Course Price  $20.00 Contact Hours  4 Instructions  Study the course, then take the test. You can also print the course and test questions and return later to take the test.

Quicklinks Print this course Take the test How to take a course

Acute Stroke

Michael Jay Katz, MD, PhD

Wild Iris Medical Education is an approved provider for paramedic and EMT continuing education in California by the California Emergency Medical Services Agency: EMS CE Provider #49-0057.
Wild Iris Medical Education is an approved provider (#0007) of continuing education by the Continuing Education Coordinating Board for Emergency Medical Services (CECBEMS).
This course is appropriate for EMTs, paramedics, and first responders.

This course includes straightforward answers to basic questions about Acute Stroke for nurses and other health professionals who advise patients over the telephone (see Part 4: Telephone Counseling).

Until recently, the medical arsenal contained few actual treatments for stroke. As Gerber (2003) wrote in her review on the history of stroke therapies:

…the only treatment option available to stroke patients during the first half of the 20th 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 for unblocking carotid arteries (endarterectomy) was improved and used widely, but this surgery was done as a preventive 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.

A dramatic step forward took place in 1996 when the FDA approved the use of a thrombolytic agent for stroke. For some patients, this drug—recombinant tissue plasminogen activator (alteplase, or rt-PA)—can reverse the neurologic effects of an acute ischemic stroke.

In earlier years, when stroke treatment revolved around rehabilitation, the watchwords for therapy were "supportive care" and "caution." Some physicians waited 12 to 24 hours to commit to a diagnosis of stroke, because transient ischemic attacks and minor strokes clear spontaneously within 24 hours.

The introduction of thrombolytic treatment changed the cautious approach to stroke management. The medication rt-PA must be administered soon after a stroke occurs, and the new paradigm considers all stroke symptoms to be potential emergencies in the class of acute myocardial infarctions. Today's watchwords are "Time lost is brain lost."

Thrombolytic treatment for the most common strokes, ischemic strokes, is time dependent. Although there has not 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 neurologic deficits and having a high rate of subsequent death and disability.

Therefore, current management of all acute stroke stresses early identification and quick, efficient treatment using blood pressure control, lytic agents, surgical and catheter procedures, and anticoagulation. The new protocols require that emergency medical (EMS) personnel, emergency department (ED) doctors and nurses, and surgical, neurologic, and radiologic specialists all be prepared to work on stroke patients quickly and efficiently (Chung & Caplan, 2007).

WHAT IS A STROKE?

A stroke—also called a cerebrovascular accident (CVA) or a "brain attack"—is an injury to the blood vessels of the brain that causes neurologic malfunctioning. In the United States, as many as 87% of all strokes are caused by the blockage of an artery feeding the brain. The resulting decrease in blood flow leads to ischemic damage in the region of the brain that is fed by the artery, and these CVAs are called ischemic strokes. Most other strokes are caused by ruptured blood vessels that bleed into the brain or into the subarachnoid space surrounding the brain, and these CVAs are called hemorrhagic strokes.

Ischemic Strokes

Ischemic strokes are usually due to blood clots or emboli that have plugged an artery. Hemorrhagic strokes are usually due to the rupture of blood vessels or aneurysms under the strain of hypertension. For the most part, both ischemic and hemorrhagic strokes give specific (focal) neurologic symptoms, because only limited sections of the brain are damaged by a typical stroke.

Besides specific neurologic problems, another characteristic of stroke is that its symptoms show up suddenly. Thus, the classic clinical picture of a stroke is the abrupt appearance of focal neurologic deficits that are ultimately found to be caused by damage to blood vessels of the brain (Kothari et al., 2006).

A transient ischemic attack (TIA) is a set of stroke symptoms that last for less than 24 hours, and usually less than 12 minutes. In a TIA, the neurologic deficits reverse spontaneously. TIAs are minor ischemic strokes, and they are most likely caused by temporary blockages of cerebral blood vessels. When the blocked blood vessel finally reopens on its own, the symptoms largely disappear, although many times silent brain damage remains. After people have a TIA, they have more than a 10% chance of having a full stroke within the next 3 months.

Ischemic strokes are sometimes categorized according to their cause. The two most common types of ischemic stroke are thrombotic strokes and embolic strokes.

THROMBOTIC STROKES: LOCAL CLOTS

Many ischemic strokes are caused by local clots or thrombi. These thrombi are usually formed along atherosclerotic plaque that has become ulcerated or disrupted, and such disruptions tend to occur in places where the blood flow is turbulent, such as at branch points of arteries.

EMBOLIC STROKES: CLOTS FROM UPSTREAM

Other ischemic strokes are caused by emboli, debris, and clots that arise elsewhere and are swept into the cerebral circulation. One common source of stroke emboli is the left atrium of the heart, where, for example, thrombi can form during atrial fibrillation. Another common source of stroke emboli is the carotid artery, from which atherosclerotic plaque and clots detach and are then carried deeper into the cerebral vasculature.

Atrial fibrillation leads to stasis of blood in the left atrium. The sluggish pools of blood tend to form clots, which can be carried through the left ventricle, into the aorta, and directly into the carotid arteries (NIH Health Images, 2007).

Hemorrhagic Strokes

The major types of hemorrhagic strokes are intracerebral hemorrhages (ICH), which are bleeds into the brain tissue, and subarachnoid hemorrhages (SAH), which are bleeds into the subarachnoid space and cerebrospinal fluid (CSF). Intracerebral hemorrhages are the more common of the two, causing approximately 10% of all acute strokes, and intracerebral hemorrhages tend to happen in the blood vessels leading to the basal ganglia and the thalamus. Intracerebral hemorrhages are typically caused by longstanding hypertension (Chung & Caplan, 2007).

Most cases of subarachnoid hemorrhage are due to ruptures of a cerebral aneurysm (NIH Health Images, 2007).

INCIDENCE OF STROKE

More than three-quarters of a million Americans had a stroke in 2005. This means that, on average, one American suffers a stroke every 40 seconds. For 600,000 people this will be their first stroke, but 180,000 of the strokes are recurrences. Eighty-seven percent of all United States strokes are ischemic, and 13% are hemorrhagic (Rosamund et al., 2008).

In the United States, between 20% and 25% of all stroke patients die within the first month after their stroke. After three months, 20% of all stroke patients are still being cared for in a hospital or other inpatient setting. Between 15% and 30% of all stroke patients will be permanently disabled. Stroke deaths steadily declined in the United States during the last half of the twentieth century.

During the last half of the twentieth century, the death rate from stroke steadily declined in the United States (NHBPEP, n.d.).

Transient ischemic attacks (TIAs) are harbingers of stroke. Fifteen percent of strokes are preceded by a TIA, and between 3% and 17% of all TIAs are followed by a stroke during the subsequent few months. One-quarter of the patients who have a TIA will die within a year.

As a class, hemorrhagic strokes are more destructive than ischemic strokes. Between 35% and 52% of hemorrhagic stroke patients die within the first month, and most of these deaths occur within the first two days. Only 20% of people suffering a hemorrhagic stroke will be functionally independent 6 months after the stoke.

Most people who have a stroke are older than 65 years, and the death rate from stroke rises with the patient's age. In developed countries, strokes are responsible for approximately 10% of all deaths. In the United States, 1 in 16 (6%) of all deaths are from stroke. This makes stroke the number 3 killer, behind heart disease and cancer. Stroke is the leading cause of serious long-term disability in the United States, and currently, approximately 3 million Americans are survivors of strokes.

The percentage of people in each age group who have had a stroke at some time in their lives. Most strokes occur in the elderly. These figures are for the United States in 2005 (NCHS, 2006).

Racial and gender groups differ in their tendencies to get strokes. In the United States, African Americans have the highest death rates from stroke. In terms of ischemic stroke, Caucasian men suffer from blocked carotid or vertebral arteries more than other groups, while women, African Americans, and Asian Americans have mores blockages of the deeper, intracranial arteries than Caucasian men. The frequency of hemorrhagic stroke is higher in African Americans and Asian Americans than in Caucasians.

