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Acute ischemic stroke: emergentevaluation and management

R. Jason Thurman, MD*, Edward C. Jauch, MD, MSDepartment of Emergency Medicine, University of Cincinnati, 231 Albert B. Sabin Way,

Cincinnati, OH 45267-0769, USA

As the third leading cause of death and number one effectuation of adult

disability in the United States and industrialized Europe, stroke inflicts a

devastating physical, emotional, and financial toll on its victims, their fam-

ilies, and healthcare systems all over the world. In 1998 alone, the U.S. pop-

ulation endured more than 600,000 strokes resulting in 158,448 deaths and

the loss of functional independence for countless others [1]. Until recently,

care for those acutely afflicted by stroke has been limited to supportive man-agement with little hope of affecting a positive outcome. The last decade has

seen the emergence of new treatments for acute stroke, however, energizing

stroke care providers and spreading a sense of optimism among those who

seek to alter the course of this terrible disease. Because effective stroke treat-

ment is extremely time-dependent, it is paramount that emergency physi-

cians understand and excel in their critical role at the forefront of stroke

management.

Epidemiology

With an estimated 750,000 new strokes and more than 1 million hospital-

izations occurring in the United States each year, the importance of stroke

as a major cause of morbidity and mortality cannot be overemphasized.

Approximately 8% of those suffering an acute stroke die within 30 days,

whereas approximately 29% of stroke patients are dead at 1 year. Of those

who survive, 16% of stroke patients require institutional care; another 31%

require assistance caring for themselves, and 20% of stroke survivors need

walking assistance [2]. Up to one third of stroke survivors suffer from majordepression, and depression is common in care providers also. The direct and

Emerg Med Clin N Am

20 (2002) 609630

* Corresponding author.

E-mail address: [email protected] (R.J. Thurman).

0733-8627/02/$ - see front matter 2002, Elsevier Science (USA). All rights reserved.

PII: S 0 7 3 3 - 8 6 2 7 ( 0 2 ) 0 0 0 1 4 - 7


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indirect economic impact of acute stroke in the United States is no less

severe, with an estimated cost of $43 billion per year.

Pathophysiology

Strokes are classified as either ischemic or hemorrhagic, with nearly 85%

being ischemic. Ischemic strokes are further divided into thrombotic strokes

(60% of ischemic strokes), caused by in situ cerebrocervical artery occlusions

usually secondary to atherosclerotic lesions, and embolic strokes (40% of

ischemic strokes), caused by obstructive emboli from proximal vessel or car-

diac sources [2]. Both subtypes of ischemic stroke result in the acute inter-

ruption of arterial blood flow to a dependent area of brain parenchyma.

Once an arterial occlusion has occurred, a heterogeneous area of hypoper-

fused tissue is created. A central zone of ischemic tissue known as the core

is completely deprived of critical oxygen and glucose delivery, and irreversi-

ble neuronal injury begins within minutes. Surrounding the core are areas of

markedly decreased perfusion where stunned brain parenchyma receives a

diminished blood supply from cerebral collateral vessels and potentially

from residual arterial flow. This area, known as the ischemic penumbra, is

potentially salvageable if significant arterial flow can be quickly restored

and thus it is the therapeutic target of most emergent stroke treatments

[3,4]. Through multiple animal studies and recent clinical experience, the

degree of neuronal injury is clearly a function of the extent and duration

of ischemia [5]. It is estimated that approximately 6 hours represents the

window of opportunity available before the penumbra is lost and irreversible

neurologic devastation occurs [4,5]. This highlights the need for speed

and efficiency in the detection of ischemic stroke symptoms, activation

of emergency medical services (EMS), emergent transport of the patient,

and rapid assessment and treatment in the emergency department. These

essential elements of acute stroke care are well summarized by the seven

step stroke chain of survival known as the Seven Ds (Table 1) [6].

Virtually every link in the chain involves the skills and efforts of emergency

physicians.

Table 1

The Seven Ds of acute stroke management

Detection The awareness of stroke signs and symptoms by the patient or bystanders

Dispatch Activation of EMS systems, priority dispatch, and rapid EMS response

Delivery Rapid transport to the appropriate facility, en-route assessment, and

prehospital notification

Door Emergency department triage

Data Emergency department evaluation (neurologic evaluationNIH Stroke

Scale, glucose, head CT, etc)

Decision Selection of appropriate therapy and interventions

Drug Delivery of therapeutics

610 R.J. Thurman, E.C. Jauch / Emerg Med Clin N Am 20 (2002) 609630


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Prehospital management

Successful stroke treatment begins with the prompt recognition of stroke

symptoms and the immediate initiation of an EMS response. First respond-

ers are of paramount importance in obtaining history and establishing the

exact time of symptom onset, which can be quite elusive once the patient has

left the scene and bystanders are unavailable for interview.

After ensuring stability of the ABCs (airway, breathing, and circulatory

system), prehospital care providers move to secondary survey, which in-

cludes a simple standardized assessment of neurologic function. One of the

first such prehospital tools, the Cincinnati Prehospital Stroke Scale (Table 2)

and others like it have proven sensitive and specific in detecting anterior cir-

culation strokes [7,8].

While en route, intravenous (IV) access is obtained, oxygen is adminis-

tered if needed, and blood glucose is checked. When stroke is strongly sus-

pected, an advanced notification is promptly made to the receiving hospital.

This critical action allows ED personnel to prepare for the arrival of the

patient, coordinate ancillary services to ensure that diagnostic imaging is

readily available, and alert the local stroke team if one is available [9]. Noti-

fication and preparation alone can save significant time. The importance of

this vital step is well underscored by the recent data suggesting that a mere

2030 minute delay in thrombolytic treatment of stroke may diminish the

chances of clinical improvement by approximately 10% [10].

