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.
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.
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.
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.
Significant medical history questions include the following:
Recent surgery (eg, carotid, cardiac)
Previous strokes
Known cardiovascular disease
Seizures
CNS infections
Use of illicit drugs
Complete medication regimen
Comorbidities related to metabolic disorders, especially diabetes
Carefully investigate onset, duration, fluctuation, and intensity of symptoms.
Reviewing the patient's medical record is extremely important for identifying deficits from previous strokes, seizures, or cardiac events. The primary care physician may have great insight into previous episodes and workup.
Attempt to clarify when symptoms first occurred, how long they lasted, if the patient recovered completely (ie, returned to baseline status), and if a pattern of escalating symptoms is present. For those who woke up or are found with symptoms, the time last known to be normal should be documented.
History of associated trauma or cardiac symptoms widens the differential diagnosis. Pertinent negative items (eg, headache, chest pain, eye pain) in the review of systems also are important.
Carotid or vertebral dissection can occur in association with both major and minor trauma. The patient may provide a history of blunt or torsion injury to the neck. Controversy exists regarding whether manipulation by a chiropractor or massage therapy increases the risk of arterial dissection.[14]
Elicit any risk factors for relevant underlying disease.
Known coagulopathy
History of arteritis
Noninfectious necrotizing vasculitis, drugs, irradiation, and local trauma are known to cause inflammatory arterial injury.
Thromboembolic risk factors such as carotid artery stenosis, venous or arterial thromboembolism, patent foramen ovale, atrial fibrillation, prior myocardial infarction, or left ventricular dysfunction.
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.
Initial vital signs should include the following:
Temperature
Blood pressure
Heart rate and rhythm
Respiratory rate and pattern
Oxygen saturation
The examiner should assess the patient's overall health and appearance, making an assessment of the following:
Attentiveness
Ability to interact with the examiner
Language and memory skills
Overall hydration status
Development
Identify signs of other active comorbidities including infections (eg, sinusitis, mastoiditis, meningitis) and vasculidities. Carotid arteries can be examined for pulse upstroke, bruit, and the presence of carotid endarterectomy scars.
Funduscopy can identify retinal plaques, retinal pigmentation, and optic disc margins.
Pupil reaction to direct and consensual light exposure can be assessed.
In addition to performing standard auscultation, examine the chest for the presence of surgical scars or presence of a pacemaker/automatic implantable cardioverter defibrillator (AICD), or other clues that the patient may have a cardiac disorder and increased risk of a cardioembolic phenomenon.
Cardioembolic events are significant causes of TIAs. Identify the rhythm for irregularity or other unusual rhythms and rates, murmurs, or rubs that might suggest valvular disease, atrioseptal defects, or ventricular aneurysm (a source of mural thrombi).
A neurologic examination is the foundation of the TIA evaluation and should particularly focus on the neurovascular distribution suggested by the patient’s symptoms. Subsets of the neurologic examination include the following:
Cranial nerve testing
Somatic motor strength
Somatic sensory testing
Speech and language testing
Cerebellar system (be sure to see the patient walk)
Mental status can be assessed formally (Mini-Mental Status Examination, Quick Confusion Scale) or as part of the patient's overall response to questions and interactions with the examiner.
The following signs may be present with cranial nerve dysfunction:
Ocular dysmotility
Forehead wrinkling asymmetry
Incomplete eyelid closure
Asymmetrical mouth retraction
Loss of the nasolabial crease
Swallowing difficulty
Lateral tongue movement
Weak shoulder shrugging
Visual field deficits
Somatic motor testing
Test muscle stretch reflexes of biceps, triceps, brachioradialis, patellar, and Achilles.
Inspect posture and presence of tremors. Test shoulder girdle, upper extremity, abdominal muscle, and lower extremity strength.
Test passive movement of major joints to look for spasticity, clonus, and rigidity.
The cerebellar system can be tested by assessing ocular movement, gait, and finger-to-nose and heel-to-knee movements, looking for signs of past-pointing and dystaxia, hypotonia, overshooting, gait dystaxia, and nystagmus.
The speech and language system can be tested to assess for both aphasia and dysarthria.
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.
