient’s blood pressure <180/105 mm Hg during the first 24 hours after an ICH.
Before using antihypertensive drugs to treat a patient’s high blood pressure, nurses should consider remedying other factors that may be elevating the blood pressure. Pain, nausea, a full bladder, or a loud environment can all raise a patient’s blood pressure. Intracranial problems, such as increased bleeding, can also raise blood pressure.
When using antihypertensive drugs, labetalol (Trandate) is commonly used when there is also tachycardia, while nicardipine (Cardene), a purely peripheral vasodilator, is used when there is bradycardia, congestive heart failure, a history of bronchospasm, or COPD (Einhorn et al., 2010; Grise & Adeoye, 2012; Owens, 2011).
After the first 48 hours, one serious complication of stroke is pulmonary embolus, which is responsible for 10% of stroke deaths. Pulmonary emboli are typically generated in lower limb or deep pelvic veins, especially in elderly patients who have been paralyzed or otherwise immobilized. Prevention of deep vein thrombosis begins in the ICU, with early patient mobilization, external compression devices, and anticoagulants (at a safe time). Comprehensive prophylaxis against deep vein thrombolysis is considered a critical component of care in the ICU of an accredited stroke center (Chaudhry et al., 2013; Lederle et al., 2011; Yeguiayan et al., 2011).
Other complications that occur frequently in ICU stroke patients include fevers, hyperglycemia, dysphagia, and infections.
Fevers give stroke patients a poorer neurological outcome, even doubling the risk of death (Prasad, 2010). Even a 1 °C rise in temperature increases patient mortality rates, so fevers are aggressively treated with antipyretic drugs. Fever can be directly caused by a stroke, but stroke patients with a fever are also examined for infections—especially, for pneumonia and urinary tract infection (Middleton et al., 2011; Phipps et al., 2011; Prasad & Krishnan, 2010).
To treat a fever, acetaminophen (Tylenol) is begun when the patient’s temperature reaches 37.5 °C (99.6 °F). Faster temperature reduction can be achieved by the use of cooling systems such as circulating cold-water blankets and cold air-forced blankets (Prasad & Krishnan, 2010).
Both hyperglycemia and hypoglycemia are associated with increased brain injury after an acute stroke.
Approximately one third of patients who present with acute stroke have hyperglycemia (i.e., blood glucose >126 mg/dL) (Staszewski et al., 2011). Hyperglycemia of >140 mg/dL increases the likelihood of a poor outcome in stroke patients, and carefully administered, rapid-acting insulin is recommended to reduce levels of blood glucose that are >180 mg/dL.
Hypoglycemia is also deleterious to an injured brain. Thus, the effects of insulin administration are closely monitored, and glucose and potassium must be available to buffer the effect of the insulin. In general, it appears that a safe target goal for blood glucose in critically ill neurological patients is between 120 and 180 mg/dL (Mayer & Schwab, 2010).
For patients who have received rtPA, their blood glucose level is checked every 1–2 hours. For other patients, blood glucose levels are checked every 6 hours (Laird & Coates, 2013; Laird et al., 2013; Staszewski et al., 2011).
Within the first three days, between 42% and 67% of acute stroke patients have dysphagia (i.e., difficulty swallowing), and dysphagia can lead to aspiration pneumonia. Swallowing difficulties can be outwardly unapparent; therefore, acute stroke patients are NPO (including no water, no ice chips, and no oral medications) until their swallowing ability has been formally evaluated. Formal evaluation is done by a speech language pathologist or a specially trained nurse using a proven assessment protocol such as the Acute Stroke Dysphagia Screen (Edmiaston et al., 2010).
After a patient has been cleared to begin oral intake, a nurse should watch for signs of swallowing difficulty—choking; coughing; a wet voice after liquids; slow or labored eating, drinking, or swallowing; or discoordinated mouth and tongue movements while eating or drinking. People are more likely to aspirate liquids than semi-solid, textured foods with the consistency of pudding, so oral intake should probably begin with semi-solids. Patients must be alert and fully awake when eating or drinking (Crary et al., 2013; Edmiaston et al., 2010; Hughes, 2011).
Acupuncture has shown promise in treating post-stroke dysphagia (Long & Wu, 2012). In one Chinese study, both traditional acupucture and electroacupuncture, using traditional points and three-needles on the forehead, have shown equivalent efficacy to each other and were more effective than rehabilitative techniques alone (Huang et al., 2010).
In the ICU, a stroke patient is at risk for infection because many levels of natural defenses have been compromised. Protective skin has been punctured with needles; protective mucosal tubes, such as urethras, have been scraped and then bypassed with catheters; and protective airway reflexes have been subdued by medicines or by the stroke itself. Reduced protective mechanisms make aspiration pneumonia and urinary tract infections the two most common infections acquired by ICU stroke patients.
Aspiration pneumonia. New fever and decreasing level of consciousness are signs that a nurse must be vigilant for in an ICU stroke patient. One out of 5 acute stroke patients develops pneumonia. If the patient has a nasogastric feeding tube, there is a 44% chance that they will develop pneumonia. Most of these pneumonias are aspiration pneumonia, meaning that they have developed from microbes aspirated from the mouth and throat. Dysphagia and reduced airway protection reflexes, due directly to the stroke or due to a reduced level of consciousness, are common precursors to aspiration pneumonia (Finlayson et al., 2011; Hoffmann et al., 2012; Wilson, 2012). A 10-point clinical scoring has been developed to facilitate predicting those at risk for pneumonia. Scores are assigned for the risk factors, including the presence of atrial fibrillation, dysphagia, male gender, and the NIHSS stroke scale (Hoffmann et al., 2012).
Dysphagia testing and oral intake restrictions and cautions are important preventive measures. Nausea and vomiting should be treated quickly. When possible, ventilated patients are kept in a semi-recumbent position and their airways are suctioned. For acute stroke patients who will be in the ICU >3 days, a new intensive prophylactic protocol—topical oropharyngeal decontamination—appears to lead to a small but significant reduction in hospital-acquired pneumonias (Mayer & Schwab, 2010).
Urinary tract infections. UTIs are another common cause of fever in acute stroke patients. Therefore, a new fever or a change in the patient’s level of consciousness should also prompt a urine screen (Poisson et al., 2010).
In the United States, the average stroke patient’s hospital stay is almost 5 days. For ICU nurses, the first 24 hours of this stay are focused on stabilizing the patient’s physiology while closely monitoring for complications. Meanwhile, besides providing acute care, physicians use the first 24–48 hours to identify the cause of the stroke and to formulate a plan to correct the cause or to otherwise reduce the risk of additional strokes.
After the first 24 hours, the nursing staff can begin to shift away from acute care and begin to monitor for other patient management issues that may arise. These include:
After the first 24 hours, patient care takes on a less-acute care routine, and it is here and in post-stroke rehabilitative care that physical and occupational therapy can make an important difference in the patient’s quality of life, even in the first few days following a stroke. Acute care takes place over the course of days, but recovery and rehabilitation takes place over the course of months and years (Alkan et al., 2013; Bernocchi et al., 2012; Dean et al., 2012; Kaltenbach et al., 2013; Kerr, 2012; Nyström, 2013).
In the United States, the average hospital stay for an acute stroke patient was 4.9 days in 2006 (CDC, 2010b). From the hospital, 30% of stroke patients were discharged home with no planned home health care, 17% were discharged home with planned home health care, 20% were discharged to a rehabilitation center, and 33% were sent to a skilled nursing facility for long-term care (Kind et al., 2010).
The balance between hospital care and home rehabilitation or skilled nursing care is different in other countries. For instance, in Canada, acute stroke patients stay in the hospital an average of 15 days when they are being cared for in a dedicated stroke unit. Canadian patients with subarachnoid hemorrhage usually stay in the hospital even longer so that they can be monitored for vasospasms, which are most common in the first 21 days after the stroke (Liu et al., 2012; Muroi et al., 2012).
Nurses are the key players in organizing a patient’s discharge from the hospital. Nurses are with the patient throughout the day, and they have seen the full range of the patient’s limitations and dependencies. While a patient is still in the hospital, nurses on the stroke team initiate the patient’s transition into the appropriate supervised rehabilitation programs. As the time of discharge approaches, nurses arrange to have a patient’s limitations assessed formally by specialists—including physical therapists, occupational therapists, speech-language pathologists, psychologists, and nutritionists. These professionals then make recommendations that can be taken into account before physicians have begun discharging the patient.
Nurses are also the family educators. Nurses explain the pathology of the patient’s particular stroke, they describe practical problems that the patient will face, and they outline the methods for preventing a recurrence of the stroke. A nurse will demonstrate how to manage continuing healthcare problems, such as changing dressings and applying topical medicines. A nurse will give advice to caregivers and family about communicating with a patient who is aphasic or who has significant motor or sensory deficits. A nurse should also check to see that follow-up visits with a physician are scheduled and that the family and patient are aware of these appointments.
In their discussions with the patient and family, a nurse should explain that almost three quarters of stroke survivors will eventually need their family’s assistance at home and that the practicalities and costs of that home help should be thought through in advance. Finally, a nurse should make sure that a social worker or community liaison provides referrals to government and nonprofit help agencies, support groups, and other helpful community resources (Kaltenbach et al., 2013; Kerr, 2012).
Discharge from the hospital is the beginning of what is often an arduous process. After a stroke, patients can be limited in their ability to interact with the world or in their ability to independently carry out their wishes. For example, they may be unable to speak clearly, or they may be unable to move one of their limbs. Recovering some of these lost skills through physical rehabilitation is one of the two primary goals of post-hospital recovery.
There is a great deal of variability in how fast and to what extent people recover after a stroke. There are, however, some general timelines of recovery. After a stroke, patients reach their maximum ability to perform activities of daily living more slowly when their stroke has left them severely disabled. Mildly disabled stroke patients tend to reach their best level of functioning two and a half months after the stroke. Moderately disabled stroke patients reach their peak in about three months. However, severely disabled stroke patients may still be improving five months after the stroke (Sugavanam et al., 2013).
It is important to remember the vital role that physical and occupational therapy professionals play in the recovery of stroke patients. As has been discussed, early mobilization and the return to activities of daily living (ADLs) as soon as possible are critical to maximize the recovery of stroke patients. Social interactions should also be encouraged—the first social interactions will, in fact, likely be with the physical therapist, occupational therapist, and/or speech-language pathologist. New approaches, including the use of robotics, computer-assisted learning, and social media approaches, are expanding the ability of PTs and OTs to better aid their clients on the path to recovery (Ayache et al., 2012).
Primary goals for occupational therapists working with post-stroke patients, whether in the acute phase, the rehabilitative phase, or the stage of continuing adjustment include:
Patients take longer to recover from more disabling strokes, and their progress is slow. Because some skills return very slowly while other abilities are never regained, post-stroke physical rehabilitation tries to help patients get on with their lives by learning substitute skills as well as by working on regaining lost skills.
As they rehabilitate their minds and bodies and learn new adaptations, patients are medically vulnerable. One fifth of the men and one quarter of the women who have had their first stroke will die within the year, and one quarter of stroke survivors will have another stroke within five years (Hassan et al., 2012). Therefore, after discharge from the hospital, patients need to embrace lifestyle and medical regimens that reduce the risk of further strokes. Prevention of additional strokes through medical rehabilitation is the second of the two goals of post-hospital recovery.
After a stroke, the patient’s health is unstable, and they are at risk for cardiovascular problems and for additional strokes. Medically, the post-hospital goals for a stroke patient are to avoid or to quickly deal with medical complications and to prevent the recurrence of strokes and TIAs. Plans to safeguard a patient’s health can be called medical rehabilitation.
As the stroke team hands a stroke patient over to a medical rehabilitation program, the patient, family, and caregivers need to be informed, educated, and kept informed. After the hospitalization is finished, these individuals will be making the day-to-day healthcare decisions for the patient, and these decisions need to be based on accurate, realistic information. For example, post-stroke patients should understand the following:
Patient education will already have begun: during a patient’s hospitalization, the stroke nurses explain the causes for the patient’s symptoms and the reasoning behind the treatments (Kerr, 2012).
The sudden influx of medical information at discharge can be overwhelming. Therefore, patients and families should be given instructions and guidelines in the form of printed materials that can be reviewed at home as long as patient can cognitively comprehend the instructions. If not, a SLP may be able to assist. Nurses should also include a list of medically accurate stroke websites; the “Resources” section at the end of the course provides some suggestions.