Emergency department management

Initial assessment

On arrival, the acute stroke patient is placed in a high acuity area and is

given the same triage priority as unstable trauma or a critical cardiac

patient. Assessment of vital signs, establishment of IV access, initiation ofcardiac monitoring, pulse oximetry measurement, and confirmation of

blood glucose are done while obtaining an accurate and focused history.

Determining the exact time of onset of the stroke symptoms along with

Table 2

The Cincinnati prehospital stroke scalea

Facial droop Have patient smile or show teeth

Normal Both sides move equally

Abnormal One side does not move as wellArm drift Patient closes eyes and holds both arms out

Normal Both sides move equally or no movement at all

Abnormal One side does not move as well or drifts downward

Speech Have patient say You cant teach an old dog new tricks

Normal Patient uses correct words without slurring

Abnormal Slurs words, uses inappropriate words, or is unable to speak

a Any one or more abnormal finding is suggestive of acute stroke.

611R.J. Thurman, E.C. Jauch / Emerg Med Clin N Am 20 (2002) 609630


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findings of any events surrounding the episode such as trauma, seizure activ-

ity, or migraine headache is the top priority of the emergency physician.

EMS personnel, family members, or bystanders are valuable sources ofinformation because the patient may be uncertain regarding the onset of the

stroke, completely unaware of the ongoing symptoms, or may be simply

unable to verbally communicate.

Supplemental history helps elicit any risk factors for acute ischemic

stroke (Table 3). Although hypertension is the most important and preva-

lent risk factor for acute ischemic stroke [11], history of prior transient ische-

mic attacks (TIAs) carries significant risk, as well [12].

Physical examinationAfter assessing the vital signs, the head and neck are examined for any

evidence of trauma. Carotid auscultation is performed to listen for bruits.

The presence of cardiac arrhythmias such as atrial fibrillation, an important

risk factor for cardioembolic stroke, is sought. A heart murmur may indi-

cate valvular problems [2]. Unequal pulses in the extremities might suggest

the presence of aortic dissection.

The importance of conducting a thorough but focused neurologic exami-

nation is underscored. Performed quickly and easily, the National Institutes

of Health Stroke Scale (NIHSS) forms the basis of the focused neurologicexamination (see Appendix A). The scale focuses on six major categories

of the neurologic examination: (1) overall level of consciousness, (2) visual

function, (3) motor skills, (4) sensation and neglect, (5) language, and (6)

cerebellar integrity [7].

The NIHSS provides an insight into the location and the size of the

underlying lesion in common ischemic stroke syndromes and even helps

identify some subtle stroke syndromes (Table 4) [13]. The scale is a strong

initial predictor of ultimate clinical outcome [14]. It also helps identify those

patients likely to respond favorably to treatment and those with increasedrisk for hemorrhagic complications after thrombolytic therapy. Widely used

by neurologists and stroke teams, NIHSS provides a powerful means of

communication between ED physicians and their consultants.

Table 3

Risk factors for ischemic stroke [7]

Modifiable Nonmodifiable

Atrial fibrillation/heart disease Age

Carotid stenosis

Diabetes mellitus Gender (male[female)

Hyperlipidemia

Hypertension Race (African American[Caucasian)

Smoking

Heavy alcohol use History of prior stroke

History of transient ischemic attacks



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Table4

Selecteduncommonclinicalstrokesyndromes[13]

Syndrome

Arterialocclusionsite

Clinicalmanifestations

Lateralmedullarysyn

drome

(Wallenburgsyndro

me)

Posteriorinferiorcerebellarartery

(oftenlesioninvertebralartery)

a)Ipsilaterallimbataxia,b)Ipsilaterallossoffacialcu

taneous

sensation,c)Hiccup,d)Ip

silateralHomesyndrome,e)Nausea/

vomiting/nystagmus,f)Con

tralaterallossofpainandtemperature

sensation,g)Dysphagia,h)

Hoarsenesswithipsilateralvocalcord

paralysis,i)Lossofipsilater

alpharyngealreflex

Lateralinferiorpontinesyndrome

Anteriorinferiorcerebellarartery

(af)Aboveplus:g)Ipsilate

ralfacialparalysis,h)Deafnessand

tinnitus,i)Ipsilateralgazep

aralysis

Lateralmidpontinesy

ndrome

Shortcircum

ferentialartery

(af)Aboveplus:g)Trigeminalnerveimpairment:Chewingd

ifficulty

(bilaterallesions)oripsilateraljawdeviationwithmouth

opened

(unilaterallesions)

Lateralsuperiorpontinesyndrome

Superiorcer

ebellarartery

(af)Aboveplus:g)Nospecificcranialnervesigns

Medialmedullarysyn

drome

Paramedian

branchesofbasilarartery

a)Contralateralhemiparesis,b)Contralaterallossofproprio

ception

andvibratorysensoryfun

ction,c)Ipsilaterallimbata

xia,d)

Ipsilateraltongueweakness

Medialinferiorpontin

esyndrome

Paramedian


(ac)Aboveplus:d)Ipsilater

algazeparalysis,e)Ipsilaterallateral

rectusparalysis,f)Gaze-evo

kednystagmus

Medialsuperiorpontinesyndrome

Paramedian


(ac)Aboveplus:d)Internuclea

rophthalmoplegia,e)Palatalmy

oclonus

Ventralmidbrainsyndrome

(Webersyndrome)

Paramedian


a)Contralateralhemiparesis,

b)Contralateralsupranuclea

rfacial

paresis,c)Ipsilateraloculom

otornervepalsy

Centralmidbrainsyndrome

(tegmentalsyndrom

e)