Atherosclerosis of carotid and vertebral arteries
Embolic sources - Valvular disease, ventricular thrombus, and thrombus formation due to atrial fibrillation
Arterial dissection
Arteritis - Inflammation of the arteries occurring primarily in elderly persons, especially women
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
Serum chemistry profile including creatinine
Coagulation studies
Complete blood count
Studies that are typically helpful and can often be performed urgently
Erythrocyte sedimentation rate (ESR)
Cardiac enzymes
Lipid profile
Screening for hypercoagulable states (particularly in younger patients with no known vascular risk factors)[2]
Protein C, protein S, antithrombin III activities
Activated protein C resistance/factor V Leiden
Fibrinogen
D-dimer
Anticardiolipin antibody
Lupus anticoagulant
Homocysteine
Prothrombin gene G20210A mutation
Factor VIII
Von Willebrand factor
Plasminogen activator inhibitor-1
Endogenous tissue plasminogen activator activity
Additional laboratory testing as needed based upon history
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
Noncontrast cranial CT scan: This test is widely and rapidly available and often serves as the initial imaging evaluation. It can aid in diagnosing the following:
A new area of ischemia or infarction
Old areas of ischemia
Intracranial mass such as tumor
Intracranial bleeding such as subdural hematoma or intracerebral hemorrhage;
MRI
MRI is more sensitive for acute ischemia, infarction, previous intracranial bleeding, and other underlying lesions than CT.
The presence of ischemic lesions on MRI appears to increase the short-term risk of stroke, highlighting its potential value in acute risk stratification.[18, 19, 20] In addition, a negative DWI image in concert with low-risk clinical features can mark those at minimal short-term stroke risk.[21]
However, MRI is less widely available on an acute basis than CT scan.
Vascular imaging
Carotid Doppler ultrasonography of the neck can identify patients in need of urgent surgical or endovascular therapy.
Transcranial Doppler can be a complementary examination evaluating patency of cerebral vessels and collateral circulation.
Computed tomographic angiography (CTA) is of increasing value in identifying occlusive disease in the cerebrovascular circulation.
Magnetic resonance angiography (MRA) is another alternative for imaging vessels in both the brain and neck.
Conventional angiography can be performed when the above modalities are unavailable or yield discordant results.
Cardiac imaging
Transthoracic or transesophageal echocardiography (TTE/TEE) can evaluate for a cardioembolic source or for risk factors such as patent foramen ovale.
12-Lead electrocardiography should be performed as soon as possible after transient ischemic attack (TIA) and can evaluate for dysrhythmias such as atrial fibrillation.
Cardiac monitoring (inpatient telemetry or Holter monitor) is recommended as "useful" in patients without a clear diagnosis after initial brain imaging and electrocardiography.
Lumbar puncture (LP) may be indicated if subarachnoid hemorrhage, infectious etiology, or demyelinating disease is to be excluded.
Electroencephalography (EEG) may be indicated to evaluate for seizure activity.
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.
Initial assessment is aimed at excluding emergent conditions that can mimic a TIA such as hypoglycemia, seizure, or intracranial hemorrhage.
Vital signs must be obtained promptly and addressed as indicated.
Cardiac monitoring can capture a relevant dysrhythmia.
Pulse oximetry can evaluate for hypoxia.
Intravenous access (if not already established by EMS) should be obtained.
Obtain a fingerstick glucose level and treat accordingly.
Laboratory studies, including CBC, coagulation studies, and electrolyte levels, should be obtained.
Obtain an ECG and evaluate for symptomatic rhythms or evidence of ischemia.
Patients may be significantly hypertensive. Unless there is specific concern for end-organ damage from a hypertensive emergency, blood pressure should be managed conservatively while ischemic stroke is being ruled out.
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]
Neurologist: There is clear consensus on the need for rapid evaluation, and patients who undergo neurology evaluation and risk stratification within 24 hours versus within a few days appear to have a significantly decreased short-term risk of stroke. Therefore, decisions regarding ED evaluation, and inpatient versus rapid outpatient follow-up, are ideally made in concert with a neurologist. International recommendations also note that immediate consultation is more cost-effective than outpatient follow-up.[17]
Primary care physician: This is the most important consultation that can occur, as the primary care physician will monitor the patient long term and ensure risk factor and lifestyle modification. In addition, rapid neurology consultation is not available in many communities, and the primary care doctor may well be primarily responsible for managing urgent risk stratification.
Cardiologist: This consultation can be considered for those with clear findings that influence stroke risk, such as atrial fibrillation, patent foramen ovale, intracardiac thrombus, or valvular abnormalities.
Vascular surgeon: This consultation should be considered for those with significant vessel stenosis or occlusion, with a goal of specialist assessment within 1 week and treatment within 2 weeks of symptom onset.[17, 25, 26] In many centers, some vascular interventions can be performed by other specialists including interventional radiologists, neuroradiologists, and cardiologists.
