Journal of the New Zealand Medical Association, 24-April-2009, Vol 122 No 1293
Preventing strokes: the assessment and management of people with transient ischaemic attack
John Gommans, P Alan Barber, John Fink
Stroke is a leading cause of death and the major cause of long term adult disability in New Zealand (NZ). The impact on individuals and their families/whānau and caregivers is substantial as approximately one-third of people with stroke will die within the first 12 months and one-third will be reliant on others for assistance with activities of daily living.1 Moreover, Demographic changes in NZ are likely to result in an increase in both stroke incidence and prevalence over coming decades.2
Transient ischaemic attack (TIA) is defined as stroke symptoms and signs that resolve within 24 hours.3 About 25% of people with ischaemic stroke have a preceding or warning TIA.2 The risk of stroke following TIA is greatest in the first 48 hours and urgent specialist assessment and initiation of treatments may prevent many of these strokes.4–6
The Ministry of Health’s Diabetes and Cardiovascular Disease Quality Improvement Plan identified a number of issues potentially affecting NZ’s ability to achieve appropriate early assessment and intervention after TIA, and prevent stroke.2 An up-to-date TIA guideline was recommended.
This review summarises the New Zealand Guideline for the Assessment and Management of People with Recent Transient Ischaemic Attack (Table 1).7 A brief User Guide is also available.8 These provide general guidance to health professionals and service providers and may not be appropriate for use in all situations. Healthcare providers will need to use clinical judgment to decide whether or not to apply guideline recommendations regarding assessments and interventions, and must consider the wishes of the patient, the individual patient circumstances, their clinical expertise, and available resources.
For full details regarding development of the guideline readers should refer to the guideline.7 In summary the authors reviewed international and NZ guidelines relating to stroke and TIA published in the last 10 years. In addition a literature search using “MEDLINE with full text” was done on 24 July 2008 for all articles published since 2005 on the topics “transient ischaemic attack” and “TIA” to identify recent evidence that may not have been included in these guidelines.
Guideline drafts were circulated during July and August 2008 to a NZ TIA Guideline advisory group, and NZ and international colleagues for comment and peer review. The NZ advisory group included representatives from people with stroke and TIA, patient support groups, Māori and Pacific people; and health practitioners working in primary care, ambulance services, emergency medicine, and internal medicine. Others consulted included PHARMAC (the NZ Government’s pharmaceutical funding agency) and DHB NZ, representing District Health Boards (DHB).
Following receipt of feedback, the guideline was then finalised by the authors and released on 24 October 2008 by the Stroke Foundation of New Zealand.
Diagnosis of TIA in primary care and emergency departments can be problematic and is likely to be only 50 to 80% accurate with frequent over-diagnosis.6,9,10
An incorrect diagnosis of TIA matters as it may expose a person to unnecessary investigations and interventions; cause anxiety regarding risk of stroke or other cardiovascular events; and impact on a person’s work, driving, travel plans or ability to obtain insurance.
A diagnosis of TIA is more likely to be correct if history confirms sudden onset of neurological symptoms with maximal deficit at onset of symptoms, which then rapidly resolve, usually within 30–60 minutes. Any progressive onset or a march of symptoms from one part of the body to another is more suggestive of epilepsy (if fast, over seconds to 1–2 minutes) or migraine (if slow, over several minutes).
Typical symptoms of a TIA involve loss of focal neurological function such as unilateral loss of movement or sensation, or loss of speech or vision (Table 2). Symptoms of generalised disturbance of neurological function such as faints, generalised weakness or numbness, bilateral blurred vision, isolated dizziness, confusion (unless mistaken for dysphasia), and “funny turns” are rarely due to TIA, unless also accompanied by focal symptoms. Similarly TIAs rarely cause “positive” symptoms such as pins and needles, limb shaking, or scintillating visual field abnormalities. Hypoglycaemia should always be excluded in people presenting with sudden onset of neurological symptoms.
Table 1. Key messages7
Table 2. TIA symptoms9,11
Note: Ataxia, vertigo, dysphagia, dysarthria, and sensory symptoms to part of one limb or the face may be consistent with TIA if they occur in conjunction with other typical symptoms.
