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| ISBN-13: | 9781472747280 |
|---|---|
| Publisher: | Bpp Learning Media Ltd (Medical) |
| Publication date: | 07/31/2016 |
| Series: | BMJ Clinical Review Series |
| Pages: | 200 |
| Product dimensions: | 8.04(w) x 11.42(h) x 0.44(d) |
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BMJ Clinical Review: Neurology and Pain
By Babita Jyoti, Michail A. Karvelis
BPP Learning Media Ltd
Copyright © 2016 BPP Learning Media LtdAll rights reserved.
ISBN: 978-1-4727-4728-0
CHAPTER 1
Diagnosis and management of transient ischaemic attack and ischaemic stroke in the acute phase
K S McArthur, clinical research fellow, T J Quinn, lecturer in geriatric medicine, J Dawson, lecturer in clinical pharmacology and stroke, M R Walters, professor of clinical pharmacology and stroke
The care of people with acute ischaemic stroke has improved dramatically in recent years. Both stroke and transient ischaemic attack (TIA) are now recognised as medical emergencies that must be treated with the same urgency as myocardial infarction. Treatments such as thrombolysis are now widely adopted and underpinned by a robust evidence base. Rapid and accurate recognition of cerebral ischaemia, prompt treatment, and referral to specialist services can reduce the risk of further events.
Although cautious optimism has replaced therapeutic nihilism, stroke remains an important cause of death and disability and improvements in stroke services are still sorely needed. There are an estimated 900 000 stroke survivors in England, half of whom are dependent on others for care at an estimated cost of £8bn per year (about &8364;9bn or $13bn). This burden will increase as population demographics change. We review the diagnosis and acute management of cerebral ischaemia drawing on evidence from original research (particularly multicentre randomised clinical trials), registry data, and systematic review and meta-analysis, and with particular attention to national and international clinical guidelines. Further discussion of the epidemiology and economical aspects of contemporary stroke care are available elsewhere; the management of intracerebral haemorrhage was reviewed in a previous BMJ article (2009;339:b2586) and is not discussed here. We will review care in hospital, rehabilitation, and secondary prevention of stroke in a second paper.
What is an acute cerebrovascular event?
The World Health Organization defines stroke as the sudden onset of focal neurological signs, of presumed vascular origin, lasting longer than 24 hours or causing death. It can be further classified as ischaemic, due to interruption of blood supply, or haemorrhagic, due to rupture of a cerebral artery. The term cerebrovascular accident is now discouraged, because there is nothing "accidental" about cerebrovascular disease. In recognition of stroke as a medical emergency the term "brain attack" has been used and seems appropriate. Symptoms of a TIA are similar to those of stroke but last less than 24 hours. Indeed, a truly "transient" ischaemic event, with no cerebral infarction, will usually manifest as a symptom complex lasting only minutes. Longer events are typically associated with infarction and should be considered "stroke"; definitions are likely to change to reflect this.
Various clinical, radiological, and pathological classification systems have been proposed to further classify stroke. The Oxford clinical classification is often used because it is simple to apply and is of prognostic use. It describes four subtypes of stroke; total anterior circulation stroke (TACS), partial anterior circulation stroke (PACS), lacunar stroke (LACS), and posterior circulation stroke (POCS) (box 1).
Once an ischaemic cause is confirmed, the nomenclature can be altered to convey greater specificityfor example, a partial anterior circulation infarct (PACI). The underlying cause in most cerebral ischaemic events is cardioembolic or atherosclerotic arterial disease, which can cause either in situ thrombosis or distal embolism. Other causes are much rarer. Common sources of cardiac emboli are atrial fibrillation, mural thrombus, and valvular heart disease and these typically involve the territory of the large intracerebral arteries, particularly the middle cerebral artery. Atherosclerotic disease typically affects the extracranial internal carotid artery but also the vertebral and basilar arteries. Lacunar infarction results from occlusion of deep perforating arteries, which arise from both the anterior and posterior circulation, and supply the white matter of the cerebral hemispheres and brainstem.
Is it an acute cerebrovascular event?