PATHOPHYSIOLOGY OF STROKE

Blood Supply to the Brain

The brain is 2% of the body's mass, but it receives 17% of the output of the heart and it consumes 20% of the oxygen supply of the body. The brain receives this large volume of blood through two major arteries, the internal carotids, that run up from the chest in the front (anterior half) of the neck and through two smaller arteries, the vertebral arteries, that run in the back (posterior half) of the neck.

The carotids 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. The anterior circulation of the brain is formed by those cerebral blood vessels that are branches of the internal carotids. The posterior circulation of the brain is formed by those cerebral blood vessels that are branches of the vertebral arteries.

Obstructions of the anterior and posterior circulations produce different neurologic deficits. Anterior strokes tend to cause motor and speech disabilities, while posterior strokes tend to cause balance, vertigo, and vision disabilities.

The first branch of the anterior circulation is the ophthalmic artery to the retina, and a blockage of the entire anterior circulation will produce a characteristic sudden and painless blindness in the eye on the side of the blockage. Beyond the ophthalmic arteries, the anterior circulation supplies the bottom and sides of the cerebral cortices. These regions include the primary motor and sensory cortices, and blockages in the anterior circulation often cut blood flow to these cortices, producing motor weakness or sensory loss on the opposite side of the body.

The posterior circulation is fed by the vertebral arteries. Blockages of the posterior circulation can produce brainstem and cerebellar problems. Blood flow reductions in these brain regions cause problems in so-called vegetative functions, such as consciousness and respiration, and also problems in balance, hearing, motor coordination, and visual perception.

At a number of points, the anterior and posterior circulations are connected. In some patients, the collateral circulation between the two can compensate for partial blockages (Kothari et al., 2006).

Disruptions of the Blood Supply

When cerebral blood flow is reduced, the affected regions of the brain stop functioning, and the patient loses the ability to perform the tasks that are localized in those regions. Loss of blood flow is ischemia, and both ischemic strokes and hemorrhagic strokes cause ischemic damage. In addition to ischemia, hemorrhagic strokes cause damage from the loose blood that is accumulating in and around brain tissues.

ISCHEMIC DAMAGE

Loss of Stored Intracellular Energy

The brain uses a lot of energy, but it can only store a small amount of it. Ischemia immediately decreases the available oxygen and glucose, and neurons run low on their ATP (intracellular energy stores) within seconds. Once the available ATP is completely used up, membranes depolarize and extracellular ions flow into the cells, which swell with the accompanying inrush of water. Massive amounts of neurotransmitters are released, and excess calcium floods the cytoplasm and sets off uncontrolled intracellular changes. In these ways, the nerve cells become damaged, but they have no energy to re-establish their metabolic equilibrium and to repair their membranes.

This worst-case scenario happens when the blood supply to the brain is cut off entirely, as occurs during cardiac arrest; here, neurons are irreversibly damaged and many of them die within a few minutes. On the other hand, after the occlusion (blockage) of a major cerebral vessel, such as occurs in an ischemic stroke, there is often sufficient remaining blood flow to delay the rate of neuronal death (Oechmichen & Meissner, 2006).

The First Response: Neurons Stop Signaling

When cerebral blood flow is reduced, electrical activity stops and the ischemic region of the brain becomes silent. For a time, the neurons are still alive in the region, but they do not have the energy to respond to stimuli or to transmit signals. Clinically, the patient has neurologic deficits, although the neurons are, at first, not irreversibly damaged. When cerebral blood flow drops below approximately one-third of normal, however, neurons are living on the edge, and many will begin to die within an hour (Arieff, 2004; Patel, 2005; Smith et al., 2005).

Reduced Blood Flow Creates an Ischemic Penumbra

Typically, a stroke does not produce the total ischemia that occurs after the heart stops beating. The cerebral circulation has interconnections and, after a stroke, blood can get to some brain regions via more than one route. In addition, strokes often leave some arteries only partly blocked. For these two reasons, most strokes reduce the blood supply to brain regions gradually.

In a typical stroke, the central core of the affected region can be entirely (or almost entirely) without oxygen and glucose. However, the edges of the core area receive some blood, although it is a reduced amount. In this border zone, neurons become silent, but not all of the neurons die quickly.

The border zone of ischemia is called the ischemic penumbra. In the penumbra, blood flow has been reduced and the local neurons have stopped functioning, but many neurons still have the potential to recover, at least for a limited time.

The Therapeutic Window After Acute Ischemia

After a stroke, the amount of irreversible damage increases steadily as long as regions remain ischemic:

• In areas with no blood flow, neurons begin to die in less than 10 minutes.
• In areas with less than 30% of normal blood flow, neurons begin to die within an hour.
• In areas with less than 40% of normal blood flow, some neurons begin to die within an hour, but others can be revived for a day or more.

Clinically, it has been found that collateral and residual blood flow can preserve many neurons in the penumbral areas for as long as 6 hours after an ischemic stroke. In this 6-hour window, treatments can reduce the amount of damage that will be irreversible. One treatment—intravenous (IV) administration of a clot-dissolving drug—has produced an eight-fold improvement in the outcomes of ischemic strokes when the drug is given within the first 3 hours after symptoms appeared.

The clot-busting drug continues to be helpful 3 to 6 hours after the onset of an ischemic stroke, but the increased bleeding caused by the drug cancels its effectiveness after about the first 3 hours (Adams, 2007); therefore, the effective clinical window for treating ischemic strokes with clot-dissolving drugs comprises the first 3 hours after the onset of the stroke.

HEMORRHAGIC DAMAGE

Cerebral hemorrhage is less common than arterial obstruction. When a cerebral blood vessel leaks, blood fills the surrounding areas and pushes on the nearby tissues. The pressure of the hematoma (extravascular pool of blood) constricts arteries and causes ischemia. A large hematoma can also squeeze brain tissue against hard surfaces of the skull and the dural septa. The effect of the pressure, the mass effect, of a hemorrhagic stroke produces more ischemia and damage. In addition, the accumulating blood filling the extravascular spaces has direct toxic effects on the neighboring brain tissue.

SIGNS AND SYMPTOMS OF A STROKE

Strokes show up as a sudden, usually painless change in a person's ability to move, feel, talk, or understand (Smith et al., 2005; Kuehl & Nolan, 2007).

STROKE SYMPTOMS

Ischemic strokes typically cause one or more of these symptoms:

• Unilateral weakness
• Unilateral numbness
• Difficulty speaking
• Vision changes
• Difficulty walking

Hemorrhagic strokes can cause the same symptoms as ischemic strokes. In addition, they may cause one or more of these symptoms:

• Severe headache
• Vomiting
• Syncope
• Increasing lethargy, stupor, or coma
• Neck stiffness
• Markedly elevated blood pressure.

Typically, the symptoms of hemorrhagic stroke worsen over the first few hours.

The underlying principles of acute stroke management are these:

• Quick and efficient treatment of a stroke can often limit or even reverse the loss of brain function.
• All potential strokes should be treated as a 911 emergency.

These principles should guide all levels of stroke management, from the patient and bystanders to the prehospital personnel to the hospital staff. The following briefly outlines the optimal roles of people at each of these levels (Adams et al., 2007; Goldstein, 2007a,b; Khaja & Grotta, 2007; Kuehl & Nolan, 2007).

QUICK RESPONSE: OVERVIEW

Patient and Bystanders

The public in general, and potential stroke patients in particular, should be taught the basic signs and symptoms of a stroke. When these signs or symptoms occur, people should call 911 without hesitating.

Prehospital Response

EMS DISPATCHERS

911 dispatchers should ask about specific signs and symptoms of stroke and should assign potential stroke the highest priority—that is, an emergency status comparable to a heart attack. One of the most important facts that dispatchers should try to ascertain from callers is the time of onset of the symptoms of a possible stroke.

EMS TECHNICIANS

EMS teams should:

• Manage airway, breathing, and circulation
• Use a standardized set of screening tests for the likelihood of stroke
• Determine the time of onset of the symptoms of any potential stroke
• Begin medical management during transport to save time
• Treat hypoxemia with supplemental oxygen
• Monitor mental status, body temperature, electrocardiogram (ECG), blood pressure, and blood glucose levels, but not treat abnormalities without guidance from ED physicians
• Immediately transport any potential stroke patients to the nearest hospital that is best able to handle acute strokes.

