Recertification Refresher

Acute ischemic stroke—swift assessment and quick action produce optimal outcomes

Carolyn Hewko, MS, PA-C

Ms. Hewko practices at Eastern Connecticut Cardiology Group in New London, Conn. The author has indicated no relationships to disclose relating to the content of this article.

The twin goals of an acute evaluation are to prevent further acute brain injury and to forestall potentially devastating neurologic sequelae.

 

Earn Category I CME credit by reading this article and the associated article and successfully completing the post-test. Successful completion is defined as a cumulative score of at least 70% correct. This material has been reviewed and is approved for 1 hour of clinical Category I (Preapproved) CME credit by the AAPA. The term of approval is for 1 year from the publication date of July 2004.

Learning objectives Describe the ischemic cascade Integrate the National Institutes of Health stroke scale (NIHSS) into the neurologic exam Review the key elements of supportive care for patients who have had a stroke

The term stroke describes a clinical diagnosis of observed loss of neurologic function due to ischemia following acute loss of circulation.¹ Stroke is third most common killer of American adults and accounted for more than 1 of every 15 deaths in the United States in 2001; approximately half of these deaths occurred out of the hospital.² Despite the high incidence of stroke, nearly two thirds of Americans are unable to identify a single warning sign of this common killer.³

The twin goals of an acute evaluation are to prevent further acute brain injury (or reverse current damaging events) and to prevent neurologic sequelae. The various possible etiologies and presentations of stroke require that clinicians keep a low threshold of suspicion of this entity (see "The anatomy and physiology of ischemic stroke").

 

The anatomy and physiology of ischemic stroke Anterior circulation includes the areas of the brain supplied by the internal carotid arteries and the majority of both cerebral hemispheres. The bifurcation of the common carotid artery leads to the internal and external carotids. The internal carotid artery (ICA) further branches into the ophthalmic artery, posterior communicating artery, and anterior choroidal artery. The internal carotid continues as the middle cerebral artery (MCA) bifurcates into the anterior cerebral artery (ACA). The MCA is the largest intracerebral vessel, supplying the lateral, frontal, parietal, and temporal lobes and the basal ganglia. The ACA supplies the medial part of the frontal and parietal lobes, most of the corpus callosum, the frontobasal cerebral cortex, deep structures, and the anterior diencephalon. The anterior choroidal artery supplies the part of the thalamus not supplied by the posterior circulation and the posterior limb of the internal capsule.   Click here to view full-size graphic   The posterior circulation is comprised of the posterior cerebral artery (PCA), which branches from the basilar artery. The PCA supplies the occipital and medial temporal lobes of the cerebral hemispheres and parts of the midbrain, subthalamic nucleus, basal nucleus, thalamus, mesial inferior temporal lobe, and occipitoparietal cortices. The two main branches of the PCA—P1 and P2—are connected by the posterior communicating artery; the anterior and posterior circulation at the base of the brain are connected by the circle of Willis. How ischemic strokes occur Ischemic strokes are the result of decreased blood flow to an area of the brain; the lessened flow cannot support metabolism with glucose and oxygen. The ischemic cascade then leaves the core infarct—the area lacking sufficient blood flow—without brain function (see table). Insufficient blood flow leads to the ischemic cascade, which begins with anaerobic metabolism and progresses as adenosine triphosphate stores are depleted, membrane ion pumps fail, and intracellular sodium and calcium levels rise. Glutamate is released as a result of this high concentration of intracellular calcium, the cells are injured, and free radicals are formed, causing neuronal and glial injury and surrounding edema. The ischemic penumbra, the area around the main infarct, may also die if blood flow is not restored within several hours.   EFFECTS OF A STROKE INDICATE THE LOCATION These signs and symptoms Indicate involvement here Aphasia, right limb weakness and sensory loss, right field visual defect, poor right conjugate gaze, difficulty reading, writing, calculating Left anterior hemisphere; anterior ICA; MCA, ACA tributaries Limb motor weakness, left motor loss, left field visual neglect, poor left conjugate gaze, unable to determine two-point stimuli on left side, difficulty drawing Right anterior hemisphere; ICA, ACA, MCA Right visual field defect, difficulty reading, naming colors or objects, occasional right-sided numbness Left posterior cerebral artery; left PCA Left limb sensory loss, left-sided neglect, left field visual defect Right posterior cerebral artery; right PCA Amnesia, double vision, nystagmus, disconjugated gaze, weakness and numbness in four limbs (or two-limb weakness on side opposite from face), dizziness, ataxia, vomiting, headache, bilateral vision disturbances Vertebrobasilar territory (posterior) Weakness in face, arm, leg on same side Internal capsule, basis pontis Numbness, decreased sensation on face, arm, leg on same side Thalamus Sudden abnormal behavior Caudate nucleus, thalamus, frontal lobe Key: ACA, anterior cerebral artery; ICA, internal carotid artery; MCA, middle cerebral artery; PCA, posterior cerebral artery. Data from Jauch,1 Selman,3 Hill,4 North American Symptomatic Carotid Endarterectomy Trial Group,8 and Weiner.9 Ischemic stroke can be caused by emboli or thrombi. A thrombosis forms in an artery after endothelial damage develops, with subsequent platelet aggregation and activation, inhibition of fibrinolysis, and blood stasis. In embolic stroke, a distal piece of thrombus or cholesterol breaks off, usually from the aortic arch, carotid bifurcation, or extracranial vessels. The thrombus travels to and lodges in an artery in the brain, compromising the blood supply to a specific area. Lacunar infarction describes a distinct syndrome of small vessel thrombosis thought to result from the occlusion of one deeply penetrating artery. The presumed mechanism is arteriolosclerosis or lipohyalinosis to the deep penetrating vessels with thrombosis of the vascular lumen. Other causes of lacunar infarcts include fibrinoid necrosis secondary to hypertension or vasculitis and amyloid angiography. A watershed infarct describes an ischemic stroke that is caused by hypoperfusion of distal territories of the brain's arteries during surgery. Other less common etiologies of stroke include hypercoagulable disorders, venous sinus thrombosis, arteritis, and fibromuscular dysplasia.

