Table of Contents

 

1. Abstract
2. Case Presentations
3. Introduction
4. Critical Appraisal Of The Literature
5. History And Definition
6. Epidemiology
7. Etiology And Pathophysiology
8. Differential Diagnosis
9. Prehospital Care
10. Emergency Department Evaluation
    1. History And Physical Examination
    2. Risk Stratification
11. Diagnostic Studies
    1. Laboratory Testing
    2. Cardiac Evaluation
    3. Brain Imaging
    4. Vascular Imaging
    5. Perfusion Imaging
12. Treatment
    1. Antihypertensive Treatment
    2. Antiplatelet Therapy
       1. Aspirin
       2. Other Antiplatelet Agents And Combinations
    3. Anticoagulation
    4. Endovascular Treatment
    5. Lipid Modification
    6. Risk Factor Control
    7. Thrombolysis
13. Disposition
14. Risk Management Pitfalls For Transient Ischemic Attack
15. Time- and Cost-Effective Strategies
16. Clinical Pathway For Transient Ischemic Attack
17. Tables and Figures
    1. Table 1. American Heart Association Classification Of Levels And Classes Of Evidence
    2. Table 2. Etiologic Subtypes Of Transient Ischemic Attack
    3. Table 3. Differential Diagnosis Of Transient Ischemic Attack
    4. Table 4. Stroke Chameleons
    5. Table 5. The ABCD2 Score
    6. Table 6. Imaging-Enhanced Risk Prediction Tools
    7. Table 7. Summary Of Types Of Imaging Used In Stroke Risk Prediction Tools
    8. Table 8. Laboratory Studies In Transient Ischemic Attack
    9. Table 9. Sources Of Cardioembolism
    10. Table 10. Summary Of Carotid Imaging Modalities
    11. Table 11. General Management Considerations For Suspected Transient Ischemic Attack
    12. Table 12. Current, Controversial, And Investigational Strategies In Transient Ischemic Attack
    13. Table 13. Novel Anticoagulants And Stroke Risk, Compared To Warfarin
    14. Table 14. Summary Of Disposition Options
    15. Figure 1. Prior And New Cerebellar Infarct On Computed Tomography And Magnetic Resonance Imaging
    16. Figure 2. Leukoaraiosis On Magnetic Resonance Imaging And Computed Tomography
    17. Figure 3. Transient Ischemic Attack On Magnetic Resonance Images
    18. Figure 4. Coronal Computed Tomographic Angiography Showing Carotid Stenosis
    19. Figure 5. Coronal Computed Tomographic Angiography Showing Severe Stenosis Of The Basilar Artery
18. References

Abstract

Transient ischemic attack represents a medical emergency and warns of an impending stroke in roughly one-third of patients who experience it. The risk of stroke is highest in the first 48 hours following a transient ischemic attack, and the initial evaluation in the emergency department is the best opportunity to identify those at highest risk of stroke recurrence. The focus should be on differentiating transient ischemic attack from stroke and common mimics. Accurate diagnosis is achieved by obtaining a history of abrupt onset of negative symptoms of ischemic origin fitting a vascular territory, accompanied by a normal examination and the absence of neuroimaging evidence of infarction. Transient ischemic attacks rarely last longer than 1 hour, and the classic 24-hour time-based definition is no longer relevant. Once the diagnosis has been made, clinical risk criteria may augment imaging findings to identify patients at highest and lowest risk of early recurrence. Early etiologic evaluation, including neurovascular and cardiac investigations, allows for catered secondary prevention strategies. Specialized transient ischemic attack clinics and emergency department observation units are safe and efficient alternatives to hospital admission for many transient ischemic attack patients.