Hospital Response

Emergency department teams should:

• Treat life-threatening conditions and stabilize the patient
• Screen for stroke with a standardized set of tests
• Determine the time of onset of stroke symptoms
• Determine the medical history and current medications of the patient
• Monitor blood pressure, ECG, blood glucose, and neurologic status
• Get prompt blood chemistries
• Get emergency CT head images
• Formulate an immediate medical and stroke management plan:
• Consider thrombolytic therapy for acute ischemic strokes
• Consider medical or surgical interventions for increased intracranial pressure from hemorrhagic strokes
• Treat co-existent problems (trauma, heart, lung, kidney, metabolic, circulatory)
• If necessary, consider quick transport to a better-equipped stroke center or neurosurgical center.

As an example of efficient acute stroke management, the section "Stroke Treatment by Remote Consultation" near the end of this course, presents the case history of a patient who came to the ED with an acute ischemic stroke. It summarizes her progression through the emergency system, including treatment with the thrombolytic drug, alteplase (rt-PA).

Use of Stroke Scales

Current recommendations emphasize that, at each step along the way, objective assessment tools—that is, stroke scales—should be used as diagnostic guides and progress measures. The Internet Stroke Center lists the recommended measurement tools for assessing the extent and the effect of strokes; the list is available at http://www.strokecenter.org/trials/scales/scales-overview.htm.

DETAILS OF EMERGENCY TREATMENT

[Sources of material in this section are, predominantly, Smith et al., 2005; Adams et al., 2007; and Goldstein, 2007a,b.]

Patient and Bystanders Response

PATIENT RESPONSE

Health professionals who care for people at risk for strokes should teach their patients the symptoms that signal a potential stroke. Tell patients to call 911, or to get someone else to call 911, if any of these symptoms occur suddenly:

• Loss of sensation on one side of their body
• Weakness or paralysis on one side of their body
• Problems walking
• Problems speaking
• Problems understanding
• Problems with vision
• A severe headache

Classic signs of a stroke (NINDS 2007).

FAMILY OR BYSTANDERS RESPONSE

People who have a stroke may be unaware of the seriousness of their sudden disability. In part, this is due to a misunderstanding of their bodies' signals; for instance, pain is a major symptom of illness, but most strokes are painless. In addition, stroke patients with damage to their nondominant parietal lobe may lose the ability to recognize that they are ill. Strokes can also cause confusion and a change in a person's level of consciousness. Therefore, it is often the family or a bystander who first recognizes that there is a medical problem and calls for help.

Time is critical in treating strokes, and the public should be taught (a) the symptoms of a stroke, and (b) to call 911 immediately if there is a possibility that a person is having a stroke. Kothari and colleagues (1999) developed a three-part test, the Cincinnati Prehospital Stroke Scale (CPSS), which is standardized and widely used as a quick way to identify stroke. The test asks potential stroke patients to:

• Smile
• Repeat a sentence
• Hold out both arms

If the problems occurred suddenly ("out of the blue"), asymmetric facial movements, an asymmetric ability to raise or hold up the arms, or slurred speech are indications of a potential stroke. (For more details, see "EMS Stroke Assessment," below.) To make these criteria more widely known and easier to remember, the CPSS test has been rephrased as the STRoke test, with the first three letters of stroke standing for:

• Smile
• Talk
• Raise arms

The public is being advised that the sudden onset of an abnormality in any of these three tests indicates a possible stroke.

In an emergency, people often feel that time is lost by waiting for an EMS team to arrive, so family members or bystanders hurriedly drive patients to the hospital themselves. 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 patient shortens the time lag between the onset of stroke symptoms and a specialist's 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 to the dispatchers automatically. At the moment, two telephone systems do not always give 911 operators the up-to-date, detailed location of callers: multi-line telephone systems (MLTS), which are used by many large organizations, and Voice over Internet Protocol (VoIP) services.

Getting help is the most important thing that a bystander can do for a stroke patient:

The one critical medical step that the public should know is how to control external bleeding. First aid providers should press on the bleeding area until either the bleeding stops or the EMS team arrives. When a person calls 911, the operator can give additional guidance for any necessary first aid (AHA 2005).

Prehospital Response: The EMS Team

The professional care of stroke patients 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 must begin within a 3-hour window after the onset of symptoms, and strokes should have the same priority of treatment as acute MIs and trauma.

Dispatchers and EMS technicians have three special tasks when managing potential stroke. First, the EMS team must make an educated assessment of the likelihood that the patient has had or is having a stroke. Second, they must try to determine either the time of onset of the stroke symptoms or the last known time when the patient was symptom-free. Third, they must expedite the patient's transport to the nearest hospital equipped to handle strokes.

Directors of EMS units should write a stroke protocol for their team. The dispatchers and technicians should practice using a standard screening test for determining the likelihood of a stroke. In addition, the region that the EMS unit covers should be mapped into districts according to the nearest emergency departments capable of treating acute stroke (Kothari et al., 2006; Crocco et al., 2007; Millin et al., 2007).

EMS DISPATCHERS

EMS operators and dispatchers have these important roles. They must:

• Choose, notify, and send the team of responders appropriate for each emergency.
• Advise the callers on possible first aid for the patient.
• Try to get critical background information about the patient.

For strokes, dispatchers should make a special effort to get an estimate of the time that potential stroke symptoms first appeared (Acker et al., 2007; Crocco et al., 2007; Millin et al., 2007).

Dispatchers must be alert to:

• Identify possible strokes
• Assign them the highest priority
• Collect critical information
• Forward a written record to the emergency department

When assigning response teams, EMS dispatchers need to assess the type and severity of the emergency. To make the most useful decisions for stroke patients, 911 operators should be trained to identify likely stroke symptoms. When a dispatcher is able to flag a possible stroke, the EMS team can be given time to review and plan during their outbound trip.

Strokes account for only 2% of all 911 calls, and this translates to only 4 to 10 stroke patients each year for the typical EMS team (Acker et al., 2007). The infrequency of stroke calls means that EMS operators will not have stroke questions at the tips of their tongues, so a written set of screening questions should be at each operator's desk.

911 OPERATOR QUESTIONS

Normally, the questions asked by a 911 operator include:

• Is the patient injured?
• Is the patient bleeding?
• Is the patient breathing normally?
• Is the patient unconscious?
• Is the patient awake and alert? (NJ EMD Cards, 2004)

When considering a stroke, the questions should also include:

• Does the patient have a new weakness of one side of the body?
• Does one side of the patient's face droop more than before?
• Is the patient's speech more slurred than before? (NJ EMD Cards, 2004)

With potential stroke, dispatchers must assign the highest priority. 911 dispatchers decide what type of response is appropriate for each emergency: they choose the skill level and equipment of the EMS response team—basic life support (BLS) or advanced life support (ALS), the type of vehicle to send, and the initial speed requirement (eg, sirens and flashing lights). 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 (Adams et al., 2007).

When available, an ALS team should be 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 the American Heart Association's advanced cardiovascular life support (ACLS) and are prepared to administer all ACLS Class I and Class II interventions on each stroke response" (Acker et al., 2007).

If a choice has to be made, 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 an EMS operator suspects that a call concerns a potential stroke, the operator begins to collect critical background information.

CRITICAL BACKGROUND INFORMATION

• The patient's medical history, asking specifically about:
  
  Past strokes
• TIAs
• Hypertension
• diabetes
• MIs and other heart problems
• atherosclerosis and peripheral artery disease
• bleeding disorders
• recent surgeries
• liver disease
• The patient's current medications, asking specifically about:
• Aspirin, anticoagulants, and antiplatelet agents
• insulin
• antihypertensives
• cocaine and other street drugs
• excess alcohol intake
• The time when the stroke symptoms first appeared and/or the last time the patient did not have symptoms
• Whether the patient has recently been injured, asking specifically about head trauma

It is essential that the dispatcher forward a written record. Written records of the information collected during the first contact with the patient can be critical for doctors making decisions about treatment. EMS operators should have a blank checklist that can be filled in with essential background information and with the results of stroke screening questions. This document is then sent electronically to the ED that is receiving the patient.

EMS TECHNICIANS

[Sources for the material in this section include Tirschwell et al., 2002; Acker et al., 2007; Crocco et al., 2007; and Millin et al., 2007.]

