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Transient Ischemic Attacks:


Transient Trouble
Or Action-Warranted Attacks?
During a Friday afternoon deposition, a 55-year-old malpractice lawyer
developed a 15-minute episode of difficulty speaking and inability to hold his pen in his
right hand. By the time a co-worker drove him to the ED to be evaluated, the episode
had completely resolvedtotal duration, about 15 minutes.
He takes 50 mg of atenolol daily for hypertension, and his only other past medical
history is a migraine headache. He has normal vital signs and a completely normal
examination, including a detailed neurologic examination. His 12-lead ECG is normal.
The patient is adamant about returning to his deposition and demands to know what
other tests or treatment are necessary and why he cant have them done by his primary
care physician on Monday.

transient ischemic attack (TIA) is a neurologic deficit caused by


ischemia to the brain that, by classic definition, completely resolves
within 24 hours. Although there is complete resolution of signs and symptoms, the incident is understandably alarming for the patient and his or her
family, raising numerous questions and sometimes panicked responses. In
contrast, because patients are usually asymptomatic by the time they present
to the ED, many physicians are underwhelmed by the situation and do not
react with appropriate immediacy.
Identifying TIA presents an opportunity to prevent a permanent brain
infarction, or strokethe leading cause of disability and third-leading cause of
death among adults in the United States.1 Traditionally, the resolution of
symptoms has been associated with TIA rather than stroke. Reversible
ischemic neurologic deficit (RIND) is occasionally used to refer to deficits that
last longer than 24 hours but completely resolve. TIA, RIND, and stroke are in
fact a continuum of one disease process. With the increasing use of magnetic
resonance imaging (MRI) evaluation of these patients, it has become clear that
some patients whose symptoms have completely resolved have, in fact, had a
brain infarction/stroke.2-4 Recent MRI data show that up to 50% of patients

Associate Editor
Andy Jagoda, MD, FACEP, ViceChair of Academic Affairs,
Department of Emergency
Medicine; Residency Program
Director; Director, International
Studies Program, Mount Sinai
School of Medicine, New York, NY.

Editorial Board
Judith C. Brillman, MD, Residency
Director, Associate Professor,
Department of Emergency
Medicine, The University of
New Mexico Health Sciences
Center School of Medicine,
Albuquerque, NM.
W. Richard Bukata, MD, Clinical
Professor, Emergency Medicine,
Los Angeles County/USC Medical
Center, Los Angeles, CA; Medical
Director, Emergency Department,
San Gabriel Valley Medical

Center, San Gabriel, CA.


Francis M. Fesmire, MD, FACEP,
Director, Heart-Stroke Center,
Erlanger Medical Center;
Assistant Professor of Medicine,
UT College of Medicine,
Chattanooga, TN.
Valerio Gai, MD, Professor and
Chair, Department of Emergency
Medicine, University of Turin,
Italy.
Michael J. Gerardi, MD, FAAP, FACEP,
Clinical Assistant Professor,
Medicine, University of Medicine
and Dentistry of New Jersey;
Director, Pediatric Emergency
Medicine, Childrens Medical
Center, Atlantic Health System;
Department of Emergency
Medicine, Morristown Memorial
Hospital.
Michael A. Gibbs, MD, FACEP, Chief,
Department of Emergency
Medicine, Maine Medical Center,

Portland, ME.
Gregory L. Henry, MD, FACEP,
CEO, Medical Practice Risk
Assessment, Inc., Ann Arbor,
MI; Clinical Professor, Department
of Emergency Medicine,
University of Michigan Medical
School, Ann Arbor, MI; President,
American Physicians Assurance
Society, Ltd., Bridgetown,
Barbados, West Indies; Past
President, ACEP.
Jerome R. Hoffman, MA, MD, FACEP,
Professor of Medicine/Emergency
Medicine, UCLA School of
Medicine; Attending Physician,
UCLA Emergency Medicine Center;
Co-Director, The Doctoring
Program, UCLA School of Medicine,
Los Angeles, CA.
Francis P. Kohrs, MD, MSPH, Lifelong
Medical Care, Berkeley, CA.
John A. Marx, MD, Chair and Chief,
Department of Emergency

October 2003
Volume 5, Number 10

Authors
Kaushal H. Shah, MD
Faculty Attending, St. LukesRoosevelt Hospital, New
York, NY.
Jonathan A. Edlow, MD, FACEP
Associate Chief of Emergency Medicine, Beth Israel
Deaconess Medical Center, Harvard Medical School,
Boston, MA.
Peer Reviewers
Andrew W. Asimos, MD
Associate Medical Director, Stroke Program
Neuroscience Institute, Carolinas Medical Center,
Charlotte, NC.
Keith Borg, MD
Chief Resident, University of Cincinnati, Cincinnati, OH.
CME Objectives
Upon completing this article, you should be able to:
1. list common symptoms that are attributable
to TIA and symptoms that are not attributable
to TIA;
2. correlate TIA symptom complexes with the
appropriate ischemic vascular territory;
3. describe the appropriate TIA evaluation given
ischemia to a particular vascular territory; and
4. identify high-risk patients who may require a
facilitated inpatient work-up.

Date of original release: October 1, 2003.


Date of most recent review: September 2, 2003.
See Physician CME Information on back page.
Medicine, Carolinas Medical
Center, Charlotte, NC; Clinical
Professor, Department of
Emergency Medicine, University
of North Carolina at Chapel Hill,
Chapel Hill, NC.
Michael S. Radeos, MD, MPH,
Attending Physician, Department
of Emergency Medicine, Lincoln
Medical and Mental Health
Center, Bronx, NY; Assistant
Professor in Emergency Medicine,
Weill College of Medicine, Cornell
University, New York, NY.
Steven G. Rothrock, MD, FACEP,
FAAP, Associate Professor
of Emergency Medicine,
University of Florida; Orlando
Regional Medical Center; Medical
Director of Orange County
Emergency Medical Service,
Orlando, FL.
Alfred Sacchetti, MD, FACEP,
Research Director, Our Lady of

Lourdes Medical Center, Camden,


NJ; Assistant Clinical Professor
of Emergency Medicine,
Thomas Jefferson University,
Philadelphia, PA.
Corey M. Slovis, MD, FACP, FACEP,
Professor of Emergency Medicine
and Chairman, Department of
Emergency Medicine, Vanderbilt
University Medical Center;
Medical Director, Metro Nashville
EMS, Nashville, TN.
Mark Smith, MD, Chairman,
Department of Emergency
Medicine, Washington Hospital
Center, Washington, DC.
Charles Stewart, MD, FACEP,
Colorado Springs, CO.
Thomas E. Terndrup, MD, Professor
and Chair, Department of
Emergency Medicine, University
of Alabama at Birmingham,
Birmingham, AL.

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address outcomes in these patients in the short or long term.


The goal of a TIA work-up and management is
to prevent more serious repeat events that lead to permanent disability. No single medicine or intervention can
prevent another episode with 100% certainty; however, the
latest expert opinion and research strongly suggests the
value of immediately initiating antiplatelet agents and riskfactor modification.9-11

with the clinical diagnosis of TIA have associated MR


findings; the longer the duration of symptoms, the more
likely the diffusion-weighted images are positive.5
The TIA Working Group recently published a statement
proposing a redefinition of TIA in light of the fact that brain
imaging can detect infarction even when the symptoms are
transient: A TIA is a brief episode of neurologic dysfunction caused by focal brain or retinal ischemia, with clinical
symptoms typically lasting less than one hour, and without
evidence of acute infarction.2 Because the resolution of
symptoms doesnt always distinguish TIA from stroke,
some neurologists advocate the same work-up and disposition for all of these patients.2
Moreover, a TIA is clearly a warning sign for future
stroke, with the risk increasing by 13- to 16-fold over
approximately four years.1,6 It is estimated that 4%-8% of
patients with TIA who go untreated will develop a stroke
within one month and 24%-29% of patients will develop
a stroke within five years.1 In a recent large cohort study
of approximately 1700 patients with the diagnosis of TIA
in the ED, the incidence of stroke in the first 90 days
was 10.5%, and half of the strokes occurred in the first
48 hours.7 Patients who experience TIAs may also suffer
short-term cardiovascular events such as myocardial
infarction, unstable angina, congestive heart failure, and
ventricular arrhythmias.
Even so, a recent study of outpatient primary care
physician management of TIAs found a disturbing 31% of
patients had no evaluation performed in the first month
after presenting with TIA.8 Unfortunately, the study did not

Critical Appraisal Of The Literature


There is a great deal written about TIAs, but large, welldesigned studies are rare. The guidelines for TIA established
by the American Heart Association and National Stroke
Association are based on weak evidence and are far from
concrete in terms of the timing of evaluations and disposition of the patient from the ED. (See Table 1.) Diagnostic
imaging studies and indications for carotid endarterectomy
are recommended, but there are no specific guidelines for
when (or how quickly) they need to be performed, due in
large part to a lack of research in this field. Many of the
guidelines are weakened by the fact that they are extrapolated from stroke or mixed stroke and TIA studies.1,2,9,11-13
Others are authored by opinion leaders whose pharmaceutical industry ties may represent a conflict of interest.
Secondary prevention guidelines are almost exclusively
based on stroke or cardiac studies.
There are no clear criteria on how to diagnose TIA; not
only do neurologists disagree with emergency physician
diagnoses, but neurologists disagree among each other.14

Table 1. Consensus Guidelines For The Management Of TIA.


Lab testing

National Stroke Association: Recommended if appropriate


imaging studies not immediately available

American Heart Association: No routine, standard evaluation;


stepwise approach tailored to history
National Stroke Association: No particular recommendations

Risk factor modification


American Heart Association: 1) Treat hypertension (over long
term) to maintain systolic BP < 140 mmHg and diastolic BP <
90 mmHg; 2) Encourage smoking cessation; 3) Maximize
treatment of coronary artery disease, cardiac arrhythmias,
congestive heart failure, and valvular disease; 4) Discourage
excessive alcohol use; 5) Treat hyperlipidemia with statin
medications if diet modification fails; 6) Tighten blood sugar
control in diabetics; 7) Encourage physical activity (30-60
minutes of exercise 3-4 times per week)
National Stroke Association: No particular recommendations

ECG
American Heart Association: Recommended
National Stroke Association: Recommended

Brain imaging
American Heart Association: CT recommended; routine MRI
use not recommended
National Stroke Association: No particular recommendations

Carotid imaging
American Heart Association: Prompt evaluation with
ultrasound, MR, or CT angiography
National Stroke Association: Urgent evaluation

Adapted from: Albers GW, Hart RG, Lutsep HL, et al. AHA Scientific Statement.
Supplement to the guidelines for the management of transient ischemic
attacks: A statement from the Ad Hoc Committee on Guidelines for the
Management of Transient Ischemic Attacks, Stroke Council, American Heart
Association. Stroke 1999 Nov;30(11):2502-2511; Feinberg WM, Albers GW,
Barnett HJ, et al. Guidelines for the management of transient ischemic
attacks. From the Ad Hoc Committee on Guidelines for the Management of
Transient Ischemic Attacks of the Stroke Council of the American Heart
Association. Circulation 1994 Jun;89(6):2950-2965; Albers GW, Caplan LR,
Easton JD, et al; TIA Working Group. Transient ischemic attackproposal for a
new definition. N Engl J Med 2002 Nov 21;347(21):1713-1716; Culebras A,
Kase CS, Masdeu JC, et al. Practice guidelines for the use of imaging in
transient ischemic attacks and acute stroke. A report of the Stroke Council,
American Heart Association. Stroke 1997 Jul;28(7):1480-1497; Brott T, Clark W,
Fagan S, et. al. Stroke: the first hours: guidelines for acute treatment.
Englewood, CO: National Stroke Association; 2000.

