Professional Documents
Culture Documents
A N E V I D E N C E - B A S E D A P P ROAC H T O E M E RG E N C Y M E D I C I N E
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
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.
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EMERGENCY MEDICINE
PRACTICE
.
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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.
Hospitalization
American Heart Association: No particular recommendations
Hemiparesis
Unilateral sensory loss
Visual field deficit (monocular blindness)
Gaze preference
Aphasia
Left-sided neglect or hemi-attention
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Prehospital Care
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.
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.
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.
Loss of consciousness
Dizziness
Generalized weakness
Mental confusion
Loss of vision with reduced level of consciousness
Incontinence of feces or urine
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)
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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
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.
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.)
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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
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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.
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.
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NO
NO
NO
NO
YES
High-risk patient?
(Includes symptoms such as: crescendo TIA,
recurrent TIA on maximum antiplatelet therapy,
and presumed cardioembolic source (e.g., atrial
fibrillation)
YES
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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
YES
Consult neurologist
Consider other antiplatelet options (Class IIa-IIb)
Clopidogrel
Combination ASA/extended-release dipyridamole
Ticlopidine
Consider other diagnoses
NO
YES
YES
NO
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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Heparin
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.
12
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
13
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Special Circumstances
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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
14
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.
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.
15
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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.)
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.
Stroke 1995 Aug;26(8):1348-1352. (Prospective, follow-up study;
728 patients)
17. Ferro JM, Falcao I, Rodrigues G, et al. Diagnosis of transient
ischemic attack by the nonneurologist. A validation study. Stroke
1996 Dec;27(12):2225-2229. (Validation study; 20 GPs and 22
neurologists)
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
16
17
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18.
COPYRIGHTED MATERIALDO NOT PHOTOCOPY OR DISTRIBUTE ELECTRONICALLY WITHOUT WRITTEN CONSENT OF EB PRACTICE, LLC
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.
79.
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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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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
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Indeterminate
Continuing area of research
No recommendations until
further research
Level of Evidence:
Evidence not available
Higher studies in progress
Results inconsistent,
contradictory
Results not compelling
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