Paramedian


a)Ipsilateraloculomotornervepalsy,b)Hemichoreaofcontralateral

limbs,c)Contralaterallossofcutaneoussensationand

proprioception

Dorsalmidbrainsynd

rome

(Parinaudsyndrome)

Usuallycausedbycompression

byextra-a

xiallesion(pinealoma)

Paralysisofupwardgaze

Locked-insyndrome

Basilararter

yocclusioncausing

bilateralv

entralpontinelesions

Completequadriplegia,inabilitytospeak,andlossofallfacial

movementsdespitenormal

levelofconsciousness:patien

tsmay

communicatewitheyeorey

elidmovements



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Level of consciousness is evaluated first. This includes an overall assess-

ment of the patients level of awareness and assignment to a category (alert,

drowsy, stuporous, or coma) along with a scoring of the patients ability toanswer simple questions and follow commands (Items 1a1c). Gaze and vis-

ual fields are assessed next as the examiner looks for evidence of gaze palsy or

a visual field cut (Items 2 and 3). These are best detected with a careful extra-

ocular movement examination and visual field testing by confrontation

(examiner faces patient and tests visual fields by bringing moving fingers in

slowly from the sides until patient detects them). The presence of a facial

palsy is sought (Item 4) by having the patient show teeth, raise eyebrows, and

squeeze eyes shut, and the differentiation between a central facial palsy (brow

spared) and peripheral facial palsy (brow and lower face involved) is noted.Motor strength is checked in all extremities (Items 58) and graded 04

according to the scale. Evaluating for pronator drift may reveal subtle

strength deficits. The examiner watches for any sign of slight pronation of the

forearm while having the patient stand (if possible) with eyes closed and arms

held outstretched 90 with palms up for 10 seconds. If the patient cannot

stand, this may be done in the same manner with the supine patient holding

the arms out 45. If no drift is present, the score is 0; some drift indicates at

least mild weakness and a score of 1 is assigned in the NIH scale. If the

patient has greater drift of the arm so that resistance against gravity isimpaired, a score of 2 is assigned. The presence of some movement, (but any

movement against gravity is absent) receives a score of 3. Absence of any

movement yields a score of 4.

Next, the extremities are quickly assessed for evidence of ataxia with

finger-to-nose coordination and heel-to-shin testing (Item 9), followed by

a rapid gross sensory examination of the face and extremities (Item 10).

The patient is then examined for evidence of neglect (the patient may un-

consciously ignore half of his or her body or the surroundings with non-

dominant hemisphere strokes) and extinction (the patient may notice astimulus of only one side of the body with simultaneous testing of both sides

if the sensory cortex is ischemic). Finally, the examiner seeks evidence of

dysarthria (Item 12) and language deficits (Item 13). By asking simple ques-

tions and having the patient attempt to repeat simple phrases, signs of dys-

arthria (slurred speech), receptive aphasia (the patient cannot comprehend

language), expressive aphasia (the patient can understand but cannot

express language), or global aphasia (the patient can neither understand nor

express language) are readily identified.

Emergent CT brain

High priority computed tomography (CT) scanning of the head is the

most important study done early in the course as most treatment algorithms

for acute stroke hinge on the presence or absence of intracranial blood on a



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brain CT study. Emergent CT brain also helps rule out nonvascular lesions

of the brain [15]. The National Institute of Neurological Disorders and

Stroke (NINDS) recommend stroke evaluation time targets that call for adoor to CT completion time of 25 minutes and a door to CT interpretation

time of 45 minutes [6,7]. These time goals stress the need for the prepared-

ness, planning, and establishment of protocols designed to streamline care

of stroke patients into rapid care pathways.

Prompt and accurate interpretation of the CT scan is critical. An

adequately trained physician who has achieved a high level of sensitivity

in detecting evidence of intracranial blood assumes this responsibility [16].

Obvious early ischemic changes such as focal hypodensity often are not

observed on initial CT; however, the presence of subtle signs helps steertherapy (Table 5) [7]. Many initial CT findings (Table 5), do not exclude the

use of thrombolytic therapy, but large areas of hypodensity or early signs of

cerebral edema or mass effect likely suggest irreversible neuronal injury that

carries a greater chance of hemorrhagic complications with the use of

thrombolytic agent.

Performance of the CT scan or its interpretation should not delay notifi-

cation of the local stroke team or the neurologist. This is especially true if

protocol design dictates the use of thrombolytic agent only by the stroke

team or the neurologist. To preserve valuable minutes, consultation occursat the moment acute ischemic stroke is suspected.

Ancillary testing

The diagnostic investigation of the stroke patient includes a measurement

of serum glucose and pulse oximetry, complete blood count, electrolyte pan-

el and renal function, coagulation testing, EKG, cardiac enzymes, and chest

radiograph [17]. These ancillary studies aid in evaluating the coexisting con-

ditions and in working quickly through the differential diagnosis of stroke

mimics (Table 6). A complete blood count screens for thrombocytopenia

(important in thrombolytic consideration) and for polycythemia-induced

hyperviscosity. Electrolyte and renal panels may identify unusual causes

Table 5

Early CT findings in ischemic stroke and treatment considerations

Subtle findings Does not exclude thrombolytic therapy

Loss of insular ribbon

Loss of gray-white interface

Loss of sulci

Dense middle cerebral artery sign Suggests large stroke, consider IAa

Hypodensity\1/3 MCA distribution Consider thrombolytics, but

increased risk of hemorrhage

Hypodensity[1/3 MCA distribution Likely contraindication to thrombolytics

Edema/mass effect/midline shift Likely contraindication to thrombolytics

a IA, intra-arterial thrombolysis.