Antithrombotics for cardioembolic source


American Heart Association: Oral anticoagulation for atrial
fibrillation
National Stroke Association: Consider acute anticoagulation

Antithrombotics for non-cardioembolic source


American Heart Association: ASA; other options: clopidogrel,
ticlopidine, or ASA plus dipyridamole
National Stroke Association: ASA; other options: clopidogrel,
ticlopidine, or ASA plus dipyridamole

Hospitalization
American Heart Association: No particular recommendations

Emergency Medicine Practice

www.empractice.net October 2003

Epidemiology, Etiology, And Pathophysiology


While the incidence of TIA in the United States is often
quoted at 300,000 per year, this is likely a gross underestimation. Some surveys suggest that almost 7% (1 in 15) of
people older than 65 years report a history of TIA.7 Of
patients who have had a stroke, 15% acknowledge a prior
TIA.16 Two separate studies determined that TIA is highly
overdiagnosed by non-neurologists.17,18 Similarly, of the
patients identified by general practitioners as having a TIA
in the Oxfordshire Community Stroke Project, only 41% had
confirmed TIA determined by the study neurologist.6 On the
other hand, in a more recent study, the ED diagnosis of TIA
was determined to be inaccurate in only 5.6% of patients by
a neurologist reviewing the ED chart (but not interviewing
the patient).7
The etiology of TIA is variable. The majority of TIAs
may result from plaque ulceration or embolism of atherosclerosis-induced platelet aggregation that temporarily
occludes blood flow. Presenting syndromes are divided into
anterior cerebral circulation (carotid artery, anterior cerebral
artery, middle cerebral artery) and posterior cerebral
circulation (vertebral arteries, basilar artery, posterior
cerebral artery). (See Table 2.) Athero-thromboembolism,
cardiogenic embolism, and small vessel disease account for
95% of TIAs.19,20 Whereas patent foramen ovales are more
likely to be present in young patients with TIAs, complex
aortic arch plaques and intra-aortic atherosclerotic debris are
now being implicated in TIAs and strokes among the
elderly with unexplained ischemic events.21,22
Approximately 2% of patients presenting with TIA
have new-onset atrial fibrillation.23 The combination of atrial
fibrillation plus prior stroke or TIA carries a 13% annual risk
of stroke in a 65-year-old male.24 Hypotension or
hypoperfusion usually results in global cerebral deficits, but
focal deficits are possible when there is relatively less
perfusion through a stenotic vessel.
Common presentations of ischemia to the anterior
circulation are often termed carotid artery syndrome.
Temporary monocular blindness (amaurosis fugax) is due to
occlusion of the ophthalmic branch of internal carotid artery,
causing retinal ischemia, and suggests atherosclerosis in the

October 2003 www.empractice.net

Table 2. TIA Syndromes.


Anterior circulation

Hemiparesis
Unilateral sensory loss
Visual field deficit (monocular blindness)
Gaze preference
Aphasia
Left-sided neglect or hemi-attention

Posterior circulation (several of the following usually present)


Hemiparesis
Quadriparesis (locked-in syndrome allows movement of
the upper lids only)
Hemisensory loss or sensory loss in all four extremities
Crossed deficits
Diplopia
Disconjugate gaze
Gaze palsy
Nystagmus
Dysarthria with dysphagia
Vertigo
Decreased level of consciousness
Limb or gait ataxia
Intractable vomiting
Adapted from: Asimos AW. Code stroke: a state-of-the-art strategy for
rapid assessment and treatment. Emerg Med Practice 1999 July;1:1-24.

Emergency Medicine Practice

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region of the carotid bifurcation.25 Patients may complain of


a shade being drawn down or vision blurred by a fog or
mist. Monoparesis and numbness of the leg are consistent
with ischemia to the anterior cerebral artery. The middle
cerebral artery ischemia classically causes hemiparesis
(including the face), aphasia (expressive or receptive), or
homonymous hemianopsia (loss of vision in the right or left
visual fields). Occasionally, language difficulties and
cognitive/behavioral changes may be present as well.
Vertebrobasilar artery syndrome is an entirely different
symptom complex due to ischemia of the posterior circulation supplying the brainstem, cerebellum, and occipital
lobes via the posterior cerebral artery, the basilar artery, and
their branches. Vertigo, dizziness, ataxia, nausea, and
vomiting are the most common symptoms but are not
diagnostic in isolation. Dysarthria, dysphagia, and diplopia
due to disconjugate gaze may also be attributed to the
posterior circulation. Posterior circulation ischemia can also
cause a contralateral homonymous hemianopia or occipital
lobe blindness.
Ischemia of the deep circulation of the brain results in
lacunes or subcortical events, most of which are asymptomatic. When they do cause symptoms, patients will
present with pure motor or sensory deficits. The classic
motor loss is unilateral, equal-intensity weakness in the face,
arm, and leg; other presentations include ataxic hemiparesis
and dysarthria/clumsy hand syndrome. The end arterioles
are thought to be damaged by lipo-hyalinosis as a result of
diabetes mellitus or hypertension.26
Based on the National Institute of Neurological
Disorders and Stroke trial, it is known that if the focal
neurologic deficit does not resolve within one hour or
rapidly improve within three hours, only 1.8% of patients

The exact work-up of TIA is also poorly established,


especially in the ED setting; the algorithm for evaluation is
based on the presumed vascular territory affected.15 It is
clear that the brain, the cerebral vasculature, and possibly
the heart should be evaluated, but the test of choice for each
and the best order of these studies have not been established. No large, prospective trials exist to recommend CT
vs. MRI or computed tomography angiogram (CTA) vs.
magnetic resonance angiogram (MRA) or transthoracic
echocardiography vs. transesophageal echocardiography.
Furthermore, the neuroimaging menu is ever-increasing.
The practice guidelines for the use of imaging in patients
with TIAs recommend CT scan of the head but acknowledge that the evidence derives from expert opinion, nonrandomized historical controls, or observations from case
series (and not empiric studies).12

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Prehospital Care

will have complete symptom resolution within 24 hours27


although the mean symptom duration of TIA in another
major study was 207 minutes.7

When paramedics are called to a patient with neurologic


deficits, three points should be kept in mind.
First, the window of opportunity for thrombolysis in
stroke is narrow. If the patient is exhibiting neurologic
deficits consistent with a vascular territory, it is impossible
to know whether the patient is having a stroke or a TIA.
Prehospital care providers should bring these patients to a
hospital (or, some say, to a stroke center) as quickly as
possible. There is a growing movement to incorporate
prehospital neurologic screens that can help determine
whether the patient is a thrombolytic candidate. Widely
used screens include the Cincinnati stroke screen, Los
Angeles Pre-hospital Stroke Screen, and the Miami EMS
Neurologic Disability Screen. An early call to the hospital
informing the staff of a possible thrombolysis candidate
is helpful.
Second, a medical assessment of the patients condition
by prehospital care providers at the scene is essential. In the
event of a true TIA, signs and symptoms often resolve
before arrival in the ED, so an accurate account of the signs
and symptoms can provide invaluable information.
Finally, prehospital care providers should be encouraged to check blood sugar levels on all patients with
neurologic deficits.

Differential Diagnosis
As Table 3 shows, not all cases of hemiparesis and speech
difficulty result from TIA or stroke; hypoglycemia is one of
the most common mimics. Other causes of focal neurologic
deficits include a post-ictal state (Todds paralysis), central
nervous system abscess, or septic emboli. Hypertensive
encephalopathy can also present with lateralizing findings
(although this rare diagnosis should be considered a
diagnosis of exclusion). Although the more common
presentations of subarachnoid hemorrhage are severe
headache, altered mental status, meningismus, and nausea/
vomiting, up to 20% can present with focal neurologic
deficits as well.28
A thorough history of the event and previous episodes
may suggest other diagnoses, such as multiple sclerosis,
complicated migraine, Mnires disease, and syncope.
Multiple sclerosis is characterized by different neurologic
manifestations at various times; these are usually more
prolonged than the typical TIA. Complicated migraines may
have a preceding aura or scintillating scotomas associated
with the neurologic deficit.29 It is generally accepted that
isolated vertigo is rarely a manifestation of TIA;29 however,
one small study of 24 elderly patients with isolated vertigo
found infarcts of the caudal cerebellum in six patients
(25%).30 If vertigo is associated with tinnitus and hearing
loss, consider Mnires disease.
Cardiac arrhythmias (e.g., ventricular tachycardia,
transient complete heart block) may cause atypical TIA
presentations (e.g., distorted vision, heavy sensation in a
limb, dizziness, uncoordinated movements).31 Arrhythmias
may reduce blood flow through a stenosed vessel, thereby
producing focal deficits in addition to global deficits
from ischemia.
If posterior circulation symptoms occur with exercise,
suspect subclavian steal syndrome; significant occlusion of
the brachiocephalic or left subclavian artery leads to reversal
of blood flow through the vertebral arteries when exercising
the ipsilateral extremity.

Emergency Department Evaluation


Initial Stabilization
Most patients with suspected TIA are not in critical condition on arrival to the ED. Although emergent stabilization is
usually not required, these patients deserve electrocardiogram (ECG) monitoring and IV access. While administering
oxygen is reasonable and appropriate, there is no evidence
to suggest it affects outcomes.

History
A thorough history is the cornerstone of care. There is no
confirmatory test for TIA; only a detailed history from the
patient and witnesses can: 1) establish the diagnosis of TIA;
2) localize the lesion(s); 3) clarify the possible etiologies
(with particular attention to anterior vs. posterior circulation
ischemia); and (4) identify high-risk patients. If the patient is
exhibiting signs of neurologic deficit on presentation, the
foremost concern is establishing the onset of the event.
Assume the patient is having an acute stroke and determine
whether he or she is a candidate for thrombolysis. (See the
July 1999 issue of Emergency Medicine Practice, Code Stroke:
A State-Of-The-Art Strategy For Rapid Assessment And
Treatment.) The time window is three hours from onset for
systemic thrombolytics (and in some institutions up to six
hours using catheter-directed intracranial thrombolysis). If
patients are thrombolytic candidates, perform an immediate
head CT to rule out hemorrhagic stroke. If the patient
awakens with neurologic deficits, assume the time of onset
to be when the patient was last known to be without
neurologic deficit.

Table 3. Differential Diagnosis Of TIA.


Structural brain lesion from tumor, hemorrhage, arteriovenous malformation, or aneurysm
Infection (focal abscess, septic emboli)
Todds paralysis (neurologic deficit status post seizure)
Epilepsy
Complicated migraine
Multiple sclerosis flare
Hypoglycemia
Syncope from any cause (especially arrhythmia)
Labyrinthine disorders (benign paroxysmal vertigo,
Mnires disease, vestibular neuronitis)
Hyperventilation/panic attack

Emergency Medicine Practice

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transient neurologic symptoms during the acute event and


go on to embolize within the next 5-7 days.

Symptoms and signs of TIA classically develop suddenly,


and the particular manifestations are determined by a
discrete ischemic distribution. TIA is also characterized by
transient deficits (usually lasting less than 30 minutes). TIA
neurologic findings are generally negative symptoms associated
with a loss of function (e.g., aphasia, weakness, numbness) as
opposed to positive symptoms (e.g., tingling or involuntary
movements). While these features are widely cited, there are
no data addressing the predictive value of this concept.
Identifying risk factors for TIA can assist in the diagnostic
process. (See Table 4.)
Non-focal signs and symptoms, such as loss of consciousness, dizziness, generalized weakness, mental
confusion, and loss of vision with reduced level of consciousness and incontinence are not typically due to a TIA.29
Similarly, the following symptoms in isolation are unlikely to
be caused by a TIA: vertigo, diplopia, dysphagia, loss of
balance, tinnitus, sensory symptoms confined to part of one
limb or the face, scintillating scotomas, amnesia, drop
attacks, and (usually) dysarthria.29 (See Table 5.)
A march of symptoms with different body parts
affected in succession is unlikely to be due to TIA and
suggests a migraine headache or seizure. A preceding
seizure may be due to a cerebral bleed or ischemia or may
cause the neurologic deficit (e.g., Todds paralysis). The
presence or absence of headache is not useful in establishing or
ruling out the diagnosis of TIA; approximately 16% of TIA
patients have a headache.32 However, headache is an
ominous sign if it is a new headache in someone older
than 50 years old. The presence of scintillating scotomas in
addition to a focal deficit suggests the diagnosis of complex
migraine over TIA. Flashing lights or wavy lines are more
consistent with migraine headache or retinal detachment
than TIA. (However, the diagnosis of new-onset complex
migraine should be left to the consultant.) Acute onset of a
worst headache of my life should prompt a subarachnoid
hemorrhage work-up with head CT followed by lumbar
puncture (if the CT scan is non-diagnostic) looking for blood
or xanthochromia.33

Identify The High-Risk Patient


One of the most important questions in the history is, Has
this ever happened before? The emergency physician must
identify a crescendo TIA, which is defined as more than three
ischemic events in a 72-hour period with an increase in frequency,
duration, or severity of symptoms.34 According to expert
opinion, this subset of patients represents an extremely
high-risk group for stroke.1,10,15,35,36
Multiple studies have attempted to delineate independent risk factors to determine a high-risk classification
(measured as risk for stroke within days to weeks). In a
retrospective study using logistic regression analysis,
Johnston et al were able to establish five risk factors for

Table 4. Risk Factors For TIA.


