Online newspaper of professor Yasser Metwally

The author:Professor Yasser Metwally

http://yassermetwally.com

INTRODUCTION

Background: A stroke is the clinical designation given to the acute loss of circulation to an area of the brain resulting in ischemia and a corresponding loss of neurologic function. Classified as either hemorrhagic or ischemic, strokes typically manifest with the sudden onset of neurological deficits, such as weakness, sensory deficit, or difficulties with language. Ischemic strokes have a heterogeneous group of causes, which include thrombosis, embolism, or hypoperfusion, while hemorrhagic strokes can be either intraparenchymal or subarachnoid.

Only in recent years have significant advances in treatment been made that enable physicians to improve significantly the outcome of this devastating disease. A new era in acute stroke care began in 1995, when the National Institute of Neurologic Disorders and Stroke (NINDS) tissue plasminogen activator (t-PA) Stroke Study Group first presented data that the early administration of t-PA benefited a carefully selected patient group with acute ischemic stroke (AIS). Currently, t-PA is the only approved therapy for AIS, but it remains underutilized. A recent study in Cleveland, Ohio reported that 1.8% of acute stroke patients received tPA. The number is likely lower in many parts of the U.S.

Pathophysiology: The brain is the most metabolically active tissue in the body. While representing only 2% of the body, it requires 15-20% of the total resting cardiac output to provide the necessary glucose and oxygen for its metabolism. Ischemic strokes result from events that limit or stop blood flow, such as embolism, thrombosis in-situ, or relative hypoperfusion. As blood flow decreases, neurons cease functioning, and irreversible neuronal ischemia and injury begin at blood flow rates of less than 18 mL/100 mg/min.

Ischemic cascade

The processes involved in injury at the cellular level are referred to as the ischemic cascade. Some of the factors thought to result in cell death and dysfunction are listed here, but others are being discovered at a rapid rate. Within seconds to minutes of the loss of glucose and oxygen delivery to neurons, the cellular ischemic cascade begins. This is a complex process that begins with cessation of the electrophysiologic function of the cells.

The cell metabolism then changes from aerobic to anaerobic. With further depletion of ATP stores, membrane ion pumps fail, leading to increased intracellular concentration of sodium and calcium. The cell begins to experience injury from calcium-mediated cytotoxic reactions and the release of excitatory neurotransmitters, specifically glutamate. These processes lead to the activation of proteases, endonucleases, phospholipases, and nitric oxide synthase and the formation of free radicals. The resultant neuronal and glial injury produces edema in the ensuing hours to days after stroke, causing further injury to the surrounding neuronal tissues.

Ischemic penumbra

An acute vascular occlusion produces heterogeneous regions of ischemia in the dependent vascular territory. The quantity of local blood flow is comprised of any residual flow in the major arterial source and collateral supply if any. Regions of the brain without significant flow are collectively referred to as the core, and it is presumed that these cells die within minutes. Zones of decreased or marginal perfusion are collectively called the ischemic penumbra. The tissue in the penumbra can remain viable for several hours, and currently studied pharmacologic interventions for preservation of neuronal tissue target the penumbra.

The administration of t-PA to the acute stroke patient allows revascularization, so that cells in the penumbra can be rescued before irreversible injury occurs. Restoring blood flow can mitigate the effects of ischemia only if performed quickly. Neuroprotective strategies are intended to preserve the penumbral tissues and attempt to extend the time window for revascularization techniques, but none have shown broad benefit in clinical trials as of this writing.

Mechanisms of stroke

• Embolic strokes

Emboli are responsible for approximately 20% of all ischemic strokes; they may be either cardiac or arterial in origin. Cardiac sources include atrial fibrillation, recent myocardial infarction (1-3% of all AMI), prosthetic valves, native valvular disease, endocarditis, mural thrombi, or dilated cardiomyopathy. Arterial sources are atherothrombolic or cholesterol emboli that develop in the arch of the aorta and in the extracranial arteries (carotid and vertebral arteries). Embolic strokes tend to have a very sudden onset, and neuroimaging may demonstrate previous infarcts in several vascular territories.

