Stroke Management Guidelines

Publication: 03/09/2007  
Next review: 01/07/2022  
Clinical Guideline
ID: 1165 
Approved By: Trust Clinical Guidelines Group 
Copyright© Leeds Teaching Hospitals NHS Trust 2019  


This Clinical Guideline is intended for use by healthcare professionals within Leeds unless otherwise stated.
For healthcare professionals in other trusts, please ensure that you consult relevant local and national guidance.

Please check the patients allergy status, as they may be allergic to Chlorhexidine, and alternative ( Providine iodine) solution will be required.
Be aware: Chlorhexidine is considered an environmental allergen.
Refer to the asepsis guidance.

Stroke Management Guidelines

  1. Making a diagnosis of stroke
  2. Decision to admit
  3. Clinical assessment
  4. Pathology  
  5. TIA and Stroke mimics
  6. Investigations
  7. Acute phase management- BP, Temperature, Blood glucose
  8. Acute phase management – parenteral fluids
  9. Early neurological deterioration
  10. Intracerebral haemorrhage
  11. Antiplatelets in stroke and TIA
  12. Thrombolysis in acute ischaemic stroke
  13. Swallow assessment
  14. Decision to start enteral feeding
  15. Decision to insert Percutaneous Endoscopic Gastrostomy (PEG)
  16. Anticoagulation following stroke
  17. Hypertension management in secondary prevention of stroke
  18. Cholesterol and stroke
  19. Carotid Surgery
  20. Stroke in Pregnancy
  21. Venous thromboembolism prevention
  22. Secondary prevention - lifestyle
  23. Driving after TIA and stroke
  24. Epilepsy after stroke
  25. Pain after stroke
  26. Skin Care
  27. Rehabilitation
  28. Treatment of spasticity
  29. Risk of recurrence and prognosis
  30. Palliative care
  31. Stroke research at LTHT


Stroke is a very complex illness involving physical, psychological and social effects.  These guidelines should help you manage the common difficulties encountered on the inpatient stroke units.  If you would like to see a particular new area covered please contact Dr. Jon Cooper.

1. Making a diagnosis of stroke

  • The diagnosis of Stroke or transient ischaemic attack (TIA) is a clinical one and it is vital that a detailed history is obtained from the patient ± eyewitnesses. The term ‘Brain Attack’ has been suggested when the symptoms and signs have persisted beyond the first hour (the duration most likely to be a genuine TIA) but not yet to 24 hours (the definition of a completed stroke) and has become more relevant as patients are seen quicker and hyperacute cerebral reperfusion therapies are now available.
  • There are four key groups of patients who present with acute neurological symptoms
    •  Those with obvious stroke i.e. patient with vascular risk factors who has sudden onset (the symptoms are maximal at onset) of a focal neurological deficit (you are able to lateralise it to one cerebral hemisphere and localise it to within that hemisphere) with symptoms which last > 24 hours and there is no other apparent cause other than a vascular event (e.g. no trauma or seizure). The specificity of the clinical diagnosis of stroke in this instance is > 95% (B).
    • Patients who have obviously not had a stroke e.g. facial weakness in lower motor distribution with unilateral auditory hyperacusis etc typical of Bell’s palsy.
    • Patients with a ‘stroke mimic’, a disorder that looks like stroke or TIA, but is due to another underlying condition (see section 4)
    • Those with an atypical stroke presentation, mistaken for something else, sometimes called the ‘stroke chameleon’.  A number of categories exist including:
  • Neuropsychiatric type features may be present or confused for them e.g. in those with abulia, emotional lability, receptive dysphasia, mutism, delirium, amnesia, reduced consciousness.
  • Abnormal movements like alien hand, limb shaking TIA, seizures at onset, spasms and various involuntary movements
  • ‘Peripheral’ disorders like acute vestibular syndrome (negative head impulse test and vasculopathy are clues to vascular aetiology), occasional isolated cranial nerve palsies, isolated monoparesis etc.
  • Atypical isolated dysarthria, dysphagia, visual loss in Anton’s or Balint’s syndromes 

The clue to an underlying stroke diagnosis will be in the sudden onset (maximal at onset) of symptoms which can be lateralised (to one cerebral hemisphere – right or left) and localised (within that hemisphere e.g. speech and language centre) in a patient with vascular risk factors or appropriate context and with negative neurological features i.e. predominantly loss of function.

  • The role of brain imaging is primarily to determine the pathological type of stroke. However, in patients where a clear history is lacking (e.g. depressed level of consciousness, aphasia, dementia) and no other source of history is available or there are atypical features (e.g. fever, progressing neurological deficit, papilloedema), cranial imaging may be used to make the primary diagnosis. 
  •  A TIA diagnosis is made when you are sure that there has been complete resolution of focal neurological symptoms within 24 hours of onset. 90% of TIAs have fully recovered by 2 hours (B).  If you are assessing a patient within 24 hours of onset and they still have symptoms at that time, then they should be managed as a ‘brain attack’. 
  • The differential diagnosis of TIA is much wider than that of stroke and the specificity of the diagnosis may be as low as 60%. Symptoms are typically negative (i.e. loss of power, speech or sensation). Most TIIAs last less than one hour.
  • Symptoms such as loss of consciousness, isolated dizziness or vertigo are unlikely to be due to a TIA.
  • It is recommended that Emergency Department staff do the Recognition Of Stroke In Emergency Room (ROSIER) score in all cases to aid diagnosis.  It has a stroke diagnosis sensitivity 92% of and specificity of 86%.

Recognition of stroke – ROSIER Score

  • The Brain Attack Team (BAT) Specialist Nurse is available 24/7 and can be contacted on: 07786250793 or bleep 2621

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2. Decision to Admit


  • Stroke (or patients with persisting symptoms at the time of assessment if < 24 hours from onset) should be viewed as a medical emergency.
  • Whenever possible patients should be assessed by the BAT Nurse with a view to direct admission to the Hyperacute Stroke Unit (HASU) on ward 21, G-Floor at Leeds General Infirmary (LGI).  No patient should be admitted without prior discussion ± review by BAT or the Stroke Physician On Call (SPOC) or nominated Senior Decision Maker.
  • Stroke unit care has been shown to reduce death and disability by about 30%1,2.  The number needed to treat (NNT) to prevent 1 death is 33, and NNT to allow 1 patient to return home independently is 20 (A).
  • Exceptions to admit to stroke unit care would be the relatively few patients for whom an accurate diagnosis and treatment would make no difference at all or those who refuse admission to hospital or are indeed otherwise well and ambulatory. The latter group of patients will generally benefit from urgent referral to the rapid access outpatient clinics (C).
  • Some patients who have atypical-stroke-like presentation, who have in-hospital events (that are not eligible for cerebral reperfusion therapy) or who are admitted to St James Hospital, but where the clinical diagnosis of stroke remains, should be discussed with BAT as above


  • TIA patients should be managed according to the specific protocols available in Emergency Department (ED), Clinical Decisions Unit (CDU) and Acute Medical unit (AMU) at both LGI and SJUH (can be accessed from the LTHT website) and referred on to rapid access neurovascular outpatient clinics. It is not necessary to admit patients who have had a single TIA.
  • Patients with multiple (particularly crescendo) TIAs, or who are in atrial fibrillation (AF), should be seen on the high stroke risk pathway – see below (C).
  • Every patient should have an ABCD2 score calculated. ABCD2 provides a simple, risk stratification which allows identification of very high-risk patients with score 4, 5, 6 or 7, who must be treated as an emergency (B).  They should be assessed and treated within 24 hours as recommended in the National Institute for health and Clinical Excellence (NICE) guideline CG68.  In order to complete assessment and investigations, TIA patients with score of 4 or more should be admitted to CDU at the LGI and reviewed by the BAT
  • Assessment includes a thorough history and examination and investigations including bloods, ECG and carotid duplex if anterior territory symptoms.  The likely interventions are emergency surgery for high grade carotid stenosis and consideration of immediate anticoagulation if in AF. Up to 67% of TIA patients are in the high-risk group with score 4 or greater (C).

Risk Factor







SBP >= 140mmHg
DBP >= 90mmHg


Clinical Features of TIA

Unilateral weakness without speech impairment
Speech impairment without unilateral weakness





>= 60 minutes
10 – 59 minutes
0-9 minutes


Diabetes Mellitus






Total ABCD 2 score



The LTHT TIA pathway

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3. Clinical Assessment

  • A full history should be carried out on admission. Obtain an accurate history of events, corroborative features where possible, identify conventional risk factors. Identification of previous stroke, dates and disability is also critical
  • Where there are communication difficulties - consider picture communication aids  (further advice is available by the Stroke Association at:
  • A full examination, including neurological assessment, is essential. The Leeds Stroke Clerking Proforma gives prompts to ensure that a comprehensive general and neurological assessment is made including a detailed neurological examination and assessment of higher mental function and swallowing including the abbreviated mental test score (AMTS) and Glasgow Coma Scale (GCS).
  • At the end of the clinical assessment the doctor should attempt to answer the following questions:
    1. Is it a stroke?
    2. What is the likely pathological type of stroke?
    3. Which part of the brain is affected (including the vascular territory)?
    4. What is the likely cause of the stroke?
    5. What are the functional consequences of the stroke?

