Transient Ischemic Attack

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Author

Joshua N Goldstein, MD, PhD, FAAEM, Assistant Professor, Harvard Medical School; Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital

CSL Behring Consulting fee Consulting

Coauthor(s)

Lauren M Nentwich, MD, Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital

Nothing to disclose.

Specialty Editor(s)

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine

eMedicine Salary Employment

J Stephen Huff, MD, Associate Professor, Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia Health Sciences Center

Nothing to disclose.

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

Nothing to disclose.

Peter MC DeBlieux, MD, Professor of Clinical Medicine and Pediatrics, Section of Pulmonary and Critical Care Medicine, Program Director, Department of Emergency Medicine, Louisiana State University School of Medicine in New Orleans

Nothing to disclose.

Chief Editor

Rick Kulkarni, MD, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital

WebMD Salary Employment

Background

A transient ischemic attack (TIA) is an acute episode of temporary neurologic dysfunction resulting from focal cerebral ischemia not associated with permanent cerebral infarction. The clinical symptoms of TIA typically last less than an hour, but prolonged episodes can occur. While the classical definition of TIA included symptoms lasting as long as 24 hours, advances in neuroimaging have suggested that many such cases represent minor strokes with resolved symptoms rather than true TIAs.

A group of cerebrovascular experts proposed a shift from the arbitrary time-based definition of TIA to a tissue-based definition in 2002 with a new definition for TIA as “a brief episode of neurological dysfunction caused by focal brain or retinal ischemia, with clinical symptoms typically lasting less than one hour, and without evidence of acute infarction.”[1] This proposed new definition was well received and endorsed by many clinicians. The American Heart Association and American Stroke Association (AHA/ASA) 2009 Guidelines endorsed this new definition with the omission of the phrase “typically less than one hour”, as there is no time cutoff that reliably distinguishes whether a symptomatic ischemic event will result in tissue infarction.

The current AHA/ASA-Endorsed Definition of TIA is as follows:

Transient ischemic attack (TIA): A transient episode of neurological dysfunction caused by focal brain, spinal-cord, or retinal ischemia, without acute infarction.[2]

For additional information, see Medscape's Stroke/Cerebrovascular Disease Resource Center.

Pathophysiology

A transient ischemic attack is a temporary reduction or cessation of cerebral blood flow in a specific neurovascular distribution due to low flow through a partially occluded vessel, an acute thromboembolic event, or stenosis of a small penetrating vessel.

Epidemiology

Frequency

United States

Between 200,000 and 500,000 TIAs per year are diagnosed in the United States.[3, 4] ED visits for TIA occur at a rate of about 1.1 visits per 1,000 US population, and TIAs are diagnosed in 0.3% of ED visits.[5] TIA carries a particularly high short-term risk of stroke, and approximately 15% of diagnosed strokes are preceded by TIAs.

International

TIA occurs in about 150,000 patients per year in the United Kingdom.[6] The population incidence likely mirrors that of stroke.

Mortality/Morbidity

The most important short-term risk from a TIA is that of stroke.[7] The early risk of stroke following TIA is approximately 4-5% at 2 days and as high as 11% at 7 days.[6, 8] Additionally, despite a public education program, many patients still do not seek medical attention after experiencing TIA symptoms. A recent population-based study of patients experiencing TIA or minor stroke found that 31% of all patients who experienced a recurrent stroke within 90 days of their first TIA or minor stroke did not seek medical attention after the initial event.[9] Public health professionals and physicians need to do more, such as promoting and participating in medical screening fairs and public outreach programs.

Race

The incidence of TIAs in blacks, 98 cases per 100,000 people, is higher than that in whites, 81 cases per 100,000 people. Controversy exists regarding whether race influences emergent workup following TIA.[10, 11]

Sex

The incidence of TIAs in men, 101 cases per 100,000 people, is significantly higher than that in women, 70 cases per 100,000 people.[12]

Age

The incidence of TIAs appears to increase with age, from 1-3 cases per 100,000 in those younger than 35 years to up to 1500 cases per 100,000 in those older than 85 years.[13] Fewer than 3% of all major cerebral infarcts occur in children. Pediatric strokes can often have quite different etiologies compared with adult strokes and are relatively more infrequent.

History

A transient ischemic attack (TIA) may last only minutes, and symptoms have often resolved before the patient presents to a clinician. Thus, historical questions should be addressed not just to the patient but also to family members, witnesses, and emergency medical services (EMS) personnel. Witnesses may have perceived abnormalities that the patient could not, such as changes in behavior, speech, gait, memory, and movement.

Physical

The goal of the physical examination is to carefully uncover any neurologic deficits, evaluate for underlying cardiovascular risk factors, and seek any potential thrombotic or embolic source of the event.