• Thrombotic strokes

Thrombotic strokes represent 60% of all ischemic strokes and include both large-vessel strokes (70%) and small-vessel or lacunar strokes (30%). They occur due to in-situ occlusions, characteristically on atherosclerotic lesions in the carotid, vertebrobasilar, and cerebral arteries, typically proximal to major branches. Thrombogenic factors include injury to and loss of endothelial cells exposing the subendothelium and platelet activation by the subendothelium, activation of the clotting cascade, inhibition of fibrinolysis, and blood stasis.

Thrombotic strokes are thought to originate frequently from ruptured atherosclerotic plaques. Intracranial atherosclerosis may be the cause in patients with widespread atherosclerosis. In other patients, especially at younger ages, other causes should be considered, including coagulation disorders (e.g., antiphospholipid antibodies, protein C deficiency, protein S deficiency), sickle cell disease, fibromuscular dysplasia, arterial dissections, and vasoconstriction associated with substance abuse.

• Lacunar stroke

Lacunar strokes represent 20% of all ischemic strokes. They occur when the penetrating branches of the middle cerebral artery, the lenticulostriate arteries, or the penetrating branches of the circle of Willis, vertebral artery, or basilar artery become occluded. Causes of lacunar infarcts include microatheroma, lipohyalinosis, fibrinoid necrosis secondary to hypertension or vasculitis, hyaline arteriosclerosis, and amyloid angiopathy. The great majority is related to hypertension. Of all stroke types, lacunar strokes have the best prognosis.

Watershed infarcts

These infarcts, also known as border zone infarcts, develop from relative hypoperfusion in the most distal arterial territories and can produce bilateral symptoms. Frequently, these are associated with surgical procedures.

Frequency:

• In the US: Approximately 700,000 strokes occur each year, including both new and recurrent cases; of these strokes, approximately 500,000 are ischemic strokes. By the year 2050, the annual number of strokes is expected to reach 1 million. Currently, there are over 4.4 million stroke survivors in the US.

• Internationally: Similar to the US, stroke is the third leading cause of death in the industrialized countries of Europe and the leading cause of adult disability. The global incidence of stroke will only increase, since the number of people older than 65 years will rise from 390 million now to 800 million by 2025, reaching 10% of the total population.

Mortality/Morbidity:

• Stroke is the third leading case of death in the US (60.2 per 100,000), following cardiac diseases and cancer-related deaths. Approximately 29% of patients die within 1 year following a stroke; this percentage rises in patients older than 65 years. Worldwide in 1990, cerebrovascular disease was the cause of death in over 4.3 million people.

• Stroke is the leading cause of disability in the US; 31% of stroke survivors need help for taking care of themselves after a stroke, 20% need some type of assistance for walking, and 16% of stroke survivors need to be placed in some form of institution providing assisted living. At least one third of stroke survivors suffer from depression.

• The direct (treatment) and indirect cost (lost productivity) of stroke in the US is approximately $ 43 billion/year.

Race: In the US, stroke has a higher incidence in the African American population than in the Caucasian population.

• In African American males, the incidence is approximately 93 per 100,000 with the death rate of approximately 51%. In African American females, incidence is 79 per 100,000 with a death rate of 39.2%. Young African Americans have a 2-3 times greater risk of ischemic stroke than the Caucasian population of the same age, and they are 2.5 times more likely to die from stroke. Adjusted for age, African Americans have 1.49 times the risk of death from stroke as Caucasians.

• In Caucasian males, the incidence is lower at 62.8 per 100,000 with death being the final outcome in 26.3% of cases. In Caucasian females, the incidence is 59 per 100,000, and the death rate is 39.2%.

• As compared to African Americans and Caucasians, Hispanics have a lower overall incidence of stroke, but more frequent lacunar stroke and at an earlier age.

Sex: In patients younger than 60 years, the incidence of stroke is greater in males (3:2 ratio).

Age:

• Stroke affects patients of all ages, including children.

• Risk of stroke increases with age, especially in patients older than 64 years, who account for 75% of all strokes.