First, a rapid assessment

A three-step process guides the evaluation of a patient with a suspected stroke: diagnosis, localization, and mechanism.⁴ The diagnostic workup can begin when the patient has been stabilized with oxygen and appropriate support and a cardiac assessment has been performed.³ The differential diagnosis of stroke includes tumor, intoxication, brain injury, seizures, hypoglycemia, syncope, electrolyte imbalance, drug effects, migraine headache, Meniere's disease, and psychiatric disorders.¹ A focused history and physical exam, described below, rule out these problems.

Treatment for stroke depends on whether the cause is hemorrhagic or ischemic, so the initial workup of suspected stroke is focused on determining the type.¹ The patient's demographic profile, the medical history, and the physical exam provide initial clues to the etiology,² which can then be pursued with brain, carotid artery, or heart imaging studies together with specific laboratory tests. Antiplatelet or thrombolytic treatment for a confirmed ischemic stroke may be initiated before an exact etiology is determined.

The history and physical exam

The first and most important step in evaluating a patient suspected of having an acute stroke is taking a thorough, immediate history, including identification and social, family, and medical histories. Both sex and ethnicity can be important etiologic clues; men and postmenopausal women are at a higher risk for hemorrhagic stroke, and persons of African, Chinese, and Japanese heritage have higher rates of vascular occlusive disease and hypertension, which are risk factors for ischemic stroke.

The patient's medical history also may offer important clues. Diabetes and coronary artery disease (CAD) can cause atherosclerosis of the extracranial vessels and increase the risk of ischemic stroke. A history of transient ischemic attacks (TIAs) with symptoms that were similar to those now present strongly suggests a thrombotic occlusive process.⁵ A history of severe, uncontrolled hypertension suggests a possible intracranial hemorrhage. A history of cardiac problems such as heart failure, rheumatic heart disease, myocardial infarction (MI), atrial fibrillation, dilated cardiomyopathy, valvular lesions, bacterial endocarditis, atrial-septal defect, and aortic aneurysm suggests possible cardioembolism.^5,6

With the relevant demographic data and medical history in hand, the clinician should determine the patient's activity at symptom onset, the temporal relationship of symptom progression, and whether either headache or loss of consciousness occurred.⁵ Embolisms frequently occur when the patient coughs, sneezes, rises during the night to urinate, or during activities performed soon after rising, such as showering.⁵ These embolic lesions typically manifest as a completed stroke with maximal deficit at onset.⁷ A hemorrhagic etiology is suggested by onset during exertion, neck rigidity, a decreasing level of consciousness or somnolence, headache, vomiting, and seizures.⁸ A lacunar thrombosis is suggested, however, if these same symptoms gradually worsen or if the patient has progressive debilitation (evolving stroke).⁹