It is recognised that in Q(2), haemorrhage and infarction can only be distinguished reliably by early CT scanning and that Q(4) may be amended following the results of investigations.

Early communication with patients and their carers is crucial. We need timely information from them and they need to know what has happened and what tests are planned.  They also need to know about other issues e.g. driving. 

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4. Pathology

  • Brain imaging must be undertaken as soon as possible if a stroke is suspected and at most within 1 hour. This will allow pathological differentiation (infarct vs haemorrhage) in the majority of cases and will facilitate selection of patients for cerebral reperfusion therapies.
  • An unenhanced CT brain scan is the first line test as it is accessible, quick and well tolerated
  • Cerebral infarction

  • Cerebral haemorrhage


  • A number of stroke classification systems exist (for example the Oxford Stroke Classification [Total Anterior Circulation Infarct, Partial Anterior Circulation Infarct, Lacunar Infarction, Posterior Circulation Infarction]) and more information can be found at:
Amarenco et al Cerebrovasc Dis 2009;27:493-501 

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5. Stroke and TIA mimics

  • A stroke mimic is not a diagnosis but an umbrella term for a number of conditions that look like a stroke (for example with a sudden onset of focal neurology) but are immediately or eventually are found not to be a vascular cause. The detail is in the history, examination and the use of brain imaging such as Magnetic Resonance Imaging, with a particular sequence called Diffusion Weighted Imaging.
  • The incidence of stroke mimics referred to a stroke unit has increased over the last decade and a half from approximately 20% (Harbison et al 2003) to 40% (Dawson et al 2016)
  • Further information can be found at:

Anathhanam and Hassan, Clinical Medicine 2017

As an aid memoir common stroke mimics include:

Differential diagnosis and stroke mimics


Clues to diagnosis



History of seizure, LOC, previous stroke, witness account



LOC, low BP, arrhythmia



Fever, changes in level of consciousness



Stressors / triggers, no anatomical deficit, changing examination,



History of migraine / tendency, fortification spectra, headache

Brain tumour


Slow onset of symptoms, seizure at onset



Low sugars, change in level of consciousness, asterixis



Sensory pattern (glove / stocking), absent reflexes,

Peripheral vestibular disorder


Positional vertigo, head thrust +ve, fatigable nystagmus



Progressive cognitive declune

Subdural haematoma


Trauma, headache, fluctuating signs, on an OAC

Drugs and alcohol


Changes in level of consciousness, myoclonus, asterixis

Transient Global Amnesia


Isolated memory impairment with functional preservation




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6. Investigations

These are graded as LEVEL 1-3. In general, you should obtain and consider the results of one level before requesting further tests.

Routine tests (GP, junior and middle grade doctors, non-specialists, specialist doctors) 

All newly diagnosed or likely stroke patients should have the following investigations performed urgently on admission:

Laboratory blood tests:

  • Full blood count (FBC)
  • Erythrocyte Sedimentation Rate (ESR)
  • C-reactive protein (CRP)
  • International normalised ratio (INR) and activated partial thromboplastin time (aPTT or APTT)
  • Plasma glucose (on admission) and fasting plasma glucose
  • Urea and electrolytes (U&E), Creatinine
  • Liver function tests (LFT)
  • Glycated haemoglobin (HbA1c)
  • Random Cholesterol (at least total and LDL)

Other investigations:

  • 12 lead Electrocardiograph (ECG)
  • An unenhanced (i.e. non-contrast) CT brain scan (post iv-contrast test can be requested on top, in the clinical suspicion of brain tumours and abscesses)

 Stratification of above investigations

  • CT brain scan – this MUST be performed ‘urgently and at most within 1 hour of arrival at hospital’ (National Clinical Guideline for Stroke prepared by the Intercollegiate Stroke Working Party, Fifth Edition 2016) or symptom recognition if the patient is already an inpatient. Presentation within 6h from last seen well or known use of anticoagulants (this does not include antiplatelet use) should urge for brain imaging at the first available slot within the hour without further delays.

For patients within 6 hours of last seen well and only after the CT brain scan has been arranged, urgent advice from the Brain Attack Team (mobile: 077 8625 0793 or switchboard) or the  Stroke Physician on-call (switchboard) should be sought, to discuss whether the patient is suitable for a carotid and intracranial CT angiogram at the same time with the brain CT scan.

  • Glucose on admission (electronic portable blood glucose meter or blood gas samlple) is an urgent test to differentiate stroke patients from those who suffer from hypoglycaemia
  • FBC, INR and aPTT results should be sent as urgent in patients who present within 6 hours from last seen well and the results should be chased. For patients on anticoagulants INR and APTT are urgent even beyond the 6-hour window

Additional tests (imaging and cardiac investigations should be requested after consultation with the Brain Attack Team, Stroke Physician or other Healthcare Professionals with relevant stroke training and experience)
The following tests should be done in selected cases:

Laboratory blood tests

  • Thyroid function tests (TFT), in patients with Atrial Fibrillation
  • Re-feeding syndrome baseline electrolytes (PO4, Mg, Adj Ca) in admitted patients who either fail their swallow assessment on admission
  • Urine dip or protein/creatinine ratio for the assessment of proteinuria (in patients with hypertension and/or diabetes)
  • Troponin I - if possible acute coronary syndrome
  • Drug screen – where relevant history or clinical suspicion (e.g. young patient with non-traumatic intracerebral haemorrhage, or young patients with acute ischemic stroke and absence of known cardiovascular risk factors).


  • Carotid duplex

All patients with anterior circulation TIAs or mild ischaemic strokes (including transient monocular blindness) with no significant disability, who might benefit from carotid endarterectomy should have carotid duplex ultrasound assessment. Patients unsuitable for carotid duplex scanning include those who are unwilling to consider carotid surgery or who are unfit for surgery due to severe co morbidity, residual disability, frailty or severe dementia.

  • Carotid and intracranial CT angiography

In patients with an anterior circulation acute ischemic stroke within 6 hours from last seen well this can potentially be an urgent test as hyperacute stroke treatment (iv-thrombolysis and ia-thrombectomy) can prevent significant disability or even reduce mortality. Data about the effectiveness of IA-MT posterior circulation are scarce but the treatment can be considered even in extended time windows up to 24 hours. In the acute phase, please seek urgent specialist’s advice.

  • Departmental chest x-ray (CXR) if history of smoking or cardio-respiratory condition.


  • Prolonged arrhythmia monitoring - if palpitations and/or paroxysmal AF (pAF) a possibility e.g. in large artery stroke (especially if has been bilateral/multiple territories) with no other aetiology. Longer monitoring periods for 7 days may be required if suspicion of pAF remains high or if there are recurrent events.  We also have an AF detector which can be accessed by contacting Liz Roberts, one of the stroke specialist nurses.
  • Trans-thoracic echocardiography (TTE), in ischemic strokes that are non-lacunar in brain imaging and with indications like the ones below: 
    • age<55
    • no evidence of large artery disease and no evidence of atrial fibrillation in at least 3 days of prolonged arrhythmia monitoring
    • evidence of multiple infarctions in different vascular territories and no evidence of atrial fibrillation in at least 3 days of prolonged arrhythmia monitoring
    • significant cardiac history
    • clinical suspicion of endocarditis (as the first line rapid assessment before a trans- oesophageal test)
    • Prosthetic valves

Requests should only be made after discussion with senior medical staff to avoid unnecessary investigations.
Advanced tests (Advise request only after consultation by a Stroke Physician or other Healthcare Professional with stroke training and experience) 

Perform only if no clear aetiological explanation and after results of other tests have been obtained. Please note that the vast majority of stroke patients will not need any of the investigations below and that there is variable evidence for many of these tests based on the type of stroke.