A number of medical conditions need to be addressed in a medical rehabilitation program. For example, patients with atherosclerotic ischemic strokes are assumed to have underlying prothrombotic conditions. For ischemic strokes not due to emboli originating in the heart, daily aspirin, aspirin plus dipyridamole (Persantine), or aspirin plus clopidogrel (Plavix) are usually prescribed (Bergman, 2011; Jauch et al., 2013). For cardioembolic ischemic strokes (e.g., from atrial fibrillation), warfarin (Coumadin) is the more effective antithrombotic medication (Bergman, 2011; Jauch et al., 2013). (Without a specific medical reason, aspirin must not be added to warfarin therapy.)
New evidence suggests that, in the future, strokes from atrial fibrillation may be more safely prevented by different antithrombotic drugs, such as vitamin K-antagonists or dabigatran (Pradaxa), or by new techniques for suppressing the arrhythmia (McArthur & Lees, 2010).
High blood pressure puts a stroke victim at risk for additional strokes; therefore, reducing hypertension is a generally accepted post-stroke goal. One common guideline suggests gradually reducing the blood pressure of a post-stroke patient over several months, with an end goal of <130/80 mm Hg. A diuretic or a diuretic plus an ACE inhibitor are usually the recommended medications. This blood pressure goal comes with caveats:
Diabetes doubles a person’s risk for having an ischemic stroke. Maintaining good glycemic control, with A1C levels <7%, will reduce the microvascular (e.g., retinal and kidney) complications of diabetes. By itself, good glycemic control has not been shown to have a large effect on reducing a diabetic patient’s risk for stroke; nonetheless, good glycemic control is recommended for all diabetic stroke patients.
Overweight patients also have an increased risk of stroke. “As with glycemic control, there are no data to confirm that weight reduction will reduce the risk of recurrent stroke. However, weight reduction is potentially beneficial for improved control of other important parameters, including blood pressure, blood glucose, and serum lipid levels” (Bergman, 2011). The recommendation is that patients maintain a body mass index (BMI) between 18.5 and 24.9 kg/m2 and a waist circumference of <102 cm (40 inches) for men and <88 cm (35 inches) for women.
For both diabetes and excess body weight, lifestyle changes (e.g., improved diet and increased exercise) are key parts of the medical rehabilitation program.
Dyslipidemia is abnormal amounts of lipids and lipoproteins in the blood. High levels of low-density lipoprotein (LDL) cholesterol, low levels of high-density lipoprotein (HDL) cholesterol, and a high ratio of total cholesterol to HDL cholesterol each put a person at risk for developing atherosclerosis of the carotid artery. Evidence is unclear, however, as to whether there is a direct relationship between specific dyslipidemias and stroke risk.
Nonetheless, drug therapy with statins does reduce a person’s risk of having an ischemic stroke. This effect is thought to be mainly a function of a statin’s antiatherothrombotic actions rather than its cholesterol-lowering actions. Current recommendations include:
Clinical depression is common after stroke; in fact, it has been estimated that as many as 40% of patients with stroke suffer treatable depression (Schneider & Schneider, 2012). Patients at high risk for clinical depression or anxiety can be identified within the first two weeks after a stroke with the brief and easy-to-use Hospital Anxiety and Depression Scale (Sagen et al., 2010). Other brief depression assessment tools have also proven useful (Flaster et al., 2013; Lincoln et al., 2013; Rashid et al., 2013; Schneider & Schneider, 2012). Post-stroke depression is usually treated with selective serotonin reuptake inhibitors, such as fluoxetine (Prozac), paroxetine (Paxil), or sertraline (Zoloft).
It is also important for all rehabilitation specialists to remain aware that a poorly understood but common after-effect of a stroke is the loss of friends and social interactions by the patient. Understanding that this may be happening can be important in the approaches therapists take during the rehabilitation process (Northcott & Hilari, 2011).
After a stroke, it is not unusual for patients to develop other medical problems. The following table shows some of these problems and the medications used to treat them.
|Source: Stein, 2008.|
|Bladder instability||Anticholinergics (e.g., oxybutynin or tolterodine)|
|Erectile dysfunction||Phosphodiesterase type 5 inhibitors (sildenafil, vardenafil)|
|Impaired mental arousal||Stimulants (dextroamphetamine, methylphenidate)|
|Muscle spasticity||Antispasmodics (e.g., baclofen, dantrolene, diazepam, tizanidine)|
|Pain syndromes||Anticonvulsants (carbamazepine, gabapentine)|
|Seizure disorders||Anticonvulsants (carbamazepine, gabapentine)|
Certain stroke patients may benefit from additional medical procedures. Carotid endarterectomy is often recommended for ischemic stroke patients with ipsilateral carotid artery stenosis >70%. Endarterectomy is also appropriate in some patients with ipsilateral stenosis between 50% and 70%. Carotid stenting is used as an alternative to endarterectomy in some medical centers (Simmons et al., 2012; Tanaskovic et al., 2011).
Patients who had a subarachnoid hemorrhage and subsequent aneurysm clipping or coil placement have a risk of recurrent bleeding. The most vulnerable patients are those who are elderly, who smoke, who are hypertensive, or who had large or multiple aneurysms. For SAH patients who were treated surgically or endovascularly, it is suggested that the status of their obliterated aneurysm be checked with imaging at three and six months after the procedure (Tanaskovic et al., 2011).
Residual movement problems, such as joint contractures, subluxations, or gait deviations, can sometimes be improved surgically, although aggressive physical therapy is usually the most successful way to regain normalized motor control. Typically, significant spontaneous recovery of motor abilities occurs in the first 6–8 weeks, and physical rehabilitation can continue the progress. By 6–9 months post-stroke, most patients have reached the peak of their recovery. Any surgical intervention is usually held until >6 months after the stroke, at which time a realistic picture of the patient’s permanent limitations becomes clearer.
Medical rehabilitation is most effective when patients make therapeutic changes in their daily lives. Smokers should quit, heavy people should lose weight, sedentary people should exercise, and high-fat, high-calorie diets should be replaced with low-fat, high-fiber diets. Each of these lifestyle modifications can slow the progression of atherosclerosis and help to maintain lower blood pressures.
These principles—stop smoking, eat a healthy diet, exercise, and maintain an optimal weight—will be familiar to most patients. It is the job of the medical rehabilitation team to work with the patient to give specificity to these familiar general statements. The medical team needs to offer practical advice that the patient can follow and that the patient believes is worth following.
Therapeutic lifestyle changes begin with smoking cessation. Carbon monoxide and other poisons in cigarette smoke damage cells throughout the body, and cigarette smoking increases the risk of all forms of stroke: the more a person smokes, the higher the risk. Therefore, stroke patients who smoke are strongly urged to stop smoking (Furie et al., 2009).
Many people find it difficult to stop smoking. A nurse or other member of the stroke team can begin by telling a patient that continued smoking increases their risk of recurrent stroke, serious heart problems, and death, while stopping smoking reduces these risks.
The nurse then asks patients who smoke if they have thought about quitting. Whatever the answer, the nurse follows with the offer, “When you would like to stop smoking, I’ll be happy to work with you to set up as effective a program as I can.”
Health counselors are encouraged to use the five As with their patients who smoke:
The American Heart Association has collected evidence demonstrating that a low-fat diet with 12 g to 33 g per day of fiber from whole foods or up to 42.5 g per day from supplements can help to reduce blood pressure, correct dyslipidemia, reduce indicators of chronic inflammation, reduce weight, and reduce the risk of coronary artery disease (Goldstein et al., 2011; Medeiros et al., 2012).
Dietary changes can reduce the risk of stroke by up to 80%. The most important food groups to include are fruits, vegetables, and soy, which clearly demonstrated a protective effect. The Dietary Approaches to Stop Hypertension (DASH) and Mediterranean diets were found to be protective as well. Low-fat diets were not found to be significantly protective if fruits and vegetables were not also included (Sherzai, 2012).
Avoiding processed, pre-cooked or prepared foods has the effect of limiting added fats and sugars. In general, a 75% plant-based diet has been recommended based on the DASH and Mediterranean diet proportions.
Source: AHA, 2011.
Dietary counseling programs can help to maintain long-term improvements in a patient’s eating habits. A dietary counseling program begins with the dietician seeing the patient (and family or caregiver, when appropriate). The dietician takes a dietary history and measures the patient’s height, weight, and waist circumference. Patients are then given diaries in which to record their complete food and drink intake for five days.
Patients mail or email their diaries to the dietician, and at the next visit, the dietician suggests specific ways that the patient can improve what and how they eat. Regular follow-up visits continue. At each visit, the patient’s height, weight, and waist circumference are measured; the patient’s progress is charted; and specific dietary recommendations are suggested. The diet rehabilitation program should continue until the patient has found a stable, healthy eating routine.
Overweight ischemic stroke patients should be encouraged to lose weight. The recommended goal is to maintain a body mass index (BMI) between 18.5 and 24.9 kg/m2 and a waist circumference for men <102 cm (40 in) and for women <88 cm (35 in).
|Measurement Units||Formula and Calculation|
|Kilograms and meters
|Formula: weight (kg) / [height (m)]2
With the metric system, the formula for BMI is weight in kilograms divided by height in meters squared. Since height is commonly measured in centimeters, divide height in centimeters by 100 to obtain height in meters.
Example: Weight = 68 kg, Height = 165 cm (1.65 m)
Calculation: 68 ÷ (1.65)2 = 24.98
|Pounds and inches||Formula: weight (lbs) / [height (in)]2 x 703
Calculate BMI by dividing weight in pounds (lbs) by height in inches (in) squared and multiplying by a conversion factor of 703.
Example: Weight = 150 lbs, Height = 5’5” (65")
Calculation: [150 ÷ (65)2] x 703 = 24.96
|* BMI is an indirect measure of body fat. The BMI of a normal person is 18.5 to 24.9 kg/m2. An overweight person has a BMI of 25 to 29.9 kg/m2. An obese person has a BMI of >30 kg/m2.|
There are no magic weight-loss diets. To lose weight, a person must always reduce their daily caloric intake. In the long run, low-carbohydrate diets (<130 g carbohydrates/day) seem to be about as effective and as safe as low-fat diets. However, without adding other features, such as increased exercise, to the weight-loss program, either variety of diet usually leads to only a modest weight loss. The American Dietetic Association recommends the USDA’s Dietary Guidelines for Americans (USDA, 2010).
The most effective way to lose weight and to maintain the lower weight is by participating in a comprehensive weight-loss program that combines low-calorie diets, behavior modification, and regular exercise. Physicians and nurses can encourage their patients in the difficult task of losing weight by checking a patient’s BMI and waist circumference at each follow-up visit.
Regular exercise helps to correct dyslipidemia. It also reduces insulin resistance, decreases platelet aggregation, aids weight loss, improves sleep, and gives people a sense of well-being. Regular physical exercise is recommended for ischemic stroke patients who are capable of it. A common recommendation is 30 minutes of moderate-intensity activity on at least three different days each week. (Brisk walking is an example of a moderate-intensity physical activity.) For patients who have residual neurological deficits after an ischemic stroke, a supervised therapeutic exercise program is usually recommended (Dean et al., 2012; MacKay-Lyons et al., 2013; Poslawsky et al., 2010).
Coordinating the various medical and lifestyle regimens that are needed to reduce the risk of another stroke can be a complex task. As an aid, medical rehabilitation can be more efficiently organized using a comprehensive disease management program that will ensure thorough medical care after a patient’s discharge (Furie et al., 2009).
One good example is the PROTECT program, which is designed for ischemic stroke patients. Developed at the UCLA Medical Center, this program begins its post-hospital care planning while the patient is still in the hospital. PROTECT uses only existing resources and personnel to create an individualized regimen of medications (antithrombotics, ACE-inhibitors, thiazide diuretics, and statins), exercise, diet, education, and regular check-ups that continue for a year.
The PROTECT program is designed to be easy to implement. Information and tools are available from the UCLA Stroke PROTECT Program website (strokeprotect.mednet.ucla.edu), including a preprinted admission order sheet, a medication algorithm, a patient tracking form, interdisciplinary sheets, patient information sheets (in English and Spanish), the draft of a letter to the primary care physician, and a discharge summary template (Alli et al., 2013; Stecker, 2010).
After a stroke, a patient may no longer be comfortable in or able to return to the environment and lifestyle that they were living before they became ill. Previously, they may have been entirely independent, able to use the bathroom, dress, eat, and travel without assistance. They could talk on the phone, write letters, and figure out their finances by themselves. Some or all of these tasks may now require assistance. Post-stroke rehabilitation programs ease a patient into a lifestyle that gives them optimal independence and protection within their capabilities.
Physical rehabilitation is needed because strokes commonly lead to functional limitations. Patients can be left with motor deficits, such as difficulty walking, speaking, or swallowing, and they can find themselves unable to perform the basic activities of daily living without assistance. Patients can also be left with sensory deficits, such as disturbances of vision or balance or a lack of perception of pain from injuries. Patients can lose cognitive abilities and become forgetful, inattentive, or unable to learn. Stroke patients can have reduced mobility and reduced ability to communicate, they may struggle with issues of incontinence or impaired sexuality, and their post-stroke lives can become narrowed, constricted, and asocial.