Clinical diagnosis
It is important to rapidly distinguish stroke from one of the numerous conditions that resemble it ("stroke mimics", box 2). In a UK observational study of 350 consecutive suspected stroke presentations to a teaching hospital at least 30% of referrals resulted in a non-stroke diagnosis. This distinction is important to allow evidence based treatment to be started early and to refer alternative conditions to the appropriate team. It may be useful to consider the definition of stroke "sudden onset, focal neurology, of presumed vascular cause". Thus, for patients with gradual onset of symptoms, who have no focal symptoms (such as those who have lost consciousness), or who give a history that suggests a nonvascular basis for the episode (seizure, migraine), stroke can probably be excluded, albeit with a few exceptions.
Formal assessment tools are available to facilitate diagnosis and are based on these simple principles. Box 3 outlines two tools commonly used in routine practice. The Face Arm Speech Test (FAST) is suitable for use by the general public and has a positive predictive value of 78% (95% confidence interval 72 to 84) for stroke while the ROSIER scale, designed for emergency department use, functions similarly well and includes a screen for common stroke mimics (but can still be administered in less than five minutes). Similar tools are available for the diagnosis of TIA but have yet to be widely adopted.
Imaging
Brain imaging is indicated to help confirm the diagnosis, identify the causes, and help initiation of evidence based treatment. The usual imaging modality is non-contrast computed tomography (CT) and this remains useful particularly in excluding intracerebral haemorrhage and important mimics such as brain metastasis. However, sensitivity for detection of ischaemia is low in the very early stages of stroke and differentiating ischaemic from haemorrhagic strokes can be difficult on CT after a period of several days. More advanced CT imaging techniques such as CT perfusion and angiography are available and are likely to be used in the future to help better select patients for some of the acute treatments discussed below. At present, however, magnetic resonance imaging (MRI) is the modality of choice. In a study of 217 sequential acute stroke patients who underwent imaging using both non-contrast CT and MRI, CT demonstrated sensitivity of 26% (95% CI 20% to 32%) compared with 83% (78% to 88%) for MRI in the detection of early ischaemia. Further, concerns that MRI may not detect intracerebral haemorrhage or proves impractical for "emergency" imaging were not supported.
Imaging of the extracranial carotid arteries is required for patients with anterior circulation stroke. Carotid endarterectomy is of proved benefit for those with at least moderate carotid stenosis ipsilateral to an ischaemic stroke in the carotid artery (?). This procedure should be performed early; further details on patient selection will be discussed in a future review. Carotid duplex ultrasonography is well tolerated and non-invasive but substantial interobserver variability limits its accuracy. Most surgical teams will require corroborative imaging, often with CT or MR angiography, before surgical intervention and many specialist centres use these as modalities of choice.
Other investigations
Electrocardiogram abnormalities may suggest a cardiac origin for thrombus. Where brain imaging and clinical presentation fit with embolic stroke, or where clinical findings suggest cardiac disease, cardiac imaging and more detailed telemetry are indicated. Routine screening for vasculitides or thrombophilia is not justified.
How should I approach suspected TIA?
Remember that all patients who have ongoing symptoms, however mild, are considered to have had stroke and urgent transfer to hospital should be arranged. Where symptoms have resolved before presentation urgent hospital transfer may not be required but rapid assessment and treatment if TIA has occurred is mandatory.
A substantial risk of stroke exists in the early period after TIA. The magnitude of risk is greater and the time to event shorter than previously recognised. A recent systematic review reported an overall 7 day stroke risk of 5.2% after TIA.
Simple stratification scores can be used to better estimate a patient's individual risk. The most commonly used (and best validated) tool is the ABCD score (table 1). ABCD estimates risk of recurrence at two days from 1% for patients with "low risk" to 8.1% for those patients with "high risk". ABCD scoring is recommended in UK national guidelines and many centres offer same day assessment of patients at highest risk of stroke. ABCD may also be useful in diagnosis. Single centre registry data (3646 patients) showed that few referrals with an ABCD score of 0 were subsequently found to have a cerebrovascular diagnosis.