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)
Antiplatelet agents are recommended rather than oral anticoagulation as initial therapy. Aspirin (50-325 mg/d), combination aspirin/extended-release dipyridamole, and clopidogrel are all reasonable first-line options (class I recommendation).
Combination aspirin/extended-release dipyridamole (Aggrenox) may be superior to aspirin alone (class IIa recommendation)[28] and can be started within 7 days of the event.[29]
Clopidogrel may be considered instead of aspirin alone (class IIb recommendation).
Aspirin in combination with clopidogrel increases the risk of hemorrhage and is not routinely recommended for patients with TIA (class III recommendation).
For those with a known cardioembolic source
Atrial fibrillation: Long-term anticoagulation with warfarin (goal INR 2-3) is typically recommended. Aspirin 325 mg/d is recommended for those unable to take oral anticoagulants.
Acute MI with left ventricular thrombus
Oral anticoagulation with warfarin (goal INR 2-3) is reasonable.
Aspirin up to 162 mg/d should be used concurrently for ischemic coronary artery disease.
Dilated cardiomyopathy: Either oral anticoagulation with warfarin (goal INR 2-3) or antiplatelet therapy may be considered.
Rheumatic mitral valve disease: Oral anticoagulation with warfarin (goal INR 2-3) is reasonable. Antiplatelet agents would not normally be added to warfarin unless patients experience recurrent embolism despite a therapeutic INR.
Mitral valve prolapse: Long-term antiplatelet therapy is reasonable.
Mitral annular calcification: Antiplatelet therapy can be considered. Those with mitral regurgitation can be considered for warfarin or antiplatelet therapy.
Aortic valve disease: Antiplatelet therapy may be considered.
Prosthetic heart valves
For mechanical prosthetic valves, oral anticoagulation with warfarin (goal INR 2.5-3.5) is recommended. For those with TIAs despite therapeutic INR, aspirin 75-100 mg/d can be added to the regimen.
For bioprosthetic valves, patients with TIA and no other source of thromboembolism can be considered for oral anticoagulation with warfarin (goal INR 2-3).
These agents inhibit platelet function by blocking cyclooxygenase and subsequent aggregation. See above for recommendations for specific agents from the American Stroke Association.
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.
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.
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.
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.
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"
ABCD2 score of 3 (Class IIa, level of Evidence C)
ABCD2 score of 0 to 2 and uncertainty that diagnostic workup can be completed within 2 days as an outpatient (Class IIa, level of Evidence C)
ABCD2 score of 0 to 2 and other evidence that indicates the patient's event was caused by focal ischemia (Class IIa, level of Evidence C)
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:
Crescendo TIAs
Duration of symptoms longer than 1 hour
Symptomatic internal carotid stenosis >50%
Known cardiac source of embolus such as atrial fibrillation
Known hypercoagulable state
Appropriate combination of the California score or ABCD score (category 4).[32]
Patients selected for outpatient care should have a clear follow-up plan and stroke prevention initiated as above, including antiplatelet medication and risk factor modification.
Patients with TIA and ipsilateral carotid artery stenosis may be candidates for urgent (< 2 wk) carotid endarterectomy. In certain patients, carotid artery stenting is a reasonable alternative. This can be discussed acutely or rapid follow-up arranged.
Patients with symptoms attributable to extracranial vertebral stenosis may be candidates for endovascular treatment, and, again, this should be arranged rapidly if available.
Antiplatelet agents should typically be initiated as soon as intracranial bleeding is ruled out. As above, the agent to be used varies with the patient and the specific indication.
Antihypertensive control should be optimized for patients with hypertension.
Lipid control should be initiated, potentially including a statin agent.
Blood glucose control should be optimized for patients with diabetes.
A smoking cessation strategy, which may include medication, should be initiated.
Heavy drinkers should eliminate or reduce alcohol consumption.
Overweight patients should be encouraged to lose weight.
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]
With passive reporting, the early risk of stroke following TIA is approximately 4% at 2 days, 8% at 30 days, and 9% at 90 days.[8] However, when patients with TIA are followed prospectively, the incidence of stroke is as high as 11% at 7 days.[6]
Patients with TIAs have an increased risk of stroke and death from coronary artery disease (depending on risk factors in the study group, approximately 6-10% per year).
Probability of stroke in the 5 years following a TIA is reported to be 24-29%.