Non-modifiable
Older age
Male sex
Heredity

Modifiable

Adapted from: Albers GW, Hart RG, Lutsep HL, et al. AHA Scientific
Statement. Supplement to the guidelines for the management of
transient ischemic attacks: A statement from the Ad Hoc Committee
on Guidelines for the Management of Transient Ischemic Attacks,
Stroke Council, American Heart Association. Stroke 1999
Nov;30(11):2502-2511.

Table 5. Symptoms Not Attributable To TIA.


Non-focal symptoms

Localize The Lesion


Determine the vascular territory (anterior or posterior
circulation) involved by matching the history and presentation with one of the syndromes described in Table 2 on page
3. The type of TIA will dictate the work-up and management plan.

Loss of consciousness
Dizziness
Generalized weakness
Mental confusion
Loss of vision with reduced level of consciousness
Incontinence of feces or urine

Following symptoms, if isolated

Clarify The Etiology


Not all ischemic events are created equal. Once the appropriate circulatory territory is identified, one must still
determine the etiology of the disturbance in blood flow.
If the maximum deficit presents immediately and there
are deficits in different neurologic territories, suspect
embolic events from a proximal source (i.e., the heart). If
there is a history of significant arthritis, consider cervical
osteophytes that mechanically compress the extracranial
vessels. Ask about recent neck trauma or injury, since many
patients with internal carotid artery dissection have

October 2003 www.empractice.net

Hypertension
Atrial fibrillation
Diabetes
Smoking tobacco
Excessive alcohol use
Hypercholesterolemia
Sedentary lifestyle

Vertigo
Diplopia
Dysphagia
Loss of balance
Tinnitus
Sensory symptoms confined to part of one limb or the face
Scintillating scotomas
Amnesia
Drop attacks
Isolated dysarthria (usually)

Adapted from: Landi G. Clinical diagnosis of transient ischaemic


attacks. Lancet 1992 Feb 15;339(8790):402-405.

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Establishing The Diagnosis Of TIA

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damage, such as papilledema, retinal hemorrhages,


or encephalopathy.40
An irregularly irregular heart rate may be due to atrial
fibrillation, with the neurologic deficit secondary to
dislodging of an atrial thrombus.
A complete neurologic examination is obviously one of
the most crucial aspects of the examination. This entails
checking mental status, cranial nerves, strength, sensation
and proprioception, reflexes, and coordination. A useful test
for upper-extremity motor function is checking for a
pronator drift. This test detects subtle weakness from an
upper motor neuron source. If the patient has unilateral
weakness, the affected forearm drifts toward pronation
when the patient closes his or her eyes and tries to keep his
or her arms supinated. When testing strength, it is more
sensitive to test wrist extensors rather than grip strength.
The patient with pseudoparalysis may demonstrate giveway weakness: initially normal strength followed by an
abrupt or stepwise loss of strength in the tested muscle
groups. This contrasts with the smooth loss of resistance in
those with true neurologic disease.41
A sensory examination should be performed, even in
difficult situations such as when patients complain that their
skin simply feels funny. Determine whether the sensory
deficit is anatomic or not. In a malingering or hysterical
patient, all sensory modalities (touch, pain, vibration, and
proprioception) disappear at a discrete border such as a
joint, skin crease, or in the midline. In true sensory loss, the
deficit demonstrates overlapping and differing borders for
the various sensory modalities.42 In the patient suspected of
non-physiologic anesthesia, consider the yes-no test. Have
patients close their eyes and say yes when they are
touched and no when they do not feel a touch. Repeated
no responses to touching a supposedly numb limb
suggests a pseudo-sensory syndrome.41 No sensation and
abnormal sensation should be documented as such.
When testing reflexes, focus on asymmetry; ongoing
ischemia will reduce reflexes, and previous ischemia with
complete infarction will heighten reflexes. The Babinski
reflex (upturning or extensor response of the big toe in
response to stroking the lateral, plantar aspect of foot)
indicates an upper motor neuron lesion in the contralateral
brain or the ipsilateral spinal cord. Gait testing is sensitive
but not specific for neurologic deficit; an abnormal gait may
be a product of weakness, sensory loss, or a vestibular,
proprioceptive, or cerebellar problem. Spatial neglect testing
is rarely performed by the emergency physician but is
highly suggestive of a contralateral parietal lesion.43 To test
spatial neglect, check the right and left visual fields simulta-

stroke in the subsequent 90 days after diagnosis of TIA in


the ED.11 They are:
Age greater than 60 years
Diabetes
Episode greater than 10 minutes in duration
Weakness with episode
Speech impairment with episode
In this analysis, the risk of stroke was 0% with no risk
factors and as high as 34% with all five risk factors. (See
Table 6.) It is important to recognize that the number of
patients with either zero or five risk factors in that study
was very small and that these criteria still need to be
validated prospectively.
Other risk factors have also been identified as high
risk for stroke, including hypertension, peripheral vascular
disease, hemispheric TIA, left ventricular hypertrophy, and
increasing number of TIAs.35,37,38
Determine whether the patient is currently taking
aspirin (ASA) on a daily basis. These patients (called ASA
failures) have failed the first-line treatment option and
deserve further work-up and/or neurologic consultation.
(See Clinical Pathway: Management Of The TIA Patient On
Aspirin on page 11.)
See Table 7 for a list of high-risk patients.

Physical Examination
Vital signs are vital. A single abnormal vital sign can alter the
differential diagnosis, the diagnostic studies ordered, the
rapidity with which treatment is initiated, and patient
disposition. For example, if the patient has a fever and
neurologic symptoms, consider infectious etiologies, such as
septic embolism.
Many patients with a stroke or TIA are hypertensive
on presentation to the ED.10,39 This may be the patients
baseline or a valuable physiologic response to cerebral
ischemia. Before considering the rare diagnosis of hypertensive emergency, look for marked elevation of blood pressures in conjunction with other signs of acute end organ

Table 6. Risk Factors For Stroke


Within 90 Days After TIA (Johnstons
High-Risk Group).

Age greater than 60 years


Diabetes mellitus
Duration of episode greater than 10 minutes
Weakness during the episode
Speech impairment during the episode

Number of risk factors


0
1
2
3
4
5

Stroke within 90 days

Table 7. High-Risk TIA Factors.

0%
3%
7%
11%
15%
34%

Crescendo TIA (more than three ischemic events in a 72hour period, with an increase in frequency, duration, or
severity of symptoms)
Recurrent TIA on maximum antiplatelet therapy
High-grade carotid artery stenosis
Presumed cardioembolic source
Johnstons high-risk group

Adapted from: Johnston SC, Gress DR, Browner WS, et al. Short-term
prognosis after emergency department diagnosis of TIA. JAMA
2000;284:2901-2906.

Emergency Medicine Practice

www.empractice.net October 2003

Diagnostic Studies
Basic Work-up In The ED
The most important immediate test is a bedside blood glucose to
rule out hypoglycemia. In addition to the blood glucose level,
the basic work-up for a patient suspected of stroke or TIA
also includes CBC for hematocrit and platelets, SMA-7 for
sodium and potassium levels, and an ECG. (See Table 8.)
While coagulation studies (PT/INR/PTT) are often ordered,
especially if unfractionated heparin is being considered, the
evidence suggests that it is neither necessary nor costeffective to get a baseline PTT in patients being started
on heparin.45
Routine CBC and SMA-7 tests are relatively quick and
inexpensive. While the results will not likely establish the
diagnosis, they might suggest other causes for a neurologic
deficit, such as a gastrointestinal bleed (causing cerebral
hypoperfusion). Low platelets or an elevated coagulation

Further Work-up
Diagnostic studies should be tailored to the vascular
distribution that is involved or other clinical suspicion (e.g.,
vasculitis or hypercoagulable state). (See Table 2 on page 3.)

Table 8. Basic TIA Work-up In The ED.

Anterior Circulation Work-up

Bedside blood glucose


Complete blood count
SMA-7
Coagulation profile
Electrocardiogram
Brain imaging (not necessarily in the ED)

October 2003 www.empractice.net

If suspicion for anterior circulation ischemia is present, the


patient will ultimately need a carotid ultrasound to assess
for stenosis of the extracranial internal cerebral artery (Class
I); the rapidity with which the test needs to be ordered and
interpreted is not known. Because 5% of patients had

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profile predispose to cerebral hemorrhage, while thrombocytosis may indicate a hypercoagulable state. If an embolic
event from endocarditis is considered, an erythrocyte
sedimentation rate or C-reactive protein may assist in the
diagnostic process.
If the patient has a fever and new murmur, obtain at
least two blood cultures to make the diagnosis of infective
endocarditis. Other simple laboratory clues to the diagnosis
of endocarditis include hematuria, red cell casts, and a
new anemia.
Obtain an ECG (Class IIa) because it may suggest the
etiology of emboli (e.g., atrial fibrillation). It is quick,
noninvasive, cheap, and always available in the ED;
moreover, it will identify rhythms that can mimic or lead to
TIAs, such as ventricular tachycardia, atrioventricular
blocks, and atrial fibrillation. A recent study found a
significant number of new diagnoses of atrial fibrillation
(2.3%) in the setting of TIA and identified independent ECG
findings that may double the stroke risk, including left
ventricular hypertrophy, atrial fibrillation, and atrioventricular conduction abnormalities.23 There is no evidence
that a chest x-ray should be done routinely, but it should be
obtained if clinically indicated.46
The noncontrast head CT scan is close to 100% sensitive
for detecting intraparenchymal blood within 5-7 days of the
infarct.47 Other lesions that mimic TIA that occasionally are
identified on head CT include tumor, some aneurysms, and
subdural hematoma.1,11,12 Since it is reasonably available,
noninvasive, fast, relatively inexpensive, and can immediately identify a hemorrhagic cerebral event, it is the preferred imaging modality in the ED (Class IIa). Although the
yield of head CT scans is only 1%, experts and American
Heart Association guidelines recommend cranial imaging
prior to discharge from the ED or hospital.1,11,12 The TIA
Working Group has advocated urgent brain imaging
(specifically MRI with diffusion-weighted images, if
available; otherwise, CT scan) in all patients suspected
of TIA.2
Some centers are using MRI as the first-line brain
imaging study in patients with TIA. MRI is more likely to
demonstrate a lesion but has a few disadvantages in the ED
setting: 1) Some machines are less reliable than CT for
detecting blood (although multimodal MRI including
gradient echo is equally or more sensitive for blood as CT);
2) they are far slower than CT scan (although speed is
continually improving); and 3) MRIs more expensive than
CT scans.12,47

neously; or check sensation with double simultaneous


stimulation and ask which hand or if both were touched.
Alternatively, ask the patient to bisect a straight line and see
if it is grossly off midline or ask them to fill in the numbers
on a clock to see if the numbers are all placed on one side of
the circle.43
The head-to-toe physical examination can be very
revealing. Signs of head or neck trauma may suggest an
evolving subdural hematoma or carotid or vertebral
dissection, respectively. If a patient complains of vertigo,
look for non-extinguishing or vertical nystagmus, as this
may result from ischemia of the brainstem or cerebellum.
Funduscopic examination may reveal cholesterol crystals
(Hollenhorst plaques), which suggest a proximal embolic
source.43 Those with subacute or chronic mass lesions may
demonstrate papilledema. If the oral examination reveals a
tongue laceration, the patient may have had a seizure.
Cervical and subclavian bruits can occasionally be
auscultated, suggesting a carotid artery source of emboli or
subclavian steal syndrome, respectively. In asymptomatic
patients, a carotid bruit is a poor predictor of stenosis;
however, in a patient with symptoms of cerebral ischemia,
the positive predictive value increases to 85% for moderateto high-grade stenosis.15,44 When a bruit is suspected, listen
for cardiac murmurs to ensure that the bruit is not simply
radiation of the murmur. Rarely, skin findings such as
splinter hemorrhages in the nail bed, Oslers nodes,
Janeway lesions, and petechiae suggest endocarditis.
A careful cardiac examination can detect an irregular
heart rate or a new heart murmur, both of which should
prompt an investigation of possible cardiac emboli.