For a stroke patient older than 65 years, 6 months after a stroke:
Rehabilitation goals include:
Physical rehabilitation programs aim to reactivate and broaden a stroke patient’s quality of life. This includes restrengthening the patient’s weakened neuromuscular, sensory, and cognitive facilities and teaching the patient ways around those residual deficits that cannot be reversed. Overall, the goal is to optimize the patient’s quality of life and the enjoyment they may gain from living it. In this regard, especially, the role of post-stroke physical and occupational therapy, as well as speech-language pathology, is difficult to overstate.
Strokes frequently reduce a patient’s independence by leaving them unable to perform certain movements. For example, they may no longer be able to grasp things with a hand, maintain balance when standing, or walk without assistance.
Overall, 65% to 75% of stroke patients will recover sufficiently to be able to walk, although some will be dependent on braces, support, or other assistance. However, to become ambulatory, patients who have motor deficits need regular range-of-motion exercises throughout the 3- to 4-month period during which their nervous systems are actively recovering. Standing and walking should be practiced as soon as possible. In some cases, electrical stimulation of muscles can help to retain muscle strength and to keep joints fully moveable (Doucet & Seale, 2012; Jonasson et al., 2012; Seyed Mansour et al., 2012; West & Bernhardt, 2012). Proprioceptive neuromuscular facilitation (PNF), which emphasizes stretching techniques to improve and enhance both active and passive range of motion, may be utilized with post-stroke patients as well, based on their individual needs and abilities (Seo et al., 2012).
When compared to the proportion of patients who recover their ability to walk unassisted, fewer patients recover satisfactory function in an upper extremity that has been disabled by a stroke. As many as one third of stroke patients who have significant dysfunction in their upper limb will not improve significantly and will always have a functionless limb (Hermann & Chopp, 2012; Tabak & Plummer-D’Amato, 2010; Shi et al., 2011).
The key to improving any of the lost motor functions is physical rehabilitation and occupational therapy. There is a wide range of specific physical rehabilitation programs, but they are all based on specifically directed movement and exercise. The most common therapeutic exercise programs focus on practical achievements, aiming to make stroke patients more mobile and more independent when performing their chosen normal activities of daily living (Alkan et al., 2013; Seyed Mansour et al., 2012; Vogel, 2012; Wolpaw, 2012).
Many training techniques have been developed for motor function improvement, but no one path to functional improvement has emerged as the standard for stroke rehabilitation (Kalra, 2010). There are, however, commonly agreed-upon principles. A recent comprehensive review found that all effective exercise techniques for reducing motor impairments and improving motor functioning share these four features:
Regardless of the particular muscles or skills to be improved, exercises designed to meet these four criteria appear to be the most effective (DeJong et al., 2011; Wolpaw, 2012).
Therapeutic exercise improves both muscle function and the lower motor neuron circuits specific to the therapeutic task. In addition, the most effective exercises work more centrally: effective physical therapy intervention appears to act as a guide for the cortical reorganization that is part of the brain’s innate recovery from a stroke.
Frontier research continues to discover details about the interactions between exercise and neural reorganization, and the new insights are being used to design novel physical therapy techniques, such as using virtual reality in exercise training (Parker et al., 2011). There are a number of virtual and computer-assisted programs that have met with significant success in allowing stroke patients to resume their chosen daily activities (Annicchiarico, 2012; Blobel et al., 2012; Cameirão, 2012; Ortner et al., 2012).
Contracting a single muscle will lead to a ballistic, uncontrolled movement. In order to achieve a smoother, more controlled movement, it is necessary to simultaneously activate antagonist muscle groups. After a stroke, the selective weakness or paralysis of muscles can impair normal agonist/antagonist activity. As a result, movements produced solely by the opposing muscles will often be poorly controlled.
In addition, limb synergies—the functional linkage of muscles during voluntary motor activities—can become disorganized after a stroke. Some studies have indicated that recognition of these functional linkages may be helpful in achieving greater recovery of mobility and range of motion (Pandian & Arya, 2012; Roh et al., 2013).
Selective bracing can help address specific gait deviation quality after a stroke that has affected the biomechanical functioning of a lower limb. Both hip and knee joint movements can be impaired in hemiplegia, but it is frequently imbalance and instability at the ankle joint that most limits gait quality. For instance, after a stroke, equinus deformity of the ankle is common, whereby either residual weakness of ankle dorsiflexor hypertonicity of plantarflexors leaves the foot excessively plantar-flexed. To counteract this deformity, the patient may benefit from lightweight ankle-foot orthoses (AFOs) in order to maintain the ankle joint in a neutral position during the gait cycle and significantly improve gait quality. When bracing intervention is not successful, surgical release of the gastrocnemius fascia can ease the plantar-flexion of an equinus deformity in cases of hypertonicity. Botulinum toxin and tibial nerve neurotomy have also been used with some success (Bollens et al., 2011; Carda et al., 2011).
Besides specialized bracing options, a wide array of technical aids is available to assist stroke patients in compensating for neuromuscular deficits. Gait and balance may be optimized with canes, walkers, or hemi-walkers, which may be modified to meet patients’ unique mobility needs. Hemi-wheelchairs, which are low to the ground, may allow patients to use their lower extremities for self-propulsion. For individuals with no functional use of their lower limbs, power wheelchairs and motorized scooters may be operated using hand, head, or mouth controls.
The engineering of assistive technologies is a creative and promising field. Research has shown that patients’ brains can directly interface with robotic devices to control upper and lower limbs for tasks such as walking and handling objects. The hope is that these devices will eventually become commercially available (Annicchiarico, 2012).
Besides causing motor deficits, strokes can leave a patient with impaired vision or with reductions in somatic or visceral sensation; it is estimated that 60% of stroke patients have sensory impairments. Glasses, hearing aids, and other assistive devices have long been used to compensate for such sensory deficits.
Recent work has taken stroke therapists in a new direction. There is now evidence that more complex sensory and cognitive problems caused by a stroke can be repaired by using compensatory therapies. This is especially important in improving executive functions, where occupational therapists can play a particularly vital role by using these compensatory strategies such as paging systems and various problem-solving strategies to maximize not only physical and mental recovery, but to affect emotional health and stability (Poulin et al., 2012).
For example, hemianopia (the loss of vision in one half of the visual field in one or both eyes) is now being treated directly with a range of new techniques. One technology uses prismatic lenses to project some of the lost visual world onto the functional part of the retina; this reduces the amount of visual space that is hidden by the hemianopia. Another technique widens the accessible visual space by training patients to increase their natural saccades (spontaneous small visual jumps made by the eye); wider saccades take in more of the visual space and increase the patient’s field of vision. In small studies, both of these new techniques appear to be effective (Kalra, 2010).
Cognitive abilities can also be impaired by strokes. Patients can have decreases in memory, attention, insight, or comprehension. Neuropsychological assessments done before a stroke patient is discharged can identify many of these problems and alert rehabilitation specialists to specific problems that need to be addressed. For example, classifying aphasia early allows patients to be enrolled in appropriate rehabilitation programs, many of which utilize specialized computer software for visual word manipulation or speech synthesis. In addition, speech language pathologists can provide a vital link, aiding both in cognitive function and recovery and in addressing specific swallowing dysfunctions that can respond to direct, speech-based techniques and interventions.
Cognitive evaluations are especially useful when counseling patients’ families and caregivers. After a stroke, patients may not be the same bright and independent people that they once were; they may appear forgetful, depressed, irrational, or aphasic. The family can be overwhelmed by the changes and unable to sort out the true deficits from the secondary effects of those deficits.
Rehabilitation specialists can help by being both realistic and constructive. To optimize improvements in a patient’s cognitive abilities, rehabilitation programs work specifically at the level at which the patient is currently functioning. Therefore, rehabilitation specialists, who can see the patient more objectively than close family or friends, must give families and caregivers a realistic yet compassionate evaluation of the patient and their capabilities. Additionally, the most effective rehabilitation will ideally include a heavy emphasis on training family and caregivers (including written instruction) in specific and practical tasks and actions that may be implemented on a long-term basis in order to optimize patient progress (DeJong et al., 2011; Hayes et al., 2011; Hoffmann et al., 2010).
Strokes, also called cerebrovascular accidents (CVAs), result from limitations in cerebral perfusion, usually due to clots. Occasionally, the reductions in perfusion are accompanied by intracranial bleeding.
Approximately 6 million Americans have had a stroke, and about 800,000 people suffer a stroke each year. Strokes do not occur equally throughout the population. Strokes are usually a condition of the elderly; the most susceptible age group is in the 80- to 84-year-old range. More women than men die of stroke each year.
Most strokes result from blockages of an artery by a local blood clot or by an embolus from the heart, aorta, or carotid artery. These strokes are called ischemic, and they are typically the product of years of atherosclerosis and hypertension. About 10% of all strokes are quite different, having been caused by intracranial bleeds. These are called hemorrhagic strokes, and they result from a ruptured cerebral artery or aneurysm. Hypertension is typically involved in generating a hemorrhagic stroke.
Symptomatically, all strokes appear as acute impairments in brain functioning. Victims may suddenly have difficulty walking, seeing, speaking, or understanding. With severe hemorrhagic strokes, the victim may lose consciousness. A common presentation of a stroke is the sudden loss of sensation or movement on one side of the body or face. Most ischemic strokes are painless, although hemorrhagic strokes can produce severe headache.
An acute ischemic stroke is a medical emergency, much like a myocardial infarction; a brain attack needs fast, organized care just as does a heart attack. The acute treatments are also similar. Both strokes and myocardial infarctions can be caused by clots obstructing arteries, both can leave some tissue underperfused, and in both, underperfused tissue can sometimes be revived if local circulation can be reestablished within a critical time window.
Like the treatment for an acute myocardial infarction, treatment for an acute stroke is given high priority by EMS teams and emergency room personnel. For a stroke, there is a 4.5-hour interval after the onset of symptoms in which thrombolytic therapy (i.e., intravenous administration of rtPA) has a chance to reopen clogged cerebral arteries and save some of the underperfused brain tissue. Given this time constraint, EMS teams have the goal of getting potential stroke victims stabilized, evaluated, and to a primary stroke center in less than an hour.
The early recognition and diagnosis of a stroke is facilitated by using standardized tests, such as the Cincinnati Prehospital Stroke Scale, which can be administered in three to five minutes using no special equipment. Such standardized diagnostic tools give accurate and reproducible predictions of the likelihood that a person has had an acute stroke. It has been shown that 911 operators can even administer the Cincinnati Prehospital Stroke Scale over the phone with the help of cooperative bystanders.
EMS responders make every attempt to transport stroke victims to primary stroke centers, which are emergency departments experienced in thrombolytic therapy for strokes. Primary stroke centers are accredited by the national Joint Commission. Accreditation signifies that the ED is part of a hospital with fully equipped stroke units, with quick access to a specialized stroke team that operates by a pre-planned written protocol for diagnosing strokes, with round-the-clock availability of emergency CT (or MRI) imaging, and with the facilities and expertise to treat ischemic strokes with intravenous rtPA. Primary stroke centers have the goal of getting eligible acute stroke patients from the door to thrombolytic treatment in less than an hour.
While making a detailed diagnosis, the first step in treating a stroke is to establish an airway, possibly by intubation. Next, one must check for evidence of head trauma and consider immobilizing the spine. If the patient’s neurological condition is deteriorating (e.g., if there is a decreasing level of consciousness, pupillary dysfunction suggesting brainstem damage, or decorticate or decerebrate posturing), there may be cerebral edema or continued hemorrhaging, so neurosurgery must be consulted.
After a brief medical history (that includes defining the time course of the onset of symptoms) and a physical exam (with special attention to the neurological and cardiac exams), stat blood work (blood glucose, serum electrolytes, renal function tests, cardiac markers, CBC, prothrombin time/INR, a PTT, and a toxicology screen if drug use is suspected) is drawn.
As in pre-hospital (i.e., EMS) stroke management, emergency department stroke care is facilitated by using standardized tests; in the ED, the recommended assessment tool is the NIH Stroke Scale, which can be administered in five to eight minutes using no special equipment. The NIH Stroke Scale quantifies the severity of a stroke, and it has been widely used to measure both deterioration and improvement of stroke patients.
The critical step in evaluating an acute stroke is making the distinction between ischemic and hemorrhagic strokes. For this, there is no clinical test: the determination must be made by CT (or MRI) imaging, as interpreted by an experienced radiologist. Emergency head imaging (usually, a noncontrast CT scan) is needed within 25 minutes of the patient’s delivery to the ED, and a completed radiologic evaluation is needed less than 20 minutes later.