Laboratory blood tests

  • Vasculitis screen- antinuclear antibody (ANA), anti-neutrophil cytoplasmic antibody (ANCA), Immunoglobulins, complement, extractable nuclear antigen (ENA) screen, cold agglutinins
  • Lupus anticoagulant, anti-phospholipid syndrome antibodies (anti-cardiolipin and anti β2-GPI), homocysteine levels
  • Thrombophilia screen – anti-thrombin III, Protein C, Protein S, Activated Protein C Resistance (APCR) and factor V Leiden
  • Flow cytometry for CD55 and CD59 (PNH testing) if evidence of haemolysis
  • Trans-oesophageal echocardiogram (TOE)


  • Bubble contrast echocardiogram- to detect PFO.
  • Trans-oesophageal echocardiogram (TOE)


  • Trans-cranial Doppler (TCD) sonography
  • MRI and MRA (magnetic resonance imaging and angiography)
  • MR with susceptibility weighted imaging (SWI) for old bleeding events (often indicates underlying cerebral amyloid angiopathy)
  • Intra-arterial cerebral arteriography 
  • CT Chest-abdomen-pelvis to exclude solid organ neoplastic disease along with proper clinical assessment for evidence of malignancy that will need different investigations (e.g. melanoma) 

Investigations are graded as routine and advanced and are available on Order Comms / ICE under adult service Neuro (including CVA)


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7. Acute phase monitoring

Blood pressure (BP), Temperature, Blood Glucose, Oxygen

There is evidence that poor outcome in acute stroke is associated with low or very high BP, high temperature, hypoxia and high blood glucose. Active monitoring and management should be the norm. (B)

  • Low BP may indicate acute myocardial infarction, hypovolaemia, sepsis or other severe illness and should be investigated and managed in line with established practice.
  • BP has a U-shaped relationship with acute stroke outcome; there is a worse outlook for low and high levels. 
  • High BP is present in up to 80% of patients acutely and the normal mechanisms for regulating cerebral blood flow are adversely affected. There is at least theoretical evidence that reducing the BP in acute stroke may reduce cerebral blood flow in critically ischaemic brain tissue. As a great deal of uncertainty exists about optimal management, it is wise to avoid initiating new treatment in the first week of stroke except in cases of intracranial haemorrhage, hypertensive encephalopathy, dissecting aortic aneurysm, acute heart failure and unstable angina/myocardial ischaemia or when thrombolysis is being considered. 
  • Before thrombolysis, If BP >180/110 on 2 readings 5-10 minutes apart, and no evident cause e.g. pain from urinary retention etc, then initiate treatment (as below) treat acutely.
  • Following and acute ICH (if presents in the first 6 hours) if SBP > 150mmHg then treat to target of 130-140mmHg as long as possible for the first 24-hours – unless:
    • GCS <5
    • Massive haematoma and death is imminent
    • Structural cause for ICH is identified
    • Immediate neurosurgical intervention is being considered

Management of hypertension during the acute phase of stroke guidelines (which includes the choice of drugs and alternatives) can be found at:


  • Pyrexia may indicate aspiration pneumonia or other sepsis, which should be treated with appropriate antibiotics after cultures have been taken according to Trust guidelines. If temperature >37.5ºC, also give oral or rectal Paracetamol.

Diabetes and hyperglycaemia

  • Hyperglycaemia could indicate previously undiagnosed diabetes mellitus or, in severe stroke, a physiological stress reaction. NICE CG68 recommends keeping blood glucose between 4 and 11 mmol/l in the acute phase.  Great care must be taken to avoid hypoglycaemia as many stroke patients would not be able to alert staff to hypo symptoms (C). 
  • See Trust guideline on hypoglycaemia:
  • 4-6 hourly capillary blood glucose (CBG) monitoring of all patients presenting with stroke and diabetes or newly recognised hyperglycaemia.
  • All TIA and Stroke patients with Type 1 Diabetes must have optimal insulin therapy.  This should be provided by either subcutaneous insulin or intravenous insulin and glucose.  If the latter is given, it must be as per the Trust IV insulin protocol
  • Refer patient to diabetes inpatient specialist nurse (DISN)/diabetes inpatient team (DIT) at earliest opportunity for individual assessment.
  • Patients with type 1 diabetes should continue their basal insulin at all times – whether receiving insulin via the subcutaneous or intravenous route – and should not have insulin omitted.
  • Continue subcutaneous basal analogue insulin (Glargine or Detemir) if patient treated with basal analogue insulin on admission.
  • Target CBG 6-12 mmol/l during enteral feeding of people with diabetes.
  • Early involvement of a dietitian to determine an appropriate feed regimen. Referral to the dietitian should be done on the following form as soon as the route of feeding is established.
  • If feed stopped for longer than 2 hours and insulin has been administered, risk of hypoglycaemia is high. Consider commencing IV 10% glucose to avoid hypoglycaemia. In people with T1DM not receiving basal insulin a VRIII should be commenced if feed turned off for greater than 2 hours. In this situation it is safest to feed over 24 hours.
  • Aim to minimise use of variable rate intravenous insulin infusions (VRIII) as far as possible – aim to establish patient on to subcutaneous insulin or glucose-lowering agents administered via the nasogastric tube (NGT) at the earliest opportunity.
  • Premixed human insulin at start and midpoint of feed, or isophane insulin at start and, if necessary, the midpoint of feed are recommended first line options for glycaemic management of patients with poorly controlled type 2 diabetes during enteral feeding.
  • Administration of soluble human insulin at the time of feed commencement is recommended for a bolus feeding regimen. For those patients prescribed Glargine or Detemir on admission to hospital and receiving continuous feeding with CBG>12 mmol/l, soluble human insulin may be administered at the start and, if necessary, midpoint of the feed.

Seek advice from pharmacy on an individual basis for administration of metformin down enteral tubes (the immediate release tablets can be crushed or dispersed in water).  There is an expensive unlicensed liquid and obviously m/r tablets cannot be crushed.
Monitor capillary glucose pre-feed and then 4-6 hourly when feed running; monitor hourly if feed unexpectedly switched off.
Involve Diabetes specialist nurses immediately in event of hypoglycaemia or recurrent hyperglycaemia (Urgent bleep: 80 6293).
Up to a quarter of acute stroke patients have undiagnosed diabetes and another quarter impaired glucose tolerance (IGT) 2(B).


  • All patients should have pulse oximetry measured at the time of initial assessment. If oxygen saturation <95% give oxygen as appropriate for severity and clinical situation (see Trust guidelines
  • Use oxygen prescription chart
  • The routine use of supplemental oxygen  is not recommended in those who are not hypoxaemic
  • Position upright at 30o on left or right and suction if required.  These measures may improve hypoxia but the underlying cause should be investigated and treated specifically. Full examination and investigation for common causes should rapidly take place. Respiratory failure should be managed according to established guidelines.
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8. Parenteral Fluids

All stroke patients should have a swallowing assessment on admission by any member of the team who has received dysphagia training.   Those patients unable to swallow safely should have parenteral fluids.  The type of fluid and amount will depend on the clinical state of hydration, U&E results, presence of sepsis, congestive cardiac failure (CCF), pyrexia or insensible losses e.g. diarrhoea.  Usually 0.9% sodium chloride is best and a rate of 1L in 12 hours is reasonable for many situations.  Subcutaneous fluids are a reasonable alternative if only a maximum of 1.5 L per day is required and the IV route is not possible (D).

Careful monitoring of urea and electrolytes (U & E), glucose, urine output and vital signs is essential.    Dehydration can worsen ischaemic brain injury by increasing viscosity and lowering blood pressure.   Hypernatraemia in stroke is usually caused by dehydration, possibly compounded by untreated diabetes.  Hyponatraemia after stroke may be due to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), drug side effects, or inappropriate fluid management and is usually transient. 

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9. Early Neurological deterioration (END)

Patients can worsen in the first few hours as the initial brain pathology progresses, but subsequent neurological deterioration should be carefully assessed. Up to 40% of hospital admitted patients deteriorate neurologically in the first day or two. Various definitions exist but 2 point rise in NIHSS or 2 point fall in GCS

There are a large number of causes, neurological and non-neurological, many of which are reversible:


  • Progression/completion of stroke.  In particular watc out for reducing coma score in those with cerebellar disease (large artery infarction or haemorrhage).  Progressive basilar thrombosis can be very successfully treated by intra-arterial thrombolysis or clot retrieval for instance several hours after onset.
  • Early recurrent event
  • Haemorrhagic transformation of infarct (occurs in 15-45%)
  • Cerebral oedema

There is no treatment proven to be effective, though raising the head of the bed to >30o is recommended.  In addition, mannitol may be used to stabilise a patient for a short period of time prior to definitive treatment such as hemicraniectomy.  The dose is 1g / kg as a 20% solution given by rapid IV infusion. A maximum of 2 infusions may be given.  Ensure the patient is catheterised.  In patients aged up to 60, hemicraniectomy has been shown to improve survival and outcome after malignant MCA occlusion. NICE guidelines can be found at:

  • Obstructive hydrocephalus
  • Epilepsy
  • Incorrect diagnosis e.g. tumour, abscess, subdural, encephalitis


  • Sepsis
  • Metabolic - Electrolyte disturbance, hypoglycaemia, dehydration
  • Adverse drug reaction
  • Hypoxaemia – pneumonia, PE, heart failure, bronchospasm
  • Hypercapnoea
  • Myocardial infarction

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10. Intracerebral Haemorrhage (ICH)