Emergency Stroke Protocol

When they reach the patient, members of the EMS response team should follow the standard protocol by assessing the situation and stabilizing the patient. In cases in which there is a question of stroke, paramedics should then make a determination of the likelihood of stroke, collect critical background information, and provide as much of the patient care as possible while en route to the hospital.

The EMS protocol for likely stroke (modified from NHTSA, 2002) includes the following:

• Orient the patient
• Check the ABCs (airway, breathing, circulation)
• Determine likelihood of stroke
• Collect critical background information
• Prepare the patient for transport
• Transport the patient
• Determine additional prehospital care

To help orient the patient, state your name and tell the patient that you are part of the emergency team that has come to help.

Always check the ABCs (airway, breathing, and circulation) first. 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. Even when the patient appears to need no airway care, the EMS response team must be alert to the sudden appearance of breathing problems.

After stabilizing the patient, determine the likelihood of stroke. EMS responders should determine 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. Without a screening test, trained paramedics recognized only 61% to 72% of strokes, but using a standardized test paramedics recognized more than 90% of strokes (Crocco et al., 2007).

First, characterize the level of consciousness using A, V, P, or U:

• Alert
• Responds to Verbal stimuli
• Responds to Painful stimuli
• Unresponsive (no gag or cough)

Second, determine for yourself the likelihood that the patient has had a stroke. (See "EMS Stroke Assessment," below.) Specifically, use the Cincinnati Prehospital Stroke Scale (Box 1).

Regardless of the information collected by the 911 dispatcher, paramedics should attempt to collect critical background information about the patient. Question whoever is available—the patient, family, or bystanders. Specific goals are to determine:

• Time of onset of symptoms
• Current medical conditions and recent surgeries
• Current medications

Because time is of the essence, get telephone numbers of relatives and witnesses. If a knowledgeable acquaintance is available, have them meet you at the receiving hospital, or, if necessary, transport them with you. For emergency treatments, it will be helpful if next-of-kin are immediately available for consent.

Written records should be kept and then passed on to the medical team at the receiving hospital. Ideally, EMS teams carry prepared checklists with the essential questions and with blank spaces for all the critical information.

When preparing the patient for transport, maintaining airway, breathing, and circulation are the first priorities. For strokes, keeping the head flat (supine, or 0° 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, transport the patient to the appropriate ED and continue the rest of the prehospital care en route.

Additional Prehospital Care

Additional prehospital care may include the following.

• 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 hypoxia (oxygen saturation <95%) with supplemental O₂. (Currently, there is no indication that supplemental oxygen will benefit a patient who already has a normal 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 (no more distal than the antecubital fossa). If the receiving hospital will need a specialized IV line, time can be saved by having the appropriate line established in advance.
• IV fluids. Treat shock or significant dehydration with balanced salt solutions (isotonic crystalloids, such as normal saline). Otherwise, either 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: First, watch for serious cardiac consequences. The brain's reaction to stroke includes an increase in the body's sympathetic tone, which predisposes a person to arrhythmias and MIs. Second, screen for cardiac causes. Strokes can be caused by pre-existing atrial fibrillation or by atherosclerosis (which can already have caused heart damage).
• Hypertension management. Hypertension is a common finding in acute stroke. However, blood pressure management is an art in stroke patients, and the choice of treatment depends on a detailed diagnosis that can only be made in a hospital. Therefore, current recommendations are that EMS personnel should not attempt to treat high blood pressure.

Transport to an Emergency Department

Transport involves choosing the best receiving hospital and then alerting the emergency department at that facility. Each EMS unit should have maps showing the nearest appropriate ED for stroke patients in any area (Adams et al., 2007; Crocco et al., 2007). Ideally, you will be near a stroke center—a hospital certified as fully equipped to deal with acute strokes. (See "Stroke Centers," below.) Other appropriate hospitals are those with:

• CT and/or MRI machines and radiologists skilled in interpreting cranial images
• Neurologists, neurosurgeons, or emergency medicine specialists skilled in diagnosing and managing strokes
• Facilities for immediate treatment of ischemic and hemorrhagic strokes
• A pre-existing plan for efficiently identifying and treating acute strokes

Clot-dissolving treatment for ischemic strokes (rt-PA) must be started no more than 3 hours after the onset of symptoms. If it is possible to reach an appropriate ED in time, EMS teams should bypass nearer hospitals. For advice in each case, consult with the best stroke ED in the area while en route.

As they work, members of the EMS team should be in contact with the destination ED. Simply notifying the receiving hospital that a potential stroke patient will be arriving has been shown to shorten the time between delivery to the hospital and receipt of treatment. Describing the patient's condition, time of symptoms onset, and medical history allows the doctors, nurses, imaging specialists, and pharmacists of the acute stroke team to mobilize.

Information goes both ways 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.

When stroke patients are more than 1 hour's travel time by ambulance from a hospital equipped to treat acute stroke, then air transport (helicopters) should be considered. Helicopters can be used to take the EMS team to the patient and then transport the patient and EMS team to a stroke center. Helicopters can also be used for secondary transport of patients from a remote receiving ED to a stroke center.

Hospital Response: Emergency Departments (EDs)

All patients with suspected acute stroke should be triaged with the same priority as patients with acute MI or serious trauma, regardless of the severity of the neurologic deficits. Approximately half of all stroke patients will not use an EMS service to come to the ED, and these people will not have been prescreened for stroke symptoms. Therefore, the ED sign-in staff should be trained and alerted to look for signs of possible stroke (Box 2) (Kothari et al., 2006; White et al,. 2007).

EMS transporters should attempt to deliver potential stroke patients to hospitals that have been designated as stroke centers. Stroke centers, by definition, have well-rehearsed protocols for dealing efficiently with stroke patients. (See "Stroke Centers," below.) However, not all regions are served by stroke centers, and even when stroke centers are accessible, approximately half of all stroke patients coming to EDs do not use EMS transportation. For these reasons, all EDs should prepare protocols for quickly assessing patients for possible stroke and for then either determining the type and severity of the stroke and treating it quickly or having the patient immediately transported to the nearest stroke center.

For patients presenting with acute stroke symptoms, the American Heart Association / American Stroke Association guidelines (Adams et al., 2007) recommend that—after stabilizing the patient's airway, breathing, and circulation—all EDs should assess the severity of the stroke using the NIHSS rating system (Box 3, below). Physicians are encouraged to quantify the severity of a patient's stroke by using a standardized stroke scale, and currently, the NIH Stroke Scale (NIHSS) is the recommended tool (Adams et al., 2007).

Standardized stroke assessment tools do not replace the neurologic exam. Instead, the stroke scale is an efficient way to determine objectively the extent of neurologic damage. The result of the initial test is an aid when choosing between available treatments, and subsequent tests can be used to quantify the amount of neurologic improvement or deterioration.

Testing via the NIHSS takes 5 to 8 minutes and requires no special equipment. On the NIHSS, points are assigned for neurologic deficits, and 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. Overall, scores <5 indicate mild neurologic impairment, 10 to 20 indicates moderate impairment, and >20 indicates severe impairment, while >22 is termed a major stroke. Box 4 presents further information about potential outcomes.

DIAGNOSING AND CATEGORIZING ACUTE STROKES

Strokes that are treated quickly have better outcomes, and the sooner the stroke is diagnosed and categorized, the sooner the appropriate treatment can be started. During the initial evaluation of a patient suspected of having a stroke, three evaluations should be going on simultaneously:

• To exclude stroke mimics (conditions that give stroke-like symptoms)
• To determine whether there has been a stroke
• To recognize other medical problems that require immediate management (Adams et al., 2007)

Stroke Mimics

Other disorders can look like stroke, especially before the time course of the symptoms and the medical history of the patient have been determined. Hypoglycemia, the aftermath of a seizure, intoxication, drug overdose, migraines, tumors, and infections (encephalitis, meningitis) can all present with stroke-like symptoms. Standardized stroke screening tools such as the CPSS and the NIHSS are independent of any information from the medical history and can help tp quickly distinguish strokes from stroke mimics (Ropper & Brown, 2005; Smith et al., 2005; Kuehl & Nolan, 2007; Saver & Kalafut, 2007).