At this point, treatment paths for ischemic and hemorrhagic stroke patients diverge. For ischemic strokes, IV recombinant tissue plasminogen activator (rtPA) should be administered to eligible patients within 4.5 hours of the onset of symptoms. To be eligible, patients must not be pregnant, must have a sufficiently high platelet count, and can have no indication of intracranial hemorrhage, no recent major surgery, no evidence of internal bleeding, no known bleeding diatheses, and no current anticoagulant therapy. After receiving IV rtPA, patients must be carefully monitored for at least 24 hours in an ICU.
For hemorrhagic strokes due to a ruptured subarachnoid aneurysm, neurosurgery is consulted for possible treatment by surgically clipping the aneurysm remnant or by endovascularly inserting a coil. For other subarachnoid hemorrhages, intracerebral hemorrhages, and ischemic strokes ineligible for rtPA treatment, patients are admitted directly to an ICU and monitored carefully.
In the ICU, stroke patients have their vital signs and neurological functioning checked regularly. The acute management of a stroke patient’s hypertension cannot be an automatic process; treatment must balance the threat of additional hypertensive tissue damage against the need to maintain adequate cerebral perfusion. Extreme hypertension is reduced gradually, but most patients are allowed to remain mildly hypertensive early in their ICU course.
Overall, 30% of strokes will deteriorate within the first 24 hours. Deteriorating vital or neurological signs can be due to cerebral edema, increased intracranial pressure, or rebleeding, as well as to cardiopulmonary problems. Neurosurgery should be involved in assessing a deteriorating patient.
In the United States, stroke patients remain in the hospital an average of five days; however, the recovery from a stroke usually requires long-term coordinated and continuing medical and physical rehabilitation. Patients who have been left with severe disabilities from their stroke may still be gradually improving more than five months afterward.
Patients frequently recover from strokes, even serious strokes, because of the ability of the brain to learn new ways to accomplish old tasks. This learning takes time, and one medical rehabilitation goal is to maintain a patient’s health sufficiently for their brain to relearn what it can; the second medical goal is to prevent additional strokes.
At the same time, the goals of physical rehabilitation are to maximize the speed at which the brain retrains itself to complete functional tasks and to substitute tasks that are more manageable for those functions that cannot be relearned.
Health professionals who advise patients over the telephone should know straightforward answers to basic questions. Here are a few important questions and answers about acute strokes.
Q:What should I do if I think I may be having a stroke?
A:A stroke is an emergency like a heart attack. Call 911 immediately, or get someone to call for you. Don’t wait for the symptoms to go away, and don’t worry that you may be mistaken: paramedics would much rather come and reassure you than see you suffer the consequences of an untreated stroke.
Q:I’m close to a hospital; shouldn’t I drive myself rather than waste time calling 911?
A:Strokes can disrupt your ability to drive, so do not drive anywhere if you think you are having a stroke. It’s also better medically for you to wait for an EMS team, so don’t let someone else drive you to a hospital if it is possible to get trained professionals to take you.
Strokes need immediate treatment, but they must be treated properly. The EMS team that comes when you call 911 knows the best first aid to administer. They know which treatments to start on the way to the hospital, they know which hospital can give you the best stroke treatments, and they will call ahead so that the hospital will be prepared to speed you past the front desk and into a treatment room.
Q:How can I tell if someone is having a stroke?
A:Strokes come on suddenly. Sometimes there is a severe headache, but many times there is no pain at all. When you have a stroke, you are suddenly not able to do something that you could do before. Classic stroke symptoms are:
A person having a stroke may show one or more of these signs. Any of the above symptoms signals an emergency, so call 911 just as you would if you saw a car accident or if a person was choking, had sudden chest pain, or became unconscious or unresponsive. You don’t have to be certain that the person is actually having a stroke.
You can watch an eight-minute online video from the National Institute of Neurologic Disorders and Stroke at stroke.nih.gov/materials/knowstrokevideo.htm. The program features experts in the field of stroke discussing the signs of a stroke and what to do if you see someone with those signs. There are also stories from people who have successfully recovered from a stroke.
Q:What first aid should I give someone with a stroke?
A:Make sure the person is in a safe place, then call 911. Calling for assistance is the most critical first aid. If the person is injured, use your hand to put pressure on any bleeding areas. The 911 operator will give you further advice about first aid.
Q:What happens when someone has a stroke?
A:A person has a stroke when a part of their brain stops getting enough blood. Usually, strokes happen all of a sudden, so the stroke patient finds that they have suddenly lost some ability. The patient may suddenly not be able to move an arm, or they may lose the ability to feel things, to speak clearly, or to walk.
Infrequently, a stroke will show up with a sudden severe headache, but most often strokes are painless, and a person may not realize they have had a stroke until they try to use one of the affected muscles. For example, they may suddenly realize that they can’t hold something in their hand, they may fall when they stand up because one of their legs isn’t working, or they may be confused or unable to talk clearly.
The best treatments for strokes need to begin quickly. If you think that you or someone around you may be having a stroke, call 911 immediately.
Q:What is a stroke? What are the different types?
A:There are two main types of stroke: ischemic and hemorrhagic.
The most common type of stroke is ischemic. In an ischemic stroke, a brain artery becomes blocked by a blood clot. The region of the brain normally supplied by that artery no longer gets enough blood, and that part of the brain becomes starved for oxygen and sugar. Without oxygen and sugar, nerve cells stop working, so the affected region of the brain can no longer performs its particular functions, such as moving an arm or a leg.
Brain cells will stop working when they get less than the normal amount of blood—even when the blood supply hasn’t stopped completely but has only been reduced. If the blood flow can be restored quickly enough, many of the brain cells will start working again and the difficulties that the person was having will go away, partly or completely. On the other hand, if it takes too long to restore the blood flow, brain cells will die. In this case, the difficulties caused by the stroke will remain.
A less common type of stroke is hemorrhagic. Hemorrhagic means “bleeding.” In a hemorrhagic stroke, an artery is torn and blood begins to leak out and form a pool in the brain. When the blood is leaking out of the artery, it is not carrying sufficient oxygen and sugar to the region that it normally supplies, and the person has the same problems as in an ischemic stroke. In addition, in a hemorrhagic stroke, the pool of blood expands and pushes on the neighboring blood vessels and brain cells. The pressure of the expanding pool of blood causes additional brain damage.
Q:What is the difference between a stroke, a brain attack, and a cerebrovascular accident (CVA)?
A:These are three different names for the same thing.
Q:I have heart disease, and my doctor said I might have a stroke. How can heart disease affect the brain?
A:Most strokes are caused by clots that become stuck inside arteries in the head and then cut off the supply of blood to the brain.
One relation of heart disease to strokes is that they can both be caused by atherosclerosis. Just as in a stroke, heart attacks and attacks of chest pain (called angina) are often caused by blood clots. Blood clots in the heart usually come from atherosclerosis. Atherosclerosis is a disease that can affect all the large arteries in the body, and some clots formed by atherosclerosis can be swept into the brain. Therefore, if a person has blood clots in their heart, then they also have a chance of getting blood clots elsewhere, such as in their brain.
Another relation between heart disease and strokes has to do with problems in the rhythm of the heartbeat. Irregular heart rhythms can cause blood clots. One particular heart rhythm irregularity, called atrial fibrillation, is notorious for putting a person at risk for having a stroke. If you have atrial fibrillation, ask your doctor how you can reduce your chance of having a stroke. And be sure to ask your doctor to teach you the warning signs of a stroke.
Q:Can a stroke be stopped?
A:A stroke is the set of symptoms that follow when a brain artery is blocked or bleeding. The brain can often recover if the cause of the stroke can be reversed and fresh blood can flow to the blood-starved areas soon enough.
When the underlying problem is a blocked artery, the stroke symptoms will sometimes lessen or even disappear if the obstructing clot is removed or dissolved quickly enough. On the other hand, bleeding arteries will sometimes stop bleeding on their own, and sometimes they can be coaxed to slow down or stop. If the bleeding can be stopped, the stroke symptoms will sometimes lessen.
All treatments depend on speed, so call 911 immediately if someone might be having a stroke.
Q:What are clot-dissolving or clot-busting drugs?
A:Clot-dissolving drugs are enzymes that break the bonds holding clots together. Clot-dissolving drugs have been used for a long time to treat blood clots elsewhere in the body. One drug has been approved by the U.S. Food and Drug Administration (FDA) for dissolving blood clots in the brain. This drug is called alteplase.
Alteplase is usually injected in a vein, and it is carried in the blood stream to the clot, where it breaks up the threads of protein that hold the clot together. Not all strokes can be treated with alteplase, and alteplase can sometimes cause bleeding in the brain. Nonetheless, when an experienced doctor recommends using alteplase for a person who has just had a stroke, the benefits outweigh the risks.
Q:My mother died of a stroke. Am I likely to have a stroke, too? What about my children?
A:People whose parents, grandparents, brothers, or sisters had a stroke have a higher risk of having a stroke themselves. You can reduce your chances of having a stroke and protect yourself and your children by paying special attention to six things in your lifestyle.
Sources of Stroke Information
Stroke Management Guidelines
Stroke Scales and Similar Tools
NIH Stroke Scale Training (free online training course)
NIH Stroke Scale Training (free on a mobile phone)
Developing a Primary Stroke Center—Guidelines
NOTE: Complete URLs for references retrieved from online sources are provided in the PDF of this course (view/download PDF from the menu at the top of this page).
Abdullah AR, Smith EE, Biddinger PD, Kalenderian D, & Schwamm LH. (2008). Advance hospital notification by EMS in acute stroke is associated with shorter door-to-computed tomography time and increased likelihood of administration of tissue-plasminogen activator. Prehospital Emergency Care, 12(4), 426–431.
Aburto-Murrieta Y, Marquez-Romero JM, Bonifacio-Delgadillo D, López I, & Hernández-Curiel B. (2012). Endovascular treatment: balloon angioplasty versus nimodipine intra-arterial for medically refractory cerebral vasospasm following aneurysmal subarachnoid hemorrhage. Vascular & Endovascular Surgery, 46(6), 460–465. doi:10.1177/1538574412454585.
Acke F, Acou M, & Hemelsoet D. (2011). Basilar artery dissection. Acta Neurologica Belgica, 111(4).
Acker III JE, et al. (2007). Implementation strategies for emergency medical services within stroke systems of care. A policy statement from the American Heart Association / American Stroke Association Expert Panel on Emergency Medical Services Systems and the Stroke Council. Stroke, 116, 3097–3115.
Agency for Healthcare Research and Quality (AHRQ). (2010) Management of patients with stroke: rehabilitation, prevention and management of complications, and discharge planning. A national clinical guideline. Retrieved from http://www.guideline.gov
Alberts MJ, Latchaw RE, Jagoda A, Wechsler LR, Crocco T, George MG, Walker MD. (2011). Revised and updated recommendations for the establishment of primary stroke centers: a summary statement from the brain attack coalition. Stroke (00392499), 42(9), 2651–2665. doi:10.1161/strokeaha.111.615336.
Alkan BM, Çulha C, & Çağlar YH. (2013). Comparison of the results of early and delayed inpatient stroke rehabilitation. Turkish Journal of Physical Medicine & Rehabilitation/Turkiye Fiziksel Tip ve Rehabilitasyon Dergisi, 59(1), 7–12. doi:10.4274/tftr.02693.
Alli O, Doshi S, Kar S, Reddy V, Sievert H, et al. (2013). Quality of life assessment in the randomized PROTECT AF (percutaneous closure of the left atrial appendage versus warfarin therapy for prevention of stroke in patients with atrial fibrillation) trial of patients at risk for stroke with nonvalvular atrial fibrillation. Journal of the American College of Cardiology (JACC), 61(17), 1790–98. doi:10.1016/j.jacc.2013.01.061.
Alspach JG. (2013). Improving recognition and response to the onset of stroke. Critical Care Nurse, 33(1), 9–13. doi:10.4037/ccn2013909.
American Heart Association (AHA). (2011). Healthy diet guidelines. Retrieved from http://www.heart.org
American Heart Association (AHA). (2010). Heart disease and stroke statistics—2010 update. Retrieved from http://www.americanheart.org
Annicchiarico R. (2012). Enhancing service delivering, improving quality of life, preserving independence through assistive technology. Studies in Health Technology & Informatics, 180, 14–18.
Aoki J & Uchino K. (2011). Treatment of risk factors to prevent stroke. Neurotherapeutics, 8(3), 463–474. doi:10.1007/s13311-011-0054-0.
AOTA. (2012). Q&A: scope of OTA practice. Retrieved from http://www.aota.org
Appelman APA, Vincken KL, Mali WPT, & Geerlings MI. (2010). Combined effect of cerebral hypoperfusion and white matter lesions on executive functioning—the SMART-MR study. Dementia & Geriatric Cognitive Disorders, 29(3), 240–247. doi:10.1159/000289813.