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completed stroke within 48 hours of TIA in the Johnston et


al study,7 the evaluation should be expeditious, especially in
high-risk patients.11 On the other hand, even if the carotid
Doppler is positive for stenosis, there is no appropriate
timing established for how quickly a person requires
carotid endarterectomy.
The accuracy of carotid ultrasound has been estimated
at 80%-95% with 89% specificity and 93% sensitivity for
high-grade stenosis using cerebral angiography as the gold
standard.15 The advantage to the procedure is that it is
noninvasive and readily available (although not always on a
24-hour basis). The disadvantage is that the specificity and
sensitivity are not as high for mild-to-moderate stenosis and
it cannot distinguish very high-grade stenosis from complete occlusion; for this reason, most vascular surgeons
require an arterial angiogram prior to surgery.
MRA and CTA are used in some centers but are
expensive and not yet recommended for first-line evaluation
of the anterior circulation.12,15 Carotid arteriogram is the gold
standard for assessing the anterior circulation; however, the
risks are not trivial. The procedure entails puncture and
catheterization of a major vessel, injection of contrast dye
and a 1% risk of stroke. This test is generally ordered by
the consultant.

emboli is best detected by transesophageal


echocardiography;15 transthoracic echocardiography is far
less sensitive. Echocardiography should be strongly
considered in young patients with TIAs because it may
reveal anomalies such as a patent foramen ovale or atrial
septal aneurysm.
If the ECG is unrevealing despite a high suspicion of
arrhythmia, consider a referral for Holter monitoring.

Posterior Circulation Work-up

Sub-acute TIA

Treatment
Hypertension
If the patients blood pressure is elevated, do not lower it
acutely unless there is a hypertensive emergency (central
nervous system bleed, hypertensive encephalopathy,
papilledema, etc.). Chronically hypertensive patients have
shifted autoregulation curves and require higher pressures
to perfuse their brains, especially when ischemic. Therefore,
although appropriate oral agents should be used over the
long term to decrease systolic blood pressure below 140
mmHg and diastolic blood pressure below 90 mmHg, urgent
control in the ED is not indicated and may be harmful, as it may
interfere with the patients ability to maintain perfusion to
the brain.

If the TIA occurred more than two weeks prior to the


patients presentation, antiplatelet therapy (see discussion
later in the text) should be initiated or adjusted. An expedited work-up can be continued as an outpatient assuming
there is reliable follow-up.15 If the TIA occurred recently
(within two weeks), attempt to classify the type of TIA.

If circulation ischemia is suspected, the vertebral and


basilar arteries need to be imaged with either transcranial
Doppler ultrasound or MRA;15 however, the studies do
not need to be performed in the ED.15 (See Clinical
Pathway: ED Evaluation Of The Acute TIA Patient on
page 10.) Transcranial Doppler ultrasound is noninvasive
and has a sensitivity of 75% for detection of significant
stenosis in the distal vertebral or basilar arteries; the
limitations include no acoustic window in 5%-10% of
patients, low spatial resolution, no established criteria,
and operator dependence.15,19
Because of cost and a lack of experience (sensitivity and
specificity levels are not known), it is unclear how well
MRA can diagnose significant stenosis. The frequency of
MRA use is institution-specific and is perhaps greater when
MRI is performed to evaluate vertebrobasilar symptoms.
Given no significant research trials supporting its utility, it
not recommended as part of the standard ED evaluation.12
The gold standard once again is cerebral angiography,
with the same disadvantages as above.

Carotid Artery Disease


There are excellent data on the long-term benefit of carotid
endarterectomy (CEA) if carotid ultrasound demonstrates

Table 9. Indications For Echocardiography


In Patients With Neurologic Events.
Patients of any age with abrupt occlusion of a major
peripheral or visceral artery (Class I)
Younger patients (typically < 45 years) with
cerebrovascular events (Class I)
Older patients (typically 45 years) with neurologic
events without evidence of cerebrovascular disease or
other obvious cause (Class I)
Patients for whom a clinical therapeutic decision
(anticoagulation, etc.) will depend on the results of
echocardiography (Class I)
Patients with suspicion of embolic disease and
cerebrovascular disease of questionable significance
(Class IIa)
Patients with a neurologic event and intrinsic
cerebrovascular disease sufficient to cause the
clinical event (Class IIb)

Embolic Event Work-up


If ischemia appears to encompass multiple vascular
distributions or CT findings are inconsistent with the clinical
picture, consider potential embolic events. A cardiac source
of emboli occurs in 6%-32% of patients presenting with
TIA.48,49 While there are no definitive studies to drive the
decision to admit or discharge, there seems to be a trend
toward more aggressive inpatient evaluation of such
patients.2,11 Obtain an ECG and consider echocardiography.
(See Table 9.) Valvular vegetation, atrial or left ventricular
thrombus, aortic arch ulcerated plaque, atrial septal
aneurysm, or patent foramen ovale as a source or cause of

Emergency Medicine Practice

Adapted from: Culebras A, Kase CS, Masdeu JC, et al. Practice


guidelines for the use of imaging in transient ischemic attacks and
acute stroke. A report of the Stroke Council, American Heart
Association. Stroke 1997 Jul;28(7):1480-1497.

www.empractice.net October 2003

Antithrombotics
The benefit of antiplatelet therapy, particularly ASA, is
accepted based on many large, well-designed, prospective
studies, but the appropriate dose remains unclear.9,11
Clopidogrel (Plavix), ticlopidine (Ticlid), or combination
ASA/extended-release dipyridamole therapy (Aggrenox)
are also frequently prescribed. There are no literature-based
criteria to determine when best to initiate a particular
antiplatelet drug after a TIA.

First-Line Agent: Aspirin


All patients with the diagnosis of TIA should be started on
antiplatelet therapy.55-58 While other antiplatelet agents have
shown promise, the first-line agent remains the costeffective ASA. ASA has been shown to reduce the incidence
of nonfatal stroke, nonfatal myocardial infarction, and death
from all vascular causes by approximately 20% compared to
placebo in multiple large prospective studies (Class I).59 The
controversial issue is not whether to start ASA but rather at
what dose. The UK-TIA Study Group (300 vs 1200) and the
Dutch TIA Trial Study Group (283 vs 30) compared low and
high doses of ASA and found no statistical difference.60,61
However, since increased doses of ASA are more
likely to cause gastrointestinal bleeding,62 it is acceptable
to prescribe 50-325 mg of ASA once per day. If there are
gastrointestinal toxicity concerns, an enteric-coated ASA
to be taken with meals is recommended. (However, some
argue against enteric-coated ASA in the ED, due to its
delay in action.) If there are significant contraindications,
such as documented hypersensitivity, liver disease,
hypoprothrombinemia, vitamin K deficiency, or bleeding
disorders, consider starting another antiplatelet medication. There has been no difference found between ASA
Continued on page 12

Cost-Effective Strategies For Managing Patients With TIA


3. Low-dose ASA seems to be as effective as high-dose ASA and
is associated with a lower rate of side-effects. Although the
newer, fancier, more expensive agentsspecifically,
ticlopidine, clopidogrel, and dipyridamoleare slightly
superior to plain ASA, they clearly add cost and possible
significant side-effects, especially when this may be a
lifelong medication.

1. Understand local and regional practices. Many neurologists


admit all of their TIA patients to the hospital, but many do not.
This goes for the primary care groups as well; there is a lot of
variability. If the primary care physician or consulting
neurologist gives the message to the patient (whom you just
discharged, and who has a bad outcome) that he or she
should have been admitted, this will not bode well for you.
Meet with these groups prospectively so everyone is playing
from the same handbook.

4. Communication is vital. Patients expectations are sometimes


more important than what transpires. For example, a patient
may be just as likely to have a stroke in the hospital as at
home. Have a meaningful conversation with patients and
their families if you are planning to discharge them. They
should have a clear understanding of reasons to return. (See
the sample discharge instructions on page 14.)

2. Understand what work-up is needed and what is realistic to


get done at your hospital. Often, an expedited outpatient
work-up can be done more easily at a small community
hospital, where lines of communication are clearer and more
direct, than at large academic centers.

October 2003 www.empractice.net

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technically successful with a high rate of bypass patency;


however, there has been no demonstrated benefit over
medical management.54 Bypass surgery is not recommended
for patients with TIAs (Class I).

occlusion greater than 70%. Unfortunately, the existing


literature falls short when establishing the appropriate time
frame for this intervention. The need for emergency
endarterectomy has not been proven. Nevertheless, some
authorities (without the support of large-scale randomized
trials) recommend an expeditious work-up in order to
accomplish urgent CEA.2,11
Four large, prospective, randomized trials show that
CEA is beneficial among patients with recent TIA and a
high-grade carotid stenosis (i.e., greater than 70%) (Class
I).50-53 However, the reduction in stroke risk is measured over
yearsnot over weeks to months. For example, the
NASCET study demonstrated an absolute risk reduction in
ipsilateral stroke of 17% and a relative risk reduction of 65%
when comparing the surgical patients to the medically
treated patients over two years.50 Patients with moderategrade stenosis (50%-69%) demonstrated a marginal benefit,
with ipsilateral stroke occurring in 15.7% of patients treated
surgically and 22.2% of patients treated medically over five
years (P = 0.045); approximately 15 patients with moderate
stenosis need to undergo CEA to benefit one patient (Class
IIb). The benefit is greater in a specific higher risk
subgroup of patients: more severe stenosis, age greater than
75, men, stroke in the past three months, and history of
hemispheric TIA as opposed to transient monocular
blindness (Class IIa). Among patients with less than 50%
stenosis, there was no statistical difference in the stroke rate
between patients who underwent surgery and those who
had maximal medical therapy (Class I). When assessing the
risk-benefit ratio of CEA, recognize that the surgeons skill
and experience in performing CEAs correlate with outcome.
Angioplasty and stenting of the carotid artery is a new
procedure that may be an alternative for patients who are
high-risk for surgery.9 Vertebrobasilar and intracranial
stenting are evolving and may soon impact the pace of
diagnostic intervention.
Extracranial-intracranial bypass surgery attempts to
improve circulation to the intracranial circulation via a
conduit from the external carotid. The surgeries have been

Triage screen: Neurologic deficits/symptoms?


referable to brain resolved?
YES

NO

Check fingerstick blood glucose level


Assume stroke and manage appropriately (Class I)

Triage to a monitored bed for nurse/


physician evaluation:
Check ABCs
Check vital signs
Obtain ECG,* CBC, SMA-7, coagulation profile
*For atrial fibrillation, anticoagulate with heparin (Class I)

History and physical exam consistent


with TIA?

NO

NO

NO

Evaluate for other diagnoses and manage appropriately

YES

Symptom episode less than 2 weeks ago?


YES

High-risk patient?
(Includes symptoms such as: crescendo TIA,
recurrent TIA on maximum antiplatelet therapy,
and presumed cardioembolic source (e.g., atrial
fibrillation)

Start ASA therapy (Class I)


Expedited outpatient work-up:
Brain imaging (Class IIa)
Evaluation based on territory affected

Start ASA therapy (Class I)


Expedited outpatient work-up or admit for facilitated
inpatient evaluation based on territory affected

YES

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Clinical Pathway: ED Evaluation Of The Acute TIA Patient

Consider neurology consult


Brain imaging (Class IIa)
Consider heparin anticoagulation (Class IIb)
Consider starting evaluation based on territory
affected

Adapted from: Brown RD Jr, Evans BA, Wiebers DO, et al. Transient ischemic attack and minor ischemic stroke: an algorithm for evaluation and
treatment. Mayo Clinic Division of Cerebrovascular Diseases. Mayo Clin Proc 1994 Nov;69(11):1027-1039.