CLINICAL PICTURE

History:

• The American Stroke Association advises the public to be aware of the symptoms of stroke that are easily recognized. The symptoms are as follows:

  • Sudden numbness or weakness of face, arm, or leg, especially on one side of the body

  • Sudden confusion, difficulty in speaking or understanding

  • Sudden deterioration of vision of one or both eyes

  • Sudden difficulty in walking, dizziness, and loss of balance or coordination

  • Sudden, severe headache with no known cause

• Focus medical history on identifying risk factors for atherosclerotic and cardiac disease, including hypertension, diabetes, tobacco intake, high cholesterol, and a history of coronary artery disease, coronary artery bypass, and atrial fibrillation. Consider stroke in any patient presenting with acute neurologic deficit or any alteration in the level of consciousness. Common signs of stroke include the following:

  • Acute hemiparesis, monoparesis, or quadriparesis

  • Complete or partial hemianopia, monocular or binocular visual loss, diplopia

  • Dysarthria or aphasia

  • Ataxia, vertigo, or nystagmus

  • Sudden decrease in consciousness

• In younger patients, elicit history of trauma, coagulopathies, illicit drug use (especially cocaine), migraines, or use of oral contraceptive or over-the-counter medications (especially those containing phenylpropanolamine).

• History also can suggest other causes of the patient’s symptoms, such as recent trauma, surgery, migraine headaches, oral contraceptive use, recent infections, or seizure activity. Family members, bystanders, and especially, prehospital personnel can provide invaluable information regarding the time and events surrounding the onset of symptoms.

• Establishing time of onset is especially critical when thrombolytic therapy is an option. If the patient awakens with the symptoms, then the time of onset is defined as the time the patient was last seen normal. Family members, coworkers, or bystanders may be required to help establish the exact time of onset, especially in right hemispheric strokes accompanied by neglect or left hemispheric strokes with aphasia.

• If the patient is a candidate for thrombolytic therapy, a thorough review of the inclusion and exclusion criteria from the NINDS trial must be performed.

Physical: Physical exam is directed towards 5 major areas: (1) assessing the airway, breathing, and circulation (ABCs), (2) identifying potential causes of the stroke, (3) identifying potential stroke mimics, such as Bell palsy, (4) defining the severity of the patient’s neurologic deficits, and (5) identifying comorbid illnesses.

• The physical examination must encompass all the major organ systems, starting with the ABCs and the vital signs. Stroke patients can quickly deteriorate; therefore, constant reassessment is critical. Ischemic strokes, unless very large, do not tend to cause immediate problems with airway patency, breathing abnormalities, or circulation issues. On the other hand, patients with intracerebral or subarachnoid hemorrhage frequently require intervention with both airway protection and ventilation.

  • Vital signs, while nonspecific, can point to impending clinical deterioration and may assist in narrowing the differential diagnosis. Many stroke patients are hypertensive at baseline, and their blood pressure can become more elevated after stroke. While hypertension is common, blood pressure decreases spontaneously over time in many patients, and medical intervention is not proven to be beneficial in these patients, in the absence of signs and symptoms of malignant hypertension.

  • Head, ears, eyes, nose, and throat examination: A careful examination of the head and neck is essential. Contusions, lacerations, and deformities may suggest trauma as the etiology for the patient’s symptoms. Auscultation of the neck may elicit a bruit, suggesting carotid disease as the cause of the stroke.

  • Cardiac: Cardiac arrhythmias, such as atrial fibrillation, are commonly found in stroke patients. Similarly, strokes may occur concurrently with other acute conditions, such as acute myocardial infarction and acute congestive heart failure. Auscultation for murmurs and gallops is crucial.

  • Extremities: Carotid or vertebrobasilar dissections, and less commonly, thoracic aortic dissections, may cause ischemic stroke. Unequal pulses or blood pressures in the extremities may reflect the presence of aortic dissections.

• The neurologic examination must be thorough, and yet this is perhaps the weakest area of training for primary care providers and emergency physicians. A directed and focused exam can be performed in minutes and not only provides great insight into the potential cause of the patient’s deficits, but it also helps determine the intensity of treatment required.

• A very useful tool in measuring neurologic impairment is the National Institutes of Health Stroke Scale (NIHSS). This scale can be easily used, is reliable and valid, provides insight to the location of vascular lesions, and can be correlated with outcome in ischemic stroke patients. It focuses on 6 major areas of the neurologic examination: (1) level of consciousness, (2) visual function, (3) motor function, (4) sensation and neglect, (5) cerebellar function, and (6) language. The NIHSS is used by most stroke teams and stroke neurologists; it enables the consultant to rapidly determine the severity and possible location of the stroke. It is strongly associated with outcome, and it can predict those patients who are likely to respond to thrombolytic therapy and those who will develop hemorrhagic complications due to thrombolytic use.