Arima H, Anderson C, Omae T, Woodward M, MacMahon S, et al. (2012). Effects of blood pressure lowering on intracranial and extracranial bleeding in patients on antithrombotic therapy: the PROGRESS trial. Stroke (00392499), 43(6), 1675–77.
ATACH. (2010). Antihypertensive treatment of acute cerebral hemorrhage. Critical Care Medicine, 38(2), 637–648.
Ayache S, Farhat W, Zouari H, Hosseini H, Mylius V, Lefaucheur J. (2012 ). Stroke rehabilitation using noninvasive cortical stimulation: motor deficit. Expert Rev Neurother, 949–972.
Bae ON, Serfozo K, Baek SH, Lee KY, Dorrance A, et al. (2013). Safety and efficacy evaluation of Carnosine, an endogenous neuroprotective agent for ischemic stroke. Stroke (00392499), 44(1), 205–212. doi:10.1161/strokeaha.112.673954.
Baldwin K, Orr S, Briand M, Piazza C, Veydt A, & McCoy S. (2010). Acute ischemic stroke update. Pharmacotherapy, 30(5), 493–514. doi:10.1592/phco.30.5.493.
Ballard DW, Reed ME, Huang J, Kramer BJ, Hsu J, & Chettipally U. (2012). Does primary stroke center certification change ED diagnosis, utilization, and disposition of patients with acute stroke? American Journal of Emergency Medicine, 30(7), 1152–1162. doi:10.1016/j.ajem.2011.08.015.
Bartolo ME. (2011). Alien hand syndrome in left posterior stroke. Neurological Sciences, 32(3), 483–486.
Beal CC. (2010). Gender and stroke symptoms: a review of the current literature. Journal of Neuroscience Nursing, 42(2), 80–87.
Béjot Y & Giroud, M. (2009). Epidemiological implications of the new definition of transient ischemic attack. Neuroepidemiology, 33(4), 358–358. doi:10.1159/000254573.
Berglund, A, Svensson, L, Sjöstrand, C, von Arbin, M, von Euler, M.et al. (2012). Higher prehospital priority level of stroke improves thrombolysis frequency and time to stroke unit: the Hyper Acute STroke Alarm (HASTA) study. Stroke (00392499), 43(10), 2666–2670.
Bergman D. (2011). Preventing recurrent cerebrovascular events in patients with stroke or transient ischemic attack: the current data. Journal of the American Academy of Nurse Practitioners, 23(12), 659–666. doi:10.1111/j.1745-7599.2011.00650.x.
Bernocchi P, Scalvini S, Tridico C, Borghi G, Zanaboni, P, et al. (2012). Healthcare continuity from hospital to territory in Lombardy: TELEMACO Project. American Journal of Managed Care, 18(3), 139.
Blobel B, Pharow P, Sousa F, Bento VF, Cruz VT, et al. (2012). The SWORD tele-rehabilitation system. Studies in Health Technology & Informatics, 177, 76–81.
Bollens B, Deltombe T, Detrembleur C, Gustin T, Stoquart G, & Lejeune TM. (2011). Effects of selective tibial nerve neurotomy as a treatment for adults presenting with spastic equinovarus foot: a systematic review. Journal of Rehabilitation Medicine (Stiftelsen Rehabiliteringsinformation), 43(4), 277–82.
Bray JE, Coughlan K, Barger B, & Bladin C. (2010). Paramedic diagnosis of stroke: examining long-term use of the Melbourne Ambulance Stroke Screen (MASS) in the field. Stroke (00392499), 41(7), 1363–66. doi:10.1161/strokeaha.109.571836.
Brenner DA, Zweifler RM, Gomez CR, Kissela BM, Levine D, et al. (2010). Awareness, treatment, and control of vascular risk factors among stroke survivors. Journal of Stroke & Cerebrovascular Diseases, 19(4), 311–320. doi:10.1016/j.jstrokecerebrovasdis.2009.07.001.
Bruce NT, Neil WP, & Zivin JA. (2011). Medico-legal aspects of using tissue plasminogen activator in acute ischemic stroke. Current Treatment Options In Cardiovascular Medicine, 13(3), 233–39. doi:10.1007/s11936-011-0122-0.
Buck B, Starkman S, Eckstein M, Kidwell, C, Haines J, et al. (2009). Dispatcher recognition of stroke using the national academy medical priority dispatch system. Stroke (00392499), 40(6), 2027–30. doi:10.1161/STROKEAHA.108.545574.
Cameirão MS. (2012). The Neurorehabilitation Training Toolkit (NTT): a novel worldwide accessible motor training approach for at-home rehabilitation after stroke. Stroke Research & Treatment, 1–13. doi:10.1155/2012/802157.
Cameron V. (2013). Best practices for stroke patient and family education in the acute care setting: a literature review. MEDSURG Nursing, 22(1), 51–55.
Carda S, Invernizzi M, Baricich A, & Cisari C. (2011). Casting, taping, or stretching after botulinum toxin type A for spastic equinus foot: a single-blind randomized trial on adult stroke patients. Clinical Rehabilitation, 25(12), 1119–27. doi:10.1177/0269215511405080.
Catangui EJ & Slark J. (2012). Nurse-led ward rounds: a valuable contribution to acute stroke care. British Journal of Nursing, 21(13), 801–5.
Centers for Disease Control and Prevention (CDC). (2012). Summary health statistics for U.S. adults: national health interview survey, 2011 vol. DHHS Publication No. (PHS) 2013–1584, Series 10, No. 256.
Centers for Disease Control and Prevention (CDC). (2011). Health Data Interactive: prevention. Retrieved from http://www.cdc.gov
Centers for Disease Control and Prevention (CDC). (2010a). Stroke: maps and statistics. Retrieved from http://www.cdc.gov
Centers for Disease Control and Prevention (CDC). (2010b). FastStats: stroke. Retrieved from http://www.cdc.gov
Cha MJ. Kim YD. Nam HS, Kim J, Lee DH, Heo JH. (2012). Stroke mechanism in patients with non-valvular atrial fibrillation according to the CHADS2 and CHA2DS2-VASc scores. European Journal of Neurology, 19(3), 473–79. doi:10.1111/j.1468-1331.2011.03547.x.
Charriaut-Marlangue C, Bonnin P, Gharib A, Leger PL, Villapol S, Pocard M, et al. (2012). Inhaled nitric oxide reduces brain damage by collateral recruitment in a neonatal stroke model. Stroke (00392499), 43(11), 3078–84. doi:10.1161/strokeaha.112.664243.
Chaudhry FS, Schneck MJ, Morales-Vidal S, Javaid F, & Ruland S. (2013). Prevention of venous thromboembolism in patients with hemorrhagic stroke. Topics in Stroke Rehabilitation, 20(2), 108–15. doi:10.1310/tsr2002-108.
Chen Y, Bogosavljevic V, Leys D, Jovanovic D, Beslac-Bumbasirevic L, Lucas C. (2011). Intravenous thrombolytic therapy in patients with stroke mimics: baseline characteristics and safety profile. European Journal of Neurology, 18(10), 1246–50. doi:10.1111/j.1468-1331.2011.03367.x.
Ching-Hui H, Putman K, Nichols D, McGinty ME, DeJong G, Smout RJ, & Horn S. (2010). Physical and occupational therapy in inpatient stroke rehabilitation: the contribution of therapy extenders. American Journal of Physical Medicine & Rehabilitation, 89(11), 887–98. doi:10.1097/PHM.0b013e3181f70fbl.
Choi HA, Ko SB, Chen H, Gilmore E, Carpenter AM, et al. (2012). Acute effects of nimodipine on cerebral vasculature and brain metabolism in high grade subarachnoid hemorrhage patients. Neurocritical Care, 16(3), 363–67.
Crary MA, Humphrey JL, Carnaby-Mann G, Sambandam R, Miller L, & Silliman S. (2013). Dysphagia, nutrition, and hydration in ischemic stroke patients at admission and discharge from acute care. Dysphagia (0179051X), 28(1), 69–76. doi:10.1007/s00455-012-9414-0.
Cruz-Flores S, Berge E, & Whittle IR. (2012). Surgical decompression for cerebral edema in acute ischemic stroke. Cochrane Database of Systematic Reviews, 1CD003435. doi:10.1002/14651858.CD003435.pub2.
Dani KA, Thomas RG, Chappell FM, Shuler K, Muir KW, & Wardlaw JM. (2012). Systematic review of perfusion imaging with computed tomography and magnetic resonance in acute ischemic stroke: heterogeneity of acquisition and postprocessing parameters: a translational medicine research collaboration multicentre acute stroke imaging study. Stroke (00392499), 43(2), 563–66.
Dávalos A & Secades J. (2011). Citicoline preclinical and clinical update 2009–2010. Stroke (00392499), 42(1 Suppl), S36–39. doi:10.1161/strokeaha.110.605568.
Dean CM, Rissel C, Sherrington C, Sharkey M, Cumming RG, et al. (2012). Exercise to enhance mobility and prevent falls after stroke: the community stroke club randomized trial. Neurorehabilitation & Neural Repair, 26(9), 1046–57. doi:10.1177/1545968312441711.
DeJong G, Ching-Hui H, Putman K, Smout RJ, Horn SD, Wenqiang T. (2011). Physical therapy activities in stroke, knee arthroplasty, and traumatic brain injury rehabilitation: their variation, similarities, and association with functional outcomes. Physical Therapy, 91(12), 1826–37. doi:10.2522/ptj.20100424.
del Zoppo GJ, et al. (2009). Expansion of the time window for treatment of acute ischemic stroke with intravenous tissue plasminogen activator: a science advisory from the American Heart Association / American Stroke Association. Stroke, 40, 2945–48.
Dhillon S. (2012). Alteplase: a review of its use in the management of acute ischemic stroke. CNS Drugs, 26(10), 899–926.
Diederich K, Frauenknecht K, Minnerup J, Schneider BK, Schmidt A, Altach E, et al. (2012). Citicoline enhances neuroregenerative processes after experimental stroke in rats. Stroke (00392499), 43(7), 1931–40.
Doucet BM & Seale J. (2012). The Free Post-Stroke Clinic: a successful teaching and learning model. Journal of Allied Health, 41(4), 162–9.
Dumont AS, Crowley RW, Monteith SJ, Ilodigwe D, Kassell NF, et al. (2010). Endovascular treatment or neurosurgical clipping of ruptured intracranial aneurysms: effect on angiographic vasospasm, delayed ischemic neurological deficit, cerebral infarction, and clinical outcome. Stroke (00392499), 41(11), 2519–24. doi:10.1161/strokeaha.110.579383.
Edmiaston J, Connor LT, Loehr L, Nassief A. (2010). Validation of a dysphagia screening tool in acute stroke patients. American Journal of Critical Care, 19(4), 357–64. doi:10.4037/ajcc2009961.
Eide PK, Bentsen G, Sorteberg AG, Marthinsen PB, Stubhaug A, Sorteberg W. (2011). A randomized and blinded single-center trial comparing the effect of intracranial pressure and intracranial pressure wave amplitude-guided intensive care management on early clinical state and 12-month outcome in patients with aneurysmal subarachnoid hemorrhage. Neurosurgery, 69(5), 1105–15. doi:10.1227/NEU.0b013e318227e0e1.
Einhorn PT, Davis BR, Wright JT Jr., Rahman M, Whelton PK, Pressel SL. (2010). ALLHAT: still providing correct answers after 7 years. Current Opinion in Cardiology, 25(4), 355–65. doi:10.1097/HCO.0b013e32833a8828.
Feng S, Yang Q, Liu M, Li W, Yuan W, Zhang S, et al. (2011). Edaravone for acute ischemic stroke. Cochrane Database of Systematic Reviews (12).
Feng W, Hendry RM, & Adams RJ. (2010). Risk of recurrent stroke, myocardial infarction, or death in hospitalized stroke patients. Neurology, 74, 588–593. doi:10.1212/WNL.0b013e3181cff776.
Finlayson O, Kapral M, Hall R, Asllani E, Selchen D, Saposnik G. (2011). Risk factors, inpatient care, and outcomes of pneumonia after ischemic stroke. Neurology, 77(14), 1338–45. doi:10.1212/WNL.0b013e31823152b1.
Flaster M, Sharma A, & Rao M. (2013). Poststroke depression: a review emphasizing the role of prophylactic treatment and synergy with treatment for motor recovery. Topics in Stroke Rehabilitation, 20(2), 139–50. doi:10.1310/tsr2002-139.
Freeman WD & Aguilar MI. (2011). Prevention of cardioembolic stroke. Neurotherapeutics, 8(3), 488–502. doi:10.1007/s13311-011-0048-y.