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of neurologic impairment such as hyponatremia and uremia. Coagulation

studies are vital in patients taking warfarin (INR must be known before

thrombolytic therapy). EKG and cardiac enzymes help identify concurrent

myocardial ischemia and underlying arrhythmias such as atrial fibrillation.

Differential diagnosis (see chapter 3)

The most common and perhaps most easily identified stroke masquerader

is hypoglycemia. The routine use of an immediate serum glucose measure-

ment in patients exhibiting alterations in their baseline neurologic statusquickly differentiates hypoglycemic patients from those with acute stroke

and prevents undesirable delays in the treatment of hypoglycemia. Hypoxia

is identified and treated promptly. Eliciting a history of seizure activity at

the onset of stroke symptoms from bystanders or EMS suggests the possi-

bility of Todds (postictal) Paralysis, which may be clinically indistinguishable

from acute stroke. Finally, complicated migraine headaches may be partic-

ularly difficult to clinically differentiate from acute stroke. Patient history,

demographics, and advanced neuroimaging techniques are sometimes help-

ful in making this distinction [7].

General management

The major focus in the initial management of acute ischemic stroke

revolves around well orchestrated coordination of patient care to ensure

Table 6

Abbreviated differential diagnosis of stroke [2,7]

Diagnosis Differential aidsHypoglycemia Finger stick serum glucose

Hyperglycemia

Complicated migraine History, young age, female gender, peripartum

Todds (postictal) paralysis History of seizure activity at stroke onset

Intracerebral hemorrhage CT scan, severe headache, moribund patient

Hypertensive encephalopathy Severe uncontrolled hypertension

Trauma Physical examination history, CT scan

Neoplasm/epidural or subdural hematoma CT scan

Encephalitis/meningitis Fever, nuchal rigidity, photophobia, CSFa

studies

Hyponatremia/uremia Electrolytes/renal panel

Toxicological History, toxicology screen

Psychiatric History, physical examination, psychiatric

meds

Bells palsy History, physical (peripheral 7th CN findings)

Arterial dissection syndromes History, physical examination, imaging studies

(CXR)

a CSF, cerebrospinal fluid.



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that physician evaluation and diagnostic testing are performed quickly.

Stroke evaluation time targets for potential thrombolytic candidates are

listed in Table 7.The ABCs are addressed first. Fortunately, the vast majority of acute

ischemic stroke patients have no major difficulties with maintaining their

airway, breathing efforts, or circulatory competence early in their clinical

course [2,6]. Problems may arise with large brainstem strokes or with very

large cortical infarcts producing vasogenic edema and mass effect, though

this complication usually does not develop until the second or third day.

Continuous cardiac monitoring of all acute stroke patients is now stan-

dard practice as arrhythmias are common. The administration of hypotonic

fluids such as D5W or excessive fluids in general is avoided to prevent theexacerbation of stroke-related brain edema [9].

Oxygen

Although in practice stroke patients are frequently placed on supplemen-

tal oxygen, there is no evidence to support the routine use of oxygen in the

absence of hypoxia [9]. Because no benefit has been established and some

evidence suggests that supernormal oxygenation might worsen outcome,

supplemental oxygen is reserved only for hypoxic patients [2].

NPO status

A major contributor to the morbidity and mortality of patients afflicted

with ischemic stroke is aspiration pneumonia as the ability to safely swallow

may be compromised. A formal swallowing evaluation is considered before

any oral intake is permitted.

Hyperthermia

Hyperthermia is controlled in all ischemic stroke patients, as an elevated

core temperature is known to be harmful in the setting of stroke. Con-

versely, some experimental studies have demonstrated a decrease in infarct

size with a lowered body temperature [9]. Possible infectious etiologies of

fever in the stroke patient should be considered and investigated as needed.

Table 7

NINDS recommended stroke evaluation targets for potential thrombolytic candidates [6,44]

Time interval Time target

Door to doctor 10 minutes

Access to neurologic expertise 15 minutes

Door to CT completion 25 minutes

Door to CT interpretation 45 minutes

Door to treatment 60 minutes

Admission to monitored bed 3 hours



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Glucose control

The finding of hypoglycemia on initial evaluation requires immediate

treatment, particularly because hypoglycemia may perfectly mimic acute

stroke. Hyperglycemia is also known to imitate stroke symptoms. Some

studies suggest that elevated serum glucose may worsen stroke outcome

by aggravating neuronal ischemia [2,9]. A serum glucose of greater than

300 mg/dL in the setting of acute ischemic stroke is treated with insulin [2].

Hypertension

There are some controversies surrounding the management of hyperten-sion in the setting of ongoing acute ischemic stroke. Many stroke victims

share hypertension as an underlying risk factor, and during an acute ische-

mic stroke these patients may exhibit even higher blood pressures than base-

line hypertension. There are no data supporting routine aggressive blood

pressure control in the setting of ischemic stroke for those patients who are

not candidates for thrombolytic therapy. Most experts maintain that signifi-

cant lowering of mean arterial pressure acutely may even be harmful. The

delicacy of poorly perfused penumbral tissue is well known. Acutely lower-

ing the blood pressure risks decreasing collateral penumbral perfusion evenfurther, leading to an exacerbation of ongoing ischemia and acceleration

and extension of neuronal death. Most of these patients have limited ability

for autoregulation of cerebral perfusion pressures as a result of chronic

hypertension. For these reasons, blood pressure management is undertaken

carefully.