Table 1. NIH Stroke Scale

Causes: Risk factors for ischemic stroke are both modifiable and nonmodifiable. Identification of risk factors in each patient can uncover clues to the cause of the stroke and the most appropriate treatment plan.

• Nonmodifiable risk factors include age, race, gender, ethnicity, sickle cell disease, fibromuscular dysplasia, and heredity.

  • Modifiable risk factors include hypertension (the most important), cardiac disease (eg, atrial fibrillation, valvular disease, mitral stenosis, structural anomalies allowing right to left shunting, such as a patent foramen ovale, atrial and ventricular enlargement), diabetes, hypercholesterolemia, history of transient ischemic attacks, carotid stenosis, hyperhomocystinemia, and lifestyle issues (eg, excessive alcohol intake, tobacco use, illicit drug use, obesity, physical inactivity). A history of migraine headaches and oral contraceptive use are additional risk factors for stroke.

WORK-UP

Lab Studies:

• Laboratory evaluation of the ischemic stroke patient should be driven by comorbid illnesses as well as the potential acute stroke.

  • Glucose and electrolytes: Hypoglycemia is the most common electrolyte abnormality that produces strokelike symptoms. It is easily corrected and leads to rapid resolution of symptoms. Electrolyte disorders, hyperglycemia, hypoglycemia, and uremia should be carefully considered as the cause of ongoing mental and physical deficits while pursuing the diagnosis of stroke.

  • Complete blood count (CBC) provides key information regarding hemoglobin and hematocrit, thus evaluating for anemia and possible deficiencies in oxygen-carrying capacity. Additionally, sickle cell disease, polycythemia, and thrombocytosis increase the risk for stroke.

  • Prothrombin time/activated partial thromboplastin time (PT/aPTT): Many patients with acute stroke are on anticoagulants, such as heparin or warfarin. Treatment decisions, such as thrombolytic use, require data on coagulation status. An elevated (ie, >1.3) international normalized ratio (INR) may preclude patients from receiving thrombolytics.

  • Cardiac enzymes: Not infrequently, patients with acute stroke also experience acute myocardial ischemia. In addition to an ECG, increased cardiac enzymes might suggest concomitant cardiac injury.

  • Arterial blood gas (ABG): In patients with suspected hypoxemia, ABG will define the severity of hypoxemia and may detect acid-base disturbance.

Imaging Studies:

• CT scan is, and probably will remain in the foreseeable future, the most commonly used form of neuroimaging in the evaluation of acute stroke patients. Noncontrast CT scan is very sensitive in detecting intracerebral and subarachnoid hemorrhage, as well as subdural hematomas. Treatment algorithms are dichotomous for the presence of intracranial blood, and most interventions for ischemic stroke require the absence of blood on CT scan.

  • While not very sensitive for early ischemia (<6 hours), several findings can suggest ischemic changes relatively early in the time course of stroke. Loss of the gray-white matter interface, loss of sulci, and loss of the insular ribbon are subtle signs of early ischemia.

  • Early mass effect and areas of hypodensity suggest irreversible injury and identify patients at higher risk of hemorrhage if given thrombolytics. Significant hypodensity on the baseline scan should prompt the physician to question the time of onset. Hypodensity in an area greater than one third of the middle cerebral artery distribution is considered by some a relative contraindication for thrombolytics.

  • A dense middle cerebral artery (MCA) sign suggests a clot in the MCA. These patients are at risk for significant hemispheric strokes. Some authorities believe that these patients may benefit most from aggressive thrombolytic therapy, including intra-arterial therapies, but this has not been specifically proved in double-blind randomized trials.

  • CT scan may demonstrate other causes of the patient’s symptoms, including neoplasms, epidural and subdural hemorrhages, aneurysms, abscesses, arteriovenous malformations, and hydrocephalus.

  • Xenon CT scan is a relatively new technique that complements the noncontrast head CT scan and provides quantitative measurement of regional blood flow. Like MRI, it is being studied for its contribution to patient selection for thrombolytic therapy and to management of medical therapies in patients with increased intracranial pressure (ICP).

  • CT angiography, while not commonly performed, can demonstrate the vascular occlusion and areas of perfusion deficits.