  • ICH accounts for about 15% of strokes and can only be diagnosed reliably with CT brain imaging.
  • Broadly, the aetiologies of ICH include:  Hypertension, cerebral amyloid angiopathy, tumours, AVMs, aneurysms and oral anticoagulants.
  • Location: subcortical (ganglionic)>lobar>cerebellar> pons
  • Haematoma expansion is the commonest cause of END and is most frequent within 4 hours but can occur upto 24 hours after the bleed.
  • The acute management of ICH is very similar to that for acute ischaemic stroke except fibrinolysis and antiplatelet agents are not given.  Blood pressure management and OAC reversal aim to reduce haematoma expansion
  • Other causes of END in ICH include peri haematoma oedema and obstructive hydrocephalus., seizures, hypoxaemia, dehydration, hyperglycaemia, fever) C).
  • ICH in a patient on anticoagulants must be discussed immediately with the Haematology Specialty Registrar and as soon as possible with the consultant in charge.   The anticoagulation should be completely reversed, although there is a risk of precipitating thrombosis in predisposed individuals.  This needs to be decided after weighing up the individualised risks and benefits of reversal as no RCTs exist (C).  It is crucial to explain the situation and options carefully to the patient and carer.
  • Reversal of anticoagulation with warfarin in patients with major bleeding requires administration of a PCC (B), and administration of intravenous rather than oral vitamin K (B). The management guidelines for anticoagulation reversal for warfarin can be found at:
  • Reversal of anticoagulation with Direct Oral Anticoagulants (DOACs) with major bleeding should be discussed with the Haematology Specialty Registrar on call
  • Patients on warfarin because of metal valve replacement should be discussed with the responsible Consultant immediately.  Liaison with cardiology and / or cardiac surgery is needed.  Reversal with PCC, as above, is generally needed but then the timing of re-anticoagulation needs individual discussion based on numerous factors including valve type and location, neurological progress etc
  • Proven DVT or PE in a patient with PICH must be discussed immediately with the consultant in charge.  The options include anticoagulation or a vena cava filter if active treatment is contemplated.  The decision will hinge on type of bleed, time from the event and estimated likelihood of recurrence.  There are no proper RCTs of the use of caval filters without anticoagulation (D).
  • Neurosurgical evacuation of most supratentorial ICHs is not effective.  However, there may be exceptions e.g. in patients with superficial bleeding who deteriorate neurologically or the development of obstructive hydrocephalus(A) 4.
  • Some patients with posterior fossa ICH benefit from clot evacuation and/or ventricular shunting.  All of these patients should be discussed with the Neurosurgeons as well as patients whose level of consciousness is deteriorating (B). 

ICH prognostic score

Hemphill et al Stroke. 2001 Apr;32(4):891-7.














>= 80











ICH volume

>= 30mL





Intraventricular blood






ICH Score


0-6 points


ICH Score

30-day mortality (%)















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11: Antiplatelets in Stroke and TIA

  • Patients with acute ischaemic stroke should be given aspirin 300mg as soon as possible within 24 hours (unless contraindicated):
      • orally if they are not dysphagia
      • PR (600mg) or NG (300mg) if they have dysphagia
    • Thereafter aspirin 300 mg daily should be continued for 2 weeks after the onset of stroke at which time long-term antithrombotic treatment should be initiated. Patients being transferred to care at home before 2 weeks should be started on long-term treatment earlier.
    • Patients with acute ischaemic stroke reporting previous dyspepsia with an antiplatelet agent should be given a proton pump inhibitor in addition to aspirin.
    • Patients with acute ischaemic stroke who are allergic to or intolerant of aspirin should be given an alternative antiplatelet agent (e.g. clopidogrel).
  • Patients with a definite or a suspected TIA
    • Should be prescribed Aspirin 300 mg once a day (or Clopidogrel 75mg, if allergic to Aspirin) until review in the TIA Service unless there are known contraindications.  Longer term they should be treated with the secondary prevention planned in the TIA Service
    • There is further recommendation (2018) that patients who have suffered a definite TIA OR who have suffered a minor ischaemic stroke (with an NIHSS score of 3 or less and no persistent disabling neurological deficit) should be given dual antiplatelet therapy with aspirin (75g) and clopidogrel (75mg) for a duration of 10-21 days (TIA) OR 22-90 days (minor stroke) followed by a single antiplatelet drug indefinitely if in sinus rhythm. This will be planned after review in the TIA Service OR the Stroke Unit

Secondary prevention antiplatelet drugs

  • In patients with Stroke or TIA, NICE guidelines for long term secondary prevention following stroke for patients in sinus rhythm  , clopidogrel 75mg once daily is recommended.
  • For people who have a contraindication or intolerance to clopidogrel, modified-release dipyridamole plus aspirin is recommended as a treatment option. For people who have a contraindication or intolerance to both clopidogrel and aspirin, modified-release dipyridamole alone is recommended as a treatment option.
  • Treatment with clopidogrel to prevent occlusive vascular events should be started with the least costly licensed preparation i.e. generic, NOT the branded form, Plavix.
  • It is worth noting that clopidogrel needs to be converted to an active metabolite and this enzymatic conversion is inhibited by some other commonly used drugs e.g. omeprazole, esomeprazole (but not other PPIs) and some SSRIs e.g. fluoxetine.  Conflicting evidence currently exists regarding whether this has a clinical effect and in whom, but there is sufficient concern that the FDA and EMEA both recommend against co-prescription and where there is a suitable alternative (e.g. using lansoprazole rather than omeprazole) 

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12. Thrombolysis in Acute Ischaemic Stroke

  • Thrombolysis with Alteplase (r-tPA) within 4.5 hours of symptom onset is recommended within its marketing authorisation if it is started as early as possible within 4.5 hours of onset of stroke symptoms.

  • Patients need to be assessed carefully for contraindications to Alteplase and also stroke severity using the National Institutes of Health Stroke Scale (NIHSS, range 0-42).  Training in NIHSS can be found at:

    Cerebral haemorrhage has to be excluded by CT scan and patients must be screened for a range of contraindications 1,2 (A).



        • Sustained hypertension n >180/110 
        • Symptoms suggestive of SAH
        • Previous ICH
        • ST elevation within the previous 3 months
        • Major head injury / trauma or stroke within 3 months
        • Major surgery within the last 14 days
        • Gastrointestinal haemorrhage within 21 days
        • Arterial puncture at a non compressible site within 7 days
        • Active bleeding or traumatic fracture on assessment
        • Seizure at onset with suspected post ictal features
        • Minor or rapidly improving symptoms
        • Active malignancy with poor prognosis
    • Radiological

      • CT brain confirming haemorrhage
      • Evolving or hypodensity suggestive of index ischaemic stroke


      • Oral anticoagulation INR >1.7
      • Heparin administration within 48 hours
      • Platelet count <100,000
      • Blood glucose <2.7 mmol/l


      • Very severe deficit at onset (NIHSS>25)
      • Poor premorbid status including severe disability
  • Trials show an increase in early mortality from intracerebral haemorrhage, although total mortality at 3 months is unchanged.  A greater proportion of patients survive with less disability.
    1:3 improved chance of benefit
    1:10 chance of good functional recovery over no treatment
    1:50 chance of significant intracranial bleed
  • Aspirin should not be given acutely if thrombolysis is being considered but delayed for 24 hours until after a second CT head has ruled out secondary haemorrhage (A).
  • The drug is given at a dose of 0.9mg/kg with 10% of the dose given as a bolus and the rest as an infusion over 1 hour.  Accurate body weight should be obtained.
  • Very close monitoring is required in the first 24 hours after the drug is given using a specific proforma (see LTHT thrombolysis guideline, appendix 4) and patients should only be admitted onto the hyperacute stroke unit on ward L21 at Leeds General Infirmary.

If you identify anyone potentially suitable for thrombolysis please contact the Brain Attack Team (BAT) immediately on 07786250793.  The Consultant Stroke Physician On Call is also available 24/7 and will be able to advise, contactable via switch board.

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13. swallowing assessment

  • Swallowing difficulties called dysphagia often occur as a result of an acute stroke.  Dysphagia may occur in up to 65% of stroke patients.  If not identified and managed, it can lead to pneumonia, poor nutrition and increased disability.  All patients admitted on the stroke pathway should have their swallow screened by an appropriately trained healthcare professional, usually a BAT Nurse, before being given any oral intake including medication.
  • The algorithm for swallow screening is outlined below, including the signs and symptoms of dysphagia.  This screen should only be completed if a patient is able to sustain an appropriate level of alertness, maintain an upright position within the chair/bed and have a clear voice quality (not wet/gurgly).
  • If the patient fails the swallow screen, on admission, they should remain NBM pending referral to SLT for a comprehensive swallow assessment.  This often involves repeated assessments, a graded approach to commencement of oral intake and on occasions instrumental assessments including videofluoroscopy or FEES.
  • If the patient fails the swallow screen and it is medically appropriate, enteral/NGT feeding should be considered and initiated within 24 hours of admission.  Once a feeding route is established please refer to dietetics for an individual feed regimen.   Please consider prescription of mouth care products such as artificial saliva, biotene gel and yellow paraffin (for lips) in any patient who is NBM.
  • Swallow screens should not be repeated unless there has been significant clinical improvement and repeat screens are always at the discretion of the stroke consultant.
  • Always seek advice from pharmacy when considering administration of medication in patients who are NBM.