Special situations such as concurrent acute myocardial infarction, con-

gestive heart failure, hypertensive encephalopathy, acute renal failure, aortic

dissection, and treatment with thrombolytic therapy call for judicious blood

pressure control during acute ischemic stroke [17]. Easily titratable pharma-cologic agents that lower mean arterial pressure gradually are recommended

(Table 8). Antihypertensive drugs known to precipitously drop the blood pres-

sure are avoided [2,6,9]. Agents such as intravenous labetalol or enalapril

Table 8

Emergent antihypertensive therapy in acute ischemic stroke [6], based on current ACLE

guidelines (nonthrombolytic candidates)

DBP[140 mm Hg Sodium nitroprusside (0.5 ug/kg/min) Reduce by approximately

10%20%

SBP[220 or DBP 121140

or MAP >130 mm Hg

Labetalol 1020 mg IV push over 12 min. May repeat or

double labetalol every 10 min to maximum dose of 150 mg.

Enalapril 1.25 mg IV push may be used as alternative therapy.

SBP\220, DBP 120,

or MAP\130 mm Hg

Antihypertensive therapy indicated only if ongoing AMI, severe

CHF, ARF [17], aortic dissection, or hypertensive

encephalopathy



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are well tolerated and are easily titrated to the desired effect. Aggressive

blood pressure control is not often warranted in the treatment of acute

ischemic stroke; almost all patients equilibrate their blood pressure on theirown over the first few hours [18]. The management of blood pressure differs

greatly in those patients who are potential candidates for thrombolytic ther-

apy, however, as discussed later.

Aspirin

The role of antiplatelet therapy in acute ischemic stroke is still being

debated. The use of aspirin has been studied for the treatment of acute

stroke, but no significant benefit was found regarding death or dependenceat 14 days or 6 months in the large International Stroke Trial (IST) [19]. A

significant benefit was discovered with aspirin use in the IST regarding the

recurrence rate of ischemic stroke within 14 days (2.8% aspirin group versus

3.9% untreated), however, suggesting that aspirin therapy has a role in the

prevention of recurrent strokes [19]. Based on these and other data, the ini-

tiation of aspirin therapy (50325 mg daily) within 48 hours of stroke onset

to prevent stroke recurrence is now advocated [20]. Although aspirin use is

to be withheld for 24 hours after thrombolytic treatment, the use of aspirin

before administration of a thrombolytic agent is not a contraindication tothrombolytic therapy. The routine use of aspirin in potential thrombolytic

candidates, however, is currently discouraged.

Anticoagulation

One of the most controversial subjects in the treatment of acute ischemic

stroke is the role of heparin and low molecular weight heparin antithrom-

botic therapy. For many years, unfractionated intravenous heparin has been

used in the treatment of acute ischemic stroke despite the lack of solid evi-dence to support any clinical benefit. In the IST, lack of significant improve-

ment in clinical outcome studies along with the potential risks of heparin use

(hemorrhage and drug-induced thrombocytopenia) has called into question

the use of heparin in stroke [21]. The efficacy of low dose and high dose sub-

cutaneous heparin in the management of acute ischemic stroke was studied.

No significant clinical benefit with regard to death or dependency was noted

in either group in the 14-day or 6-month outcome measures. There was an

observed benefit in recurrence of ischemic stroke in the IST, but this was off-

set by a similar magnitude of increased hemorrhagic strokes and fatalextracranial bleeds [19]. The bleeding complications observed with heparin

were also found to be dose-related in the IST. Critics of this study maintain

that the anticoagulant effects were not monitored and that mandatory CT

scans did not take place before randomization [22]. Although this short-

coming in the study may account for some hemorrhagic complications,

it does not change the fact that clinical outcome measures did not improve at



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6 months in the heparin treated patients. There is no strong evidence to

support the use of unfractionated heparin in cardioembolic strokes [2022].

Many recent clinical trials have assessed the efficacy of low molecularweight heparins (LMWHs) in acute ischemic stroke. A study by Kay et al

examining nadroparin (Fraxaparine) for acute stroke treatment demon-

strated a significant positive dose-dependent effect at 6 months in the treat-

ment groups [23]. Unfortunately, a larger multicenter trial of Fraxaparine

with a similar study design (the Fraxiparine in Ischemic Stroke Study) failed

to reproduce these results [24]. The Trial of Org 10172 in Acute Stroke

Treatment (TOAST) tested the efficacy of the LMWH danaparoid (ORG

10172). The treatment group did show an increase in favorable outcomes

at 7 days, but this benefit did not extend out to 3 months. Despite failureto show a significant improvement in clinical outcome for stroke, many

studies have shown a clear benefit associated with the use of LMWH in

stroke patients for DVT and PE prophylaxis.

There are no definitive data to confirm a significant improvement in

clinical outcome in patients with acute ischemic stroke treated with either

unfractionated heparin or LMWHs. No recommendation can be made at

the present time to support the use of unfractionated heparin or LMWHs

in the setting of acute ischemic stroke except for the prophylaxis of

DVT and PE. Many clinicians continue to use these medications for thetheoretical benefit of anticoagulation in patients with cardioembolic

stroke and thromboembolism. Results of ongoing research trials are

eagerly awaited.