Frese EM, Fick A, & Sadowsky HS. (2011). Blood pressure measurement guidelines for physical therapists. Cardiopulm Phys Ther J, 22(2), 5–12.
Frontera JA. (2012). Metabolic encephalopathies in intensive care. CONTINUUM: Lifelong Learning in Neurology, 18(3), 611–39.
Furie KL, Wilterdink JL, & Kistler JP. (2009). Secondary prevention of stroke: risk factor reduction. In BD Rose (ed), UpToDate. Waltham MA: UpToDate. Retrieved from http://www.uptodate.com
Geeganage CM, Diener HC, Algra A, Chen C, Topol EJ, et al. (2012). Dual or mono antiplatelet therapy for patients with acute ischemic stroke or transient ischemic attack: systematic review and meta-analysis of randomized controlled trials. Stroke (00392499), 43(4), 1058–1066.
Gerber CS. (2003). Stroke: historical perspectives. Critical Care Nursing Quarterly, 26(4), 268–275.
Gilboy N, Tanabe P, Travers D, Rosenau A. (2011). Emergency severity index (ESI): a triage tool for emergency department care implementation handbook (4th ed.). Rockville, MD: Agency for Healthcare Research and Quality.
Go AS, Mozaffarian D, Roger VL, Benjamin EJ, Berry JD, Borden WB, Turner MB. (2013). Heart disease and stroke statistics—2013 update: a report from the American Heart Association. Circulation, 127(1), e6–e245. doi:10.1161/CIR.0b013e31828124ad.
Gocan S & Fisher A. (2008). Neurological assessment by nurses using the National Institutes of Health Stroke Scale: implementation of best practice guidelines. Canadian Journal of Neuroscience Nursing, 30(3), 31–42.
Goldstein LB, Bushnell CD, Adams RJ, Appel LJ, Braun LT, et al. (2011). Guidelines for the primary prevention of stroke: a guideline for healthcare professionals from the American Heart Association / American Stroke Association. Stroke (00392499), 42(2), 517–84. doi:10.1161/STR.0b013e3181fcb238.
Gounis MJ & Wakhloo AK. (2010). Advances in interventional neuroradiology. Stroke (00392499), 41(2), e81–87. doi:10.1161/strokeaha.109.574319.
Govindarajan P, Desouza NT, Pierog J, Ghilarducci D, Johnston SC. (2012). Feasibility study to assess the use of the Cincinnati stroke scale by emergency medical dispatchers: a pilot study. Emergency Medicine Journal, 29(10), 848–50. doi:10.1136/emermed-2011-200150.
Grise EM & Adeoye O. (2012). Blood pressure control for acute ischemic and hemorrhagic stroke. Current Opinion in Critical Care, 18(2), 132–138.
Hansen JM, Schytz HW, Larsen VA, Iversen HK, Ashina, M. (2011). Hemiplegic migraine aura begins with cerebral hypoperfusion: imaging in the acute phase. Headache: The Journal of Head and Face Pain, 51(8), 1289–96. doi:10.1111/j.1526-4610.2011.01963.x.
Hassan AE, Chaudhry SA, Grigoryan M, Tekle WG, Qureshi AI. (2012). National trends in utilization and outcomes of endovascular treatment of acute ischemic stroke patients in the mechanical thrombectomy era. Stroke (00392499), 43(11), 3012–17. doi:10.1161/strokeaha.112.658781.
Hayes S, Donnellan C, & Stokes E. (2011). The measurement and impairment of executive function after stroke and concepts for physiotherapy. Physical Therapy Reviews, 16(3), 178–90. doi:10.1179/1743288x11y.0000000030.
Hays AN. (2011). Review of Intracerebral hemorrhage. Neurology, 77(3), 303–04.
Heidenreich P, Trogdon J, Khavjou O, Butler J, Dracup K, et al. (2011). Forecasting the future of cardiovascular disease in the United States: a policy statement from the American Heart Association. Circulation, 123(8), 933–44.
Heiss WD, Brainin M, Bornstein NM, Tuomilehto J, Hong Z. (2012). Cerebrolysin in patients with acute ischemic stroke in Asia: results of a double-blind, placebo-controlled randomized trial. Stroke (00392499), 43(3), 630–36.
Hermann DM & Chopp M. (2012). Promoting brain remodelling and plasticity for stroke recovery: Therapeutic promise and potential pitfalls of clinical translation. The Lancet Neurology, 11(4), 369–80. doi:10.1016/s1474-4422(12)70039-x.
Hess DC, et al. (2006). Telestroke: extending stroke expertise into underserved areas. Personal view. Lancet Neurology, 5, 275–78.
Hoffmann S, Malzahn U, Harms H, Koennecke HC, Berger K, Kalic M, Heuschmann PU. (2012). Development of a clinical score (A2DS2) to predict pneumonia in acute ischemic stroke. Stroke (00392499), 43(10), 2617–23.
Hoffmann T, Bennett S, Koh C, McKenna K. (2010). A systematic review of cognitive interventions to improve functional ability in people who have cognitive impairment following stroke. Topics in Stroke Rehabilitation, 17(2), 99–107. doi:10.1013/tsr1702-99.
Hornik A, Morgan C, Platakis J, Morales-Vidal S. (2013). Pearls on primary stroke center. Topics in Stroke Rehabilitation, 20(2), 124–30. doi:10.1310/tsr2002-124.
Huang Z, Huang F, Yan HX, Min Y, Gao Y, Tan BD, Qu F. (2010) [Dysphagia after stroke treated with acupuncture or electric stimulation: a randomized controlled trial]. [Article in Chinese]. Zhongguo Zhen Jiu, 30(12), 969–73.
Hughes SM. (2011). Management of dysphagia in stroke patients. Nursing Older People, 23(3), 21–24.
Internet Stroke Center (ISC). (2010). Stroke scales & clinical assessment tools. Retrieved from http://www.strokecenter.org
Ireland S, MacKenzie M, Gould L, Dassinger D, Koper A, LeBlanc K. (2010). Nurse case management to improve risk reduction outcomes in a stroke prevention clinic. Canadian Journal of Neuroscience Nursing, 32(4), 7–13.
Jauch EC, Saver JL, Bruno A, Connors JB, Demaerschalk BM, et al. (2013). Guidelines for the early management of patients with acute ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke (00392499), 44(3), 870–947. doi:10.1161/STR.0b013e318284056a.
Johansson BB. (2011). Current trends in stroke rehabilitation: a review with focus on brain plasticity. Acta Neurologica Scandinavica, 123(3), 147–59. doi:10.1111/j.1600-0404.2010.01417.x.
Joint Commission on Accreditation of Healthcare Organizations (JCAHO). (2010). Standards FAQs for primary stroke centers. Retrieved from http://www.jointcommission.org
Jonasson I, Baigi A, Marklund B, Månsson J. (2012). A new primary care model the rehabilitation of strokepatients[sic] impaired arm and hand function—a pilot study. Nordic Journal of Nursing Research & Clinical Studies/Vård i Norden, 32(2), 15–20.
Jones SP, Jenkinson AJ, Leathley MJ, Watkins CL. (2010). Stroke knowledge and awareness: an integrative review of the evidence. Age & Ageing, 39(1), 11–22. doi:10.1093/ageing/afp196.
Judd SE, Kleindorfer DO, McClure LA, Rhodes JD, Howard G, Cushman M, Howard VJ. (2013). Self-report of stroke, transient ischemic attack, or stroke symptoms and risk of future stroke in the reasons for geographic and racial differences in stroke (REGARDS) study. Stroke (00392499), 44(1), 55–60. doi:10.1161/strokeaha.112.675033.
Kalra L. (2010). Stroke rehabilitation 2009: old chestnuts and new insights. Stroke, 41, e88–e90.
Kaltenbach L, Reeves MJ, Smith EE, Fonarow GC, Schwamm LH, Peterson ED. (2013). Assessing stroke patients for rehabilitation during the acute hospitalization: findings from the Get with the Guidelines Stroke Program. Archives of Physical Medicine & Rehabilitation, 94(1), 38–45. doi:10.1016/j.apmr.2012.06.029.
Kerr P. (2012). Stroke rehabilitation and discharge planning. Nursing Standard, 27(1), 35–39.
Kind AJH, et al. (2010). Discharge destination’s effect on bounce-back risk in Black, White, and Hispanic acute ischemic stroke patients. Archives of Physical Medicine and Rehabilitation, 91, 189–195.
Koennecke HC, Belz W, Berfelde D, Endres M, Fitzek S, et al. (2011). Factors influencing in-hospital mortality and morbidity in patients treated on a stroke unit. Neurology, 77(10), 965–72. doi:10.1212/WNL.0b013e31822dc795.
Koga M, Toyoda K, Yamagami H, Okuda S, Okada Y, et al. (2012). Systolic blood pressure lowering to 160 mmHg or less using nicardipine in acute intracerebral hemorrhage: a prospective, multicenter, observational study (the Stroke Acute Management with Urgent Risk-factor Assessment and Improvement-Intracerebral Hemorrhage study). Journal of Hypertension, 30(12), 2357–64. doi:10.1097/HJH.0b013e328359311b.
Korja M, Silventoinen K, Laatikainen T, Jousilahti P, Salomaa V, Kaprio J. (2013). Cause-specific mortality of 1-year survivors of subarachnoid hemorrhage. Neurology, 80(5), 481–86. doi:10.1212/WNL.0b013e31827f0fb5.
Kothari RU, Pancioli A, Liu T, Brott T, & Broderick J. (1999). Cincinnati Prehospital Stroke Scale: reproducibility and validity. Annals of Emergency Medicine, 33(4), 373–378.
Kwon HG & Jang SH. (2012). Motor recovery mechanism in a quadriplegic patient with locked-in syndrome. Neurorehabilitation, 30(2), 113–17.
Lahr MMH, Luijckx GJ, Vroomen PC. van der Zee DJ, Buskens E. (2012). Proportion of patients treated with thrombolysis in a centralized versus a decentralized acute stroke care setting. Stroke, 43(5), 1336–40. doi:10.1161/strokeaha.111.641795.
Laird EA & Coates V. (2013). Systematic review of randomized controlled trials to regulate glycaemia after stroke. Journal of Advanced Nursing, 69(2), 263-277. doi:10.1111/j.1365-2648.2012.06091.x.
Laird EA, Coates V, & Chaney D. (2013). Systematic review of descriptive cohort studies on the dynamics of glycaemia among adults admitted to hospital with acute stroke. Journal of Advanced Nursing, 69(3), 500–13. doi:10.1111/j.1365-2648.2012.06094.x.
Langhorne P, Bernhardt J, & Kwakkel G. (2011). Stroke rehabilitation. Lancet, 377(9778), 1693–1702.
Latchaw RE, et al. (2009). Recommendations for imaging of acute ischemic stroke: a scientific statement from the American Heart Association. Stroke, 40, 3646–78.
Lauritzen M, Dreier JP, Fabricius M, Hartings JA, Graf R, Strong AJ. (2011). Clinical relevance of cortical spreading depression in neurological disorders: migraine, malignant stroke, subarachnoid and intracranial hemorrhage, and traumatic brain injury. Journal of Cerebral Blood Flow and Metabolism, 31(1), 17–35. doi:10.1038/jcbfm.2010.191.
Lederle FA, Zylla D, Macdonald R, Wilt TJ. (2011). Venous thromboembolism prophylaxis in hospitalized medical patients and those with stroke: a background review for an American College of Physicians clinical practice guideline. Annals of Internal Medicine, 155(9), 602–15.
Lee KY, Bae ON, Serfozo K, Hejabian S, Moussa A, et al. (2012). Asiatic acid attenuates infarct volume, mitochondrial dysfunction, and matrix metalloproteinase-9 induction after focal cerebral ischemia. Stroke (00392499), 43(6), 1632–38.
Leira EC, Ludwig BR, Gurol ME, Torner JC, Adams HP. (2012). The types of neurological deficits might not justify withholding treatment in patients with low total National Institutes of Health Stroke Scale scores. Stroke, 43(3), 782–86.
Lincoln NB, Brinkmann N, Cunningham S, Dejaeger E, De Weerdt W, et al. (2013). Anxiety and depression after stroke: a 5-year follow-up. Disability & Rehabilitation, 35(2), 140–45. doi:10.3109/09638288.2012.691939.
Liu G, Wang Z, Wang Y, Xu L, Wang X, et al. (2012). Systematic assessment and meta-analysis of the efficacy and safety of Fasudil in the treatment of cerebral vasospasm in patients with subarachnoid hemorrhage. European Journal of Clinical Pharmacology, 68(2), 131–39. doi:10.1007/s00228-011-1100-x.