The fact that the increased risk occurs so soon after TIA tells us that same day assessment should be the aim for patients with TIA, although the practicalities of referral and investigation of stroke will vary according to the local facilities available. UK guidelines (National Institute for Health and Clinical Excellence and Scottish Intercollegiate Guidelines Network) suggest starting all patients on antiplatelet treatment (aspirin 300 mg) and referring them for urgent specialist assessment. NICE recommends that patients with ABCD scores greater than 4 be assessed within 24 hours. Delivery of these targets on a nationwide and fully inclusive basis will require substantial investment in services.
The landmark EXPRESS study compared stroke events in Oxford, UK, before and after a move from their standard to an immediate access, comprehensive, TIA assessment service. An 80% reduction in recurrent stroke at 90 days was demonstrated with no increase in adverse events (fig 1). Although we extrapolate these results from a single centre with caution, it is worth noting that if outcomes were replicated across all UK stroke centres 10 000 stroke events could be prevented annually.
How will specialist services manage the patient with suspected stroke or TIA?
The aim of specialist stroke assessment is confirmation of stroke diagnosis, identification of the causes, and timely initiation of evidence based treatment.
Brain imaging should be performed with minimal delay to distinguish ischaemic from haemorrhagic stroke. Even when the patient is not eligible for thrombolysis, imaging within 24 hours (although ideally as soon as possible) is the most cost effective strategy. The need for imaging in transient ischaemic attack is more contentious. In our unit we routinely scan anyone with symptoms lasting more than one hour before starting secondary prevention.
Patients with TIA
Treatments are aimed at preventing a further event, similar to the secondary treatments given to patients following acute stroke. In those with confirmed atrial fibrillation or mural thrombus anticoagulants are warranted. Antiplatelet or anticoagulant drugs may be considered in all patients, as may lipid lowering therapy, antihypertensive therapy, carotid surgery, treatment of diabetes, and advice about diet, lifestyle, and smoking cessation. A recent focus of research has been the potential benefits of early antiplatelets, statins, and antihypertensives. The marked reduction in stroke rate seen in EXPRESS may have been caused by immediate delivery of these therapies (patients were given medication at clinic review). We await results of ongoing trials, although emergent stroke data suggest that "acute" prescription of antihypertensives may have no clinical benefit.
Patients with acute ischaemic stroke
Within the first hours to days, proved treatments for acute ischaemic stroke include admission to a dedicated stroke unit; administration of intravenous tissue plasminogen activator (rt-PA); antiplatelet agents; and surgical decompression of massive cerebral oedema (table 2).
Aspirin
A systematic review of antiplatelets after ischaemic stroke (n=43 041) demonstrated that for every 1000 patients treated acutely with aspirin (160-300 mg) 13 fewer deaths occurred by the end of follow-up, which is a modest but important effect at a population level. UK guidelines recommend that patients with acute ischaemic stroke are prescribed aspirin 300 mg daily for two weeks, followed by a long term secondary preventative antiplatelet strategy. Aspirin should be withheld for 24 hours after thrombolysis. Where a patient's swallowing is impaired to a degree that precludes oral administration, rectal preparations may be used. In patients unable to take aspirin, alternatives such as clopidogrel may be used. There is no evidence to support the use of early anticoagulation as a treatment for acute ischaemic stroke.
Thrombolysis
Intravenous tissue plasminogen activator (rt-PA) alteplase is beneficial if given within 4.5 hours of acute ischaemic stroke in selected patients. In Europe, rt-PA is licensed for the treatment of acute ischaemic stroke provided it is administered within three hours of symptom onset, but many centres will administer it up to 4.5 hours based on evidence. The benefits of rt-PA are in reducing longer term disability and not in improved survival or in immediate improvement in neurological impairment (although anecdotally this has been observed). Two recent pooled meta-analyses of the major thrombolysis trials (n=2775 and n=3670) have demonstrated clear benefit of thrombolysis with significantly better outcomes seen with early treatment (table 3) In the larger analysis the odds ratios of a favourable outcome with rt-PA were 2.55 (95% CI 1.44 to 4.52) for 0-90 minutes, 1.64 (1.12 to 2.4) for 91-180 minutes, 1.34 (1.06 to 1.68) for 181-270 minutes, and 1.22 (0.92 to 1.61) for 271-360 minutes in favour of the rt-PA group. Trials have reported that mortality rates at three months are equivalent to placebo.
