Cerebrovascular Events (Stroke)

Stroke refers to a clinical syndrome, of presumed vascular origin, typified by rapidly developing signs of focal or global disturbance of cerebral functions lasting more than 24 hours or leading to death. A stroke results either from ischaemic infarction of part of the brain or from intracerebral haemorrhage. It leads to the rapid onset of signs and symptoms of focal brain damage. Ischaemic infarction may be caused by atheroma or thrombo-embolism (and more rarely by trauma, infection or tumours). Cerebral infarction accounts for 69% of strokes, primary haemorrhage for 13%, subarachnoid haemorrhage for 6%, and 12% are of uncertain type.¹

In a young patient, consider especially: vasculitis, thrombophilia, subarachnoid haemorrhage, venous-sinus thrombosis or carotid artery dissection (e.g. via near-strangling or fibromuscular dysplasia).

• Thrombosis in-situ.
• Athero-thromboembolism (e.g. from carotid arteries).
• Heart emboli (atrial fibrillation, infective endocarditis, myocardial infarction).
• Central nervous system bleed (hypertension, head injury, aneurysm rupture).
• Sudden blood pressure drop by more than 40mmHg.
• Vasculitis, e.g. giant cell arteritis.
• Venous-sinus thrombosis.

• Stroke is a major cause of mortality and morbidity in the United Kingdom. The annual incidence is 1.5/1000 overall, rising rapidly with age to 10/1000 at age 75 years.

Risk Factors

• Hypertension
• Smoking
• Diabetes Mellitus
• Heart disease (valvular, ischaemic, atrial fibrillation)
• Peripheral vascular disease
• Past transient ischaemic attack: approximately 15% of ischaemic strokes are preceded by a transient ischaemic attack.² The greatest risk is within the first 72 hours after the TIA.
• Polycythaemia vera
• Carotid artery occlusion: carotid bruit
• The combined oral contraceptive pill
• Hyperlipidaemia
• Excess alcohol
• Clotting disorders

• Either sudden onset or a step-wise progression of symptoms and signs over hours (or even days) is typical.
• Focal signs relate to distribution of the affected artery, but collateral supplies may cause variation in the presentation.
• Cerebral hemisphere infarcts (50%) may cause: contralateral hemiplegia which is initially flaccid (floppy limb, falls like a dead weight when lifted) then becomes spastic; contralateral sensory loss; homonymous hemianopia; dysphasia.
• Brainstem infarction (25%): wide range of effects which include quadriplegia, disturbances of gaze and vision, locked-in syndrome (aware but unable to respond). Lateral Medullary Syndrome from vertebrobasilar occlusion.
• Lacunar infarcts (25%): small infarcts around basal ganglia, internal capsule, thalamus and pons. May cause pure motor, pure sensory, mixed motor and sensory signs, or ataxia. Intact cognition/consciousness.

• The two types of stroke are not reliably distinguishable clinically but pointers include:
  • Haemorrhagic stroke: meningism, severe headache and coma within hours
  • Ischaemic stroke: carotid bruit, atrial fibrillation, past transient ischaemic attack
• CNS tumour
• Subdural bleed
• Todd's palsy
• Consider drug overdose if comatose.

• Full blood count: thrombocytopenia, polycythaemia. Test for sickle cell disease.
• ESR: giant cell arteritis (consider temporal lobe artery biopsy, start steroids).
• Hypoglycaemia, hyperglycaemia and hyperlipidaemia.
• Syphilis: active, untreated.
• Hypertension: hypertensive retinopathy, large heart on chest x-ray, ventricular hypertrophy on ECG. Raised blood pressure may be an acute result of stroke, and therefore should not be treated unless sustained. Treatment of raised blood pressure soon after a stroke may lead to a worse prognosis.³
• Emboli from the left atrium may have caused the stroke. Look for a large left atrium on chest x-ray and consider echocardiography.
• Post-myocardial infarction: mural thrombus is best shown by echocardiography. In stroke due to atrial fibrillation or mural thrombus, a CT scan should be performed to exclude a haemorrhagic stroke, and then aspirin started.⁴
• CT scan provides evidence of haemorrhage within the first 48 hours in up to 98% of patients with subarachnoid haemorrhage. CT scan is considered superior to MRI in this context.⁵ Full anticoagulation should be delayed in order to avoid bleeds into infarcts.
• Brain imaging should be undertaken as soon as possible in all patients, at least within 24 hours of onset unless there are good clinical reasons for not doing so. Brain imaging should be undertaken as a matter of urgency if the patient:
  • Is currently taking anticoagulant treatment
  • Has a depressed level of consciousness
  • Has papilloedema, neck stiffness or fever
  • Has indications for thrombolysis or early anticoagulation
  • Has a known bleeding tendency
  • Has unexplained progressive or fluctuating symptoms
  • Has severe headache at onset
• Infective endocarditis: 20% of those with endocarditis present with CNS signs due to septic emboli from valves.
• Carotid duplex ultrasound: in stroke or TIA in carotid territory.