Liu J, Wu B, Feng H, You C. (2011). Spinal subdural hematoma following cranial surgery: a case report and review of the literature. Neurology India, 59(2), 281–84.
Lloyd-Jones D, Adams RJ, Brown TM, et al. (2010.) Heart disease and stroke statistics––2010 update: A report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation, 121, e1–e170.
Long YB & Wu XP. (2012). A meta-analysis of the efficacy of acupuncture in treating dysphagia in patients with a stroke. Acupuncture in Medicine, 30(4), 291–97. doi:10.1136/acupmed-2012-010155.
Lukovits TG & Goddeau RP, (2011). Critical care of patients with acute ischemic and hemorrhagic stroke: update on recent evidence and international guidelines. Chest, 139(3), 694–700. doi:10.1378/chest.10-1530.
Lutsep HL, Altafullah IM, Roberts R, Silverman IE. Turco MA, Vaishnav AG. (2013). Neurologic safety event rates in the SENTIS trial control population. Acta Neurologica Scandinavica, 127(2), e5–e7. doi:10.1111/ane.12005.
Ma Y, Zechariah A, Qu Y, Hermann DM. (2012). Effects of vascular endothelial growth factor in ischemic stroke. Journal of Neuroscience Research, 90(10), 1873–82. doi:10.1002/jnr.23088.
MacKay-Lyons M, Thornton M, Ruggles T, Che M. (2013). Non-pharmacological interventions for preventing secondary vascular events after stroke or transient ischemic attack. Cochrane Database of Systematic Reviews, (3).
Magauran BG & Nitka M. (2012). Stroke mimics. Emergency Medicine Clinics of North America, 30(3), 795–804. doi:10.1016/j.emc.2012.06.006.
Martini SR, Flaherty ML, Brown WM, Haverbusch M, Comeau ME, Sauerbeck LR, et al. (2012). Risk factors for intracerebral hemorrhage differ according to hemorrhage location. Neurology, 79(23), 2275–82. doi:10.1212/WNL.0b013e318276896f.
Mattle HP, Arnold M, Lindsberg PJ, Schonewille WJ, Schroth G. (2011). Basilar artery occlusion. Lancet Neurology, 10(11), 1002–14. doi:10.1016/s1474-4422(11)70229-0.
Mayer SA & Schwab S. (2010). Advances in critical care and emergency medicine. Stroke, 41, e74–e76.
Mazya M, Egido JA, Ford GA, Lees KR, Mikulik R, et al. (2012). Predicting the risk of symptomatic intracerebral hemorrhage in ischemic stroke treated with intravenous alteplase: safe implementation of treatments in stroke (SITS) symptomatic intracerebral hemorrhage risk score. Stroke (00392499), 43(6), 1524–31.
McArthur K & Lees KR. (2010). Advances in emerging therapies 2009. Stroke, 41, e67–e70.
Mears GD, Rosamond WD, Lohmeier C, Murphy C, O’Brien E, Asimos AW, Brice JH. (2010). A link to improve stroke patient care: a successful linkage between a statewide emergency medical services data system and a stroke registry. Academic Emergency Medicine, 17(12), 1398–1404. doi:10.1111/j.1553-2712.2010.00925.x.
Medeiros F, Marcela, Fraulob JC, Trindade, M. (2012). How can diet influence the risk of stroke? International Journal of Hypertension, 1–7. doi:10.1155/2012/763507.
Menon RS. (2010). Cerebral amyloid angiopathy. eMedicine. Retrieved from http://emedicine.medscape.com
Merenda A & DeGeorgia M. (2010). Craniectomy for acute ischemic stroke: how to apply the data to the bedside. Current Opinion in Neurology, 23(1), 53–58. doi:10.1097/WCO.0b013e328334bdf4.
Middleton S, McElduff P, Ward J, Grimshaw JM, Dale S, et al. (2011). Implementation of evidence-based treatment protocols to manage fever, hyperglycaemia, and swallowing dysfunction in acute stroke (QASC): a cluster randomised controlled trial. Lancet, 378(9804), 1699–1706.
Millin MG, Gullett T, & Daya MR. (2007). EMS management of acute stroke—out-of-hospital treatment and stroke system development. Prehospital Emergency Care, 11(3), 318–25.
Mingfeng H, Zhixin W, Qihong G, Lianda L, Yanbin Y, Jinfang F. (2012). Validation of the use of the ROSIER scale in prehospital assessment of stroke. Annals of Indian Academy of Neurology, 15(3), 191–95. doi:10.4103/0972-2327.99713.
Mink J & Miller J. (2011). Stroke, part 1: opening the window of opportunity for treating acute ischemic stroke. Nursing, 41(1), 25–33. doi:10.1097/01.nurse.0000391397.75203.54.
Mokin M, Kass-Hout T, Kass-Hout O, Dumont TM, Kan P, et al. (2012). Intravenous thrombolysis and endovascular therapy for acute ischemic stroke with internal carotid artery occlusion: a systematic review of clinical outcomes. Stroke (00392499), 43(9), 2362–68. doi:10.1161/strokeaha.112.655621.
Müller-Barna P, Schwamm LH, & Haberl RL. (2012). Telestroke increases use of acute stroke therapy. Current Opinion in Neurology, 25(1), 5–10.
Muroi C, Seule M, Mishima K, & Keller E. (2012). Novel treatments for vasospasm after subarachnoid hemorrhage. Current Opinion in Critical Care, 18(2), 119–26.
Murphy SL, Xu J, & Kochanek KD. (2013). Deaths: final data for 2010, National Vital Statistics Reports, 61(4).
National Center for Health Statistics (NCHS). (2012). Health, United States, 2011: with special feature on socioeconomic status and health. Retrieved from http://www.cdc.gov
National Heart, Lung, and Blood Institute (NHLBI). (2013). 2012 fact book. Retrieved from http://www.nhlbi.nih.gov
National Highway Traffic Safety Administration (NHTSA). (2002). EMT basic curriculum. Retrieved from http://www.nhtsa.gov
National Institutes of Health (NIH). (2011a). Types of aneurysms. Retrieved from http://www.nhlbi.nih.gov
National Institutes of Health (NIH). (2011b). What are the signs and symptoms of atrial fibrillation? Retrieved from http://www.nhlbi.nih.gov
National Institutes of Health (NIH). (2009). Stroke: challenges, progress and promise. Retrieved from http://stroke.nih.gov
National Institute of Neurologic Diseases and Stroke (NINDS). (2013). What you need to know about stroke. Retrieved from http://www.ninds.nih.gov
National Institute of Neurologic Diseases and Stroke (NINDS). (2010). Stroke information page. Retrieved from http://www.ninds.nih.gov
National Library of Medicine (NLM). (2010). MedlinePlus: stroke. Retrieved from http://www.nlm.nih.gov
National Stroke Association (NSA). (2009). What is stroke? Retrieved from http://www.stroke.org
Nguyen HP, Zaroff JG, Bayman EO, Gelb AW, Todd MM, Hindman BJ. (2010). Perioperative hypothermia (33 degrees C) does not increase the occurrence of cardiovascular events in patients undergoing cerebral aneurysm surgery: findings from the Intraoperative Hypothermia for Aneurysm Surgery Trial. Anesthesiology, 113(2), 327–42. doi:10.1097/ALN.0b013e3181dfd4f7.
Nijboer JM & ten Duis HJ. (2010). Patients beyond salvation? various categories of trauma patients with a minimal Glasgow Coma Score. Injury, 41(1), 52–57. doi:10.1016/j.injury.2009.05.030.
Northcott S & Hilari K. (2011). Why do people lose their friends after a stroke? International Journal of Language & Communication Disorders, 46(5), 524–34. doi:10.1111/j.1460-6984.2011.00079.x.
Nudo RJ. (2011). Neural bases of recovery after brain injury. Journal of Communication Disorders, 44(5), 515–20. doi:10.1016/j.jcomdis.2011.04.004.
Nyström AK. (2013). Fall risk six weeks from onset of stroke and the ability of the Prediction of Falls in Rehabilitation Settings Tool and motor function to predict falls. Clinical Rehabilitation, 27(5), 473–79. doi:10.1177/0269215512464703.
Oechmichen M & Meissner C. (2006). Cerebral hypoxia and ischemia: the forensic point of view: a review. Journal of Forensic Science, 51(4), 880–887.
Oh H & Seo W. (2010). Changes in the acute functional and cognitive disability states of severe hemorrhagic stroke patients. Journal of Neuroscience Nursing, 42(5), 245–54. doi:10.1097/JNN.0b013e3181ecaf81.
Oliveira-Filho J & Samuels OB. (2009). Fibrinolytic (thrombolytic) therapy for acute ischemic stroke. In BD Rose (ed.), UpToDate. Waltham, MA: UpToDate. Retrieved from http://www.uptodate.com
Olkowski BF, Devine MA, Slotnick LE, Veznedaroglu E, Liebman KM, Arcaro ML, Binning MJ. (2013). Safety and feasibility of an early mobilization program for patients with aneurysmal subarachnoid hemorrhage. Physical Therapy, 93(2), 208–15. doi:10.2522/ptj.20110334.
Ortner R, Irimia DC, Scharinger J, Guger C. (2012). A motor imagery based brain-computer interface for stroke rehabilitation. Studies in Health Technology & Informatics, 181, 319–23.
Osman MM, Lulic D, Glover L, Stahl CE, Lau T, van Loveren H, Borlongan CV. (2011). Cyclosporine-A as a neuroprotective agent against stroke: its translation from laboratory research to clinical application. Neuropeptides, 45(6), 359–68. doi:10.1016/j.npep.2011.04.002.
Owens WB. (2011). Blood pressure control in acute cerebrovascular disease. Journal of Clinical Hypertension (Greenwich, CT), 13(3), 205–11. doi:10.1111/j.1751-7176.2010.00394.x.
Palka I, Nessler J, Nessler B, Piwowarska W, Tracz W, Undas A. (2010). Altered fibrin clot properties in patients with chronic heart failure and sinus rhythm: a novel prothrombotic mechanism. Heart, 96(14), 1114–18. doi:10.1136/hrt.2010.192740.
Panagos PD. (2012). Transient ischemic attack (TIA): the initial diagnostic and therapeutic dilemma. American Journal of Emergency Medicine, 30(5), 794–99. doi:10.1016/j.ajem.2011.03.004. doi:10.1016/j.ajem.2011.03.004.
Pandian S & Arya KN. (2012). Relation between the upper extremity synergistic movement components and its implication for motor recovery in poststroke hemiparesis. Topics in Stroke Rehabilitation, 19(6), 545–55. doi:10.1310/tsr1906-545.
Parker J, Mountain G, & Hammerton J. (2011). A review of the evidence underpinning the use of visual and auditory feedback for computer technology in post-stroke upper-limb rehabilitation. Disability & Rehabilitation: Assistive Technology, 6(6), 465–72. doi:10.3109/17483107.2011.556209.
Patel MD, Rose KM, O’Brien EC, Rosamond WD. (2011). Prehospital notification by emergency medical services reduces delays in stroke evaluation: findings from the North Carolina Stroke Care Collaborative. Stroke (00392499), 42(8), 2263–68.
Pezzotti W & Freuler M. (2012). Using anticoagulants to steer clear of clots. Nursing, 42(2), 26–35. doi:10.1097/01.NURSE.0000410303.18542.9e.
Phipps MS, Desai RA, Wira C, Bravata DM. (2011). Epidemiology and outcomes of fever burden among patients with acute ischemic stroke. Stroke (00392499), 42(12), 3357–62.
Poisson SN, Johnston SC, & Josephson SA. (2010). Urinary tract infections complicating stroke: mechanisms, consequences, and possible solutions. Stroke (00392499), 41(4), e180–184. doi:10.1161/strokeaha.109.576413.
Poslawsky IE, Schuurmans MJ, Lindeman E, & Hafsteinsdóttir TB. (2010). A systematic review of nursing rehabilitation of stroke patients with aphasia. Journal of Clinical Nursing, 19(1–2), 17–32. doi:10.1111/j.1365-2702.2009.03023.x.
Poulin V, Korner-Bitensky N, Dawson D, & Bherer L. (2012 ). Efficacy of executive function interventions after stroke: a systematic review. Top Stroke Rehabil, 19(2), 158–71.
Prasad K & Krishnan PR. (2010). Fever is associated with doubling of odds of short-term mortality in ischemic stroke: an updated meta-analysis. Acta Neurologica Scandinavica, 122(6), 404–08. doi:10.1111/j.1600-0404.2010.01326.x.
Rafter RH & Kelly TM. (2011). Nursing implementation of a Telestroke program in a community hospital in the U.S. Journal of Nursing Management, 19(2), 193–200. doi:10.1111/j.1365-2834.2011.01233.x.