• MRI with magnetic resonance angiography (MRA) is a major advance in the neuroimaging of stroke. MRI not only provides great structural detail but also can demonstrate impaired metabolism. A major limitation of MRI is its availability and the skills required to interpret the images.

  • Diffusion-weighted MRI can detect areas of ischemic brain injury more quickly than standard MRI or CT by detecting changes in water molecule mobility. These sequences in combination with perfusion MRI, which yields areas of diffusion-weighted imaging/perfusion-weighted imaging (DWI/PWI) mismatch, can theoretically identify potentially salvageable tissues.

  • Perfusion MRI: With the use of injected contrast material, it can demonstrate areas of decreased perfusion.

  • MR angiography: This noninvasive technique demonstrates vascular anatomy and occlusive disease of the head and neck without the need for contrast material.

• Cerebrovascular angiography: Angiography not only provides useful information of the extracranial and intracranial vasculature, but it is now used to assist in intra-arterial therapies, using both intra-arterial thrombolytics and investigational catheter devices.

• Digital subtraction angiography is considered the definitive method for demonstrating vascular lesions, including occlusion, stenoses, dissections, and aneurysms. It requires special facilities and a skilled operator. It carries a risk of stroke in 1-2% of patients.

• MR spectroscopy is an experimental technique, which may have a potential for distinguishing areas of salvageable neurons from those that are irreversibly injured.

• Carotid duplex scanning is one of the most useful tests in evaluating stroke patients. Increasingly, it is being performed earlier in the evaluation, not only to define the cause of the stroke but also to stratify patients for either medical management or carotid endarterectomy (CEA), if they have carotid stenoses. Patients with symptomatic critical stenoses on carotid duplex scanning may require anticoagulation before CEA is performed.

• Transcranial Doppler (TCD): TCD studies can assess the location and degree of arterial occlusions in the extracranial carotid and large intracranial vessels, including the middle cerebral and vertebrobasilar arteries. It can also be used to detect restoration of flow after thrombolytics.

• The use of single-photon emission computed tomography (SPECT) in stroke is still relatively experimental and available only at select institutions; it can define areas of altered regional blood flow.

Other Tests:

• Additional laboratory tests are tailored to the individual patient. They may include rapid plasma reagent (RPR), fasting lipid profile, sedimentation rate, lipid profile, pregnancy test, antinuclear antibody (ANA), rheumatoid factor, and homocysteine. In select patients with possible hypercoagulable states, protein C, protein S, antithrombin III, and Factor V Leiden testing may be required. These blood abnormalities mainly contribute to venous thrombosis but may be relevant in patients with cardiac shunts or cerebral venous thromboses. The anticardiolipin antibody and the lupus inhibitor, both antiphospholipid antibodies, correlate with arterial strokes, as well as DVT, pulmonary embolism, MI, and miscarriages.

• Echocardiography: Transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE) are useful tools in evaluating patients with possible cardiogenic sources of their stroke. TEE is more sensitive than TTE and can evaluate the aortic arch and thoracic aorta for plaques or dissections.

• ECG: Stroke and cardiovascular disease share many risk factors. An ECG may demonstrate cardiac arrhythmias, such as atrial fibrillation, or may indicate acute ischemia. All stroke patients should have an ECG as part of their initial evaluation.

Procedures:

• Lumbar puncture (LP): An LP is required to rule out meningitis or subarachnoid hemorrhage when the CT scan is negative but the clinical suspicion remains high. Performing an LP on acute stroke patients will preclude them from receiving thrombolytics.

MANAGEMENT

Medical Care: Medical care for AIS occurs on a continuum, beginning in the prehospital setting and ending at home after discharge.

• Prehospital care personnel are critical elements in the AIS chain of survival. Emergency medical services (EMS) personnel should begin with the ABCs and, once the patient is stable, should perform a more directed assessment and administer supportive treatment.

  • Prehospital stroke scales, such as the Cincinnati Prehospital Stroke Scale or Los Angeles Prehospital Stroke Scale, can be useful in identifying potential stroke patients. Providing supplemental oxygen when indicated, establishing IVs, measuring serum glucose, and administering glucose (and usually thiamine) in hypoglycemic patients are elements of prehospital stroke care.