The evidence for recommendations is graded using the following scale. For complete definitions, see back page. Class I: Definitely
recommended. Definitive, excellent evidence provides support. Class II: Acceptable and useful. Good evidence provides support. Class III:
May be acceptable, possibly useful. Fair-to-good evidence provides support. Indeterminate: Continuing area of research.

This clinical pathway is intended to supplement, rather than substitute for, professional judgment and may be changed depending
upon a patients individual needs. Failure to comply with this pathway does not represent a breach of the standard of care.

Copyright 2003 EB Practice, LLC. 1-800-249-5770. No part of this publication may be reproduced in any format
without written consent of EB Practice, LLC.
Emergency Medicine Practice

10

www.empractice.net October 2003

Interpret distribution of TIA symptoms

Specific distribution of symptoms?

YES

Evaluate depending upon anterior vs. posterior circulation

Consult neurologist
Consider other antiplatelet options (Class IIa-IIb)
Clopidogrel
Combination ASA/extended-release dipyridamole
Ticlopidine
Consider other diagnoses

NO

Symptoms in multiple territories?

YES

YES

Obtain transesophageal echocardiography or place on


Holter monitor (can be done as inpatient)
Consider angiogram

NO

Other symptoms or distribution of


symptoms unclear?

Consult neurologist
Consider other antiplatelet options (Class IIa-IIb)
Clopidogrel
Combination ASA/extended-release dipyridamole
Ticlopidine
Consider other diagnoses

Adapted from: Brown RD Jr, Evans BA, Wiebers DO, et al. Transient ischemic attack and minor ischemic stroke: an algorithm for evaluation and
treatment. Mayo Clinic Division of Cerebrovascular Diseases. Mayo Clin Proc 1994 Nov;69(11):1027-1039.

The evidence for recommendations is graded using the following scale. For complete definitions, see back page. Class I: Definitely
recommended. Definitive, excellent evidence provides support. Class II: Acceptable and useful. Good evidence provides support. Class III:
May be acceptable, possibly useful. Fair-to-good evidence provides support. Indeterminate: Continuing area of research.

This clinical pathway is intended to supplement, rather than substitute for, professional judgment and may be changed depending
upon a patients individual needs. Failure to comply with this pathway does not represent a breach of the standard of care.

Copyright 2003 EB Practice, LLC. 1-800-249-5770. No part of this publication may be reproduced in any format
without written consent of EB Practice, LLC.
October 2003 www.empractice.net

11

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Clinical Pathway: Management Of The TIA Patient On Aspirin

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Continued from page 9

Heparin

and warfarin in the prevention of recurrent stroke or


TIA;63-65 however, given the increased side-effects with
warfarin, ASA is preferred.

Heparin use remains controversial as there are no large,


prospective, randomized, controlled trials demonstrating benefit
for patients with TIA, especially given the risks of bleeding.1,71
Some experts argue that, similar to unstable angina, patients
with crescendo TIA need immediate anticoagulation with
heparin (assuming a non-hemorrhagic head CT) in addition
to a facilitated hospital work-up. However, there is no clear
evidence in the literature for this contention. As one expert
recently stated, The value of intravenous heparin for highrisk subsets of acute TIA patients is unsettled and merits
additional clinical trials.72
Heparin offers no overall benefit over ASA for acute
stroke patients with atrial fibrillation.73,74 The group that has
been shown to benefit from anticoagulation (but not
necessarily heparin) includes patients with atrial fibrillation
and a recent TIA or minor stroke based on the European
Atrial Fibrillation Trial (Class I). In this trial, 1007 patients
with atrial fibrillation and recent TIA or minor stroke were
randomized to receive either anticoagulation (the method of
which was left to physicians choice) or ASA or placebo. The
annual rate of outcome events over 2.3 years was 8% in the
anticoagulation group, 15% in the ASA group, and 19% in
the placebo group.75 No strong evidence exists to support
giving either unfractionated or low-molecular-weight
heparin over simply starting warfarin. If warfarin is
contraindicated, ASA is still recommended for TIA or stroke
prevention. Anticoagulation is not recommended for
patients with bacterial endocarditis.76
Based on the EAFT study, the use and benefit of
heparin and warfarin has been extrapolated to include
other cardioembolic TIAs (i.e., mechanical prosthetic heart
valves, recent myocardial infarction, left ventricular
thrombus, dilated cardiomyopathies, and marantic endocarditis). Although data are lacking, the target INR for
patients with mechanical valves is higher (3-4). Anticoagulation for these high-risk sources of embolization seems
reasonable but is not based on randomized clinical trials.
Similarly, experts in the field have recommended heparin
treatment for patients with crescendo TIAs while an
evaluation for carotid stenosis is conducted, but this, also, is
not grounded in medical evidence.1,10,34
From the emergency perspective, heparin is generally
initiated for TIA after consultation with a neurologist. There
are no clear data to support a particular method or dose
of heparin administration in patients with TIA; some
centers give heparin with a bolus, others start an infusion
without giving a bolus. It is advised to follow the common
practice at your institution or consult a neurologist for
appropriate dosing.

Second-Line Agents
The ESPS-1 and ESPS-2 Trials have shown that extendedrelease dipyridamole, a cyclic nucleotide phosphodiesterase
inhibitor, can reduce the risk of stroke by 38% and 37%,
respectively, when taken in combination with ASA (Class
I).66,67 ESPS-2 was done to compare the combination drug
with ASA alone; this trial found that a significant decrease in
stroke, death, or stroke and death together occurred with
combination therapy compared to dipyridamole alone or
ASA alone. Based on these results, the dipyridamole and
ASA combination may be superior to ASA alone for
secondary prevention of TIA/stroke. However, it is still not
considered first-line therapy due to its cost and because the
results have not been confirmed by further studies. The
most common side-effects are headache and gastrointestinal
events, but compared to ASA alone, the gastrointestinal
bleeds were less frequent and less severe. The dose of
dipyridamole was extended-release 200 mg PO BID and the
dose of ASA was 25 mg PO BID.
Ticlopidine (250 mg BID) is an antiplatelet agent that
inhibits adenosine phosphate-dependent platelet activation.
It is slightly more effective than ASA alone for preventing
recurrent TIA.68,69 However, due to its cost and side-effects, it
is not a first-line agent.69 Diarrhea is the most common sideeffect. Neutropenia is the most serious complication. In one
study, neutropenia occurred in approximately 2.4% of
patients taking ticlopidine, but it always occurred in the first
three months and was reversible when the medication was
discontinued.9 Ticlopidine has also been associated with
thrombotic thrombocytopenic purpura.9 For these reasons,
ticlopidine is reserved for patients who have a cerebrovascular event while on ASA or those with ASA intolerance
(Class IIa). Patients on ticlopidine should have a CBC with
differential checked every two weeks for the first 90 days.
This should be clearly stated in the discharge instructions if
the therapy is initiated in the ED.
Clopidogrel 75 mg per day is also an adenosine
phosphate inhibitor that is structurally similar to ticlopidine
but does not cause neutropenia. The CAPRIE Trial compared clopidogrel to ASA and found a small relative risk
reduction of 8.7% for ischemic stroke, myocardial infarction,
or vascular death (the absolute risk fell from 5.83% with
ASA to 5.32% with clopidogrel) (Class IIa).70 Of note, TIA
patients were not eligible for the study, and the relative risk
reduction in the stroke subgroup was non-significant.70 The
most common side-effects are rash and diarrhea. While the
safety profile of clopidogrel is at least as good as ASA, the
role of clopidogrel remains unclear because of cost and a
marginal benefit in absolute risk reduction. For patients who
are ASA failures or are intolerant, clopidogrel remains a
useful possibility.
The PRoFESS study, which is scheduled to start in the
fall of 2003, will include a comparison of clopidogrel to the
extended-release dipyridamole/ASA combination.

Emergency Medicine Practice

Risk Factor Modification


Risk factor modification should be strongly encouraged.
This includes long-term (not acute) reduction of both
systolic and diastolic blood pressure under 140 mmHg
and 90 mmHg, respectively; blood sugar control in both
type I and type I diabetics; and smoking cessation. (See also
the American Heart Association guidelines in Table 1 on
page 2.)

12

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the dose of ASA has not been shown to be of benefit.60,61


There are no prospective, randomized clinical trials to
guide management decisions in this scenario. Anticoagulation with warfarin is generally not indicated. The large
SPIRIT Trial, which randomized patients to either ASA or
warfarin to prevent recurrent TIA/stroke, was discontinued
prematurely due to excess cerebral hemorrhage in the
warfarin arm of the study.80 Other therapies include risk
factor modification to maximize blood pressure control,
tightening blood sugar control in diabetics, and lowering
cholesterol levels in patients with hypercholesterolemia
with statin drugs.
Because ASA failures have a more complex TIA
pattern or another diagnosis, further investigation may be of
value. MRA of extracranial and intracranial vessels or
carotid and vertebral angiography should be considered
because ultrasound can miss high cervical lesions and
bifurcation stenosis.15 In addition, strongly consider
neurology consultation for ASA failures. Similarly, if a TIA
occurs while the patient is on clopidogrel, combination
ASA/extended-release dipyridamole, or warfarin, consider
involving a neurologist in the decision-making for further
antiplatelet or anticoagulation treatment.

Young TIA Patients


In young patients (less than 50 years old) with TIA-type
symptoms, broaden the differential diagnosis and the workup for etiologies of ischemia. (See Table 10.) A clear etiology
is found in approximately 75% of cases.77
Headache and neck pain with or without a history of
trauma warrant evaluation for carotid artery and vertebral
artery dissection. Spontaneous dissection accounts for 10%24% of ischemic events in young and middle-aged patients.78 Classically, patients with carotid artery dissection
usually present with the triad of: 1) unilateral head, face, or
neck pain; 2) partial Horners syndrome; and 3) amaurosis
fugax (although only one-third of patients present in the
classic manner).78 On the other hand, patients with
vertebral artery dissection present with an occipital headache and brainstem ischemia.78 Treatment often includes
anticoagulation, although no studies have shown that it
improves outcome.
Consider cardiac etiologies in young patients with
transient or permanent focal neurologic deficits, especially
patent foreman ovale or atrial septal aneurysm. Hypercoagulable states may also cause TIA in the young; the most
common deficiencies include protein C, protein S, and
antithrombin III. As many as 30% of patients under the age
of 45 with a history of TIAs may have a clotting disorder.79
However, tests for these and other conditions should not occur in
the ED because the results of some of the tests are
uninterpretable when obtained in the acute setting.
There is no definite indication for routine brain MRI for
young patients with TIA, although it can be useful to
diagnose certain TIA mimics such as multiple sclerosis.

Controversies/Cutting Edge
Non-TIA Syndromes
Transient global amnesia, which is the acute onset of
amnesia but preservation of self-identity without other
neurologic deficits, usually lasts 6-12 hours; after resolution,
the patient is amnesic only to the event.81 This phenomenon
was once thought to be due to transient ischemia of the
posterior cerebral arteries (temporal lobes or thalamic
areas); however, transient global amnesia is no longer
considered a TIA and does not require a TIA work-up.29
The underlying pathophysiology remains obscure. It is
not unreasonable for the emergency physician to order a
head CT for these patients to rule out intracranial pathology
because some cases are caused by trauma. Before making
the diagnosis of transient global amnesia, consider the
possibility of ischemia-related aphasia mimicking
global confusion.
Drop attacks were once considered basilar artery
TIAs but are now known to be atonic seizures.29,81 These
brief spells of sudden loss of muscle tone cause the patient
to drop to his knees without loss of consciousness.