Algorithm for swallowing assessment

Teaspoon 1:
No attempt to swallow
Water leaks from lips
Multiple swallows

Teaspoon 2:
No attempt to swallow
Water leaks from lips
Multiple swallows

Teaspoon 3:
No attempt to swallow
Water leaks from lips
Multiple swallows

½ glass of water (100mls):
No attempt to swallow
Water leaks from lips
Multiple swallows

No symptoms of dysphagia:
Proceed to teaspoon 2

No symptoms of dysphagia:
Proceed to teaspoon 3

No symptoms of dysphagia:
Proceed to ½ glass of water

No symptoms of dysphagia:
Commence Normal Fluids

If facial weakness is present commence on Cat C Puree Diet and refer to SLT.

If no facial weakness commence on Normal Diet but ensure observation of initial meal.

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14.  Decision to start enteral feeding

  • Up to half of stroke patients develop dysphagia.  Most survivors recover safe swallowing within three weeks.  Dysphagia is associated with aspiration pneumonia and malnutrition.
  • If the swallow is unsafe within 24 hours fine bore nasogastric (NG) feeding should be considered.  Decisions should involve patients, and where this is not possible, their family and carers.
  • Misplacement of NGTs has now been declared a ‘never event’ by the National patient safety agency (NPSA).  The Trust NGT guideline should be followed in all cases and only fully trained staff should use them. These can be found at:

Initial placement must be checked by either aspirating secretions with pH <5 or doing a CXR and checking carefully that it is in the stomach.  The commonest reason for misplacement in the lungs is misreading the CXR.  All staff who are ever asked to check NGT position MUST undertake mandatory training in NGT placement.
Please refer to ward dietitian once a decision has been made to place an NG tube: http://lthweb/sites/nutrition-and-dietetics/dietetic-referral

If out of hours (Friday after 16.00 - Monday after 09.00) please commence the LTHT ICP Adult Out of Hours Enteral Tube Feeding available at:

This ICP requires clinical assessment and management of the patients risk of refeeding syndrome following the further trust guideline at: 
Guidelines for the prevention of aspiration in adults is available at:

Any patient who is nil by mouth needs artificial saliva and chlorhexidine mouthwash regularly (C).

Patients’ previous medication should be reviewed.  Any medication which cannot safely be stopped must be given by feeding tube or parenterally (see below). 
If a patient is unable to tolerate a NGT consider:

A. using mittens. The Trust guideline is at:  


B. a nasal loop device (or bridle). The Trust guideline is at:
Patients receiving NG feeding in whom a prolonged period of enteral feeding is anticipated or who do not tolerate and NGT with mittens or bridle should be considered for percutaneous endoscopic gastrostomy (PEG) feeding.  Early PEG feeding within the first two weeks is not indicated unless NG feeding proves impossible, as it is associated with slightly worse outcomes (FOOD trial) (A).

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15. Decision to insert Percutaneous Endoscopic Gastrostomy (PEG)

  • PEG is a safe and effective method of providing long term enteral nutrition or an alternative route if NGT is not tolerated.  PEG has increased risk compared to NG tubes, with 1-2% mortality and 5-15 % morbidity (mainly infection and bleeding).
  • Studies have shown the superiority of PEG over NG feeding in nutritional terms, although the effect on final outcome is not marked.  The FOOD trial showed that early PEG feeding was associated with worse outcome 1.  PEG feeding should be considered when the patient has a prospect of longer-term survival and:
    • enteral feeding is likely to be required for several weeks
    • or the NG tube is causing distress
    • or the NG tube falls out repeatedly or is difficult to replace, once mittens and/or a nasal bridle have been attempted if appropriate.
  • Absolute contra-indications to PEG feeding include:
    • severe oesophageal or stomach pathology or surgery that would make the procedure technically impossible.
    • bleeding diathesis (INR> 1.3, platelets <50)
    • portal hypertension and/or ascites
    • bowel ileus or obstruction
    • morbid obesity
    • severe decompensated cardio-respiratory disease
  • If a PEG is being considered, referral should be made to the Endoscopy department. 

Further information can be found in the trust Enteral Tube Feeding Policy:

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16: Oral Anticoagulants (OAC) following Stroke

Indications for anticoagulation
Indications for which anticoagulation should be considered following stroke/TIA are as follows:

Indication related to stroke

Decision maker

AF (Paroxysmal/Permanent and Atrial Flutter)-

Non-specialist decision maker

Anterior transmural MI/LV Thrombus

Senior clinical decision made on a case by case basis

Arterial dissection

Senior clinical decision made on a case by case basis


Senior clinical decision made on a case by case basis

Atrial septal aneurysm with PFO

Senior clinical decision made on a case by case basis

Atrial Fibrillation - decision whether to anticoagulate a patient

  • Patients with atrial fibrillation (AF) and ischaemic stroke are at high risk of recurrent stroke.  They should be considered for long term anticoagulation with a DOAC (direct oral anticoagulant) or warfarin (suggested INR 2.5, range 2-3). 
  • This gives the greatest protection from further ischaemic strokes compared to standard treatment with antiplatelets (reduces the risk of recurrent stroke in clinical trials by approximately 2/3).
  • This decision needs careful thought and good communication with the patient or proxy decision maker and should usually be led by the patients treating consultant. 
  • In each case a carefully individualised assessment and communication of risk/benefit is essential. 

The following validated tools are available to assist in decision making:

Other situations which require careful consideration and senior discussion regarding whether or not to anticoagulate a patient are:

  • Recent active peptic ulcer
  • Recurrent falls (If cause now addressed may not be relevant but if ongoing or significant injuries sustained)
  • Extreme frailty or high MRS
  • Dementia
  • Proliferative retinopathy
  • Poor compliance with medication previously (Consider compliance aids - liase with pharmacist)
  • Accelerated Hypertension
  • Alcoholism

Choice of Agent

DOAC (formerly referred to as NOAC)
Usually the first line choice for non-valvular atrial fibrillation, DOACs have been shown to be as effective as warfarin in stroke prevention, whilst having a similar risk profile. They are specifically recommended over warfarin in the following circumstances:

  • Lifestyle issues which make INR monitoring difficult
  • ADR from warfarin
  • Wide fluctuations in INR (e.g. time in therapeutic window <65%)
  • Patients who frequently require drugs which interact with warfarin
  • Poor compliance, though this needs careful thought as the NOACs have shorter half-lives so beneficial anticoagulant effect wears off quicker. It is therefore crucial to emphasise strict adherence.

The DOACs include factor Factor Xa antagonists (e.g. rivaroxaban, apixaban, edoxaban - the major drawback to these drugs is a lack of a clinically proven antidote) and direct thrombin inhibitors (DTIs e.g. dabigatran). Please see the following for general information on the various choices:

Some patients may not be able to take a DOAC (often due to significant CKD, patient preference, allergy, other dual indication for which DOAC is not licensed).

Patient information to aid decision making can be found here:

Antiplatelets AND anticoagulation
It is usually suggested that an antiplatelet is discontinued on commencing anticoagulation. Antiplatelet agents and Anticoagulants should only be given together in exceptional circumstances, such as with certain cardiac conditions, as bleeding complications are excessively high. ALWAYS confirm the indication for this.

When/How to commence anticoagulation after stroke/TIA

Anticoagulation should not generally be used in the acute phase after large vessel ischaemic stroke (e.g. greater than 1/3 of an areterial territory involvement), even in patients with atrial fibrillation, because of the risk of haemorrhagic transformation.   Intracerebral haemorrhage must be excluded with a CT scan in every case.  The decision to anticoagulate a patient should be made by the treating consultant. General consensus and European Cardiology Society guidelines (image form these) suggest the following approach:

Guidelines available at:

For specific advice on initiation of your chosen agent or any bleeding or complications please refer to the leeds anticoagulant guidelines at

Follow up

All patients on an oral anticoagulant (particularly the frail and elderly) should have an annual review of stroke vs bleeding risk and need for treatment.