  • Equally important is prehospital notification of a stroke patient. This allows for early activation of stroke teams and mobilization of necessary resources, such as CT scan.

• The goal of acute stroke management in the emergency department is rapid and efficient care. Continuing from the assessment of the ABCs, stroke patient evaluation and treatment should be performed within 1 hour from presentation as shown below.

Table 2. NINDS Recommended Stroke Evaluation Targets for Potential Thrombolytic Candidates

Again, general management is a team effort with the nursing and physician staff closely working together. General stroke care issues are outlined in the table below.

Table 3. General Management of Acute Stroke Patients

• Hypoglycemia and hyperglycemia need to be identified and treated early in the evaluation. Not only can both produce symptoms that closely mimic an ischemic stroke, but both can also aggravate ongoing neuronal ischemia. Administration of glucose in hypoglycemia produces profound and prompt improvement, while insulin should be started for stroke patients with hyperglycemia.

• Hyperthermia is infrequently associated with stroke but can cause increased morbidity. Administration of acetaminophen, by mouth or per rectum, is indicated in the presence of fever.

• Supplemental oxygen is needed only when the patient has a documented oxygen requirement. No evidence to date suggests that supernormal oxygenation improves outcome, and some studies suggest it may worsen outcome.

• Blood pressure management is delicate and controversial. Many patients will be hypertensive on arrival. Recent American Stroke Association guidelines have reinforced the need for caution in lowering blood pressures acutely. Table 4 shows current recommendations for both thrombolytic and nonthrombolytic candidates.

• In a small proportion of stroke patients who are relatively hypotensive, pharmacologically increasing blood pressure may improve flow through critical stenoses.

Table 4. Blood Pressure Management (adopted from ACLS guidelines)

Surgical Care: Surgical intervention is rarely required urgently in acute ischemic strokes; however, current recommendations suggest that neurosurgical care should be available within 2 hours when needed, e.g. to evaluate surgical options in symptomatic hemorrhagic conversion following tPA.

• Increased ICP is a life-threatening event occurring in up to 20% of all strokes and more commonly occurs in large, hemispheric strokes. Edema and herniation are the most common causes of early mortality in patients with hemispheric stroke.

  • Patient position, hyperventilation, hyperosmolar therapy, and rarely, barbiturate coma, may be used, as in patients with increased ICP secondary to closed head injury.

  • Recent reports of hemicraniectomy to treat life-threatening ICP have suggested decreased length of ICU stay and mortality, if surgery is performed before clinical deterioration.

• Selected patients with either hemorrhagic transformation or intracerebral hemorrhage after thrombolytic therapy may benefit from surgical evacuation of the hematoma, but this has not been proven prospectively in randomized, double-blind trials.

• If neurosurgical care is not available in house, a transfer policy is required to expedite patient transfer when neurosurgical expertise is needed.

Consultations: Consultations are tailored to individual patient needs.

• In the first hours of acute stroke, an experienced professional sufficiently familiar with stroke, or a stroke team should be available within 15 minutes of the patient’s arrival in the emergency department.

• Within the first day of hospitalization, physical medicine and rehabilitation (PM&R), occupational therapy, physical therapy, and speech therapy experts are often consulted.

• Consultation of cardiology and vascular surgery or neurosurgery may be warranted based on the results from TTE/TEE and carotid duplex scanning.

• During hospitalization, additional useful consultations include home health care coordinator, rehabilitation coordinator, social worker, psychiatrist (commonly for depression), and dietitian.

Diet:

• In acute stroke patients, aspiration is a risk. As such, all stroke patients should be given nothing by mouth (NPO) until a swallowing assessment is performed.

• Due to temporary dysphagia, a temporary feeding tube may be required.

• If the patient remains at a significant aspiration risk for the foreseeable future, a percutaneous endoscopic gastrostomy feeding tube may be required.

• A dietitian can help identify a diet that not only addresses the aspiration risk but also ensures adequate caloric intake to help prevent poststroke malnutrition.

• The dietitian also must consider special dietary needs of patients with hypertension, diabetes, and hyperlipidemia.

Activity: Activity is tailored to the severity of stroke.

• Aspiration precautions, with the head of the bed elevated to 30 degrees, need to be observed.

• Physical therapy will test and suggest level of activity. This should be performed within the first 24 hours of hospitalization.