The physical exam should include the cardiovascular and neurologic systems, with close attention paid to the extremities.^3,9 A diagnosis of cardioembolism is suggested by telltale signs from the heart and extremities; particular attention must be paid not only to detecting murmurs, but also to the character and quality of all heart sounds and carotid bruits.^5,9 The facial arteries on the lower jaw and superficial temporal arteries should be palpated for stenosis and symmetry.⁵ Cyanotic, cold, or gangrenous fingers or toes indicate embolism or severe peripheral vascular disease, while small peripheral nodules are a sign of endocarditis.⁵ A funduscopic retinal exam is useful for finding end-organ damage from hypertension or diabetes.⁴ Signs of hyperlipidemia, including xanthomata and corneal arcus, can also be noted.⁴

A full neurologic assessment is the focus of the physical examination. Higher cortical function may be evaluated by asking the patient to read aloud or write a brief paragraph, to name objects, and to repeat a phrase or sentence.⁵ The National Institutes of Health stroke scale (NIHSS) is a reliable and valid tool for assessing prognosis and also can help to localize the lesion (see Figure 1). The six focal points of the NIHSS include level of consciousness, visual function, motor function, sensation, neglect, cerebellar function, and language. A score greater than 20 indicates a severe neurologic deficit.

 

FIGURE 1 NIH Stroke Scale
INSTRUCTIONS	SCALE DEFINED	SCORE
LOC
	0–Alert, keenly responsive 1–Not alert but arousable by minor stimulation 2–Not alert, requires stimulation, or is obtunded 3–Unresponsive or responds only with reflex motor or autonomic effects
LOC questions
Ask the patient the month and his/her age	0–Answers both correctly 1–Answers one correctly 2–Answers both incorrectly
LOC commands
Ask patient to open and close the eyes and to grip and release the nonparetic hand	0–Performs both tasks correctly 1–Performs one task correctly 2–Performs both incorrectly
Best gaze
Test only horizontal eye movements	0–Normal 1–Partial gaze palsy 2–Total gaze palsy
Visual fields
Test upper and lower quadrants by confrontation, using finger counting or visual threat	0–No visual loss 1–Partial hemianopsia 2–Complete hemianopsia 3–Bilateral hemianopsia
Facial palsy
Ask the patient to show teeth or raise the eyebrows and close the eyes	0–Normal symmetric movement 1–Minor paralysis 2–Partial paralysis 3–Complete paralysis of one or both sides
Motor function, arm
Extend the patient’s arm out, flexed 90 degrees (sitting) or 45 degrees (supine), with palms down. Release, encourage patient to hold the position, and watch for drift	0–No drift for full 10 sec 1–Drifts down within 10 sec but does not come to rest 2–Some effort against gravity 3–No effort against gravity; arm falls 4–No movement	Left arm Right arm
Motor function, leg
Leg is positioned at 30 degrees (supine)	0–No drift for full 5 sec 1–Drifts down within 5 sec but does not come to rest 2–Some effort against gravity 3–No effort against gravity; leg falls immediately 4–No movement	Left leg Right leg
Limb ataxia
Perform finger-nosefinger and heel-shin tests on both sides, scoring ataxia only if it is present disproportionate to weakness	0–Absent 1–Present in one limb 2–Present in both limbs
Sensation
Use pinprick to test arms (not hands), legs, trunk, and face	0–Normal 1–Mild or moderate loss of sensation 2–Severe or total sensory loss
Best language
Ask the patient to describe the events in a picture, or name items on a naming sheet, or read sentences on a sheet of paper	0–Normal 1–Mild or moderate aphasia; some loss of fluency 2–Severe aphasia 3–Global aphasia; mute
Dysarthria
Ask the patient to read or repeat several words	0–Normal 1–Mild or moderate (slurs some words or can be understood with some difficulty) 2–Severe (mute or unintelligible in the absence of, or disproportionate to, dysphasia)
Extinction and inattention (Neglect)
Previous items may provide sufficient information to gauge neglect	0–Normal 1–Inattention or extinction to bilateral simultaneous stimulation in one of the sensory modalities 2–Profound hemi-inattention to more than one modality; does not recognize own hand or orients to only one side of space
Key: LOC, level of consciousness; NIH, National Institutes of Health.
Adapted from the NIH Stroke Scale, National Institutes of Health, Institute of Neurological Disorders and Stroke. Available at: http://www.ninds.nih.gov/doctors/index.htm . Accessed June 10, 2004.