Aspirin Failures
Patients who have a TIA while on ASA (considered ASA
failures) pose a management dilemma. Some practitioners
increase the ASA dose, while others switch to or add
clopidogrel 75 mg daily, ticlopidine 250 mg BID or dipyridamole/ASA 200/25 mg BID. However, simply increasing

Table 10. TIA Etiologies In Children


And Young Adults.

Congenital heart disease with cerebral thromboembolism


Drug abuse (e.g., cocaine)
Clotting disorders
Carotid artery or vertebral artery dissection
SCUBA diving
CNS infection
Neurofibromatosis
Vasculitis
Idiopathic progressive arteriopathy of childhood
(moyamoya)
Fibromuscular dysplasia
Marfans syndrome
Tuberous sclerosis
Tumor

Advanced Imaging Modalities


Diffusion-weighted magnetic resonance imaging (DW-MRI)
is the latest imaging modality presently being investigated
for the evaluation of TIA and stroke. By detecting random
diffusion of water, DW-MRI can detect ischemic lesions
within minutes of the event, whereas CT and conventional
(T2-weighted) MRI require 8-12 hours to demonstrate the
lesion.82 DW-MRI localizes the lesion more often than CT in
cases of TIA, small-vessel disease, and brainstem events; in
one study of 42 TIA patients who were evaluated with DWMRI, lesions were found in approximately 50% of them.5
Even more impressive is the information gained by

Adapted from: Naradzay JFX. Transient ischemic attack.


Emedicine.com 2001.

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Special Circumstances

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medical systems.11 This has initiated a trend toward a lower


threshold for hospitalization.
Another retrospective study of 168 patients with stroke
or TIA over one year examined whether admission was
medically justified and found that 63 admissions (39%)
were justified. However, it was not possible to stratify which
patients conditions would worsen based on the ED
evaluations.85 While this study has been used to argue that
all patients with TIAs should be admitted, the vast majority
of justified admissions had the diagnosis of stroke; 70% of
the admissions for TIAs or non-hemorrhagic stroke were not
medically justified.
The tools currently available to predict which patients
will have poor short-term outcomes are imperfect. In
addition, one study demonstrated that only 50% of strokes
after a TIA are in the same vascular territory (e.g., left
carotid, right carotid, vertebrobasilar).86 In short, the
literature has not clearly described how to identify the highrisk patient who requires admission.85
Could a subsequent stroke be treated with prompt
thrombolysis if the patient is admitted as opposed to
returning from home? This important question also remains
to be answered in the literature. There are no large, prospective, randomized trials that have demonstrated a benefit
with hospital admission for expedited work-up or significant detriment with discharge to home with close primary
care or neurology follow-up. As a result, the decision to
admit or discharge for an outpatient work-up is presently
institution- or physician-driven. Given the medicolegal
climate, it makes sense for the emergency physician to
speak directly to the primary care physician or neurologist
who will orchestrate an expedited workup if the patient is

comparing DW-MRI with perfusion MRI. If the perfusion


scan lesion is larger than the diffusion-weighted scan lesion,
there is risk of extending the infarct due to inadequate
perfusion. This patient population potentially requires more
aggressive interventions. Gradient-echo and EPI susceptibility-weighted imaging are becoming increasingly added to
the overall MRI menu (so-called multi-modal MRI) in
stroke and TIA patients.

Disposition
Opinions regarding the need to admit patients with
TIAs run hot; however, the literature does not currently
provide clear answers. Leading textbooks are conservative
or ambiguous; some suggest that all patients with newonset TIAs warrant hospital admission,28 while others
allow patients who are not high risk to be evaluated
as an outpatient,34 and still others do not clearly discuss
disposition.83,84 Often the determining factors are how
quickly an outpatient evaluation can be done, how reliable
the patient is, and how connected the patient is to the
primary care physician and the medical system. Some
experts claim that the real benefit of admission is ensuring a
prompt TIA work-up. Regardless of disposition, patients with a
diagnosis of TIA should be started on ASA, assuming no
contraindications exist.
In a 2002 study by Johnston, an alarming 5% of patients
with TIA returned to the ED within two days with a stroke,
and 10.5% had a stroke within the first 90 days.11 The author
has subsequently recommended hospitalization if the
appropriate evaluation cannot be conducted within 24
hours as an outpatient, which is unlikely to occur in most

Sample Discharge Instructions For TIA Patients


Your preliminary diagnosis is Transient Ischemic Attack (TIA).
Recommendations
Continue to take your usual medications, especially the blood pressure pills.
Stop smoking cigarettes or cigars.
Discontinue excessive alcohol use and binges.
Increase physical activity as tolerated.
Take 325 mg of aspirin daily with food (unless your physician instructs otherwise).
Rememberit is very important to follow up with your primary care physician / neurologist in 24-48
hours for further testing!
IMPORTANT
Return to the Emergency Department immediately by calling 911 if:
you cannot talk properly, move a part of your body, see properly, or walk properly.
you are confused, dizzy, or pass out (lose consciousness).
Return to the Emergency Department even if you have these symptoms for only a brief period.
Emergency Medicine Practice

14

www.empractice.net October 2003

Ten Pitfalls To Avoid


to speak and hold an object with her right hand. Patients who
have just suffered from an acute neurologic deficit may
understandably be quite anxious.

1.The symptoms only lasted a few minutes, so I didnt think it


was a TIA.
The next day, during a second episode, when the symptoms
didnt go away, the TIA was obvious to everyone, including the
patients lawyer son. TIAs are, by definition, short. Even though
the textbooks allow for 24 hours of symptoms, the large
majority last less than one hour. Although duration beyond 10
minutes was identified in one study as a risk factor for stroke,7
even a very short TIA can portend a bad outcome.

6.I didnt think he needed an ECG because there was no chest


pain or palpitations.
Without appropriate testing, atrial fibrillation might go
unnoticed. ECG is a cheap, useful test that may identify an
unsuspected rhythm disturbance.
7.I thought when I discharged the patient that shed get the
carotid noninvasives the next day.
The patient left a message with the vascular lab and didnt
hear back until four days later, by which time she had a major
stroke at home. Know what your system is capable ofand
what it isnt. Know what the patient and/or family is capable of
doing before you make a plan that can easily fail.

2.I thought it was just a migraine.


True, the patient did have a mild headache associated with
the transient weakness and aphasia, but some patients with
TIA (or stroke) will have an associated headache, even if theres
no bleed. Migraine and seizures are major diagnostic
competitors, but there are often distinguishing features,
such as less rapid onset,positive rather than negative
symptoms, and duration.

8.I didnt realize that he had two other episodes on the two
previous days.
Be sure to ask the patient and his or her familyand be sure
to check the triage notes, too. Some categories of TIA patients
should almost always be treated more aggressively, such as
this one with crescendo TIA.

3.The physical examination was normal.


The physical examination is usually normalthats why
theyre called transient ischemic attacks. This diagnosis is
often made purely on the basis of the history. You wouldnt
dismiss a patients complaint of exertional substernal chest
pressure just because the examination was normal.

9.I thought that ticlopidine was better than just plain aspirin;
how did I know the patient would become neutropenic?
While the newer, more expensive antiplatelet agents have
some benefit over old-fashioned, inexpensive, low-dose ASA,
they have serious side-effects. Keep it simple; unless there is a
contraindication to ASA or the patient has already failed ASA,
ASA is first-line therapy.

4.I didnt consider TIA because the patient was so young.


This one had a TIA from a vertebral artery dissection, which
followed a minor fall on the ski slopes. Just like young patients
occasionally have myocardial infarction or pulmonary
embolism, young patients sometimes have TIA based on
traditional peripheral vascular or cardiac causes. Other
etiologies in young patients with TIA include carotid artery
dissections, hypercoagulable states, or patent foramen ovale.

10.I didnt think the neurologist would want to see


the patient.
Because TIAs can be so complex, maintain a low threshold
for consultation and even admission.

5.I thought it was just an anxiety attack.


Of course the patient was anxious; she had just lost her ability

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on antiplatelet therapy (ASA) and advised to modify risk


factors and return immediately for recurrent symptoms.
Early follow-up should be ensured. Also, it is generally
agreed upon that patients with transient monocular
blindness are low-risk for recurrent or serious TIA or
stroke.87 The three-year risk of stroke after medical management of transient monocular blindness is half that of
transient hemispheric ischemic attack, and the risk is even
lower if a CEA is indicated and performed.25 These patients
can be safely discharged home on ASA if an expedited
outpatient work-up with carotid ultrasonography and
possible vascular surgery consultation can be established.
In general, neurologic consultation is not essential for
every TIA patient; however, maintaining a low threshold is
recommended because TIAs are complex, and significant
differences in opinion exist as to their appropriate manage-

being discharged.
The disposition of some subgroups of patients with
TIAs, however, is fairly straightforward and minimally
controversial. The high-risk group with crescendo TIAs
should be admitted (based more on expert opinion than on
large clinical trials) for a facilitated hospital evaluation and
possible interventions.10,34 Most patients with new-onset
atrial fibrillation or flutter in the setting of neurologic
deficits should be admitted to monitored beds. (Consider
cardiology consultation.) While atrial fibrillation and flutter
have a very low yearly incidence of embolic events, it is
prudent to admit patients who present with neurologic
symptoms and let the consultant decide on cardiac imaging
and possible anticoagulation.
On the other end of the spectrum, patients who are not
candidates for surgery or anticoagulation can be discharged

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ment. Provide clear written and verbal discharge instructions to any TIA patient who is released. (See the sample
discharge instructions on page 14.)

should carry more weight than a case report.


To help the reader judge the strength of each reference,
pertinent information about the study, such as the type of
study and the number of patients in the study, will be
included in bold type following the reference, where
available. In addition, the most informative references cited
in the paper, as determined by the authors, will be noted by
an asterisk (*) next to the number of the reference.

Summary
TIAs are complicated entities. Histories are often vague, and
there are usually minimal, if any, concrete physical, laboratory, or radiologic findings. Even if the diagnosis is abundantly clear, the management of these patients is quite
variable, and few definitive guidelines exist. However, just
as angina may be the precursor to a myocardial infarct, TIAs
may presage an impending stroke.
All emergency physicians should be able to: 1) elicit the
key historical facts to make the diagnosis and distinguish it
from other causes of transient neurologic abnormalities; 2)
identify the involved vessel and cerebral distribution; 3)
determine the most appropriate evaluation; 4) identify
groups that require anticoagulation, surgical intervention, or
simple antiplatelet therapy; 5) distinguish patients who
need a facilitated hospital work-up from those who can
safely be discharged to obtain an expedited outpatient
work-up; and 6) determine when to enlist the assistance of
specialists (i.e., the neurologist).
One of the most contentious aspects of the work-up
involves what should be done in the ED or hospital vs.
the outpatient setting. Perhaps the most compelling factor
may relate to the adequacy of follow-up. A stable patient
without high-risk factors (such as those found in Table 6
and Table 7 on page 6) whose private physician will see
him or her quickly and order appropriate tests may not
require an inpatient evaluation. Patients with high-risk
features or those without a primary care provider or who
belong to a clinic where urgent follow-up is not ensured
may require a more aggressive diagnostic approach from
the emergency physician.

1.