In addition to stroke screening tools, the history of the symptoms and the medical history of the patient are usually strong clues to the diagnosis when they are available. Strokes tend to have a characteristic overall presentation.

Ischemic strokes cause an abrupt onset of focal (specific) neurologic deficits; even those ischemic strokes that develop over time usually progress in abrupt steps. In contrast, tumors, abscesses, and demyelinating disorders can cause focal deficits, but the symptoms from these disorders typically worsen gradually, over a period of days or longer. Focal deficits can also be caused by hypoglycemia, epidural hematoma, peripheral and cranial neuropathies (eg, Bell's palsy), and migraines. Each of these nonstroke conditions should be considered and ruled out.

In contrast to ischemic strokes, hemorrhagic strokes tend to worsen gradually. Intracerebral hemorrhages frequently progress quickly during the first several hours; the classic presentation of an intracerebral hemorrhage is the sudden appearance of a focal neural deficit that worsens or spreads quickly in minutes or hours. Symptoms of subdural hematomas, however, can appear and worsen gradually over days or weeks.

Hemorrhagic strokes often present with severe headache and vomiting in addition to neurologic deficits. Other causes of neurologic deficits with headache and/or vomiting include migraine, hypertensive encephalopathy, giant-cell arteritis, and subdural or epidural hematomas. Headaches are also common after seizures.

Hemorrhagic strokes commonly cause an impaired level of consciousness. Besides hemorrhagic stroke, the major causes of coma are intoxication and cranial trauma. Other common causes of a reduced level of consciousness include epilepsy, drug overdose, diabetes, and severe infections. Meningitis and encephalitis can also change a patient's level of consciousness, as will systemic hypotension.

Finally, remember that acute systemic illnesses will often unmask or reactivate focal neurologic deficits from a previous stroke. Thus, other illnesses can make it appear as if the patient has suffered a new stroke.

Stroke Assessment Protocol for All Hospitals

To help in their decision as to where to take potential stroke patients, the EMS system should be given a summary of all stroke plans for the EDs in their region. Approximately half of acute stroke patients do not arrive at EDs via the EMS system. Therefore, although not all EDs are equipped to manage acute strokes, all EDs need a stroke assessment protocol: regardless of its capabilities, each hospital with an ED may have to deal with stroke patients, and each ED needs a written plan that details its level of acute stroke management.

For any patient presenting to an ED with acute stroke symptoms, the American Heart Association and the American Stroke Association (Adams et al., 2007) recommend that after stabilizing the patient's airway, breathing, and circulation all EDs should assess the severity of the stroke using the NIHSS rating system. A trained member of the ED staff can make this assessment in 5 minutes. Patients with a reduced level of consciousness should also be rated on the Glasgow Coma Scale. This is a 3-minute task for a trained staff member. (See "ED Consciousness Assessment," below.)

Speed remains critical. Many patients with ischemic strokes can be helped by quick treatment with a drug that lyses (disintegrates) blood clots, and many patients with hemorrhagic stroke deteriorate rapidly and need specialized neurologic care in an intensive care unit (ICU). For acute strokes of all types, the recommended timetable calls for a complete evaluation and treatment plan to be completed within 60 minutes of the patient's arrival at the ED.

Hospitals not equipped to carry through a complete stroke evaluation and subsequent treatment should have a protocol in place for a fast initial evaluation followed by the immediate transport of acute stroke patients to the nearest hospital that has the needed facilities.

ED Consciousness Assessment: Glasgow Coma Scale

For hemorrhagic strokes, the Glasgow Coma Scale is an important guide for predicting the neurologic outcome. This scale is not a diagnostic tool, and it does not replace the neurologic exam. Instead, the Glasgow Coma Scale is a widely used and standardized way of quantifying the severity of the injury underlying a patient's change of consciousness (Smith & Grady, 2005; Bleck, 2007).

The Glasgow Coma Scale has been a part of neurologic practice for thirty-five years as an objective and reproducible way to describe a patient's level of consciousness and arousal. Administering the scale takes 3 to 5 minutes and requires no special equipment. External stimuli are given to a patient, and the tester rates three neurologic aspects of the patient's response: eye opening, limb movement, and vocalization. A sample scoring form is available at http://www.strokecenter.org/trials/scales/glasgow_coma.pdf.

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 neurologic deficiency. (This is opposite to the NIHSS, in which higher scores indicate more severe deficits.)

Glasgow Coma Scale scores less than 9 indicate coma. Patients with scores less than 5 have a greater than 85% chance of dying in the first 24 hours, while patients with scores over 11 have a greater than 85% chance of recovering with no worse than a moderate disability.

Stroke Assessment Protocol for Stroke Hospitals

When a potential stroke patient enters a hospital with the staff and facilities to treat acute ischemic strokes, the ED staff begins a protocol that can lead directly to the administration of a thrombolytic drug.

Typically, such hospitals have a stroke team with two divisions. A code team (a neurologist or ED stroke specialist and a neurology nurse) always available to respond to a page and institute emergency care. There is also a larger support team, 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 (Lutsep & Clark, 2007).

Step I: Assessment, History, Physical Exam, and Labs

A stroke page is initiated either from an incoming EMS vehicle or from the ED triage person. The stroke code team then reports to the ED, joins the ED receiving team, and begins the acute stroke protocol. The first part of the stroke protocol includes administering the NIHSS to rate the severity of the stroke (Box 5). Patients with a reduced level of consciousness should also get a Glasgow Coma Scale score. Additionally, critical background information (time of onset of symptoms, medical history, and current medications) are collected.

These steps are followed by (or done concurrently with) a complete neurologic exam and a selected clinical exam that includes an ECG, because cardiac problems are common in people with stroke. (In this time-limited stage, a chest x-ray is warranted only when needed for immediate decisions about heart or lung problems.) Meanwhile, a selected set of blood tests is processed. (The ED stroke protocol should describe when to expand the basic stroke blood tests to include toxicology screening, liver function tests, lumbar puncture, or a pregnancy test.)

For speed and efficiency, the ED should have standing written orders for Step 1 of the acute stroke protocol. These orders can be enacted while the code stroke team is reporting to the ED (Lutsep & Clark, 2007).

During the brief physical exam, certain features deserve special attention (Chung et al., 2007; Jauch et al., 2007):

• Vital Signs
• Oxygen saturation (pulse oximetry) must be monitored continuously because all attempts to limit or reverse ischemic damage depend on having an optimal oxygen concentration in the circulation
• Blood pressure is often elevated in a stroke. Pressures of >220 mm Hg may be a result of, or a cause of, intracerebral hemorrhage.
• Fever can be caused by bleeding into the ventricles.
• Head
• In relation to stroke, loss of consciousness can be caused by a subarachnoid hemorrhage, an ischemic stroke with blockage of the basilar artery (supplying the brainstem), or increased intracranial pressure.
• Severe headache often accompanies hemorrhagic strokes.
• Contusions or tongue lacerations may be a result of a seizure.
• Signs of head trauma may be clues as to the cause of the presenting symptoms.
• Neck
• Carotid bruits can indicate atherosclerotic artery disease.
• Jugular venous distension (JVD) can indicate congestive heart failure.
• Heart
• In addition to doing a cardiac physical exam, including auscultation, 12-lead ECG recordings should be taken for all stroke patients.
• Atrial fibrillation puts a patient at risk for stroke, and conversely, acute strokes can cause arrhythmias.
• Patients with coronary artery disease have a high risk of stroke, and an acute MI can precipitate a stroke. Conversely, strokes can lead to myocardial ischemia.
• Abdomen
• Vomiting is common in hemorrhagic strokes, but it is rare in ischemic strokes.
• Skin
• Jaundice (liver disease), 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.

The two critical laboratory tests for acute stroke patients are blood sugar levels and coagulation studies (Kothari et al., 2006; Adams et al., 2007). A serum glucose level should be determined for all patients who appear to have had a stroke, because either extreme of blood sugar should be treated. Hypoglycemia can mimic a stroke by causing focal neurologic deficits, while persistent hyperglycemia will worsen stroke damage.