Confirming the diagnosis

An early imaging study is required to differentiate ischemia from hemorrhage so that appropriate treatment may be initiated rapidly. The ideal imaging modality for stroke must be able to rule out intracranial hemorrhage, confirm ischemic pathology, (intracranial artery disease, ischemic tissue injury, decreasing perfusion), and require no more than 20 minutes.¹⁰ Although magnetic resonance plus diffusion-weighted imaging (MR-DWI), perfusion-weighted imaging (PWI), and MR angiography meet these criteria,¹⁰ CT is the preferred imaging study in the emergency department (ED) because of its speed, availability, and ability to confirm bleeding (despite its inability to confirm ischemia).^11,12 MRI is more sensitive at detecting early infarct but is more expensive than CT. A suspected cardioembolism must be investigated with chest radiography^13,14 and with continuous ECG for intermittent atrial fibrillation. Transesophageal echocardiography is the most sensitive test for cardioembolic sources.¹³

A CBC, erythrocyte sedimentation rate, serum electrolyte values, liver function tests, serum glucose levels, and a coagulation profile should be obtained to rule out anemia, polycythemia, hypercoagulable states, and infection.¹⁵ Serum homocysteine levels and a complete hematologic workup may be indicated in a young patient to rule out premature atherosclerotic disease.²

Treating the ischemic attack: Emergent care and after

Antiplatelet therapy continues to be the mainstay of treatment for ischemic stroke. Aspirin administered within 48 hours of symptom onset and continued for 10 to 28 days has been shown to reduce death and both long- and short-term dependency.^13,16 Ticlopidine (Ticlid), 250 mg twice a day, clopidrogrel (Plavix), 75 mg/d, and the combination of aspirin plus extended-release dipyridamole (Aggrenox) are also effective therapies in some patients.¹⁷ Studies have shown both fewer recurrences and a better side-effect profile with antiplatelet agents than with other drugs. A low dosage of aspirin (75-150 mg/d) is protective and forestalls the apparent dosage-related effects of dyspepsia and constipation.¹⁸

In addition to its role in the treatment of acute stroke, antiplatelet therapy has a role in preventing subsequent strokes. A meta-analysis showed a 25% reduction in serious vascular events among patients using antiplatelet therapy who had had an acute stroke or vascular disease.¹⁸ With the relatively low risk of complications on low-dosage antiplatelet therapy, this should be a mainstay of prevention after a stroke, an MI, or a TIA and in patients at high risk for stroke.

In a landmark trial, 624 patients with stroke were randomly assigned to receive either recombinant tissue plasminogen activator (rt-PA) or placebo.¹⁹ Those patients who received rt-PA were found to be at least 30% more likely to have minimal or no disability at 3 and 12 months than were the placebo-treated patients, and mortality at 12 months was not significantly different between the rt-PA group and the placebo group. The results indicated a sustained benefit of rt-PA.

The only FDA-approved agent for acute ischemic stroke is rt-PA in dosages of 0.9 mg/kg up to a maximum of 90 mg; 10% of the total dose is given as a bolus, and the remainder is infused over 1 hour. No other drugs that affect coagulation (including heparin, warfarin, or aspirin) should be given for 24 hours after initiation of rt-PA therapy (see Table 1). Only a small percentage of stroke patients are candidates for rt-PA therapy, however, because of time constraints and risks associated with administering the drug in error to patients with hemorrhagic rather than ischemic stroke.

 

TABLE 1 The use of rt-PA

Indicated in Clinical diagnosis of stroke; hemorrhage and edema excluded by CT Age >18 y, with consent Symptom onset of <3 h Conditions needed IV access with two peripheral lines, continuous BP monitoring, no other thrombotic treatment for 24 h. Infusion of rt-PA must stop and cryoprecipitate must be given if there is further neurologic decline; no urethral catheterization for 2 h. Contraindications BP >185/110 mm Hg at time of treatment Coma or stupor Elevated INR GI bleeding within past 21 d Heparin use Platelet count <100,000 mL or hematocrit <25% Prior intracranial hemorrhage Prolonged PTT Rapidly improving or minor symptoms Recent MI Serum glucose level <50 or >400 mg/dL Stroke or head injury within 3 mo Surgery within 14 d

Key: INR, international normalized ratio; MI, myocardial infarction; PTT, partial thromboplastin time; rt-PA, recombinant tissue plasminogen activator.