Acute Stroke Management

• Patients should be admitted to hospital (ideally a stroke unit for initial care and treatment, unless the diagnosis will make no difference to management, e.g. where optimal management is palliative care).⁶
• Aspirin (300 mg) should be given as soon as possible after the onset of stroke symptoms once a diagnosis of primary haemorrhage has been excluded. Antiplatelet therapy should then be continued indefinitely. Aspirin should be delayed for 24 hours following thrombolysis.
• Anticoagulants should not be started until brain imaging has excluded haemorrhage, and usually not until 14 days have passed from the onset of an ischaemic stroke.⁷
• Unless there are contraindications, thrombolytic treatment appears to be effective in improving prognosis after an acute stroke. ⁸ Treatment with alteplase should only be given provided that:
  • It is administered within three hours of onset of stroke symptoms (unless as part of a clinical trial)¹
  • Haemorrhage has been definitively excluded
• Drugs depressing the function of the central nervous system (e.g. anxiolytics and tranquilisers) and new prescriptions for sedatives should be avoided.
• Patients with TIA, or patients with a stroke who have made a good recovery when seen, should be assessed and investigated in a specialist service (e.g. neurovascular clinic) as soon as possible within seven days of the incident.

Secondary Prevention of Stroke and TIA

• All patients should have an individualised strategy for stroke prevention that should be implemented within a maximum of 7 days of acute stroke or TIA.
• All patients should be given appropriate advice on lifestyle factors, including: stopping smoking, regular exercise, diet and achieving a satisfactory weight, reducing the intake of salt, and avoiding excess alcohol.
• All patients should receive regular review and treatment of risk factors for vascular disease for the rest of their lives after a stroke with inclusion on a stroke register and a minimum of annual follow-up.
• Blood pressure. All patients who have a high blood pressure persisting for over two weeks should be treated. The British Hypertension Society guidelines are:⁹
  • In non-diabetic people with hypertension, the optimal blood pressure treatment goals are systolic blood pressure less than 140 mmHg and diastolic blood pressure less than 85 mmHg.
  • For patients with diabetes mellitus and high blood pressure, the optimal goals of control are 130/80.
  • Further reduction of blood pressure should be undertaken using a thiazide diuretic (e.g. bendroflumethiazide or indapamide) or an ACE inhibitor (e.g. perindopril or ramipril) or preferably a combination of both, unless there are contraindications.
• Anti-thrombotic treatment:
  • All patients with ischaemic stroke or TIA who are not on anticoagulation, should be taking an antiplatelet agent i.e. low-dose aspirin (e.g. 75mg). Where patients are intolerant of aspirin, an alternative antiplatelet agent (e.g.clopidogrel 75mg daily and/or dipyridamole MR 200mg twice daily) should be used. Patients with an occlusive stroke (not due to atrial fibrillation) should receive aspirin and dipyridamole for two years before reverting to aspirin alone.¹⁰
  • Anticoagulation should be started in every patient with persistent or paroxysmal atrial fibrillation (valvular or non-valvular) unless contraindicated. Anticoagulants should not be used for patients in sinus rhythm unless there is a major source of cardiac embolism. Anticoagulants should not be started until brain imaging has excluded haemorrhage, and usually not until 14 days have passed from the onset of an ischaemic stroke.
• Anti-lipid agents:
  • Treatment with a statin should be given to patients with ischaemic stroke or TIA, and total cholesterol of >3.5mmol/L unless contraindicated.¹¹

Long-term Management

• Patients and their carers should have their individual psychosocial and support needs reviewed on a regular basis. This will include mood (depression and anxiety), cognitive impairment, pain, communication difficulties, continence, functional ability, equipment needs and social integration.
• Patients should continue to have access to specialist care and rehabilitation after leaving hospital.
• Any patient with reduced function at 6 months or later after stroke should be assessed for a period of further targeted rehabilitation.
• Independence should be encouraged. As patients become more active, consideration should be given to withdrawal of physical and psychological support, enteral tubes, cessation of therapy and withdrawal of personal support.
• All patients should receive an annual flu vaccination.
• Information and support needs
  • Patients who make a satisfactory recovery from their stroke must not drive for 1 month after the stroke. Patients with residual disability at one month after a stroke must inform the DVLA and will only be able to resume driving after formal assessment.¹²
  • The needs of the carers should be considered from the outset.
  • Health and social services professionals should ensure that patients and their families have information about the statutory and voluntary organisations offering services specific to these needs.