Before using a thrombolytic agent (rt-PA) to treat an ischemic stroke, a platelet count can warn of the possibility of inducing or worsening hemorrhage. If there are reasons to suspect pre-existing bleeding abnormalities (eg, from liver disease, recent warfarin therapy, or a known coagulopathy), then the patient's prothrombin time (usually given as the international normalized ration, INR) should also be measured before giving the patient rt-PA.

Getting other basic stroke blood chemistry results should not be allowed to delay treatment with rt-PA. The other tests that should be requested, however, are a complete blood count, serum electrolytes, renal function tests (blood urea nitrogen and creatinine levels), cardiac enzymes, and activated partial thromboplastin time.

Additional tests may be warranted by the specific situation. For example, an examination of the cerebrospinal fluid can be used to diagnose a suspected subarachnoid hemorrhage even when the CT scan does not show blood. For young or middle-aged patients, consider a toxicology screening test for street drugs. For women of childbearing age, a pregnancy test should be done.

Step 2: Brain Imaging

If the patient has been diagnosed with an acute stroke, the next question is which immediate treatments will be of most benefit. The critical distinction is between ischemic stroke, in which clot-dissolving therapies can be effective, and hemorrhagic stroke, in which clot-dissolving therapies can worsen the damage.

Brain imaging is the fastest way to distinguish between ischemic and hemorrhagic strokes, because bleeds (hematomas) show up clearly. Either CT or MRI can be used for diagnostic studies, but a noncontrast CT scan is usually the most practical (Arieff, 2004; Kothari et al., 2006; Chung et al., 2007; Khaja & Grotta, 2007).

CT scans can detect intracerebral bleeds greater than 1 cm in size and can identify 95% of all subarachnoid bleeds. Nonbleeding ischemic damage, however, is not easily seen in CT scans for 6 to 12 hours after the onset of a stroke.

A transverse (axial) noncontrast CT scan of a patient with a hemorrhagic stroke. Blood is seen as light areas along the left cerebral ventricle. The front of the head is at the top of the image. (Neurology Image Library 2004, © 2008 The Internet Stroke Center at Washington University, used by permission.)

The time goal for Step 2 in the treatment of an acute stroke is 45 minutes. Specifically, it is recommended that a CT scan be completed within 25 minutes of the patient's arrival at the ED, and the interpretation by an expert should be available within 20 minutes of the scan's completion.

There should be a standing order for a CT scan for all stroke patients, as well as a plan for getting the scan read quickly. This means that an experienced CT technician and a radiologist must always be available. (For speed, it may be most efficient for members of the stroke code team to transport stroke patients directly to the CT scanner themselves (Lutsep & Clark, 2007).

In some hospitals, MRI scans are being used as first-line brain imaging for acute strokes. MRI and CT show intracerebral hemorrhages equally well. On the other hand, MRI is better able to detect acute ischemia than is CT. MRI is also better at detecting infarcts in those brain regions fed by the posterior cerebral circulation.

Currently, MRI is less widely available and is more expensive than CT scans. In addition, certain patients cannot be subjected to MRI: MRI scans cannot be done on patients with cardiac pacemakers or metal implants, and it is difficult or contraindicated in some patients with impaired consciousness, respiratory or hemodynamic instability, vomiting, or agitation.

THERAPY FOR ISCHEMIC STROKE

Saving the Penumbra

An ischemic stroke usually causes a gradient of decreased blood flow. In an ischemic stroke, the central area (the core) served by the blocked artery or arteries receives the least oxygenated blood—often none at all. At the same time, the periphery of the fields of the blocked arteries can still be receiving sufficient blood flow to keep brain tissue alive; these peripheral areas are the penumbra of the stroke.

Neurons are sensitive to decreases in oxygen and glucose, and even small decrements in local blood flow will stop neurons from being able to transmit signals. For this reason, the entire field of the blocked arteries in an ischemic stroke will stop functioning.

Often, the core of the stroke infarcts fairly rapidly, because any brain tissue that is receiving no blood flow begins to die in less than 10 minutes. The penumbra, however, can still be receiving sufficient blood flow to keep 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.

Current treatments of ischemic stroke try to reperfuse the penumbral regions of the brain before the blood-starved neurons die. At the moment, the main reperfusion technique is thrombolysis, or dissolving the arterial obstructions with a clot-lysing drug (Bravata et al., 2002; Arieff, 2004; Smith, 2007; White et al., 2007).

Thrombolysis

Treatment with a thrombolytic drug improves the outcome of patients with acute ischemic strokes (Adams et al., 2007; Grotta & Marler, 2007; Khaja & Grotta, 2007; Mecozzi et al., 2007; Smith, 2007; White et al., 2007). Three months after treatment, 80% of patients will survive. Of the survivors, 60% will be independent in their activities of daily living, 20% will be moderately dependent on others, and 20% will be completely dependent. Approximately one-third of the survivors will be almost normal neurologically (Saver & Kalafut, 2007).

As many as a quarter of the ischemic stroke patients seen in the ED arrive within 3 hours of the onset of their symptoms. If these strokes can be diagnosed within the 3-hour window, then it is possible to consider using drugs to lyse the obstructing clots. Currently, recombinant tissue plasminogen activator (rt-PA) is the only thrombolytic agent with FDA approval for use in ischemic stroke. The American Heart Association / American Stroke Association guidelines recommend administering intravenous rt-PA (0.9 mg/kg, maximum dose 90 mg) to selected patients within 3 hours of onset of ischemic stroke (Adams et al., 2007).

Eligibility

Three hours is the time window in which treatment with rt-PA can be started. The EMS team may already have discovered the time of onset of the patient's stroke, but the ED team should attempt to confirm the time. Patients who are awake can often give enough information to estimate a time of onset. Witnesses or family members are also potential sources of information, in person or by telephone.

If the patient is aphasic or comatose and if no one witnessed the onset of symptoms, then the time of onset is taken to be the last time the patient was known to be symptom-free. For patients who awaken with stroke symptoms, the time of onset is taken to be the time they went to bed.

For a patient whose symptoms are progressing, the time of onset is the first appearance of any symptoms. When a stroke patient has had a previous transient ischemic attack (TIA) that resolved completely, the time of stroke onset is taken to be the onset of the current symptoms.

Two things are necessary for the safe use of rt-PA: the accurate diagnosis of an acute ischemic stroke, and the adherence to a set of inclusion and exclusion criteria describing which ischemic stroke patients should receive rt-PA. Eligibility criteria for rt-PA include having normal blood levels of glucose, acceptable numbers of platelets, and normal clotting functions studies. The patient must not be at risk for bleeding from recently healed surgeries or internal injuries. Any indication of intracranial hemorrhage is an absolute contraindication for rt-PA. In addition, the patient should not have significant hypertension (Saver & Kalafut, 2007). See Box 6.

Treatment Plan

In a stroke center, rt-PA should be given intravenously for those ischemic stroke patients who are eligible. The recommended does is 0.9 mg/kg, with 10% given as a bolus and the remainder infused over >1 hour (Saver & Kalafut, 2007). The total amount of rt-PA given should not exceed 90 mg. The rt-PA must be administered promptly, therefore stroke EDs must have a plan in place for getting the drug from the pharmacy quickly at any hour (Lutsep & Clark, 2007). Procedures that have a risk of inducing bleeding, such as inserting Foley catheters or nasogastric tubes, should be done before administering rt-PA.

Patients who are being treated with rt-PA need to be monitored closely in an ICU for at least 24 hours. Their vital signs should be checked every 15 minutes for 2 hours, every 30 minutes for the next 6 hours, and once every hour for the following 16 hours. In addition, a neurologic assessment should be done when the vital signs are taken.

Blood pressure should be maintained at less than 180/105 mm Hg. Antiplatelet drugs and anticoagulants should not be given during the first 24 hours, and arterial punctures should not be done. Likewise, intra-arterial catheters, nasogastric tubes, and indwelling bladder catheters should not be inserted during the first 24 hours. Even in the best of circumstances, almost one-third of patients will develop oozing from around IV lines and at venous puncture sites after rt-PA treatment.

Symptoms that warn the physician to stop the rt-PA infusion and to get an emergency CT scan include severe headache, acute hypertension, nausea, or vomiting. After treatment with rt-PA, there is a ten-fold increase in the risk of developing intracerebral hemorrhaging (6.4% with rt-PA versus 0.6% without rt-PA). This new hemorrhaging may cause sudden hypertension, headache, nausea, or vomiting, and the patient's neurologic condition can deteriorate.