Ideally, any neurologic deficits should be recorded with the aid of a formal and reproducible stroke scale, such as the National Institutes of Health Stroke Scale (NIHSS). A stroke scale prompts the examiner to be thorough and allows different examiners to reliably repeat the examination during subsequent phases of the evaluation. Any neurologic abnormalities should suggest the diagnosis of stroke (or ongoing neurologic event) rather than TIA.

Causes

The transient ischemic attack (TIA) workup is focused on emergent/urgent risk stratification and management. A number of potential underlying causes can be rapidly identified.

Laboratory Studies

Ruling out metabolic or drug-induced etiologies for symptoms consistent with a TIA is important. Most importantly, a fingerstick blood glucose should be checked for hypoglycemia. Serum electrolytes should be sent to investigate for electrolyte derangements.

Emergency presentation

Studies that are typically helpful and can often be performed urgently

Additional laboratory testing as needed based upon history

Imaging Studies

National recommendations for urgent evaluation of the patient with a transient ischemic attack (TIA) include imaging of the brain within 24 hours of symptom onset; preferably MRI with diffusion-weighted imaging (DWI), but, if this is not available, then a CT scan should be obtained.[2, 17] The cerebral vasculature should be imaged urgently, preferably at the same time as the brain. Brain imaging can identify an area of ischemia in up to 25% of patients, and TIA mimics may be identified as well. Vessel imaging can identify a stenosis or occlusion that requires early intervention.

Brain imaging

Vascular imaging

Cardiac imaging

Transthoracic or transesophageal echocardiography (TTE/TEE) can evaluate for a cardioembolic source or for risk factors such as patent foramen ovale.

Other Tests

Prehospital Care

Emergency Department Care

Global CNS depression and airway or cardiac compromise are not typically features of a transient ischemic attack (TIA). In fact, the level of consciousness and neurologic examination are expected to be at the patient's baseline.

For acute ischemic stroke, the American Heart Association recommends initiating antihypertensive therapy only if blood pressure is more than 220/120 mm Hg, or mean arterial pressure greater than 130 mm Hg. Unless a comorbid cardiac or other condition requiring blood pressure lowering is a concern, allowing the patient's blood pressure to autoregulate at a higher level (during the acute phase) may help maximize cerebral perfusion pressure.[23]

Brain imaging is recommended within 24 hours of symptom onset. While MRI with DWI is preferred, a noncontrast head CT as a widely accessible study, is a reasonable first choice when MRI is not readily available.[2, 24]

Consultations

Medication Summary

Medical management is aimed at reducing both short- and long-term risk of stroke. Antithrombotic therapy should be initiated as soon as intracranial hemorrhage has been ruled out, given the high short-term risk of stroke following TIA. One set of guidelines from the American Stroke Association (and supported by the American Academy of Neurology) is summarized below:[27]

Noncardioembolic TIA (or for those in whom no source is determined)

For those with a known cardioembolic source

Class Summary

These agents inhibit platelet function by blocking cyclooxygenase and subsequent aggregation. See above for recommendations for specific agents from the American Stroke Association.

Aspirin (Anacin, Ascriptin, Ecotrin, Bufferin, Bayer Aspirin)

Clinical Context:  Blocks prostaglandin synthetase action, which, in turn, inhibits prostaglandin synthesis and prevents formation of platelet-aggregating thromboxane A2.

Aspirin 25 mg/dipyridamole 200 mg (Aggrenox)

Clinical Context:  Drug combination with antithrombotic action. This combination may be superior to aspirin alone in preventing cardiovascular events following TIAs.

Aspirin irreversibly inhibits formation of cyclooxygenase, thus preventing formation of thromboxane A2, a platelet aggregator and vasoconstrictor. Platelet-inhibition lasts for life of cell (approximately 10 d).

Dipyridamole is a platelet adhesion inhibitor that possibly inhibits RBC uptake of adenosine, itself an inhibitor of platelet reactivity. In addition, may inhibit phosphodiesterase activity leading to increased cyclic-3',5'-adenosine monophosphate within platelets and formation of the potent platelet activator thromboxane A2.

Each capsule contains 25 mg aspirin and 200 mg dipyridamole for total of 50 mg aspirin and 400 mg dipyridamole to be given per day.

Clopidogrel (Plavix)

Clinical Context:  Selectively inhibits ADP binding to platelet receptor and subsequent ADP-mediated activation of glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation.

Dipyridamole (Persantine)

Clinical Context:  Administer to complement usual warfarin therapy. Inhibits platelet adhesion, which may inhibit adenosine uptake by RBCs. May increase cyclic-3',5'-AMP within platelets and formation of potent platelet activator thromboxane A2. May reduce the risk of stroke when used as monotherapy instead of aspirin.