In addition to administering appropriate drug therapy to treat ischemia in the ED, important hospital care includes encouraging early patient mobility and self-care, facilitating communication in patients who have aphasia, and initiating rehabilitation.²⁰

The complications and sequelae of stroke

Cardiac and pulmonary problems are the most common complications of acute ischemic stroke and are an important cause of secondary morbidity and mortality.²¹ Approximately half of patients who have had a stroke will also have CAD; MI or other ischemia will complicate 3% of hospital stays for stroke patients.²¹ Deep venous thrombosis and pulmonary embolism are also important causes of death in patients with acute stroke. Prophylaxis includes early ambulation if possible, antiembolism stockings, and aspirin. Electrical stimulation and external pneumatic calf compression devices are also effective.^21,22

Aspiration pneumonia kills 6% of patients with acute stroke; dysphagia must be addressed with postural or dietary changes or with swallowing exercises.²² Decubitus ulcers occur in 14.5% of hospitalized stroke patients.²⁰ Important measures to prevent ulcers include putting stroke patients on flat beds, repositioning them every 2 hours, providing body support, applying lotion, and using gel pads to keep their skin cool and dry.

Adequate nutrition is also an important management goal; half of stroke victims in inpatient rehabilitation centers are malnourished. Hypoalbuminemia and hyperglycemia are important problems to watch for and correct.²⁰

Prevention and patient education

Although some risk factors for stroke are modifiable, such as hypertension, others are not (see Table 2).

 

TABLE 2 Possible and confirmed risk factors for stroke
Alcohol use Age >64 y Cardiac disease Diabetes History of transient ischemic attacks	Hyperhomocysteinemia Hyperlipidemia Hypertension Migraine headache Oral contraceptive use Smoking

Hypertension Controlling BP is the most important factor in risk reduction, and the degree of hypertension is proportional to the increased risk of stroke. In the United Kingdom TIA (UK-TIA) trial, risk for recurrent stroke increased by 28% for every 10 mm Hg increase in BP above 120/80 mm Hg.²¹ Recently issued guidelines from the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) have established 120/80 mm Hg as the upper limit for normal BP.²²

Researchers in the Perindopril Protection Against Recurrent Stroke Study (PROGRESS) sought to determine the best antihypertensive therapy in patients within 5 years of either a TIA or a stroke. The researchers found that use of a diuretic added to perindopril reduced the risk of stroke;²³ an ideal antihypertension regimen seems to be an ACE inhibitor combined with a diuretic.

Atrial fibrillation Twenty to 30 million Americans have atrial fibrillation,²⁴ which is likely to be associated with 15% of all ischemic strokes and with 30% of those in the elderly.²⁰ Because atrial fibrillation has been shown to be an independent risk factor for embolic stroke, it should be medically treated; both warfarin (Coumadin) and aspirin are used (see Table 3).²⁵

 

TABLE 3 Anticoagulation choices for atrial fibrillation

Age <65 y, no risk factors: aspirin, 325 mg/d Age >65 y, with or without risk factors: warfarin, to international normalized ratio 2-3

Note: Risk factors include stroke, diabetes, hypertension. Contraindications to warfarin are patient nonadherence, GI bleeding, pregnancy, alcoholism, coagulopathy, history of bleeding during anticoagulation, and recent surgery.

Hyperlipidemia Statins, particularly pravastatin (Pravachol) and simvastatin (Zocor), have been beneficial for secondary stroke prevention, even among patients whose serum cholesterol levels are within normal reference ranges. A large meta-analysis of nonstatin cholesterol-lowering agents did not, however, show a stroke-reducing effect.²⁶

Carotid stenosis This condition may be responsible for 20% to 30% of strokes.²⁴ Carotid endarterectomy is an important therapeutic modality in many patients because even with medical management, including aspirin, 325 mg/d, there is still a 10% risk of ipsilateral stroke within 5 years of the diagnosis.

Patient education about risk factors and their management are the keys to stroke prevention. For example, cigarette smoking directly increases the risk of stroke, but that risk decreases 2 to 5 years after smoking cessation. As little as several hours a week of moderate physical activity can counteract the risk for stroke associated with a sedentary lifestyle. ²⁴

 

KEY POINTS in this article Once stroke is diagnosed, its etiology—either hemorrhagic or ischemic—must be identified before treatment is initiated. Despite the availability of more advanced modalities, CT is the most commonly ordered imaging study because of its cost, availability, and accuracy in ruling out hemorrhage. Though antiplatelet therapy remains the cornerstone of treatment for stroke, the thrombolytic agent rt-PA has been shown to improve outcomes if given within 3 hours of symptom onset.

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24. Go AS, Hylek EM, Phillips KA, et al. Prevalence of diagnosed atrial fibrillation in adults: national implications for rhythm management and stroke prevention: the AnTicoagulation and Risk Factors in Atrial Fibrillation (ATRIA) Study. JAMA. 2001; 285:2370-2375.

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Carolyn Hewko. Acute ischemic stroke--swift assessment & quick action produce optimal outcomes. JAAPA July 2004;17:19-25.

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