These signs and symptoms should trigger an immediate CT scan and blood work to check platelet count and coagulation function. Emergency neurosurgical and hematologic consults should be called to advise on the immediate treatment plan (Saver & Kalafut, 2007).

Future Treatments for Ischemic Stroke

Therapy for acute strokes is an active area of research, and a number of techniques are currently being tested to improve the rate of recanalization of blocked cerebral arteries. One line of research attempts to enhance the effects of intravenous rt-PA with additional antithrombotic drugs or ultrasonic energy. Another research program is exploring the use of intra-arterial rt-PA after treatment with intravenous rt-PA.

In a different approach, endovascular mechanical extraction techniques have already been used to remove clots from large cerebral arteries. In addition, brain imaging or higher resolution is being developed to better match patients, therapeutic techniques, and time windows (Grotta & Marler, 2007).

Another promising area of research is the field of neuroprotection— techniques and pharmaceuticals that prolong the life of those neurons that are receiving reduced blood flow. One result of ischemia is that nerve cells depolarize, causing a destructive release of excess neurotransmitters, so drugs that selectively block excitatory neurons are being tested as neuroprotective agents (Lutsep & Clark, 2006).

Another possible neuroprotection technique is to lower the patient's body temperature. In some hypothermic situations (eg, after having been buried in an avalanche) patients have successfully been revived even when their brains had suffered more than 2 hours of oxygen deprivation (Oechmichen & Meissner, 2006). Animal studies have shown that it may be possible to produce a controlled hypothermia that will sometimes act as a temporary neuroprotectant.

THERAPY FOR HEMORRHAGIC STROKE

Hemorrhagic strokes cause brain injury by ischemia, pressure, and the toxic effects of free blood. A hemorrhagic stroke diminishes blood flow to the arterial field beyond the leak or rupture. At the same time, the mass of the increasing hematoma constricts other arteries (further reducing blood flow), compresses the brain against stiff surfaces (bone and dural flaps), and increases intracranial pressure. In addition, the leaked blood, which is now extravascular, imbalances the composition of the extracellular fluid and is destructive to neurons.

Currently, there is no standard way to treat hemorrhagic stroke. The treatment goals are to stop or decrease the bleeding and to remove the extravascular blood, but the appropriate plan of action must be decided on an individual basis.

Patients with hemorrhagic stroke should be admitted to an ICU. Their circulation must be kept well oxygenated, and their blood levels of nutrients, especially glucose, maintained in a healthy range. In general, a stroke patient's blood pressure should be kept within normal limits, but the effective management of the blood pressure and fluid levels of a patient with an intracerebral hemorrhage is a case-by-case balancing act.

Vital signs and cardiac functioning must be monitored regularly. Complications such as airway problems, increased intracranial pressure, and deep-vein thrombosis must be recognized quickly and dealt with effectively. Seizures are common, and their results are damaging, so anti-seizure prophylaxis (eg, phenytoin) is often instituted. Surgery is sometimes recommended for cerebellar hemorrhages.

Two early tests are the best prognosticators of the outcome of hemorrhagic strokes. Together, the volume of the intracranial bleed, as determined by CT or MRI, and the score on the Glasgow Coma Scale give a good prediction of the likelihood of death within the next 30 days.

TREATMENT OF ACUTE COMPLICATIONS

Approximately one-quarter of all acute stroke patients will deteriorate over the 24 hours following onset, and most patients diagnosed with an acute stroke should not be released from the ED but be directly hospitalized. Those few patients who are released should first be evaluated for the likelihood that they will develop a subsequent stroke.

Watchful monitoring and quick reaction to developing complications are the basis of acute care for stroke patients. The majority of acute stroke patients can be properly evaluated, monitored, and treated in medical units, which ideally will have staff trained in comprehensive stroke care.

Other patients—those with serious strokes, with hemorrhagic strokes, or post emergency treatment—should be monitored in an ICU. For these patients, the vital signs, neurologic assessments, blood values, and CT images that were determined in the ED can only be used as baseline values, and details of the patient's medical status must constantly be updated and reevaluated. Moreover, acute stroke patients come to the ED with a variety of concurrent medical problems, and these disorders add to the conditions that must be watched and treated.

Although the details vary, there are some general recommendations regarding complications that commonly arise in the first day of caring for an acute stroke patient (Kothari et al., 2006; Adams et al., 2007; Goldstein, 2007a, 2007b; Jauch et al., 2007; Khaja & Grotta, 2007).

Airway Maintenance and Ventilatory Support

Self-regulated breathing can be a problem for stroke patients, especially patients with hemorrhagic stroke or with damage to the brainstem. Such patients will usually have impaired consciousness or impaired airway reflexes, and an endotracheal tube should be inserted if the patient's airway or breathing mechanisms are compromised. The need for endotracheal intubation, however, is a poor sign, and approximately half of the acute stroke patients who are intubated die within 30 days.

Dysphagia

One-third of stroke patients have dysphagia (difficulty swallowing), and this can lead to aspiration pneumonia. Pneumonia is one of the most common complications of stroke, and it is a frequent cause of mortality.

Dysphagia is most common in those patients who also have breathing problems, although it can occur in patients with a seemingly normal level of consciousness. Warning signs of dysphagia and the accompanying potential for aspiration include difficulty speaking, a weak voluntary cough, and drooling. A good test for dysphagia is to watch the patient attempt to swallow a small amount (3 oz) of water. Even when patients appear successful in swallowing the water, if the voice is wet there is risk for aspiration. Patients should be NPO until their swallowing ability has been assessed.

Supplemental Oxygen

Poor oxygenation of brain tissue is one of the major causes of the neurologic deficits of a stroke, and longer times of oxygen insufficiency produce more irreversible damage. Therefore, it is critical to maintain a normal blood oxygen saturation of >95%. Hypoxia is treated with supplemental oxygen. Currently, it is not clear whether either supplemental or hyperbaric oxygen is helpful for stroke patients who already have normal blood oxygen saturations.

Temperature

Acute stroke patients with fever tend to have poorer neurologic outcomes. The current recommendation is to treat fevers with antipyretic drugs. Fever can be directly caused by a stroke, but stroke patients with a fever should also be assessed for infections.

Cardiac Monitoring

Strokes are often associated with heart problems, such as atrial fibrillation and coronary artery disease, and the initial screening of a potential stroke should include a cardiac exam, an ECG, and blood tests for cardiac markers. Conversely, strokes can cause arrhythmias and MIs. Therefore, stroke patients should have regular vital-sign checks and continuous cardiac monitoring to catch developing arrhythmias or acute coronary syndromes.

Hypertension

As many as 60% of all acute stroke patients have systolic blood pressures >160 mm Hg, and both extremes of blood pressure—hypertension and hypotension—will increase the likelihood that an acute stroke has a poor neurologic outcome.

Currently, recommendations for treating hypertension are tentative, and the consensus is to treat hypertension cautiously. The immediate treatment of high blood pressure should be tempered by the observation that hypertension declines spontaneously in many stroke patients during the first 24 hours.

Generally, it is suggested that markedly high blood pressures (>220 mm Hg systolic, or >120 mm Hg diastolic) should be lowered gradually by about 15% during the first 24 hours after an ischemic stroke. Patients with intracerebral hemorrhages are usually treated more aggressively for hypertension in an attempt to decrease the blood pressure's contribution to intracranial pressure; here, the goals are to maintain systolic pressure <180 mm Hg and diastolic pressure <105 mm Hg.

Blood Glucose

Both hypoglycemia and hyperglycemia are associated with increased brain injury after an acute stroke. Approximately one-third of the patients who present with acute stroke have hyperglycemia. Management of hyperglycemia in stroke patients is essentially the same as in other acutely ill patients.

Specifically, hyperglycemia of >140 mg/dl increases the likelihood of a poor outcome in stroke patients, and carefully administered insulin is recommended to reduce higher levels of blood glucose. Because hypoglycemia is also harmful to an injured brain, the effects of insulin must be closely monitored, and glucose and potassium should be available to buffer the effect of the insulin.