Rasalkar DD & Chu WC. (2012). Imaging in children presenting with acute neurological deficit: stroke. Postgraduate Medical Journal, 88(1045), 649–60. doi:10.1136/postgradmedj-2011-130087.
Rashid N, Clarke C, & Rogish M. (2013). Post-stroke depression and expressed emotion. Brain Injury, 27(2), 223–38. doi:10.3109/02699052.2012.729287.
Rist PM, Buring JE, Kase CS, Kurth T. (2013). Effect of low-dose aspirin on functional outcome from cerebral vascular events in women. Stroke (00392499), 44(2), 432–36. doi:10.1161/strokeaha.112.672451.
Roger VL, Go AS, Lloyd-Jones DM, Benjamin EJ, Berry JD, et al. (2012). Executive summary: heart disease and stroke statistics—2012 update: a report from the American Heart Association. Circulation, 125(1), 188–97.
Roh J, Rymer WZ, Perreault EJ, Yoo SB, Beer RF. (2013). Alterations in upper limb muscle synergy structure in chronic stroke survivors. J Neurophysiol, 109(3), 768–81.
Roots A, Bhalla A, & Birns J. (2011). Telemedicine for stroke: a systematic review. British Journal of Neuroscience Nursing, 7(2), 481–89.
Roots A, Thomas L, Jaye P, Birns, J. (2011). Simulation training for hyperacute stroke unit nurses. British Journal of Nursing, 20(21), 1352–56.
Ropper AH & Samuels MA. (2009). Cerebrovascular diseases. Spontaneous subarachnoid hemorrhage (ruptured saccular aneurysm). Adams and Victor’s principles of neurology (9th ed.). New York: McGraw-Hill, Ch. 34.
Sagen U, et al. (2010). Early detection of patients at risk for anxiety, depression and apathy after stroke. General Hospital Psychiatry, 32(1), 80–85.
Sahota P & Savitz SI. (2011). Investigational therapies for ischemic stroke: neuroprotection and neurorecovery. Neurotherapeutics, 8(3), 434–51. doi:10.1007/s13311-011-0040-6.
Saposnik G, Guzik AK, Reeves M, Ovbiagele B, & Johnston SC. (2013). Stroke prognostication using age and NIH Stroke Scale SPAN-100. Neurology, 80(1), 21–28.
Schellinger PD, Bryan RN, Caplan LR, Detre JA, Edelman RR, et al. (2010). Evidence-based guideline: the role of diffusion and perfusion MRI for the diagnosis of acute ischemic stroke: report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology, 75(2), 177–85. doi:10.1212/WNL.0b013e3181e7c9dd.
Schjolberg A & Sunnerhagen KS. (2012). Unlocking the locked in; a need for team approach in rehabilitation of survivors with locked-in syndrome. Acta Neurologica Scandinavica, 125(3), 192–98. doi:10.1111/j.1600-0404.2011.01552.x.
Schneider MA & Schneider MD. (2012). Recognizing poststroke depression. Nursing, 42(12), 60–63. doi:10.1097/01.NURSE.0000422646.06254.1c.
Schwamm LH, et al. (2009). Recommendations for the implementation of telemedicine within stroke systems of care: a policy statement from the American Heart Association. Stroke, 40, 2635–60.
Searls DE, Pazdera L, Korbel E, Vysata O, Caplan LR. (2012). Symptoms and signs of posterior circulation ischemia in the New England Medical Center posterior circulation registry. Archives of Neurology, 69(3), 346–51. doi:10.1001/archneurol.2011.2083.
Seo K, Lee J, Lee S. (2012). Impact of PNF-based walking exercise on a ramp on gait performance of stroke patients. Journal of Physical Therapy Science, 24(12), 1243–46.
Seyed Mansour R, Leyla S, Sadat MH, Iman R, Maryam T, et al. (2012). The effect of neurofeedback therapy accompanying conventional occupational therapy on improving hand function in stroke patients: a pilot study [Farsi]. Pejouhandeh, 17(2), 1p.
Shah LI & Christensen M. (2012). Ineffective cerebral perfusion related to increased intracranial pressure secondary to subarachnoid haemorrhage: an examination of nursing interventions. Singapore Nursing Journal, 39(2), 15–24.
Sherzai A, Heim L, Boothby C, Dean SA. (2012). Stroke, food groups, and dietary patterns: a systematic review. Nutrition Reviews, 70(8), 423–35. doi:10.1111/j.1753-4887.2012.00490.x.
Shi Y, Tian J, Yang K, Zhao Y. (2011 ). Modified constraint-induced movement therapy versus traditional rehabilitation in patients with upper-extremity dysfunction after stroke: a systematic review and meta-analysis. Arch Phys Med Rehabil, 92(6), 972–82.
Shulkin DJ, Jewell KE, Alexandrov AW, Bernard DB, Brophy GM, et al. (2011). Impact of systems of care and blood pressure management on stroke outcomes. Population Health Management, 14(6), 267–75. doi:10.1089/pop.2010.0068.
Sidney S, Rosamond WD, Howard VJ, Luepker RV. (2013). The "heart disease and stroke statistics—2013 update" and the need for a national cardiovascular surveillance system. Circulation, 127(1), 21–23. doi:10.1161/circulationaha.112.155911.
Siket MS & Edlow JA. (2013). Transient ischemic attack: an evidence-based update. Emergency Medicine Practice, 15(1), 1–26.
Siket MS & Edlow JA. (2012). Transient ischemic attack: reviewing the evolution of the definition, diagnosis, risk stratification, and management for the emergency physician. Emergency Medicine Clinics of North America, 30(3), 745–70. doi:10.1016/j.emc.2012.05.001.
Silva GS, Farrell S, Shandra E, Viswanathan A, Schwamm LH. (2012). The status of Telestroke in the United States: a survey of currently active stroke telemedicine programs. Stroke (00392499), 43(8), 2078–85.
Simmons BB, Gadegbeku AB, Cirignano B. (2012). Transient ischemic attack: part ii: risk factor modification and treatment. American Family Physician, 86(6), 527–32.
Sorensen AG & Heiss WD. (2010). Advances in imaging 2009. Stroke, 41, e91–e92.
Staszewski J, Brodacki B, Kotowicz J, Stepien A. (2011). Intravenous insulin therapy in the maintenance of strict glycemic control in nondiabetic acute stroke patients with mild hyperglycemia. Journal of Stroke & Cerebrovascular Diseases, 20(2), 150–54. doi:10.1016/j.jstrokecerebrovasdis.2009.11.013.
Stecker EC. (2010). Finding a balance in long-term anticoagulation therapy. American Journal of Managed Care, 16, S278–83.
Stein J. (2008). Stroke. In chapter 49 of WR Frontera, JK Silver, and TD Rizzo Jr. (eds.), Essentials of physical medicine and rehabilitation (2nd ed.). Philadelphia: Saunders.
Steiner T & Bosel J. (2010). Options to restrict hematoma expansion after spontaneous intracerebral hemorrhage. Stroke, 41, 402–409.
Sugavanam T, Mead G, Bulley C, Donaghy M, Van Wijck F. (2013). The effects and experiences of goal setting in stroke rehabilitation—a systematic review. Disability & Rehabilitation, 35(3), 177–90. doi:10.3109/09638288.2012.690501.
Sukhotinsky I, Yaseen MA, Sakadzić S, Ruvinskaya S, Sims JR, et al. (2010). Perfusion pressure-dependent recovery of cortical spreading depression is independent of tissue oxygenation over a wide physiologic range. Journal of Cerebral Blood Flow and Metabolism, 30(6), 1168–77. doi:10.1038/jcbfm.2009.285.
Summers D, et al. (2009). Comprehensive overview of nursing and interdisciplinary care of the acute ischemic stroke patient: a scientific statement from the American Heart Association. Stroke, 40, 2911–2944.
Sunderrajan N, Chang T, Caserta F, Kowalski RG, Carhuapoma JR, & Tamargo RJ. (2013). Improved aneurysmal subarachnoid hemorrhage outcomes: a comparison of 2 decades at an academic center. Journal of Critical Care, 28(2), 182–88. doi:10.1016/j.jcrc.2012.05.008.
Tabak R & Plummer-D’Amato P. (2010). Bilateral movement therapy post-stroke: underlying mechanisms and review including commentary by Cauraugh JH, Giuffrida C, and Waller SM. International Journal of Therapy & Rehabilitation, 17(1), 15–23.
Tan XX, Zhong M, Zheng K, Zhao B. (2011). Computed tomography angiography based emergency microsurgery for massive intracranial hematoma arising from arteriovenous malformations. Neurology India, 59(2), 199–203.
Tan Y & Christensen M. (2012). The pathophysiology of ischaemic stroke: considerations for emergency department advanced practice nursing. Singapore Nursing Journal, 39(2), 31–39.
Tanaskovic S, Isenovic ER, Radak, D. (2011). Inflammation as a marker for the prediction of internal carotid artery restenosis following eversion endarterectomy—evidence from clinical studies. Angiology, 62(7), 535–42.
Thaler DE & Kent DM. (2010). Rethinking trial strategies for stroke and patent foramen ovale. Current Opinion in Neurology, 23(1), 73–78. doi:10.1097/WCO.0b013e3283352dbc.
Thaler DE, Ruthazer R, Di Angelantonio E, Donovan JS, Griffith J, et al. (2013). Neuroimaging findings in cryptogenic stroke patients with and without patent foramen ovale. Stroke (00392499), 44(3), 675–80. doi:10.1161/strokeaha.112.677039.
Thome J & Doppler E. (2012). Safety profile of Cerebrolysin: clinical experience from dementia and stroke trials. Drugs of Today, 48, 63–69.
U.S. Department of Agriculture (USDA). (2010). Dietary guidelines for Americans. Retrieved May 2013 from http://www.health.gov/dietaryguidelines/.
van de Port IG, Valkenet K, Schuurmans M, Visser-Meily JM. (2012). How to increase activity level in the acute phase after stroke. J Clin Nurs, 21(23–24), 3574–78. doi:10.1111/j.1365-2702.2012.04249.x.
Vergouwen MD, Algra A, & Rinkel GJ. (2012). Endothelin receptor antagonists for aneurysmal subarachnoid hemorrhage: a systematic review and meta-analysis update. Stroke (00392499), 43(10), 2671–76.
Vogel G. (2012). Can we make our brains more plastic? Science, 338(6103), 36–39.
Wang QS, Chen C, Chen XY, Han JH, Soo Y, Leung TW, et al. (2012). Low-molecular-weight Heparin versus aspirin for acute ischemic stroke with large artery occlusive disease: subgroup analyses from the Fraxiparin in Stroke Study for the Treatment of Ischemic Stroke (FISS-tris) Study. Stroke (00392499), 43(2), 346–49.
Wess C, Sarnthein J, Krayenbühl N, Scholz M, Kunze E, & Meixensberger J. (2010). Spectral iEEG markers precede SSEP events during surgery for subarachnoid hemorrhage. Clinical Neurophysiology, 121(12), 2172–76. doi:10.1016/j.clinph.2010.04.031.
West T & Bernhardt J. (2012). Physical activity in hospitalised stroke patients. Stroke Research & Treatment, 1–13. doi:10.1155/2012/813765.
Westover MB, Bianchi MT, Shafi M, Hoch DB, Cole AJ, Chiappa K, Cash SS. (2013). Inferring seizure frequency from brief EEG recordings. Journal of Clinical Neurophysiology, 30(2), 174–77. doi:10.1097/WNP.0b013e3182767c35.
Williams LS & Rudd AG. (2010). Advances in health policy and outcomes 2009. Stroke, 41, e77–e80.
Wilson RD. (2012). Mortality and cost of pneumonia after stroke for different risk groups. Journal of Stroke & Cerebrovascular Diseases, 21(1), 61–67.
Wolpaw JR. (2012). Harnessing neuroplasticity for clinical applications. Brain: A Journal of Neurology, 135(4). doi:10.1093/brain/aws017.
Yeguiayan JM, Benatru I, Guiu B, Taam JA, Albertini S, Freysz M, Giroud M. (2011). Recombinant tissue plasminogen activator for both pulmonary and cerebral embolism. American Journal of Emergency Medicine, 29(8), 961.e961–964. doi:10.1016/j.ajem.2010.08.020.
Yeo LLL, Paliwal P, Teoh HL, Seet RC, Chan BPL, et al. (2013). Timing of recanalization after intravenous thrombolysis and functional outcomes after acute ischemic stroke. JAMA Neurology, 70(3), 353–358.
Zahuranec DB, Morgenstern LB, Sánchez BN, Resnicow K, White DB, & Hemphill JC III. (2010). Do-not-resuscitate orders and predictive models after intercerebral hemorrhage. Neurology, 75(7), 626–633. doi:10.1212/WNL.0b013e3181ed9cc9.