Feinberg WM, Albers GW, Barnett HJ, et al. Guidelines for the
management of transient ischemic attacks. From the Ad Hoc
Committee on Guidelines for the Management of Transient
Ischemic Attacks of the Stroke Council of the American Heart
Association. Circulation 1994 Jun;89(6):2950-2965. (Practice
guideline, systematic review)
2.* Albers GW, Caplan LR, Easton JD, et al; TIA Working Group.
Transient ischemic attackproposal for a new definition. N Engl J
Med 2002 Nov 21;347(21):1713-1716. (Historical article; commentary)
3.
Davalos A, Matias-Guiu J, Torrent O, et al. Computed tomography in reversible ischaemic attacks: clinical and prognostic
correlations in a prospective study. J Neurol 1988 Jan;235(3):155158. (Prospective; 219 patients)
4.
Dennis M, Bamford J, Sandercock P, et al. Computed tomography
in patients with transient ischaemic attacks: when is a transient
ischaemic attack not a transient ischaemic attack but a stroke? J
Neurol 1990 Jul;237(4):257-261. (Prospective; 184 patients)
5.
Kidwell CS, Alger JR, Di Salle F, et al. Diffusion MRI in patients
with transient ischemic attacks. Stroke 1999 Jun;30(6):1174-1180.
(Comparative; 42 TIA patients, 23 stroke patients)
6.
Dennis M, Bamford J, Sandercock P, et al. Prognosis of transient
ischemic attacks in the Oxfordshire Community Stroke Project.
Stroke 1990 Jun;21(6):848-853. (Follow-up study; 184 patients)
7.* Johnston SC, Gress DR, Browner WS, et al. Short-term prognosis
after emergency department diagnosis of TIA. JAMA 2000 Dec
13;284(22):2901-2906. (Cohort study; 1707 patients)
8.
Goldstein LB, Bian J, Samsa GP, et al. New transient ischemic
attack and stroke: outpatient management by primary care
physicians. Arch Intern Med 2000 Oct 23;160(19):2941-2946.
(Retrospective; 176 patients)
9.* Albers GW, Hart RG, Lutsep HL, et al. AHA Scientific Statement.
Supplement to the guidelines for the management of transient
ischemic attacks: A statement from the Ad Hoc Committee on
Guidelines for the Management of Transient Ischemic Attacks,
Stroke Council, American Heart Association. Stroke 1999
Nov;30(11):2502-2511. (Practice guideline)
10. Borg KT, Pancioli AM. Transient ischemic attacks: an emergency
medicine approach. Emerg Med Clin North Am 2002 Aug;20(3):597608. (Systematic review)
11.* Johnston SC. Clinical practice. Transient ischemic attack. N Engl J
Med 2002 Nov 21;347(21):1687-1692. (Systematic review)
12. Culebras A, Kase CS, Masdeu JC, et al. Practice guidelines for the
use of imaging in transient ischemic attacks and acute stroke. A
report of the Stroke Council, American Heart Association. Stroke
1997 Jul;28(7):1480-1497. (Practice guideline)
13. Brott T, Clark W, Fagan S, et. al. Stroke: The First Hours. Guidelines
for Acute Ttreatment. Englewood, CO: National Stroke Association;
2000. (Systematic review)
14. Kraaijeveld CL, van Gijn J, Schouten HJ, et al. Interobserver
agreement for the diagnosis of transient ischemic attacks. Stroke
1984 Jul-Aug;15(4):723-725. (Comparative; 56 patients, 8
observers)
15.* Brown RD Jr, Evans BA, Wiebers DO, et al. Transient ischemic
attack and minor ischemic stroke: an algorithm for evaluation and
treatment. Mayo Clinic Division of Cerebrovascular Diseases.
Mayo Clin Proc 1994 Nov;69(11):1027-1039. (Systematic review)
16. Brainin M, McShane LM, Steiner M, et al. Silent brain infarcts and
transient ischemic attacks. A three-year study of first-ever
ischemic stroke patients: the Klosterneuburg Stroke Data Bank.
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728 patients)
17. Ferro JM, Falcao I, Rodrigues G, et al. Diagnosis of transient
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References
Evidence-based medicine requires a critical appraisal of the
literature based upon study methodology and number of
subjects. Not all references are equally robust. The findings
of a large, prospective, randomized, and blinded trial

Table 11. Disclosure Of Off-Label Usage.


Clopidogrel: indicated for patients with recent stroke
(but not TIA specifically) to reduce the rate of new
ischemic stroke.
Dipyridamole: given alone (as opposed to its extendedrelease formulation in combination with ASA), it is not
indicated for patients with TIAs.
Heparin (unfractionated): indicated for patients with atrial
fibrillation but not for TIA or crescendo TIA.
Heparin (low molecular weight): not indicated for atrial
fibrillation or TIA.
Warfarin: indicated for prevention and treatment of
thromboembolic complications associated with atrial
fibrillation and to reduce the risk of stroke after a myocardial
infarction but not specifically after a TIA.

Emergency Medicine Practice

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www.empractice.net October 2003

Martin PJ, Young G, Enevoldson TP, et al. Overdiagnosis of TIA


and minor stroke: experience at a regional neurovascular clinic.
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N Engl J Med 1985 Nov 7;313(19):1191-1200. (Randomized,
controlled trial; 1377 patients)
55.* No authors listed. Collaborative overview of randomised trials of
antiplatelet therapyI: Prevention of death, myocardial
infarction, and stroke by prolonged antiplatelet therapy in various
categories of patients. Antiplatelet Trialists Collaboration. BMJ
1994 Jan 8;308(6921):81-106. (Meta-analysis)
56. Puranen J, Laakso M, Riekkinen P Sr, et al. Risk factors and
antiplatelet therapy in TIA and stroke patients. J Neurol Sci 1998
Feb 5;154(2):200-204. (Multicenter, randomized, controlled trial;
1306 patients)
57. Sivenius J, Riekkinen PJ Sr, Laakso M. Antiplatelet treatment in
elderly people with transient ischaemic attacks or ischaemic
strokes. BMJ 1995 Jan 7;310(6971):25-26. (Randomized, controlled
trial; 1306 patients)
58. Warlow C, Wardlaw J. The drug trials that have influenced our
clinical practice in acute ischaemic stroke. Thromb Haemost 1997
Jul;78(1):558-561. (Review)
59. Stachenko SJ, Bravo G, Cote R, et al. Aspirin in transient ischemic
attacks and minor stroke: a meta-analysis. Fam Pract Res J 1991
Jun;11(2):179-191. (Meta-analysis)
60. No authors listed. United Kingdom transient ischaemic attack
(UK-TIA) aspirin trial: interim results. UK-TIA Study Group. Br
Med J (Clin Res Ed) 1988 Jan 30;296(6618):316-320. (Prospective,
40.

17

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blinded, randomized, controlled trial; 2435 patients)


No authors listed. A comparison of two doses of aspirin (30 mg vs.
283 mg a day) in patients after a transient ischemic attack or
minor ischemic stroke. The Dutch TIA Trial Study Group. N Engl J
Med 1991 Oct 31;325(18):1261-1266. (Prospective, double-blind,
randomized, control trial; 3131 patients)
62. No authors listed. Swedish Aspirin Low-Dose Trial (SALT) of 75
mg aspirin as secondary prophylaxis after cerebrovascular
ischaemic events. The SALT Collaborative Group. Lancet 1991 Nov
30;338(8779):1345-1349. (Multicenter, randomized, controlled
trial; 1360 patients)
63. Mohr JP, Thompson JL, Lazar RM, et al. Warfarin-Aspirin
Recurrent Stroke Study Group.A comparison of warfarin and
aspirin for the prevention of recurrent ischemic stroke. N Engl J
Med 2001 Nov 15;345(20):1444-1451. (Multicenter, randomized,
controlled trial; 2206 patients)
64. Liu M, Counsell C, Sandercock P. Anticoagulants for preventing
recurrence following ischaemic stroke or transient ischaemic
attack. Cochrane Database Syst Rev 2000;(2):CD000248. (Cochrane
systematic review; nine trials included)
65. Algra A, de Schryver EL, van Gijn J, et al. Oral anticoagulants
versus antiplatelet therapy for preventing further vascular events
after transient ischaemic attack or minor stroke of presumed
arterial origin. Cochrane Database Syst Rev 2001;(4):CD001342.
(Cochrane systematic review; four trials included)
66. Sivenius J, Riekkinen PJ, Smets P, et al. The European Stroke
Prevention Study (ESPS): results by arterial distribution. Ann
Neurol 1991 Jun;29(6):596-600. (Prospective, multicenter,
randomized, controlled trial; 2500 patients)
67.* Diener HC, Cunha L, Forbes C, et al. European Stroke Prevention
Study. 2. Dipyridamole and acetylsalicylic acid in the secondary
prevention of stroke. J Neurol Sci 1996 Nov;143(1-2):1-13.
(Prospective, multicenter, randomized, controlled trial; 6602
patients)
68. Gent M, Blakely JA, Easton JD, et al. The Canadian American
Ticlopidine Study (CATS) in thromboembolic stroke. Lancet 1989
Jun 3;1(8649):1215-1220. (Prospective, multicenter, randomized,
controlled trial; 1072 patients)
69. Bellavance A. Efficacy of ticlopidine and aspirin for prevention of
reversible cerebrovascular ischemic events. The Ticlopidine
Aspirin Stroke Study. Stroke 1993 Oct;24(10):1452-1457. (Prospective, multicenter, randomized, controlled trial; 3069 patients)
70.* No authors listed. A randomised, blinded, trial of clopidogrel
versus aspirin in patients at risk of ischaemic events (CAPRIE).
CAPRIE Steering Committee. Lancet 1996 Nov 16;348(9038):13291339. (Prospective, multicenter, randomized, controlled trial;
19,185 patients)
71. Biller J, Bruno A, Adams HP Jr, et al. A randomized trial of aspirin
or heparin in hospitalized patients with recent transient ischemic
attacks. A pilot study. Stroke 1989 Apr;20(4):441-447. (Pilot study,
prospective, randomized, control; 55 patients)
72. Hart RG, Easton JD. Do we really need a better way to give
heparin in acute cerebral ischemia? Stroke 2002 Mar;33(3):659-660.
(Comment, editorial)
73. Berge E, Abdelnoor M, Nakstad PH, et al. Low molecular-weight
heparin versus aspirin in patients with acute ischaemic stroke and
atrial fibrillation: a double-blind randomised study. HAEST Study
Group. Heparin in Acute Embolic Stroke Trial. Lancet 2000 Apr
8;355(9211):1205-1210. (Multicenter, randomized, controlled trial;
449 patients)
74. Saxena R, Lewis S, Berge E, et al. Risk of early death and
recurrent stroke and effect of heparin in 3169 patients with acute
ischemic stroke and atrial fibrillation in the International Stroke
Trial. Stroke 2001 Oct;32(10):2333-2337. (Multicenter, randomized,
controlled trial; 3169 patients)
75.* No authors listed. Secondary prevention in non-rheumatic atrial
fibrillation after transient ischaemic attack or minor stroke. EAFT
(European Atrial Fibrillation Trial) Study Group. Lancet 1993 Nov
20;342(8882):1255-1262. (Prospective, multicenter, randomized,
controlled trial; 1007 patients)
76. Stein PD. Antithrombotic therapy in valvular heart disease. Clin
Geriatr Med 2001 Feb;17(1):163-172, viii. (Systematic review)
77. Carolei A, Marini C, Ferranti E, et al. A prospective study of
cerebral ischemia in the young. Analysis of pathogenic determinants. The National Research Council Study Group. Stroke 1993
Mar;24(3):362-367. (Prospective; 333 patients)
78. Schievink WI. Spontaneous dissection of the carotid and vertebral
arteries. N Engl J Med 2001 Mar 22;344(12):898-906. (Systematic

review)
De Lucia D, Renis V, Belli A, et al. Familial coagulation-inhibiting
and fibrinolytic protein deficiencies in juvenile transient ischaemic
attacks. J Neurosurg Sci 1996 Mar;40(1):25-35. (Prospective,
randomized, controlled trial; 150 patients)
80. No authors listed. A randomized trial of anticoagulants versus
aspirin after cerebral ischemia of presumed arterial origin. The
Stroke Prevention in Reversible Ischemia Trial (SPIRIT) Study
Group. Ann Neurol 1997 Dec;42(6):857-865. (Prospective,
multicenter, randomized, controlled trial; 1316 patients)
81. Rowland LP. Merrits Neurology. 10th ed. Philadelphia: Lippincott,
Williams & Wilkins; 2000. (Textbook)
82. Lecouvet FE, Duprez TP, Raymackers JM, et al. Resolution of early
diffusion-weighted and FLAIR MRI abnormalities in a patient
with TIA. Neurology 1999 Mar 23;52(5):1085-1087. (Case report,
review)
83. Goetz CG, Pappert EJ, eds. Textbook of Clinical Neurology. 1st ed.
Philadelphia: W.B. Saunders Co.; 1999. (Textbook)
84. Braunwald E, Fauci A, Kasper D, et al, eds. Harrisons Principles of
Internal Medicine. 15th ed. New York: McGraw-Hill, Inc.; 2001.
(Textbook)
85.* Henneman PL, Lewis RJ. Is admission medically justified for all
patients with acute stroke or transient ischemic attack? Ann Emerg
Med 1995 Apr;25(4):458-463. (Retrospective; 168 patients)
86. Cillessen JP, Kappelle LJ, van Swieten JC, et al. Does cerebral
infarction after a previous warning occur in the same vascular
territory? Stroke 1993 Mar;24(3):351-354. (Prospective, multicenter,
randomized, controlled, trial; 2993 patients)
87. Streifler JY, Eliasziw M, Benavente OR, et al. The risk of stroke in
patients with first-ever retinal vs hemispheric transient ischemic
attacks and high-grade carotid stenosis. North American
Symptomatic Carotid Endarterectomy Trial. Arch Neurol 1995
Mar;52(3):246-249. (Prospective, randomized, controlled trial;
129 patients)

61.