The limited time window for delivery of thrombolytic therapy is a major barrier to its delivery. The risk: benefit ratio beyond 4.5 hours has not been fully established and ongoing clinical trials aim to provide further evidence. Patients older than 80 years were excluded from most of the clinical trials. Non-randomised observational data suggest that their risk: benefit ratio is similar to that of other patients (fig 2 ) and many centres will give thrombolysis to selected older patients. However, data from randomised studies are lacking and we await results of the third international stroke trial.
Many clinicians fear the potential for iatrogenic intracerebral haemorrhage after thrombolysis and patient selection guidance is designed to minimise this risk. A list of contraindications to thrombolysis is shown in table 4 . For many of these, as we have gained more experience with thrombolysis, conditions that were previously "absolute" contraindications to rt-PA are now deemed "relative" contraindications. Because this is an evolving landscape, we advise referral of all hyperacute suspected strokes to a specialist team unless there is substantial premorbid disability. As the benefits of rt-PA are in reducing disability, this approach is not routinely used in patients who are already functionally impaired.
(Continues...)
Excerpted from BMJ Clinical Review: Neurology and Pain by Babita Jyoti, Michail A. Karvelis. Copyright © 2016 BPP Learning Media Ltd. Excerpted by permission of BPP Learning Media Ltd.
All rights reserved. No part of this excerpt may be reproduced or reprinted without permission in writing from the publisher.
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Table of Contents
Contents
About the publisher, iii,About The BMJ, iii,
About the editors, vi,
Introduction to Neurology and Pain, vii,
Diagnosis and management of transient ischaemic attack and ischaemic stroke in the acute phase K S McArthur, T J Quinn, J Dawson, M R Walters, 1,
Post-acute care and secondary prevention after ischaemic stroke K S McArthur, T J Quinn, P Higgins, P Langhorne, 7,
Posterior circulation ischaemic stroke Áine Merwick, David Werring, 14,
The management of spasticity in adults Krishnan Padmakumari Sivaraman Nair, Jonathan Marsden, 23,
First seizures in adults Heather Angus-Leppan, 30,
Drug treatment of epilepsy in adults Dieter Schmidt, Steven C Schachter, 37,
Management of chronic epilepsy Fergus J Rugg-Gunn, Josemir W Sander, 53,
Chronic migraine Todd J Schwedt, 58,
Pharmacological prevention of migraine Nathan Fenstermacher, Morris Levin, Thomas Ward, 68,
Cluster headache Alexander D Nesbitt, Peter J Goadsby, 72,
Thunderclap headache Anne Ducros, Marie-Germaine Bousser, 78,
Restless legs syndrome Guy Leschziner, Paul Gringras, 83,
Neuropathic pain: mechanisms and their clinical implications Steven P Cohen, Jianren Mao, 88,
Management of lumbar spinal stenosis Jon Lurie, Christy Tomkins-Lane, 100,
Opioids for low back pain Richard A Deyo, Michael Von Korff, David Duhrkoop, 112,
Trigeminal neuralgia Joanna M Zakrzewska, Mark E Linskey, 124,
Painful diabetic neuropathy Amanda Peltier, Stephen A Goutman, Brian C Callaghan, 131,
Fibromyalgia Anisur Rahman, Martin Underwood, Dawn Carnes, 140,
Complex regional pain syndrome Stephen Bruehl, 148,
Polymyalgia rheumatica Sarah L Mackie, Christian D Mallen, 161,
Temporomandibular disorders Justin Durham, Toby R O Newton-John, Joanna M Zakrzewska, 168,
Management of chronic pain in older adults M Carrington Reid, Christopher Eccleston, Karl Pillemer, 176,
Cancer induced bone pain Christopher M Kane, Peter Hoskin, Michael I Bennett, 184,