• Increase activity if tolerated as per the suggestions of the rehabilitation coordinator with the goal of mobilizing the patient as early as possible. At discharge, encourage patients to increase activity as tolerated.

MEDICATION

While only one drug, t-PA, has demonstrated efficacy and effectiveness in treating acute ischemic strokes and is approved by the FDA, other medications are equally important in the acute management of stroke. National consensus panels have included antihypertensives, anticonvulsants, and osmotic agents in their recommendations. Additional agents may be required for comorbid illnesses in many stroke patients.

FOLLOW-UP

Further Inpatient Care:

• Inpatient care is tailored to the severity of the acute stroke and comorbid illnesses. Some recent studies suggest that admission to a dedicated stroke unit with specially trained staff may reduce morbidity and mortality, although many of these studies are not randomized and prospective and many originate outside the US, where comparison to general medical or neurology wards may not be directly comparable to those in the US.

• The goals of early supportive care after admission (adapted from the American Stroke Associations guidelines) include the following:

  • Observe changes in the patient’s condition that might prompt different medical or surgical interventions. Of note, 25% of patients worsen in the first 24-48 hours after admission.

  • Facilitate medical or surgical measures aimed at improving outcome after stroke. This includes evaluation for carotid stenoses and cardioembolic sources.

  • Institute measures to prevent subacute complications. Foley catheters increase the risk for UTI and should be used only when absolutely necessary. Sequential compression stockings, subcutaneous heparin, and low–molecular-weight heparin in bedridden patients decrease the risk of deep vein thrombosis.

  • Initiate therapies to prevent recurrent stroke.

  • Begin efforts to restore neurological function through rehabilitation or other techniques. This includes occupational, physical, and speech therapy.

• Acute hospitalization is an opportune time to consider smoking cessation.

• Further inpatient care is directed towards other potential comorbid conditions and risk factor reduction. This includes managing hypertension, diabetes, hypercholesterolemia, and cardiac arrhythmias or diseases.

• Depression is prevalent in stroke survivors. It should be addressed with survivors and their family during hospitalization.

Further Outpatient Care:

• Poststroke outpatient care largely focuses on rehabilitation and recurrent stroke prevention. Rehabilitation planning begins within the first day of the acute stroke.

• The American Stroke Association guidelines for rehabilitation focus on 6 major areas, which are as follows:

  • Preventing, recognizing, and managing comorbid conditions and medical complications

  • Training for maximum independence

  • Facilitating maximum psychosocial coping and adaptation by patient and family

  • Preventing secondary disability by promoting community reintegration, including resumption of home, family, recreational, and vocational activities

  • Enhancing quality of life in view of residual disability

  • Preventing recurrent stroke and other vascular conditions

In/Out Patient Meds:

• Patients discharged from the hospital after ischemic stroke should be considered for antiplatelet medications unless contraindicated. Current choices include the following:

  • Aspirin, taken daily in low-to-medium doses (50-325 mg), is an effective and inexpensive first-choice agent for reducing recurrent stroke risk.

  • Newer antiplatelet agents, such as clopidogrel (Plavix) and ticlopidine (Ticlid) are effective in reducing recurrent stroke but may cause significant side effects that must be monitored, including severe neutropenia (ticlopidine) and TTP. Other antiplatelet agents, such as dipyridamole in combination with low-dose aspirin, have been introduced with similar efficacy but without the hematologic side effects.

• Initiating long-term anticoagulation (eg, warfarin) reduces the risk of recurrent stroke in patients at risk for cardioembolic stroke.

  • In patients with atrial fibrillation, the recommended target international normalized ratio (INR) is in the range of 2-3. In patients with mechanical prosthetic valves, target INR is in the range of 2-3.5, depending on the type of valve.

  • Patients with rheumatic valvular heart disease, cardiomyopathy, arrhythmias, or heart failure should also be considered for long-term anticoagulation. Patients without one of these indications for anticoagulation do not appear to benefit from warfarin therapy, judging by preliminary results of the WARSS (Warfarin Aspirin Recurrent Stroke Study).

• Additional outpatient medications should be tailored to the patient’s comorbid conditions and to risk factors identified during hospitalization.

• Use of HMG-coreductase inhibitors has been proven to be beneficial in reducing the rates of stroke in patients with coronary artery disease and elevated or high-normal low-density lipoprotein (LDL) cholesterol.