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17. Hypertension management in Secondary Prevention of Stroke

  • Epidemiological studies have demonstrated a linear relationship between arterial blood pressure and incidence of stroke - for each 7 mmHg rise in usual diastolic BP, the risk of stroke doubles. There is robust evidence from primary prevention trials that treatment of hypertension lowers the risk of a first stroke.
  • Other evidence suggests that this relationship with BP also holds true for the recurrence of stroke or TIA after an index event. There are now secondary prevention trials, which have demonstrated the benefit of BP lowering in this group.
  • There remain no definitive data to guide decisions regarding the optimum time period for starting antihypertensive therapy after stroke to achieve optimal BP figure in acute ischaemic stroke. BP should be lowered rapidly in patients with ICH
  • Optimal BP control is considered to be systolic < 130 and diastolic < 80 mmHg. However, recent studies have shown further risk reduction can be achieved by lowering BP even in patients with “normal” BP. It is often worth considering a 24 hour BP recording especially where casual readings vary, there may be a white coat effect, or if there are features of postural hypotension.
  • Where possible, recommend treatment with drugs taken only once a day
  • In patients aged < 55, ACE inhibitors or angiotensin 2 receptor blockers (ARBs) are first line. Amlodipine, a calcium channel blocker (CCB) would be the usual first line agent in those aged over 55 and in Afro-Caribbean people, unless other compelling indications exist. If side effects or evidence of heart failure, use of a diuretic -chlorthalidone (12.5 - 25.0 mg once daily) or indapamide (1.5 mg modified-release or 2.5 mg once daily) in preference to a conventional thiazide diuretic such as bendroflumethiazide or hydrochlorothiazide.
  • Usually, 2 or more agents are needed to achieve adequate control. Second line is alternative i.e. CCB if thiazide first used of vice versa. ACE inhibitors are an equally good alternative second line. For treatment of resistant hypertension after three drugs have already been prescribed - consider further diuretic therapy with low-dose spironolactone (25 mg once daily) if the blood potassium level is 4.5 mmol/l or lower. Use particular caution in people with a reduced estimated glomerular filtration (eGFR) rate because they have an increased risk of hyperkalaemia. Consider higher-dose thiazide-like diuretic treatment if the blood potassium level is higher than 4.5 mmol/l. Refer to NICE clinical guideline 127 for more detailed information.
  • It has also been shown the importance of 24 hour control and this is better achieved with calcium channel blockers or diuretics.
  • Other medication may be used tailored to other pathologies e.g. beta blocker in those with IHD/CCF, alpha blocker in benign prostatism and ACE inhibitor in diabetes

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18. Cholesterol and Ischaemic Stroke

High cholesterol is a less significant risk factor for stroke than for ischaemic heart disease in epidemiological studies.
The role of cholesterol lowering with statins in stroke disease has now been clarified by the HPS. Statins reduce further vascular events by 25%, the NNT to prevent one vascular event is 18 over 5 years.

If measured in the first 48-72 hours, the cholesterol value is likely to be accurate.  After that time, the acute phase response suppresses cholesterol levels and level should be checked 3 months or so later to obtain a representative value. 
A fasting sample is not needed but check full lipid profile, at least before starting treatment.

Common causes of secondary hyperlipidemia:

  • hypothyroidism
  • nephrotic syndrome
  • excessive alcohol
  • uncontrolled diabetes
  • liver disease and
  • nephrotic syndrome

Appropriate investigations should be considered on an individual basis.

Patients who need referral to a specialist clinic are those with:

  • Total cholesterol >7.5 mmol/litre and family history of premature coronary heart disease. [Think of familial hypercholesterolaemia (NICE guideline CG71)]
  • Total cholesterol concentration >9.0 mmol/litre or non-HDL cholesterol >7.5 mmol/litre even in the absence of a first-degree family history of premature coronary heart disease