Case Presentations

A 59-year-old obese woman presents to your community hospital ED after experiencing a distinct episode in which her left hand felt “clumsy,” along with a left facial droop and left-sided numbness. She denies experiencing frank weakness and states that the symptoms resolved in less than 10 minutes. She mentions a similar episode 2 weeks ago and is concerned because both her parents and an older sibling experienced significantly disabling ischemic strokes. Her vital signs and point-of-care glucose were within normal limits, and her ECG showed sinus rhythm. Her physical exam, including a detailed neurologic exam, was largely unrevealing, with no facial asymmetry, unilateral weakness, sensory loss, or dysmetria appreciated. A noncontrast cranial CT scan of the brain was remarkable only for nonspecific subcortical and periventricular white matter changes without evidence of acute or old infarction, mass, or hemorrhage. Although she was relieved to learn that she has not had a stroke, she is concerned that this may be a precursor of a more serious event. She does not have a primary care physician and states that she has not seen a physician in several years. She asks whether this was a “mini stroke” and, if yes, what the chances are that she will have a stroke in the future.

An 80-year-old man with a history of diabetes, carotid stenosis status post right carotid endarterectomy, and pacemaker-dependent cardiomyopathy presents after multiple brief episodes of garbled speech over the past week. He states that each episode resolved completely before recurring and that he is presently symptom-free. While in the ED, he experiences a 5-minute episode of right hemiparesis and then, once again, normalizes. His vital signs remain stable, and your physical exam is notable for a high-pitched carotid bruit on the right and a stroke scale of zero. A noncontrast CT scan of the brain shows no evidence of infarction. You have no inhouse neurology, and your carotid duplex lab has closed for the evening. How do you proceed?

A 72-year-old woman with a history of hypertension, diabetes, coronary artery disease, and chronic kidney disease presents shortly after experiencing a 20-minute episode of slurred speech and right facial droop. She denies experiencing similar events in the past, but she does endorse a transient episode of vision loss a week ago, intermittent vertigo, and left-sided weakness last month. On exam, her blood pressure is 178/100 mm Hg, her heart rate is 80 beats per minute and regular, and the ECG shows a sinus rhythm. Her stroke scale is zero, and noncontrast cranial CT scan shows an old small cerebellar infarct. It is Friday evening, and you have no inhouse neurology and no MRI capabilities overnight. The patient attributes her symptoms to stress and states that she has experienced anxiety and palpitations recently. She asks if it is necessary for her to be admitted or whether she can seek follow-up with her primary care physician next week.

Introduction

A transient ischemic attack (TIA) may not seem significant to patients and providers, but it should always be considered a true medical emergency. Caused by temporary focal central nervous system hypoperfusion, a TIA is often a warning of an impending stroke. Patients presenting to the emergency department (ED) with TIA are at highest risk of stroke within the next 48 hours,¹ and thus, it is critically important for the emergency clinician to recognize this opportunity to initiate primary stroke prevention strategies. Since the 2008 issue of Emergency Medicine Practice on TIA was published, there have been numerous studies focusing on improving risk stratification and early management strategies in TIA. This update will provide the best available evidence on diagnosing and managing TIAs.

For more information on current strategies for management of stroke, refer to the July 2012 issue of Emergency Medicine Practice, “Four Evolving Strategies In The Emergent Treatment Of Acute Ischemic Stroke,” the April 2012 issue of Emergency Medicine Practice, “Carotid And Vertebral Arterial Dissections In The Emergency Department,” and the May 2012 issue of EM Practice Guidelines Update, “Current Guidelines On Atrial Fibrillation In The Emergency Department.”

Critical Appraisal Of The Literature

The American Heart Association / American Stroke Association (AHA/ASA) released its current recommendations for the evaluation of TIA in a Scientific Statement published in the journal, Stroke, in 2009² and released guidelines for the prevention of stroke following TIA in 2011,³ also in Stroke. The current recommendations are supported by an increasingly robust body of clinical research. The AHA/ASA classification of recommendations and level of evidence are shown in Table 1.

A literature search was performed in September 2012 using PubMed, The National Guidelines Clearinghouse (www.guidelines.gov), and the Cochrane Library. The search was limited to human studies and reviews published in the English language since 2008 using the MeSH term TIA. The search yielded more than a thousand publications, of which hundreds were reviewed. Most were excluded based on reviewing the title, and those most relevant to emergency medicine were included. Preference was given to studies focusing on the diagnostic evaluation, risk stratification, and management of TIA. Additional articles were included if they were judged to be needed for completeness or historical reference.