Increased Intracranial Pressure (ICP)

Hemorrhagic strokes can increase intracranial pressure (ICP) and this will manifest as neurologic deterioration. Deterioration can be monitored quantitatively by repeatedly applying the NIHSS and the Glasgow Coma Scale.

Treatments for increased ICP include positioning the patient nearly upright, controlling pain and agitation, and avoiding techniques and situations that increase intrathoracic pressure. (Moving some stroke patients to an upright posture worsens their neurologic status, so position changes must be done cautiously.)

Other possible treatments include: reducing the extravascular fluid volume with IV mannitol or hypertonic saline; inducing respiratory alkalosis with forced hyperventilation; sedating with barbiturates; reducing any hypertension; directly draining some CSF; or performing a craniotomy to decompress the intracranial space mechanically. All these treatments have considerable risks, and they should only be applied by experienced neurologic specialists and in ICUs equipped to handle neurologic crises (Evans et al., 2007).

STROKE CENTERS

When the care described above is available in a community, the overall outcome of acute stroke improves. High quality stroke care—ie, the care recommended by the American Heart Association and the American Stroke Association—requires a specially trained staff, appropriate facilities, and planned protocols, as well as practice and experience.

Most hospitals cannot afford the specialized staff and do not see enough cases of stroke to maintain the needed levels of practice and experience for emergency acute stroke treatment. It has been suggested that only certain hospitals take on the responsibility of maintaining the complement of people and technologies needed to treat acute strokes. These hospitals are called primary stroke centers (PSCs) (Gerber, 2003; Goldstein, 2007a, 2007b).

Primary Stroke Centers (PSCs)

Emergency departments vary in their ability to manage acute strokes, so there is currently a push to develop a core of primary stroke centers throughout the United States To standardize the requirements for a topnotch primary stroke center, the Joint Commission (formerly JCAHO) has developed a program to certify and designate particular EDs as primary stroke centers.

As of February 2008, 648 hospitals across the United States have been accredited as PSCs. Six states—Delaware, North Dakota, New Hampshire, New Mexico, Vermont, and Wyoming—still have no nationally accredited PSCs. The goal is to have a specialized stroke center within 100 miles of all cities in the United States (Adams et al., 2007).

To be certified as a PSC, emergency departments must be able to deliver basic stroke care. CT scanning must be available for emergency use and there should be experienced neuroradiologists on call. The ED must have a stroke team with neurologists or specially trained emergency physicians and with neurology nurses. The ED or its hospital must be equipped and staffed to treat ischemic stroke patients quickly with IV thrombolytic drugs. The hospital must also have medical units that can care for uncomplicated stroke patients. Finally, either in the hospital or within secondary transport range, there must be a neurosurgical team, endovascular surgeons, and a neurosurgical ICU.

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 a standardized record of its patients, their treatments, and the outcomes; these records are used to monitor the performance of the center (Joint Commission, 2007).

PRIMARY STROKE CENTER TIMETABLE

Primary stroke centers are dedicated to quick, efficient care. The recommended time targets for key steps in the management of acute stroke are (Adams et al., 2007; Jauch et al., 2007):

TIME TAKEN FOR KEY MANAGEMENT STEPS

• From the door to a physician: 10 minutes
• From the door to a completed CT: 25 minutes
• From the door to a CT scan reading by a specialist: 45 minutes
• From the door to thrombolytic treatment: 60 minutes
• From the door to admission to a monitored bed: 3 hours

TIME TO SPECIALIST CONSULTATION WHEN NEEDED

• Neurologist: 15 min
• Neurosurgeon: 2 hours

Comprehensive Stroke Centers (CSC)

A primary stroke center has the ability efficiently to diagnose and categorize strokes and to quickly administer certain acute therapies, most notably, intravenous rt-PA. Hemorrhagic strokes and ischemic strokes with major complications need a higher level of care, with dedicated neurologic ICUs and experienced neurosurgeons, endovascular surgeons, and neuroradiologists. Hospitals with these advanced stroke facilities are called comprehensive stroke centers (CSCs) (Smith 2007, White et al. 2007).

More hospitals have the staff and facilities to become primary stroke centers than 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 rt-PA. Patients with complex strokes, hemorrhagic strokes, and complications from rt-PA treatments would be rapidly transferred to the affiliated comprehensive stroke center.

STROKE TREATMENT BY REMOTE CONSULTATION

The time-dependent stroke treatments, such as intravenous rt-PA, are only recommended for hospitals with experienced staff and well-equipped facilities. Ideally, the treatment of acute stroke should be done in primary stroke centers. However, many areas of the country are far from primary stroke centers. One technique for extending the range of acute stroke treatments, especially the administration of thrombolytic agents, into rural areas, is video consultation.

The following 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 fine example of how remote consultation can take time-dependent stroke therapy far beyond the communities near primary stroke centers.

A LEGAL NOTE

Malpractice suits have been brought for failure to offer or to administer rt-PA to eligible patients (Saver & Kalafut, 2007). When it is consistent with the best clinical practice, thrombolytic therapy can be administered even if the patient is unable to authorize it and a legally authorized representative is not available. However, "best clinical practice" has not yet (as of February 2008) been firmly established across the United States.

The FDA guidelines are not precise, and, although the American Heart Association / American Stroke Association recommendations have begun to take hold, they are relatively new. Therefore, as a legal safeguard, physicians should remember to discuss treatment options—including getting a second opinion and transferring the patient to another institution—with patients and family when there is sufficient time, and then to document either the discussions or the need for immediate treatment without these discussions (Weintraub, 2006).

SUMMARY

An acute ischemic stroke is a medical emergency much like an MI: a brain attack needs fast, organized care just as does a heart attack. Both types of vascular accident can be caused by clots obstructing arteries, and both can leave some tissue underperfused but potentially revivable if circulation can be re-established within a critical time window.

Like the treatment for an acute MI, treatment for an acute stroke should be given high priority by EMS teams. There is a 3-hour interval after the onset of a stroke in which thrombolytic therapy (ie, intravenous rt-PA) can reopen clogged cerebral arteries and save at least some of the underperfused brain tissue. EMS teams should have the goal of getting potential stroke patients stabilized, preliminarily evaluated, and to a primary stroke center in less than an hour.

Speedy, accurate stroke diagnosis is facilitated by using standardized tests, such as the Cincinnati Prehospital Stroke Scale, which can be administered in 3 to 5 minutes using no special equipment. Such standardized diagnostic tools give accurate and reproducible predictions of the likelihood that a person has had a recent stroke. It has been shown that EMS operators can effectively administer the Cincinnati Prehospital Stroke Scale over the phone with the help of cooperative bystanders.

Emergency departments experienced in thrombolytic therapy for strokes can be accredited as primary stroke centers by the Joint Commission. Accreditation signifies that the ED is part of a hospital with specialized stroke units. The ED must have access to a specialized stroke team that operates by a pre-planned written protocol for diagnosing strokes using CT (or MRI) imaging, and for treating ischemic strokes with intravenous rt-PA. Primary stroke centers have the goal of getting appropriate acute stroke patients from the door to thrombolytic treatment in less than an hour.

As in prehospital (EMS) stroke management, ED stroke care is facilitated by using standardized tests, especially the NIH Stroke Scale, which can be administered in 5 to 8 minutes using no special equipment. The NIHSS quantifies the severity of a stroke and can be used to measure objectively both deterioration and improvement. The critical distinction between ischemic and hemorrhagic strokes must be made by CT or MRI imaging, as interpreted by an experienced radiologist.

Management of ischemic stroke can often take place in a medical unit. In all cases, the best outcomes require experienced, attentive care of airways, blood pressure, blood glucose, and concurrent cardiac problems.

Primary care centers should be able to mobilize neurosurgical care within 2 hours. Management of hemorrhagic stroke should take place in an ICU with the staff and facilities for dealing with increased intracranial pressure (Adams et al., 2007; Chung & Caplan, 2007; White et al., 2007). Hospitals with these advanced capabilities are called comprehensive care centers.

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.

Advice and Triage Questions

Informational Questions

Posted April 18, 2008

Expires April 1, 2010

Copyright © 2008 Wild Iris Medical Education. All rights reserved.