Table 3. TIA differential diagnosis6,9
People with TIA are at risk of stroke and other cardiovascular events including myocardial infarction and sudden death. This risk can be as high as 12% at 7 days and 20% at 90 days.12–14 About half of these strokes will occur within the first 48 hours and up to 85% of strokes that follow TIA will be fatal or disabling.4,13 This risk is higher than that for chest pain. TIA warrants urgent attention.
All people with suspected TIA should have a full assessment that includes determination of their stroke risk, using the ABCD2 tool, at the initial point of health care contact whether first seen in primary or secondary care (Table 4). The ABCD2 score can identify those most at risk of stroke following TIA; usually those with unilateral weakness and/or speech disturbance, especially if symptoms are prolonged.4,15
Use of the ABCD2 tool also facilitates accurate diagnosis as it identifies people who are more likely to have a true TIA.4,16 This is because its discriminating factors include symptoms and signs commonly seen in definite TIAs such as unilateral weakness and speech disturbance, and the focus on neurological symptoms of longer duration excludes most people with seizures and syncope. Furthermore, older people, and those with high blood pressure and/or diabetes are more likely to have cerebrovascular disease.
Table 4. ABCD2 tool for stroke risk after TIA4
Table 5. Stroke risk according to ABCD2 scores4
It is important that clinicians recognise that the ABCD2 tool is an aid to and not a substitute for clinical decision making in individual patients. Other factors not included in the ABCD2 tool also contribute to an increased risk of stroke (Table 6). High risk groups include people with persistent symptoms when first seen, ABCD2 score of 4 or more, crescendo TIAs (two or more TIAs within a week), atrial fibrillation or who are already on anticoagulation therapy. Lower risk is indicated by an ABCD2 score of 3 or less, or late presentation such as more than 1 week after their last TIA.
Table 6. Risk of stroke following TIA7
The most cost-effective service is immediate specialist assessment for all people identified as high risk (a 7-day stroke risk of >4%) including those with an ABCD2 score of 4 or more.3 Therefore, the urgency of assessment should be according to an individual’s risk of stroke (Table 5). Most people at high risk should be transferred urgently to hospital to facilitate rapid specialist assessment and treatment within 24 hours; preferably to an open-access specialist TIA clinic or a short stay unit.7,17
Most people at low risk of stroke may initially be managed in the community and referred to a specialist clinic, and should be seen within 7 days.7 If the treating doctor has ready access to brain and carotid imaging, and is confident about the diagnosis and implementing recommended treatments, then some people with TIA who are assessed as low risk may not require specialist review.7
Based on a generally accepted figure of $50,000 per new stroke in direct health costs funded by District Health Boards (DHBs), a relatively low number of strokes need to be prevented after TIA to justify intensification of services for people with TIA.2 Each DHB should have locally agreed protocols for the assessment and management of people with recent TIA, irrespective of where they are initially seen.7
Vascular risk factors—All people with TIA should be assessed for vascular risk factors at their first assessment including; hypertension, atrial fibrillation, ischaemic heart disease and/or peripheral vascular disease, diabetes, cholesterol, smoking history, and alcohol consumption.
Routine investigations—Investigations are necessary to exclude other diagnoses and to determine the potential cause of the event (Table 7). Further investigations may be warranted if clinical history, imaging and routine investigations do not adequately identify the underlying cause.