Acute Ischemic Stroke/TIA

5. Statins

  • Unless statins are contra-indicated, atorvastatin 20-80mg od should be prescribed in all patients.
  • In the presence of risk factors associated with statin intolerance starting with atorvastatin 20mg od and gradually up-titrating the dose is suggested. Risk factors associated with statin intolerance include:
    1. advanced age (>70 years)
    2. female sex
    3. history of creatine kinase elevation or family history of muscle disorders
    4. vitamin D deficiency
    5. renal and hepatic impairment
    6. untreated hypothyroidism
    7. disorders of calcium homeostasis
    8. alcohol abuse
    9. Asian ethnicity
    10. low body mass index
    11. genetic polymorphisms (e.g., genes associated with drug and muscle metabolism)
    12. surgery with severe metabolic demands
    13. heavy and/or unaccustomed exercise and interactions with concomitant medication
    • When facing statin intolerance, check for hypothyroidism, vitamin D deficiency, renal disease, and excessive physical activity.
    • In case of known statin intolerance to at least two different statins, consider starting rosuvastatin at a dose of 5mg od when the patient has recovered from all his previous intolerance symptoms.
    • Aim of statin treatment is >40% reduction in non-HDL cholesterol.
    • Over the age of 80, patients should be assessed individually on their ability to benefit from statin treatment. Unless someone has a life expectancy exceeding 2 years, they are unlikely to benefit.
    • PCSK9 inhibitors are expensive, only recently approved monoclonal antibodies for patients with hyperlipidaemia or hypercholesterolaemia that meet very specific criteria.
    • Ideally stroke patients from the LTHT catchment area, with any of the following
      1. Primary heterozygous-familial hypercholesterolaemia and LDL persistently >3.5 mmol/litre
      2. Primary non-familial hypercholesterolaemia with recurrent cardiovascular events or polyvascular disease and LDL persistently >3.5 mmol/litre
      3. Mixed dyslipidaemia with recurrent cardiovascular events or polyvascular disease and LDL persistently >3.5 mmol/litre
      4. Primary non-familial hypercholesterolaemia or mixed dyslipidaemia and LDL persistently >4.0 mmol/litre despite maximal tolerated lipid-lowering therapy.
    • Ezetimibe should be used only in people who also have familial hypercholesterolaemia.
    • For secondary stroke/TIA prevention, patients should not be prescribed fibrates, bile acid sequestrants, nicotinic acid or omega-3 fatty acid compounds.
    • RCP Guidelines on Stroke 2016: ‘People with primary intracerebral haemorrhage should avoid statin treatment unless it is required for other indications.’
    • There is no evidence from randomised controlled trials looking specifically at the question of statin treatment post ICH. Data from meta-analysis that include primary and secondary cardiovascular risk reduction trials suggest that the ICH risk might not be affected by statin treatment unless high doses are used.
    • anterior circulation TIA or ischaemic stroke
    • reasonable recovery i.e. not severely disabled
    • 70 – 99% ipsilateral carotid stenosis (NASCET criteria) if event more than 2 weeks ago. Patients with occluded carotid do not benefit from CEA.
    • 50 - 99% stenosis if event was < 2 weeks ago (A).
    • Stroke is a recognised complication of pregnancy, contributing to more than 12% of all maternal deaths with estimated incidence rates that vary considerably from 4.3 to 210 strokes per 100 000 deliveries.
    • Atherosclerosis is rare in young adults, and so other causes of stroke become increasingly likely (see above)
    • Aetiological factors important in pregnancy include hypercoagulability due to maternal physiological changes, pre-eclampsia and eclampsia, cerebral venous thrombosis, paradoxical embolism, postpartum cerebral angiopathy and peripartum cardiomyopathy.
    • Management of patients with pregnancy related stroke should generally proceed as for nonpregnant patients, although there are a number of important areas specific to pregnancy:
      • Pregnancy is associated with an increased risk of both ischaemic and haemorrhagic stroke, the majority occurring in the third trimester or puerperium.
      • Stroke accounts for more than 12% of all maternal deaths. 
      • Stroke can present in a similar way to other more common complications of pregnancy, such as eclampsia, and should therefore be considered in all cases of neurological deterioration.
      • Investigation should proceed as in the non-pregnant state, with special consideration of the pregnancy-specific causes outlined.
    • Graduated pressure stockings have been shown NOT to result in any reduction in proximal DVT in the recently published CLOTS trial 1.
    • The CLOTS3 trial showed that intermittent pneumatic compression (IPC) stockings reduce VTE risk significantly and even have a small effect on reducing mortality.  They should be offered to all immobile stroke patients and prescribed on the medication chart.  Exceptions include if the patient has peripheral vascular disease, skin ulcers, high falls risk etc.  The IPCs should be removed once the patient is mobile, or if there are any side effects.
    • Early use of heparin is associated with no overall benefit because of bleeding risk. The greatest risk of haemorrhagic transformation of infarct (HTI) is in the first two weeks.  After that, it is reasonable to give enoxaparin 40mg sc od to patients who remain at high risk i.e. those who are immobile, CCF etc (A).  This dose should be reduced to 20mg if patient weighs <40kg or if creatinine clearance <30ml/min.  The license states a duration of two weeks only as this was the duration of the trials.  Thrombocytopenia and hyperkalaemia are very rare complications of longer courses so monitor.
    • No smoking
    • Daily moderate physical activity ≥30 minutes
    • Healthy nutrition (scoring within the top 40% of a healthy diet score)
    • Moderate alcohol consumption (men, 5-30 g/d; women, 5-15 g/d) and
    • BMI <25 kg/m2
    • It is very important from a medico-legal point of view that all patients in whom a stroke or TIA is diagnosed should be advised to stop driving immediately. This advice should be recorded in the notes. A clear record on the clinical findings (in particular visual acuity, field defect, visual inattention, cognitive deficits) should be recorded to assist in any future recommendation about driving
    • All patients with residual disability at 1 month must be advised to inform the driver and vehicle licensing agency (DVLA). Patients should also be advised to read their insurance documents to see if notification of the TIA or stroke to them is required. The regulations relating to fitness to drive are being updated on a regular basis and you should look at the DVLA website before giving out any specific advice.
    • For Group 1 drivers (under 7.5 t) the minimum period off the road after a TIA is 1 month or 3 months in the case of recurrent TIAs. In the case of patients with stroke, again the minimum time is 1 month but they must also have made a recovery which is compatible with driving. Particular care should be taken to check that there isn’t a persisting visual field defect, sensory inattention or proprioceptive loss or significant incoordination of the limbs.
    • For Group 2 drivers (i.e. HGV) the duration off the road will be determined by the DVLA but is likely to be a minimum of 1 year and they may be asked to undergo an exercise ECG. Although taxi drivers operate on Group 1 licences, the local taxi licensing authorities are encouraged to apply Group 2 standards.
    • Any patient who has had a post stroke seizure must have a period of 1 year without seizures before applying to have their license reinstated (for group 1 licenses).  A patient with a group 2 licence must be free from seizures for 10 years without taking medication.
    • Any patient with a homonymous visual field defect who wishes to return to driving should be referred to optometry for formal assessment of their visual fields, unless they have another impairment that would make driving unsafe.  A person who has had a stable homonymous visual field defect that does not satisfy the driving standard for more than 1 year may make an exceptional circumstances application for an on road driving assessment.  They will need clinical confirmation of full functional adaptation – as evidenced by normal performance in all activities.  Details of this are contained in the ‘at a glance’ guide on the DVLA website (see link above).
    • There are regional specialist driving assessment centres for patients who may want to return to driving.  Patients may self refer to these specialist centres (see below for the Yorkshire centre).  The cost of an assessment is £75-£100 if the patient self refers.  Alternatively, the DVLA may require an assessment to be undertaken as part of the ongoing licensing process after a stroke following a medical report, in which case the patient does not have to pay.
      The assessment is performed by a specifically trained therapist and is in two parts.  The first part consists of an interview and assessment of physical problems followed by a battery of cognitive and perceptual tests.  The second part is driving in normal road conditions (usually 45-60 minutes).  The centre has two manual and four automatic cars which can be adapted in a number of ways to allow for various disabilities.
    • Suitable patients should be made aware of the blue badge parking scheme and the Motability scheme
    • It is estimated that between 3-30% of patients after stroke may develop post stroke epilepsy, depending upon the underlying cerebrovascular disease and can occur in the very acute stages and years after stroke. About 5-10% of patients present with in the first 2-weeks (early post stroke seizures) with initial stroke severity, large volume infarct size and cerebral haemorrhage increasing the risk. Most of these will occur in the first 24-hours.
    • Late onset seizures, distant from the index stroke confers a risk of epilepsy (a predisposition to recurrent seizures) that will develop in a smaller number, with approximately 2% / year risk
    • Most seizures post stroke are focal onset (from a focal area of injured brain) and impaired awareness (formerly known as complex partial) with or without focal to bilateral tonic-clonic* (formerly known as secondary generalisation) . Prolonged post-ictal (confusional) states can occur, particularly in older patients and Todd’s paresis can often mimic fresh stroke, especially in patients with established stroke disease.
    • The diagnosis can be challenging and almost certainly requires a witness account. One should be alerted to seizures mimicking stroke and unmasking other disorders such as non-convulsive status epilepticus or other intracranial pathology like encephalitis.
    • There are no evidence based guidelines for the use of anti-epileptic drugs in post stroke seizures or epilepsy. If treatment is initiated it should be tailored to the individual patient (age, sex, potential drug-drug interaction, side effects) starting at a low dose and titrating the dose slowly See NICE CG 137 which can be found at:
    • Status epilepticus is defined as generalised seizures lasting more than 30 minutes, or repeated seizures with failure to regain consciousness between seizures.   Status epilepticus should be managed as per the NICE guidance.
    • *International League Against epilepsy 2017 revised classification. Further details can be found at:
    • Urinary incontinence occurs in up to 60% of patients admitted to hospital immediately after stroke. In 20% of these people there may have been urinary incontinence prior to the stroke.  Continence problems can arise from the lack of mobility/dexterity, difficulty in communicating basic needs as well as the micturition pathways being damaged after stroke. A full multidisciplinary assessment of the problem is needed and careful recording of findings, contributory factors (usually several) and management plan using Trust documentation.
    • Continence problems should be considered in light of other pre-existing problems. Careful history will often distinguish urge from genuine stress incontinence (GSI) in women and obstructive prostatic symptoms in men.
    • Simple continence promotion measures, such as regular toileting, provision of aids and good bowel care are essential. Urinary tract infection (UTI) must be excluded by through test of urine (TTU) (and culture if TTU positive).  Persistent urinary incontinence should be investigated with abdominal and rectal examination and measurement of residual volume using a bladder scanner.  Women with GSI need an assessment of vulva and vagina by a suitably qualified doctor. A referral to urogynaecology may be needed and pelvic floor exercises provided.  It is essential for the nurses to formally record a continence chart/diary.
    • Detrusor instability resulting from the stroke presents with urgency and frequency.  It can be treated with bladder retraining and/or anticholinergic medication such as oxybutinin XL, tolterodine, trospium or solifenacin (A).  All of these drugs commonly cause side effects of confusion, dry mouth, dizziness and constipation. In addition, in those patients with significant prostatic hypertrophy, urinary retention may occur. These drugs should not be used in those with a high residual volume on post micturition bladder ultrasound as they may precipitate retention.  Mirabegron is a newly available alternative if anticholinergic medication is not tolerated.
    • Urinary catheterisation should be avoided wherever possible as it delays spontaneous recovery and can damage the urethra and sphincter mechanisms.  Indwelling catheters should be reserved for patients with a high risk of sacral skin ulceration or to maintain comfort and dignity in unconscious patients.  Refer to urology in men with prostatic symptoms/signs and retention if not resolving or failed trial without catheter (TWOC).
    • Individual, comprehensive assessment of patient and carer.  This will include correctly identifying and assessing co-morbid conditions, pre-morbid state physical functioning, cognitive and emotional state and social circumstances.
    • Prevention of avoidable complications such as pressure sores and shoulder subluxation.
    • Full involvement of the interdisciplinary team in screening for the impairments caused by stroke including dysphagia, visual inattention and depression.
    • Agreeing appropriate goals and timescales for achievement.
    • Delivering the rehabilitation plan through appropriate nursing and therapy interventions and optimising the individual’s environment.
    • Supporting the individual and carers emotionally and practically.
    • Effective multidisciplinary discharge planning involving the hospital and community rehabilitation teams and social services.
    • Ongoing support and rehabilitation in the community where further goals are achievable.
    • It is still a widely held belief that ‘recovery after stroke occurs in the first 3 to 6 months’. This can be emotionally very damaging to patients many of whom have achieved important improvements well after this time.
    • Recognise that fatigue and reduced concentration / attention span are very common but ‘invisible’ stroke related problems. For many patients they become the major issue, especially after discharge.
    • 8% risk of further stroke in the first year
    • 5% risk of MI per year.
    • 8% risk of stroke in first month,
    • 5% risk in rest of year
    • 5% risk of MI a year.
    • unconscious at presentation
    • bilateral signs
    • bilateral upgoing plantar reflexes
    • gaze palsies
  • B. PCSK9 Inhibitors (NICE Technology appraisal guidance TA393 and TA 394) – PCSK9 Inhibitors

    should be referred to the ‘Innovative Medicines Clinic (PCSK9 inhibitors / statin intolerance)’ currently run by Dr Rani Khatib (Consultant Pharmacist in Cardiology & Cardiovascular Clinical Research) and Professor Prof Alistair S Hall (Cardiologist) for further assessment and potential treatment.

    C. Other medication

    D. Lifestyle measures

    Offer advice on lifestyle factors that may modify lipid levels (healthy diet, increased physical activity, weight loss, reduced alcohol consumption and smoking cessation). However statin treatment should not be delayed for managing modifiable risk factors.

    Spontaneous Non-traumatic Intracerebral Haemorrhage (ICH)

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    19. Carotid Surgery in Stroke

    Carotid endarterectomy has a role in preventing stroke in patients with recent  carotid territory ischaemic cerebrovascular events 1,2  
    Surgery should be considered for those with:

    Particularly high-risk patients are those with frequent TIAs, cerebral rather than ocular symptoms and ulcerated rather than smooth stenosis.  Modern surgical techniques including surgery under local anaesthesia have improved operative outcomes.   As can be seen below, benefit falls off rapidly with time from the event.  Surgical advice should be sought for those patients who may benefit from surgery.   This should be same day in the case of high stroke risk TIAs.

    Ipsilateral ischaemic stroke and operative stroke or death 3

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    20. Stroke in Pregnancy

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    21. Venous thromboembolism (VTE) Prevention

    Venous thromboembolism is the term for deep vein thrombosis (DVT) and pulmonary embolism (PE). Although heparin and low molecular weight heparin prevent DVT in immobile stroke patients, the risk of fatal PE is lower than the risk of intracranial haemorrhage in the first 2 weeks or so.   Therefore heparin prophylaxis should not be routinely used in the first 2 weeks but reconsider and perform a risk assessment after that time using the Trust VTE risk tool.

