 
|
|
|
|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| 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.
MethodFor 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 TIADiagnosis 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
Risk of stroke after TIAPeople 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
Urgency of assessmentThe 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
InvestigationsVascular 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
Secondary prevention measuresSeveral 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
Driving adviceAll 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
SummaryPeople 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: john.gommans@hawkesbaydhb.govt.nz
References:
|
|
|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| | Current
issue | Search journal |
Archived issues | Classifieds
| Hotline (free ads) Subscribe | Contribute | Advertise | Contact Us | Copyright | Other Journals |
|