Table 7. Routine investigations for TIA17,18
Brain imaging—All people with TIA should have brain imaging, either magnetic resonance imaging (MRI) or computerised tomography (CT).7 If at high stroke risk this should be done urgently, but certainly within 24 hours. If low stroke risk this should be done within 7 days.7 CT imaging is widely available, reliably identifies many diagnoses that mimic TIA and should be undertaken early in all patients.17 However, MRI with diffusion weighted imaging is the imaging strategy of choice and can detect ischaemic changes consistent with infarction in up to two thirds of those with TIA.3,18 Patients with severe comorbidities may not be appropriate for scanning if the results would not change management.3
Carotid imaging—Carotid imaging is recommended for people with anterior circulation TIA symptoms such as dysphasia, transient monocular blindness, and most with unilateral weakness, if they are fit for surgery.18 Carotid imaging should be done in appropriate people within 1 day if high risk or 7 days if low risk.7
Several interventions are of proven effectiveness in preventing stroke and other cardiovascular events after a TIA. Assuming that these effects are independent, use of these interventions in appropriate people following TIA or stroke have been predicted to reduce the long-term group risk of recurrent stroke by up to 80%. Analysis gives an estimated number needed to treat (NNT) of about 5 at 5 years and 3 at 10 years.19 There is evidence that initiating secondary stroke prevention therapies in hospital results in high rates of adherence to therapy at follow-up.20
Although the high risk of stroke early after TIA indicates a need for urgent diagnostic workup and rapid intervention to prevent further events, to date there are no large randomised trials of urgent treatments after TIA. However, meta-analysis confirms that urgent assessment and intervention by specialised stroke services is associated with the lowest risk of early stroke.21
Recent studies also confirm that it is feasible to reorganise or create services that facilitate urgent assessment and early initiation of secondary preventative therapy, and that by doing so the risk of stroke after TIA may be significantly reduced, possibly by as much as 80%.5,6
The following recommendations should be considered for all people after TIA but treatment decisions must be tailored to the needs of individuals. For example some people may not be able to tolerate all recommended therapies and the long term goal of reducing future cardiovascular events must be balanced against potential immediate hazards of therapies such as bleeding, falls and fractures, delirium, and electrolyte disturbances.
Begin Early Aggressive Treatment to “BEAT” TIA—Treatment must be initiated at first contact whether the person with TIA attends their GP, emergency department, out-of-hours medical centre, or similar providers. Follow-up is recommended, either in primary or secondary care, within 1 month so that medication and other risk factor modification can be reassessed.22
Behaviour change and lifestyle modification—Every person with TIA should be assessed and informed of their risk factors for stroke and other cardiovascular events, and possible strategies to modify these. This includes; assistance with smoking cessation via nicotine replacement therapy, other replacement aid and/or behavioural therapy; a diet that is low in fat and sodium, but high in fruit and vegetables; a weight-reducing diet for people with an elevated body mass index; increasing regular exercise and physical activity; and avoiding excessive alcohol consumption.7,18 For Māori and Pacific people, involvement of whānau and culturally appropriate service providers is advised, where these are available.
Anti-platelet agents—Aspirin remains the cheapest and most widely used anti-platelet agent and is recommended for all people with suspected TIA unless contraindicated; 300 mg stat if aspirin naïve and 75–150 mg daily.7
If the person has fully recovered, it is reasonable to start aspirin pending brain imaging due to the high risk of early stroke, as 99% of strokes after TIA are ischaemic and intracerebral haemorrhage (ICH) rarely causes TIA.3,4 Furthermore, inadvertent short-term use of aspirin in stroke patients subsequently shown to have ICH has not been shown to cause harm.23
If TIA occurs in a person already on aspirin, either add dipyridamole or change to clopidogrel. Aspirin plus modified release dipyridamole twice daily and clopidogrel alone are more effective than aspirin alone, although the numbers needed to treat (NNT) are greater than 100 to obtain benefit above aspirin alone.17
Dipyridamole is funded by PHARMAC as a 150mg SR tablet in NZ whereas available evidence supports a 200 mg modified release dose given twice daily.24 There is a significant dropout rate with dipyridamole therapy due largely to headache. Adherence may be improved if people are advised that side effects may resolve after several days therapy or if dose is temporarily reduced and reintroduced gradually, for example using dipyridamole 150 mg SR once daily at night for 1 week before increasing to twice daily.
Clopidogrel alone is as effective as combination aspirin plus dipyridamole, and is better tolerated.25 The recommended dose is 300 mg stat and 75 mg daily. At the time of writing, PHARMAC special authority approval is required for funding of clopidogrel. Some people may choose to pay for clopidogrel.