There exists heterogeneity in the primary outcome measures in the current body of TIA literature. Most studies focus on recurrent events or disabling stroke, but the timeframe is often variable, with 2, 7, 30, and 90 days being the most commonly reported. Although studies with each of the time points are included in this review, emphasis is placed on 2 and 7 days, as they are most relevant to emergency medicine.

Risk Management Pitfalls For Transient Ischemic Attack

1. “The patient denied symptoms of a stroke, so I did not consider TIA.”
2. In TIA, history is often difficult, with vague symptoms that may not be suspected to be of ischemic etiology if they are not meticulously ascertained by an astute provider. Patients may dismiss or even fail to recognize certain symptoms.
3. “Although the patient reported multiple, brief episodes, she felt normal in the ED, so I sent her home.”
   Stuttering symptoms are of particular concern and warrant aggressive care. Be sure to ask about multiple episodes and take them very seriously, even if the patient is normal at the time of the ED encounter.
4. “I thought the patient’s neurologic examination was normal.”
   Subtle, persistent neurologic deficits are frequently missed in the ED—in over a quarter of TIA patients in 1 study. Performing a stepwise, thorough, and complete neurologic examination can help reduce the incidence of missed ischemic stroke.
5. “The patient was too young to be having a TIA.”
   Though TIA and stroke are far more common in the elderly, they can occur in young adult and pediatric patients. Consider arterial dissection, structural heart defects, and hereditary or acquired thrombophilias in these patients.
6. “The CT scan was normal, so I told him to follow up with neurology in a few weeks.”
   In patients with clinically silent infarctions, CT is falsely negative in at least one-third of cases. Patients receiving only a CT scan in the ED should be seen by a neurologist within 48 hours for additional etiologic testing and complete risk stratification.
7. “The ECG showed a sinus rhythm, so I didn’t pursue cardioembolic causes further.”
   Paroxysmal atrial fibrillation is a common cardioembolic culprit in TIA patients without evidence of large-vessel disease. A single 12-lead ECG is insufficient, and these patients should be considered for prolonged Holter or event monitor recording following discharge.
8. “I discharged the patient because the neurologist said the ABCD2 score wasn’t high enough to admit.”
   The ABCD2 score is a useful research tool and may serve as an adjunct to available imaging for risk stratification, but it should not be used as a threshold by which to screen patients for hospital admission.
9. “The symptoms lasted only 4 hours, so I knew it had to be a TIA.”
   The revised AHA/ASA-endorsed definition of TIA has moved away from a time-based definition to a tissue-based definition, wherein the arbitrary timeline of 24 hours no longer applies. In fact, the vast majority of TIAs last < 1 hour, and beyond that, infarction is much more likely.
10. “The patient was already taking aspirin, so I didn’t think there was anything to add.”
    It is still possible to have a TIA or ischemic stroke while already on antiplatelet therapy, and these patients should be considered for alternative antiplatelet agents such as clopidogrel or aspirin/dipyridamole combination therapy. Additional secondary prevention measures include lipid modification, antihypertensive therapy, selective anticoagulation, and lifestyle modification measures.
11. “TIA is a diagnosis to be worked up either as an inpatient or an outpatient, but not in the ED.”
    Since the risk of ischemic stroke following a TIA is highest within the first 48 hours, the emergency clinician is often the only provider to evaluate the patient in this narrow window of opportunity. Patients should receive frontloaded care and protocolized ED observation units offer a rapid, safe, and efficient means by which to conduct a complete evaluation.

Tables and Figures

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 should carry more weight than a case report.

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

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3. * Furie KL, Kasner SE, Adams RJ, et al. Guidelines for the prevention of stroke in patients with stroke or transient ischemic attack: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2011;42(1):227-276. (Guideline)
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83. Kang DW, Yoo SH, Chun S, et al. Inflammatory and hemostatic biomarkers associated with early recurrent ischemic lesions in acute ischemic stroke. Stroke. 2009;40(5):1653-1658. (Prospective; 153 patients)
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