Subarachnoid haemorrhage

Subarachnoid haemorrhage should be considered in any patient presenting with sudden-onset, severe and unusual headache with or without any associated alteration in consciousness.

• If subarachnoid haemorrhage is suspected:
  • CT brain scan: immediately if the patient has impaired consciousness and within 12 hours in all patients. If the CT scan is negative or equivocal, lumbar puncture should be undertaken 12 or more hours after onset. Spectrophotometry should be used to permit detection of small amounts of xanthochromia.
  • An MRI brain scan should not be used to diagnose subarachnoid haemorrhage.
• Once the diagnosis is confirmed:
  • Oral nimodipine 60 mg four-hourly is given, unless there are specific contraindications.
  • Anti-fibrinolytic agents (A) and steroids (D) should not be given.
  • All patients should be discussed with a neurosurgeon immediately.
  • Imaging of cerebral vessels should be undertaken at the neurosciences centre.
  • A ruptured aneurysm should be treated by endovascular or surgical obliteration as determined by the neurovascular team.
  • All patients should be monitored for the development of treatable complications, especially hydrocephalus, cerebral ischaemia, electrolyte imbalance and hypotension.

Surgical

• Surgical intervention should be considered in cases of supratentorial haemorrhage with mass effect or posterior fossa/cerebellar haematoma.
• Neurosurgical opinion should be sought for cases of secondary hydrocephalus.
• Carotid endarterectomy¹³
  • Any patient with a carotid artery territory stroke but without severe disability should be considered for carotid endarterectomy.
  • Carotid duplex ultrasound should be performed on all patients being considered for carotid endarterectomy and confirmed with magnetic resonance angiography or with a second ultrasound.
  • Carotid endarterectomy should be considered where carotid stenosis is measured at greater than 70% as measured using the European Carotid Surgery Trialists and 50% as measured using the North American Symptomatic Carotid Endarterectomy Trial Collaborators methods.
  • Carotid endarterectomy should be performed as soon as the patient is fit for surgery, preferably within 2 weeks of the cerebravascular event.
  • Carotid angioplasty or stenting is an alternative to surgery but should only be carried out in specialist centres.

• Patients who have suffered a stroke remain at an increased risk of a further stroke (between 30 and 43% risk within five years).¹ The risk of a further stroke is highest early after the stroke or TIA.¹³
• Patients with TIA and stroke also have an increased risk of myocardial infarction and other vascular events.
• By 6 months over half of stroke survivors will need some help with activities of daily living. 15% will have communication impairments and 53% motor weakness and many will have problems with mood or cognition.
• Other complications for the patient include: thromboembolism, pneumonia, depression, contractures, bladder and bowel problems (e.g. incontinence, constipation) and bed-sores.
• Morbidity within the carers is high. Stress, which is only partly relieved by respite admissions.

• Mortality: 20% at 1 month and then 5-10% per year thereafter.¹
• Full recovery 40%.¹
• Drowsiness suggests a poorer prognosis.

• See Stroke Prevention and Primary prevention of cardiovascular disease.

Quality and outcomes framework guidance: Stroke and TIA (February 2006):

• STROKE 1: The practice can produce a register of patients with stroke or TIA; 2 points.
• STROKE 11: The percentage of new patients with a stroke who have been referred for further investigation; 2 points; payment stages 40-80%.
• STROKE 5: The percentage of patients with TIA or stroke who have a record of blood pressure in the notes in the preceding 15 months; 2 points; payment stages 40-90%.
• STROKE 6: The percentage of patients with a history of TIA or stroke in whom the last blood pressure reading (measured in the previous 15 months) is 150/90 or less; 5 points; payment stages 40-70%.
• STROKE 7: The percentage of patients with TIA or stroke who have a record of total cholesterol in the last 15 months; 2 points; payment stages 40-90%.
• STROKE 8: The percentage of patients with TIA or stroke whose last measured total cholesterol (measured in the previous 15 months) is 5 mmol/l or less; 5 points; payment stages 40-60%.
• STROKE 12: The percentage of patients with a stroke shown to be non-haemorrhagic, or a history of TIA, who have a record that an anti-platelet agent (aspirin, clopidogrel, dipyridamole or a combination), or an anti-coagulant is being taken (unless a contraindication or side-effects are recorded); 4 points; payment stages 40-90%.
• STROKE 10: The percentage of patients with TIA or stroke who have had influenza immunisation in the preceding 1 September to 31 March; 2 points; payment stages 40-85%.