Intravenous thrombolytic therapy

Background and literature review of thrombolytic therapy

In 1995, the National Institute of Neurological Disorders and Stroke

(NINDS) rt-PA Stroke Study Group published the landmark study of

thrombolytic therapy for acute ischemic stroke. FDA approval of a single

pharmacotherapy for acute stroke followed. Using rt-PA (alteplase) within

a strict set of guidelines and treatment parameters, the NINDS trial demon-

strated a significant benefit in clinical outcome at 3 months for acute ische-

mic stroke patients. The NINDS trial consisted of two major parts. Part 1

enrolled 291 patients and assessed the clinical efficacy of rt-PA as indicated

by a four-point improvement in the NIH Stroke Scale over established base-line or a complete resolution of neurologic deficit at 24 hours. This part of

the NINDS trial demonstrated no significant difference between treatment

and placebo groups at 24 hours. Statistically significant improvement in

clinical outcome, however, was seen in the treatment group at 3 months

in four independent stroke outcome measures (NIHSS, modified Rankin

scale, Barthel index, and Glasgow outcome scale). Part 2 of the NINDS trial



13/22

enrolled 333 patients and used a global test statistic to ascertain clinical out-

come at 3 months using the same four clinical assessment scales. The long-

term 3-month clinical benefit of rt-PA noted in Part 1 of the NINDS trialwas confirmed in Part 2 [25]. Clinical benefit is sustained at 1 year for

patients treated with rt-PA, with a 30% greater likelihood of minimal or

no disability at 12 months than the placebo group [26].

In the NINDS trial, the incidence of the most feared side effect of throm-

bolytic therapy, symptomatic intracerebral hemorrhage (ICH) occurred ten-

fold in the treatment group versus placebo (6.4% versus 0.6%). Despite these

complications, there was no significant difference in mortality at 3 months

between the treatment and placebo groups (17% versus 21%, respectively)

and no increase in the severely disabled group was observed [25]. Overall theNINDS trial showed that patients with acute ischemic stroke treated with

rt-PA following a strict established protocol were 30% more likely to have

minimal or no neurologic deficit at 3 months than the placebo group while

suffering no increase in overall mortality.

One of the hurdles to the widespread use of rt-PA for acute ischemic

stroke patients is that many other trials have not reflected similar benefits,

whereas some have shown an alarming rate of ICH in the treatment groups.

Three other major trials of intravenous rt-PA (the European Cooperative

Acute Stroke Study [ECASS I] [27], ECASS II [28], and the AlteplaseThrombolysis for Acute Noninterventional Therapy in Ischemic Stroke

[ATLANTIS] trial [29]) failed to demonstrate a statistically significant

improvement in clinical outcome at 3 months in rt-PA treated patients versus

placebo [17]. In a recent publication Katzan et al reported that 15.7% of rt-

PA treated ischemic stroke patients among 29 Cleveland area hospitals devel-

oped symptomatic ICHs [30]. Many clinicians continue to believe that the

evidence presented in these negative trials may offset the positive results of

the NINDS trial. None of these trials, however, maintained the strict guide-

lines put forth by the NINDS investigators. ECASS I, ECASS II, and theATLANTIS trial all involved patients treated well beyond the 3-hour win-

dow of the NINDS trial, with only a combined 14% of patients treated with

rt-PA within 3 hours of stroke symptom onset in these trials compared with

99.7% in the NINDS trial [17]. In addition to the time window, many other

NINDS protocol violations have occurred in comparative trials, including an

astonishing 50% protocol deviation rate in the Cleveland area study [31].

Since 1996, numerous U.S. and Canadian centers have experienced sim-

ilar success with the use of rt-PA following the NINDS protocol. Albers et

al recently reported the results of the phase IV STARS study, which enrolled389 patients and demonstrated a significant improvement in clinical out-

come at 3 months and a low rate (3.3%) of symptomatic ICH [32]. These

positive results were achieved despite a longer median stroke onset to treat-

ment time (2 hours, 44 minutes) and a 32.6% protocol violation rate. Of

these violations, however, only 13.4% consisted of treatment beyond the

3-hour window.



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There are investigators that argue against thrombolytic treatment because

the exact location of the underlying obstructive vascular lesion is not known,

noting that intravenous rt-PA might not be as effective in large vessel occlu-sions and these patients should not be exposed to the risk for the complica-

tions of thrombolytic therapy [33]. In the NINDS trial patients with all major

subtypes of stroke including those caused by large vessel occlusion benefited

from thrombolytic therapy [17]. The technology to precisely localize arterial

occlusions is restricted by the lack of availability of institutional resources.

This could prevent countless stroke patients from receiving beneficial ther-

apy. Even as the research on the optimal use of rt-PA in acute ischemic stroke

continues, currently intravenous rt-PA administered within the NINDS

guidelines is the best available treatment offering hope for a better outcomefollowing acute stroke [34]. Based on available data, the treatment of acute

ischemic stroke with thrombolytic therapy carries the Grade A recommenda-

tion of the Stroke Council of the American Heart Association provided that

the NINDS inclusion criteria and protocol guidelines are met by qualified

treating physicians in capable treating facilities [35].

Administration of intravenous thrombolytic therapy

Having established the diagnosis of acute ischemic stroke, the ED physician

is now confronted with the critical decision whether to proceed with thrombo-

lytic therapy or pursue supportive care. If less than 3 hours have passed since

the exact time of symptom onset and the patient is at least18 years of age, then

IV thrombolytic treatment must be considered. If available, stroke team mem-

bers or neurologists must be involved in this decision-making process. The

final decision is made only after extensive and informative discussion with the

patient (if possible) and family members has taken place.

The patient and the family members are informed of the potential risksand possible benefits of thrombolytic therapy, and this interaction is docu-

mented. The patient and family are informed of:

1. The fact there is a 30% greater chance of improved clinical outcome at 3

months and 1 year with rt-PA treatment

2. The fact there is a tenfold greater risk for symptomatic ICH within 36

hours in patients treated with the use of thrombolytic therapy

3. The fact there is no significant difference in mortality rate at 3 months

or 1 year despite the increased rate of hemorrhages with rt-PA treat-ment

4. The rationale behind the use of rt-PA for acute ischemic stroke given the

significant morbidity and mortality risk for the underlying stroke and

the use of rt-PA [31]

5. The individual patient risk to benefit profile may neither be clearly de-

fined nor always predicted



15/22

A subgroup of patients within the accepted NINDS criteria carries a

higher risk for hemorrhage, and a lower chance of benefiting from rt-PA

therapy. Increased risk for hemorrhage is associated with the presence ofsignificant findings on early CT scan, treatment beyond 3 hours of symptom

onset, NIHSS[22, and elevations in post-thrombolytic blood pressure [7].