Ticlopidine (Ticlid)

Clinical Context:  Second-line antiplatelet therapy for patients who cannot tolerate or do not respond to aspirin therapy. In some circumstances, it can be an alternative to clopidogrel.

Class Summary

These agents are used to prevent venous thrombosis, pulmonary embolism, and thromboembolic disorders.

Warfarin (Coumadin)

Clinical Context:  Interferes with hepatic synthesis of vitamin K-dependent coagulation factors. Used for prophylaxis and treatment of venous thrombosis, pulmonary embolism, and thromboembolic disorders.

Further Inpatient Care

While controversy exists regarding the need for admission, there is no controversy regarding the need for urgent evaluation, risk stratification, and initiation of stroke prevention therapy.[30, 31, 2, 32]

When one community implemented a strategy to ensure patients were seen within an average of 1 day, compared with an average of 3 days, the 90-day stroke risk fell from 10% to 2%.[33] Another initiated a program to admit patients to a "rapid evaluation unit," which dropped the 90-day stroke risk from 9.7% to 4.7%.[34] Others have suggested similar benefits from rapid follow-up.[35]

The availability of local resources determines whether this urgent evaluation should occur as an inpatient, in an ED observation unit, or in rapid follow-up. In order to determine appropriate disposition, the emergency physician should determine necessary workup, then discuss with the neurologist or primary care doctor how best to ensure this occurs promptly.[36] In addition to the rapidity of the risk stratification workup, the emergency physician should also consider the potential benefit of decreased time to thrombolysis in hospitalized patients diagnosed with TIA who develop a new stroke in the first 24-48 hours after diagnosis.

One randomized controlled trial of an emergency department diagnostic protocol found that they could reduce cost, length of stay, and provide appropriate risk stratification by performing this workup in an ED observation unit (with neurology consultation) rather than in an inpatient unit.[37]

A number of patients present to the ED with a "transient neurological disturbance" that does not represent a true TIA, and these can be difficult to distinguish for the busy emergency practitioner. In addition, an emergent and comprehensive workup of all patients with "possible TIA" may not be the most cost-effective or appropriate use of limited local resources. The emergency practitioner should use appropriate risk stratification to ensure that emergent diagnostic and therapeutic interventions are targeted to the highest risk patients. A number of risk stratification scores are available to assist in this task, but the most widely validated is the ABCD2 score.[38, 39, 19]

Table 1. ABCD2 Score


View Table

See Table

Individuals with an ABCD2 score higher than 6 had an 8% risk of stroke within 2 days, while those with an ABCD2 score less than 4 had a 1% risk of stroke within 2 days. Some of these patients with lower scores may well have non-TIA events rather than true TIAs.[40] It has been proposed that this scoring system can be used to risk-stratify ED patients for emergent workup.[38, 41] Additionally, it has been shown that the ABCD2 score may help to predict the severity of recurrent stroke after TIA.[42, 43]

However, some groups have noted that the short-term stroke risk after TIA can be worrisome, even in those with a low ABCD2 scores.[44, 45]

Additionally, abnormalities on brain imaging can highlight patients diagnosed with a TIA who are at increased risk of early stroke and should also be taken into consideration. It has been shown that patients with transient neurological deficits who are found to have infarcts on DWI have a worse prognosis with higher rates of recurrent TIA and stroke compared to patients experiencing either an ischemic stroke or a TIA without evidence of infarction on DWI.[20, 19]

The American Heart Association[2] comments "It is reasonable to hospitalize patients with TIA if they present within 72 hours of the event and any of the following criteria are present"

The National Stroke Association consensus guidelines for the management of TIAs recommends the consideration of hospitalization of patients with their first TIA within the past 24-48 hours to facilitate possible early treatment with tPA and other medical management for recurrent symptoms and to expedite risk stratification and implementing secondary prevention (category 4). For patients with a recent (within 1 wk) TIA, the guidelines recommend a timely hospital referral with hospitalization for the following:

Further Outpatient Care

Inpatient & Outpatient Medications

Transfer

Decisions made regarding ED evaluation and inpatient versus rapid outpatient follow-up should ideally be made in consultation with a neurologist. It may be that the only way to access expedited evaluation and workup is via interfacility transfer to hospital with the appropriate resources. The National Stroke Association consensus guidelines recommend that “Hospitals and general practitioners should agree on a local admissions policy and a local protocol for referral to specialist assessment clinics for patients with TIA who do not require hospital admission" (category 4).[32]

Prognosis

References

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A: Age >60 y 1 point
B: Blood Pressure >140/90 mm Hg 1 point
C: Clinical Features
Unilateral weakness2 points
Speech disturbance without weakness1 point
D: Duration
>60 minutes 2 points
10-59 minutes1 point
D: Diabetes 1 point
Total0-7 points