Emergency Medicine Practice

79.

Physician CME Questions


49. TIA is defined as a brief episode of neurologic
dysfunction caused by focal brain or retinal ischemia,
with clinical symptoms typically lasting less than one
hour, and without evidence of acute infarction.
a. True
b. False
50. Resolution of symptoms:
a. occurs only with TIAs and not with strokes.
b. occurs with TIAs and sometimes even with
strokes.
c. often occurs with strokes and rarely with TIAs.
d. is used to distinguish a TIA from a stroke.
51. Which of the following symptom complexes is not
associated with ischemia of the posterior circulation?
a. Vertigo, dizziness, ataxia, nausea, and vomiting
b. Dysarthria, dysphagia, and diplopia due to
disconjugate gaze
c. Temporary monocular blindness
d. Contralateral homonymous hemianopia or
occipital lobe blindness.
52. All of the following are true regarding hypertensive
TIA patients except:
a. urgent control in the ED is indicated.
b. urgent control in the ED may interfere with the
patients ability to maintain perfusion to the brain.
c. urgent control in the ED is only indicated if there is
a hypertensive emergency.
d. the consultant should initiate appropriate therapy
to decrease blood pressure over the long term.

18

www.empractice.net October 2003

54. Which of the following is/are important aspects in the


prehospital care of potential TIA/stroke patients?
a. Rapid transport to the treating facility, as thrombolysis has a narrow window of opportunity
b. A medical assessment, because signs and symptoms of TIA often resolve before arrival in the ED
c. Checking blood sugar levels
d. All of the above

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of Pediatric Respiratory Emergencies
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Presented by Ghazala Q. Sharieff, MD, FACEP, FAAP, FAAEM

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55. Many large, randomized, controlled trials demonstrate the benefit of heparin for patients with TIA.
a. True
b. False

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56. TIA neurologic findings are generally positive (e.g.,


tingling or involuntary movements) rather than
negative (e.g., aphasia, weakness, numbness).
a. True
b. False

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57. A crescendo TIA (more than three ischemic events in


a 72-hour period with an increase in frequency,
duration, or severity of symptoms) represents an
extremely high-risk group for subsequent stroke.
a. True
b. False

Emergency physicians must recognize and manage a wide


variety of pediatric respiratory emergencies. Differences in
anatomy and disease patterns between adults and children
can complicate this important task. The emergency
physician must understand the etiologies and significance
of pediatric respiratory emergencies and employ rational
diagnostic modalities and therapeutic interventions.

58. The basic work-up for a patient suspected of stroke or


TIA includes all of the following except:
a. blood glucose level.
b. CBC.
c. carotid arteriogram.
d. SMA-7.
e. ECG.

Presented by:
Ghazala Q. Sharieff, MD, FACEP, FAAP, FAAEM,
Clinical Assistant Professor, University of Florida,
Jacksonville, FL. Dr. Sharieff is Chair of the American
College of Emergency Physicians Pediatric Emergency
Medicine Section and is board certified in emergency
medicine and pediatric emergency medicine.

59. All of the following are correct regarding the presence


of headache except:
a. It rules out the diagnosis of TIA.
b. It is an ominous sign if it is a new headache in
someone older than 50 years.
c. It should prompt a subarachnoid hemorrhage
work-up if it is described as the worst ever.
d. It may suggest a diagnosis of complex migraine
rather than TIA if there are scintillating scotomas
in addition to a focal deficit.

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participant before the session begins.
What if you cant save the date? No problem! Each
registrant will also receive a free CD of the audio
seminar that can also be shared with colleagues who
arent available at conference time! Listen once or use
the CD to train others as many times as youd like!
The audio conference and CD are ideal for seasoned
professionals and residency programs alike.

60. The first-line antiplatelet agent for TIA is:


a. clopidogrel.
b. aspirin.
c. ticlopidine.
d. combination ASA/extended-release dipyridamole.

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61. A thorough patient history is essential to:


a. establish the diagnosis of TIA.
b. localize the lesion(s).
c. clarify the possible etiologies.
d. identify high-risk patients.
e. all of the above.

October 2003 www.empractice.net

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New from the Publisher of


Emergency Medicine
Practice: Special Audio
Conference and CD Package!

53. Which of the following is the most common


TIA mimic?
a. Hypoglycemia
b. Todds paralysis
c. Hypertensive encephalopathy
d. Mnires disease

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Physician CME Information

62. Which of the following symptom complexes is not


associated with ischemia of the anterior circulation?
a. Temporary monocular blindness
b. Monoparesis and numbness of the leg
c. Hemiparesis, aphasia, or homonymous
hemianopsia
d. Vertigo, dizziness, ataxia, nausea, and vomiting

This CME enduring material is sponsored by Mount Sinai School of Medicine and
has been planned and implemented in accordance with the Essentials and
Standards of the Accreditation Council for Continuing Medical Education. Credit
may be obtained by reading each issue and completing the printed post-tests
administered in December and June or online single-issue post-tests
administered at www.empractice.net.
Target Audience: This enduring material is designed for emergency medicine
physicians.

63. Ticlopidine:
a. is slightly more effective than ASA alone.
b. has fewer side-effects than ASA.
c. costs less than ASA.
d. all of the above.

Needs Assessment: The need for this educational activity was determined by a
survey of medical staff, including the editorial board of this publication; review
of morbidity and mortality data from the CDC, AHA, NCHS, and ACEP; and
evaluation of prior activities for emergency physicians.
Date of Original Release: This issue of Emergency Medicine Practice was published
October 1, 2003. This activity is eligible for CME credit through October 1,
2006. The latest review of this material was September 2, 2003.

64. In which of the following subgroups of TIA patients


is admission least necessary?
a. Patients with crescendo TIAs
b. Patients with monocular blindness
c. Patients with new-onset atrial fibrillation or flutter
d. Patients in whom ASA therapy has failed

Discussion of Investigational Information: As part of the newsletter, faculty may


be presenting investigational information about pharmaceutical products that
is outside Food and Drug Administration approved labeling. Information
presented as part of this activity is intended solely as continuing medical
education and is not intended to promote off-label use of any pharmaceutical
product. Disclosure of Off-Label Usage: This issue of Emergency Medicine Practice
discusses some off-label uses of pharmaceutical products (see Table 11).
Faculty Disclosure: In compliance with all ACCME Essentials, Standards, and
Guidelines, all faculty for this CME activity were asked to complete a full
disclosure statement. The information received is as follows: Dr. Asimos reports
that in the past, he and a program with which he is affiliated have received
consultation fees, educational grants, and honoraria from Boehringer Ingelheim
Pharmaceuticals, Inc. Dr. Shah, Dr. Edlow, and Dr. Borg report no significant
financial interest or other relationship with the manufacturer(s) of any
commercial product(s) discussed in this educational presentation.

Class Of Evidence Definitions


Each action in the clinical pathways section of Emergency Medicine Practice
receives an alpha-numerical score based on the following definitions.
Class I
Always acceptable, safe
Definitely useful
Proven in both efficacy and
effectiveness
Level of Evidence:
One or more large prospective
studies are present (with
rare exceptions)
High-quality meta-analyses
Study results consistently
positive and compelling
Class II
Safe, acceptable
Probably useful
Level of Evidence:
Generally higher levels
of evidence
Non-randomized or retrospective studies: historic, cohort, or
case-control studies
Less robust RCTs
Results consistently positive
Class III
May be acceptable
Possibly useful
Considered optional or
alternative treatments
Level of Evidence:
Generally lower or intermediate
levels of evidence

Case series, animal studies,


consensus panels
Occasionally positive results

Accreditation: Mount Sinai School of Medicine is accredited by the Accreditation


Council for Continuing Medical Education to sponsor continuing medical
education for physicians.

Indeterminate
Continuing area of research
No recommendations until
further research

Credit Designation: Mount Sinai School of Medicine designates this educational


activity for up to 4 hours of Category 1 credit toward the AMA Physicians
Recognition Award. Each physician should claim only those hours of credit
actually spent in the educational activity. Emergency Medicine Practice is approved
by the American College of Emergency Physicians for 48 hours of ACEP Category
1 credit (per annual subscription). Emergency Medicine Practice has been reviewed
and is acceptable for up to 48 Prescribed credit hours by the American Academy
of Family Physicians. Emergency Medicine Practice has been approved for 48
Category 2-B credit hours by the American Osteopathic Association.

Level of Evidence:
Evidence not available
Higher studies in progress
Results inconsistent,
contradictory
Results not compelling

Earning Credit: Two Convenient Methods

Significantly modified from: The


Emergency Cardiovascular Care
Committees of the American Heart
Association and representatives
from the resuscitation councils of
ILCOR: How to Develop EvidenceBased Guidelines for Emergency
Cardiac Care: Quality of Evidence
and Classes of Recommendations;
also: Anonymous. Guidelines for
cardiopulmonary resuscitation and
emergency cardiac care. Emergency
Cardiac Care Committee and
Subcommittees, American Heart
Association. Part IX. Ensuring
effectiveness of community-wide
emergency cardiac care. JAMA
1992;268(16):2289-2295.

Print Subscription Semester Program: Paid subscribers with current and


valid licenses in the United States who read all CME articles during each
Emergency Medicine Practice six-month testing period, complete the posttest and the CME Evaluation Form distributed with the December and June
issues, and return it according to the published instructions are eligible for
up to 4 hours of Category 1 credit toward the AMA Physicians Recognition
Award (PRA) for each issue. You must complete both the post-test and CME
Evaluation Form to receive credit. Results will be kept confidential. CME
certificates will be delivered to each participant scoring higher than 70%.
Online Single-Issue Program: Paid subscribers with current and valid
licenses in the United States who read this Emergency Medicine Practice CME
article and complete the online post-test and CME Evaluation Form at
www.empractice.net are eligible for up to 4 hours of Category 1 credit
toward the AMA Physicians Recognition Award (PRA). You must complete
both the post-test and CME Evaluation Form to receive credit. Results will
be kept confidential. CME certificates may be printed directly from the Web
site to each participant scoring higher than 70%.

Emergency Medicine Practice is not affiliated with any pharmaceutical firm or medical device manufacturer.
President and CEO: Robert Williford. Publisher: Heidi Frost. Research Editors: Ben Abella, MD, University of Chicago; Richard Kwun, MD, Mount Sinai School of Medicine.

Direct all editorial or subscription-related questions to EB Practice, LLC: 1-800-249-5770 Fax: 1-770-500-1316 Non-U.S. subscribers, call: 1-678-366-7933
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Emergency Medicine Practice (ISSN 1524-1971) is published monthly (12 times per year) by EB Practice, LLC, 305 Windlake Court, Alpharetta, GA 30022. Opinions expressed are not necessarily
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substitute, professional judgment. It covers a highly technical and complex subject and should not be used for making specific medical decisions. The materials contained herein are not
intended to establish policy, procedure, or standard of care. Emergency Medicine Practice is a trademark of EB Practice, LLC. Copyright 2003 EB Practice, LLC. All rights reserved. No part of this
publication may be reproduced in any format without written consent of EB Practice, LLC. Subscription price: $299, U.S. funds. (Call for international shipping prices.)

Emergency Medicine Practice

20

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