Anticoagulation—Warfarin is recommended for every person with TIA if atrial fibrillation (paroxysmal or permanent) or other cardiac source of emboli is identified, unless contraindicated.7 Brain imaging must be done first to exclude haemorrhage or other pathology. The potential risks and benefits of anticoagulation therapy should be discussed with the person and where appropriate their family/whānau, and this discussion and its outcome should be documented. A target INR of 2.5 (range 2–3) is recommended.
Blood pressure-lowering treatments—All people with TIA, either normotensive or hypertensive, should receive blood pressure-lowering therapy, unless contraindicated by symptomatic hypotension.3,7,17 Treatment should be initiated at first contact but BP should not be lowered rapidly.
More than one drug is frequently required to lower BP to optimum levels and an ACE-inhibitor with a thiazide diuretic is an appropriate combination. The absolute target BP level is uncertain and should be individualised, but benefit has been associated with an average reduction of about 10/5 mmHg, and normal BP levels have been defined as <120/80 mmHg.17
Individual blood pressure targets should take into account the number and dose of medications as well as comorbidities and frailty, especially in older people.
Cholesterol-lowering treatment: Therapy with a statin is recommended for all people after TIA.7 At the time of writing, PHARMAC funds simvastatin as initial statin therapy in NZ. The recommended starting dose is 40 mg, although a lower dose (20 mg and titrate up) may be more appropriate in older people or those with frailty. PHARMAC special authority approval is required for more intensive therapy with atorvastatin 80 mg daily. Benefit occurs even in those with normal baseline cholesterol. The LDL cholesterol (optimal level <2.5 mmol/L) should be used to monitor therapy.
Carotid surgery—People with TIA who have at least 50% symptomatic carotid stenosis should be assessed and if a surgical candidate, be referred for carotid endarterectomy (CEA) within 1 week (one day if high risk), and receive treatment within a maximum of 2 weeks of onset of symptoms.7
The benefit from CEA is highly dependent on time since the presenting symptom and the degree of stenosis. The absolute risk reduction from CEA is reduced by half if surgery is delayed beyond 2 weeks and further reduced by half if it is delayed beyond 4 weeks.26 The benefit of CEA is substantial for people with 70–99% stenosis of the symptomatic internal carotid artery with NNT of 6 to prevent one ipsilateral stroke, or any stroke or surgical death.26
The benefit from CEA is much lower in patients with 50–69% stenosis; NNT 24 to prevent one ipislateral ischaemic stroke, or 14 to prevent one stroke of any origin, including surgical death.26
All people with TIA should have their driving status assessed and be advised about the impact of their TIA on their ability to drive; this advice should be documented (Table 8). Heath practitioners should refer to the Land Transport NZ document Medical Aspects of Fitness to Drive for full advice regarding driving after a TIA, which is also available online.27
Table 8: Summary of recommendations for driving after TIA27
People with recent TIA are at risk of stroke and other cardiovascular events, and those identified as at high risk should be managed as a medical emergency. Urgent specialist assessment and rapid initiation of secondary prevention measures can prevent strokes. Begin Early Aggressive Treatment to BEAT TIA. Based on a generally accepted figure of $50,000 per new stroke in direct health costs funded by District Health Boards (DHBs), a relatively low number of strokes need to be prevented after TIA to justify intensification of services for people with TIA. The full guideline and user guides are freely available at www.stroke.org.nz
Declaration: The authors wrote the NZ TIA Guideline on behalf of the Stroke Foundation of New Zealand under contract to the Ministry of Health, and currently act as honorary medical advisors for the Stroke Foundation (JG Central, PAB Northern, and JF National).
Author information: John Gommans, General Physician and Geriatrician, Hawke’s Bay District Health Board, Hastings; P Alan Barber, Neurological Foundation Professor of Clinical Neurology, University of Auckland, and Stroke Neurologist, Auckland District Health Board, Auckland; John Fink, Stroke Neurologist, Canterbury District Health Board, Christchurch
Acknowledgements: We are grateful to the writers, consumers, and commentators for their generous voluntary contribution of time and expertise in the preparation of the TIA guideline.
Correspondence: Dr John Gommans, Hawke’s Bay Hospital, Private Bag 9014, Hastings, New Zealand. Phone: 06 8781332. Fax: 06 8781319. Email: email@example.com
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