Factors associated with a worse prognosis regardless of thrombolytic treat-

ment include diabetes mellitus, advanced age, uncontrolled hypertension,

higher NIHSS scores, and early CT findings of edema, hypodensity, or a

dense middle cerebral artery sign [7,32,36]. The presence of any or a combi-

nation of these factors are carefully considered before recommending

thrombolytic therapy.

Blood pressure management in the thrombolytic candidate carries a spe-cial significance, as one of the contraindications to thrombolysis is uncon-

trolled hypertension at the time of treatment. The preintervention blood

pressure is gently lowered to a systolic blood pressure of\185 mm Hg and

a diastolic blood pressure of\110 mm Hg [35]. Recommendations for

thrombolytic candidates adopted from ACLS guidelines are presented in

Table 10. If aggressive measures are required to lower the patients blood

pressure to less than 185/110 in the pretreatment window, the patient is

excluded from thrombolytic therapy.

After all inclusion and exclusion criteria are considered (Table 9) and therisks and benefits of thrombolytic therapy have been weighed and discussed

Table 9

Indications and contraindications to thrombolytic therapy in acute ischemic stroke [25]

Indications

Acute ischemic stroke within 3 hours from symptom onset.

Age greater than 18 years old (rt-PA has not been studied in pediatric stroke)

Contraindications

Evidence of intracranial hemorrhage on pretreatment evaluation

Suspicion of subarachnoid hemorrhage

Recent stroke, intracranial or intraspinal surgery, or serious head trauma in the past 3 months

Major surgery or serious trauma in the previous 14 daysa

Arterial puncture at a noncompressible site or lumbar puncture in the last 7 daysa

Major symptoms that are rapidly improving or only minor stroke symptoms (NIHSS \4)a

History of intracranial hemorrhage

Uncontrolled hypertension at the time of treatment

Seizure at the stroke onset

Active internal bleeding

Intracranial neoplasm, arteriovenous malformation, or aneurysm

Known bleeding diathesis including but not limited to:

Current use of anticoagulants or an International Normalized Ratio (INR)[1.7 or

a prothrombin time (PT)[15 seconds

Administration of heparin within 48 hours preceding the onset of stroke and an elevated

activated partial thromboplastin time at presentation

Platelet count\100,000 mm3

a In the NINDS trial, not present in current package insert.



16/22

with the patient and family, the treatment decision is made. The recom-

mended dosing of intravenous rt-PA in acute ischemic stroke is the following:

Total dose 0.9 mg/kg (90 mg maximum)

10% of total dose given IVP over 12 minutes

90% remainder as an infusion over 1 hour

rt-PA is packaged in 50-mg and 100-mg vials. After the treatment dosageis established, the excess rt-PA is removed and discarded before drug admin-

istration to prevent overdose.

Intra-arterial thrombolytic treatment (see also chapter 9)

The use of intra-arterial thrombolytic drugs to facilitate clot lysis is

currently under investigation. Using a tiny catheter, skilled interventionalneuroradiologists are able to identify the obstructive lesion. Local infusion

of thrombolytic agents proximal, distal, and into occlusive cerebrovascular

clots follows. Although intra-arterial thrombolytic therapy is limited

to centers possessing the necessary angiographic resources, the initial

trials assessing the efficacy of intra-arterial thrombolysis are promising

[37,38].

The largest randomized trial of intra-arterial thrombolytic therapy to

date is the Prolyse in Acute Cerebral Thromboembolism II (PROACT II)

trial that screened 12,323 patients, sending 474 to arteriography and treating121 with intra-arterial thrombolytics [37]. Intra-arterial prourokinase was

used in patients with angiographic evidence of middle cerebral artery occlu-

sion or a first-order MCA branch. Intravenous heparin was used concomi-

tantly with the intra-arterial drug, and therapy was begun within 6 hours of

stroke symptom onset. At the 2-hour assessment, the prourokinase group

showed a 67% rate of partial or complete lysis of clot compared with

Table 10

Emergent antihypertensive therapy in acute ischemic stroke [6] (thrombolytic candidates)

Pretreatment Labetalol 1020 mg IVP, 12 doses orSBP[185 mm Hg or Nitro paste 12 or

DBP[110 mm Hg Enalapril 1.25 mg IVPb

Post-treatmenta

DBP[140 mm Hg Sodium nitroprusside (0.5 ug/kg/min)

SBP[230 mm Hg or

DBP 121140 mm Hg

Labetalol 1020 mg IVP and consider a Labetalol drip at 12

mg/min

SBP 180230 mm Hg or

DBP 105120 mm Hg

Labetalol 10 mg IVP, may repeat and double up to a maximum

dose of 150 mg

a Monitor vitals every 15 min for 2 hours, then every 30 min for 6 hours, then every hour for

16 hours.b Not in the current AHA Guidelines.



17/22

18% of the heparin-only group [37]. On outcome measures, the treatment

group enjoyed a 40% rate of favorable outcome defined as the ability to

live independently at 3 months as opposed to 25% in the heparin-onlygroup. A significant fivefold increase in ICH was noted in the treatment

group also.