• Medications to address hypertension, hyperlipidemia, and diabetes should all be reviewed with the patient prior to discharge.

Transfer:

• EMS triage and transfer of stroke patients is an important issue in stroke care. The recommendation for the establishment of stroke centers has helped define for consideration the elements of both primary and secondary stroke centers. The reader is referred to the chapter by Dr. Helmi Lutsep on stroke team creation and management.

• EMS agencies are likely to be asked to triage potential stroke patients to centers that have demonstrated capabilities to evaluate and treat stroke patients in a timely fashion.

• As part of each hospital’s stroke protocol and pathway, criteria for patient transfer to other medical facilities must be established before the actual need.

  • Hospitals without neuroimaging capabilities should stabilize and immediately transfer potential stroke patients to centers with CT scan availability.

  • Hospitals without intensive care units or access to timely neurosurgical expertise should transfer patients who are candidates for thrombolytics or who have received thrombolytics to institutions that can provide those services.

  • Patients with large hemispheric strokes who may be at significant risk for edema and increased intracranial pressure and who may require neurosurgical expertise should be transferred before clinical deterioration occurs.

Deterrence/Prevention:

• The acute hospitalization is focused not only on treating the acute stroke but also on identifying risk factors for recurrent stroke and to begin modifying these risk factors if possible.

Complications:

• Complications following a stroke can be divided into those occurring acutely, typically within 72 hours, and those occurring later.

  • Acute complications include cerebral edema, increased ICP and possible herniation, hemorrhagic transformation, aspiration pneumonia, and seizures.

  • Postthrombolytic complications center around bleeding. Of greatest concern is intracerebral hemorrhage, typically occurring within the first 12 hours from treatment. Other potential sites of bleeding include GI tract, GU tract (associated with Foley catheters), and skin, typically at IV sites.

  • Subacute complications include pneumonia, deep venous thrombosis and pulmonary emboli, urinary tract infections, decubitus ulcers, contractures, spasticity, joint problems such as the shoulder-hand syndrome, and malnutrition.

  • A significant number of stroke survivors also experience depression. Identification and treatment of depression is extremely important in maximizing the quality of life, not only for stroke survivors, but also for their families and care providers.

Prognosis:

• The prognosis after an acute ischemic stroke varies greatly, depending upon the premorbid condition, stroke severity, age, and poststroke complications.

• Mortality: In the Framingham and Rochester stroke studies, overall stroke mortality at 30 days was 28%. Ischemic stroke mortality at 30 days was 19%. One-year survival for ischemic strokes in the Framingham study was 77%.

• Morbidity: In stroke survivors from the Framingham Heart Study, 31% needed help caring for themselves, 20% needed help when walking, and 71% had impaired vocational capacity in long-term follow-up.

Patient Education:

• Education is paramount in the fight to prevent and treat stroke. Education must include all elements of the stroke chain of survival. While medical education is often difficult and requires constant reinforcement, it has potential for minimizing the stroke burden.

• Public education is perhaps the hardest of all. Presently, the American Stroke Association, through Operation Stroke, is reaching to large metropolitan communities to promote stroke awareness and to develop coordinated stroke care within the region.

• Public education must involve all age groups. Incorporating stroke into basic life support (BLS) and cardiopulmonary resuscitation (CPR) curricula is just one way to reach a younger audience. Avenues to reach an audience with a higher stroke risk include using the local churches, employers, and senior organizations to promote stroke awareness.

• Prehospital care providers are essential to timely stroke care. Course curriculum for prehospital care providers is beginning to include more information on stroke than ever before. Through certification and ACLS instruction, as well as continuing medical education classes, prehospital care providers can remain current on stroke and promote stroke awareness in their own communities.

• Physician and nursing staff involved with stroke patients, both in the emergency department and in the hospital, should participate in scheduled stroke education to maintain the required skills to effectively treat stroke patients and to remain current on medical advances

References

1. Adams HP Jr, Brott TG, Furlan AJ, et al: Guidelines for thrombolytic therapy for acute stroke: a supplement to the guidelines for the management of patients with acute ischemic stroke. A statement for healthcare professionals from a Special Writing Group of the Stroke Council, American Heart As. Circulation 1996 Sep 1; 94(5): 1167-74.

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