Assessment of the efficacy and safety of intra-arterial rt-PA in acute stroke

treatment is now being conducted in several trials. The observed benefit of

thrombolytic therapy noted within a 6-hour treatment window potentially

increases the pool of stroke patients eligible for thrombolytic treatment. The

intra-arterial treatments are found to be effective in large artery obstructions.

This is encouraging, as intravenous thrombolytic therapy is known to have

a lower recanalization rate in larger arterial occlusions [3].Another intriguing possibility is the use of intravenous rt-PA followed by

intra-arterial treatment. In this scenario, ED physicians and stroke special-

ists begin intravenous thrombolytic therapy while awaiting the assembly

of an interventional neuroradiology team. This practice introduces the op-

portunity for the initiation of intravenous therapy at outlying hospitals

followed by transport to stroke centers with intra-arterial treatment capabil-

ities [39]. Although limited by small sample sizes, two recent publications

reported positive outcomes of combined therapy. In the EMS Bridging

Trial, 35 patients were randomized to receive either placebo or 0.6 mg/kgof intravenous rt-PA within 3 hours of symptom onset. Cerebral angiography

was then performed, and if an arterial occlusion was identified, the patient

received IA-tPA. Improved recanalization rates and improved 3-month out-

comes were observed in the combined IV-IA tPA therapy group [38]. A retro-

spective analysis by Ernst et al looked at 20 consecutive patients treated with

combined IV and IA rt-PA within 3 hours of symptom onset. The initial

dose of intravenous rt-PA was 0.6 mg/kg (60 mg maximum dose) with a

15% bolus followed by a 30-minute infusion. All 20 patients received angiog-

raphy, and 16 of these were treated with intra-arterial rt-PA (up to 0.3 mg/kg). Again, favorable outcomes were observed as 50% of enrolled patients

recovered to a 2-month modified Rankin scale of 02 (minimal or no disabil-

ity) [40]. The median NIHSS was 21 in the study population compared with

a median NIHSS score of 14 in the NINDS trial, suggesting that the com-

bined approach of intravenous and intra-arterial therapy may play a signifi-

cant role in improving outcomes in more severe strokes involving larger and

more proximal arterial occlusions. Both studies reported excellent door to

treatment times, likely contributing to the positive results of these analyses

and further illustrating the importance of time in treating acute ischemicstroke.

Intra-arterial thrombolytic treatment has indeed shown early promise in

clinical practice. At the present time, this potentially valuable therapy is lim-

ited to major stroke treatment centers, but as research is advanced and more

interventional neuroradiologists are trained, intra-arterial thrombolysis is

likely to become a significant part of acute stroke treatment.



18/22


19/22

prioritization, and management. At the hospital level, emergency physicians

and neurologists must strive together to establish and practice well-

constructed stroke protocols and treatment guidelines. The implementationof stroke code teams enlisting the departments of Emergency Medicine,

Neurology, Radiology, skilled nursing staff, and hospital administration is

imperative to streamline acute stroke patients into optimal care scenarios.

These multidisciplinary teams serve as leaders in the advancement of stroke

care within their local healthcare systems and communities. Through the

creation of well-organized stroke code systems encompassing the prehospi-

tal, ED, and inpatient arenas, stroke teams provide the framework for rapid

and effective acute stroke care.

A vigorous involvement of emergency physicians is critical in the successof stroke treatment. Emergency physicians must become experts in the diag-

nosis and management of acute ischemic stroke and play a leadership role in

advancing the use of thrombolytic therapy. In recognizing and embracing

their critical function at the forefront, emergency physicians will entrench

themselves in the exciting and evolving world of the interventional care of

acute ischemic stroke for years to come.

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Appendix A: The NIH Stroke Scale

Category Description Score

1a Level of consciousness Alert 0

Drowsy 1

Stuporous 2

Coma 3

1b LOC questions (Month, age) Answers both correctly

Answers one correctly

Incorrect on both

0

1

2

1c LOC commands (Open, close

eyes, show thumb)

Obeys both correctly

Obeys one correctly

Incorrect on both

0

1

2

2 Best gaze (Follow finger) Normal 0Partial gaze palsy 1

Forced deviation 2

3 Best visual (Visual fields) No visual loss 0

Partial hemianopia 1

Complete hemianopia 2

Bilateral hemianopia 3

(continued on next page)



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Appendix A (continued)

Category Description Score

4 Facial palsy (Show teeth, raisebrows, squeeze eyes shut)

NormalMinor

Partial

Complete

01

2

3

5 Motor arm lefta Raise 90, hold

10 seconds)

No drift 0

Drift 1

Cant resist gravity 2

No effort against gravity 3

No movement 4

6 Motor arm righta (Raise 90,

hold 10 seconds)

No drift 0

Drift 1



No movement 4

7 Motor leg lefta (Raise 30, hold

5 seconds)

No drift 0

Drift 1



No movement 4

8 Motor leg righta (Raise 30,

hold 5 seconds)

No drift 0

Drift 1



No movement 4

9 Limb ataxia Absent 0

Present in one limb 1

Present in two limbs 2

10 Sensory (Fine touch to face,

arm, leg)

Normal 0

Partial loss 1

Severe loss 2

11 Extinction/neglect (Double

simultaneous testing)

No neglect 0

Partial neglect 1

Complete neglect 212 Dysarthria (Speech clarity to

mama, baseball, huckleberry,

tip-top, fifty-fifty)

Normal articulation 0

Mild to moderate dysarthria 1

Near to unintelligible or worse 2

13 Best languageb (Name items,

describe pictures)

No aphasia 0

Mild to moderate aphasia 1

Severe aphasia 2

Mute 3

Total 042

a For limbs with amputation, joint fusion, etc, score a 9 and explain.b

For intubation or other physical barrier to speech, score a 9 and explain.


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