    Stroke patients are at high risk of venous thromboembolism (VTE) so any leg swelling should be carefully evaluated.  D-dimer may be used if there is clinical suspicion, but it is frequently elevated in acute stroke limiting its value in decision making.  It has high negative predictive value (if low, VTE very unlikely) but poor positive predictive value (high value not specific, so need further investigation).  This would lead on to doppler scan of popliteal fossa.  Any unexplained hypotension or hypoxaemia (as well as pleuritic chest pain, dyspnoea or haemoptysis) should result in action to positively rule out PE.

    Symptomatic venous thromboembolism should be managed with low molecular weight heparin and an oral anticoagulant - must always be discussed with a Consultant.  Some patients have an absolute contraindication to anticoagulation and in these cases a vena cava filter may be considered.

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    22. Secondary Prevention - lifestyle measures

    Patients need advice about what they can do themselves to reduce risk of a further vascular event.  There are a number of areas to discuss and the advice you give should be recorded in the medical notes. Some plans, a general outline and potentially the first steps (e.g Nicotine Replacement Therapy for smoking cessation) can start on the patient’s admission but continuation through the community and GP services is essential.

    A holistic lifestyle approach has been shown to be more beneficial than the treatment of single risk factors. Patients that manage to achieve all the following targets of lifestyle:

    have a 70-80% reduced stroke risk compared to those who do not fulfil any.

    ‘ONEYOU’ is a site operated by Public Health England. It provides useful advice and support (e.g. face to face free sessions) for people who want to make healthy lifestyle changes.
    Information for ‘ONEYOU’ services in Leeds is available on .

    The Stroke Association also has useful information which can help:

    Smoking is the greatest cause of preventable morbidity and premature death in UK according to data from the Health and Social Care Information Centre.  It is a major contributory factor in hypertension, atherosclerosis as well as malignancies. 

    All patients should have a record of smoking history.  If still smoking, advice to stop must be recorded in the notes. There is good evidence that smoking cessation advice from health professionals is effective in helping smokers stop.

    If the patient is ready to stop and will consider active support, please give them the Leeds ‘ONEYOU’ smoking cessation service details and contact information below:

    Contact Free Phone 0800 1694219

    Alternatively, patients can find their local Stop Smoking Service by call the NHS Smokefree Helpline on 0300 123 1044 or visiting .

    If the patient is keen to start smoking cessation during admission and agrees with organised support, please consider prescribing varenicline, nicotine replacement therapy (NRT) or bupropion according to current practice recommendations. Combinations of the three options should not be used although the combination of different NRT methods is allowed.

    Varenicline or combination NRT (a patch plus a short-acting preparation) have been shown to be the most effective treatments. Current NRT guidance for adults in Leeds Teaching Hospitals NHS Trust can be found on . There is no evidence about superiority of any of the NRT forms over others.

    There is no local Varenicline guidance, so prescription and advice should be based on other official sources like current BNF (British National Formulary) guidance. According to NICE Technology appraisal guidance [TA123]: ‘Varenicline for smoking cessation’, the prescription of Varenicline should normally only be as part of a behavioural support programme.


    Excess alcohol consumption is a risk factor for stroke. Apart from stroke, increased regular alcohol consumption increases the chances of several health problems (including mouth, throat and breast cancer).
    Binge drinking is associated with increased risks of death from long term illness, accidents and injuries.
    Recommend to patients to stay within safe alcohol consumption limits, which are ≤14 units/week for both men and women (UK Chief Medical Officers’ Low Risk Drinking Guidelines, August 2016).
    On one can find plenty of information like the ‘Useful contacts for alcohol problems’ section (groups, roganizations, national help line etc.).
    The national alcohol helpline is called Drinkline. This is a free service where anyone can talk in complete confidence about his own or someone else's drinking problem.Telephone 0300 123 1110 (weekdays 9am to 8pm, weekends 11am to 4pm).

    Physical activity

    Patients should be advised to increase levels of physical activity within existing limitations of functional capacity. The American Heart Association recommends a combination of aerobic training, treadmill walking and adjunctive muscular strength and endurance exercises. The training should be tailored to the patient’s deficits post stroke and this includes the frequency and intensity, apart from the type of exercises.

    It should be clear to patients that exercising can start with very low targets such as brisk 10min walks 5 times a week and they can gradually build on that.

    On top of that patients should be encouraged to increase their daily lifestyle activities (e.g, walking breaks at work, use of stairs, gardening, household duties).

    Stroke Association provides useful information on exercise post stroke along with contact details for more information on clubs, organisations and resources on chair-based exercises online:

    Useful tips are also available from the American Stroke Association online:


    Patients who have had a stroke should be encouraged to follow a healthy diet. This includes not only the type of selected food (e.g. more fruits and vegetables) but also the way of cooking (e.g. avoiding fried foods).

    Salt restriction is also encouraged as increased intake can increase blood pressure. However recommendations about the daily suggested intake vary significantly between the American Heart Association and the UK Stroke Association.

    More details about diet can be found at:

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    23. Driving after stroke or TIA

    The William Merritt Disabled Living Centre
    St Mary's Hospital,
    Greenhill Road,
    Armley, Leeds LS12 3QE
    Tel: 0113 305 5288
    Fax: 0113 2319291


    Unlike driving, there is no aviation mandate, though air travel is generally discouraged for around 3 months following acute stroke but this is not a statutory requirement like driving.  People should always be advised to check carefully with their travel insurance company to ensure adequately covered.

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    24.  Epilepsy and Stroke

    See NICE CG137

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    25.  Pain after Stroke

    Pain after stroke may be related to pre-existing painful conditions or directly to the stroke.  Most pain is mechanical and is related to reduced mobility.  Common pre-existing conditions such as osteoarthritis (OA) knee may be exacerbated after stroke.  All patients should be regularly assessed for pain.  Dysphasic patients unable to communicate should be observed for physical signs of pain.

    Central Post-Stroke Pain is often described as a burning or prickling sensation and may be precipitated by touch.  Allodynia (non noxious stimulus e.g. light stroking of skin felt as pain) is a common feature.  Central pain may respond to tricyclic antidepressants such as amitriptylline 10-25mg nocte, or gabapentin up to 1.8g (B).  Gabapentin requires dose adjustment depending on eGFR.

    Shoulder pain may be the result of adhesive capsulitis of the shoulder and / or rotator cuff tendonitis. It can affect arm recovery. Appropriate support and positioning of the arm and other physiotherapy methods are important aspects of reducing the risk of shoulder pain.  It is important that the affected arm is supported during any changes in posture (including when examining the patient e.g. chest examination).  In established shoulder pain, simple analgesia and nonsteroidal anti-inflammatory drugs (NSAIDs) are the first line of treatment.  Transcutaneous electrical nerve stimulation (TENS) may help as can intra-articular steroids (triamcinolone 40 mg to glenohumeral joint or subacromial space depending on the specific clinical findings)  Slings and strapping do not generally help and may cause the flexed postural deformity in the affected arm.

    Autonomic disturbances may accompany pain.  These include peripheral vasomotor changes producing changes in skin temperature and colour together with swelling. 

    All pain is worse if accompanied by depression or anxiety so screen for mood disorders in all cases.

    Section 35: Urinary Incontinence in Stroke

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    26.  Skin care

    Many stroke patients are vulnerable to skin damage due to immobility, sensory impairment, malnutrition, incontinence, poor peripheral circulation and cognitive impairment.  All patients should have a risk assessment carried out by nursing staff on admission.  This should be the Braden scale combined with professional judgement.  If you have any concerns about skin integrity, please let the nursing staff know immediately. 

    The Trust pressure sore prevention guidelines are available at:

    There are also specific guidelines for managing people with skin care problems due to incontinence at:

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    27.Rehabilitation (see NICE CG162)

    Stroke rehabilitation is an educational and problem-solving approach for individuals to enable them to achieve their optimum physical, psychological and social function. The principal aims of rehabilitation are to identify the impairments that limit activities such as daily tasks; optimise physical and psychological functioning; and modify personal and environmental factors to enable greater participation and quality of life for people recovering from strokes.
    It involves active change by the disabled person to acquire the skills necessary to participate in society, and the use of resources to reduce societal barriers (Rehabilitation Advisory Group NHS Executive 1997).
    Stroke rehabilitation requires significant input from the patient as well as considerable healthcare resources; therefore, rehabilitation services must ensure that they are effective. Furthermore, for stroke rehabilitation to be worthwhile, the changes made must persist after discharge as measured by reintegration into the community. And, after returning home, patients who wish to resume work must be able to do so; therefore the impact of the stroke on return to work must be minimised.
    Stroke rehabilitation aims to assist individuals in reducing the limitations placed on their activities and participation in society by the stroke. The effect of rehabilitation can be measured at several levels – impairment, activity and participation.

    Rehabilitation may also involve specialist equipment such as assistive technology, including environmental control equipment, wheelchairs and functional orthotics. These can be accessed through the Stroke Units and LTHT Specialist Rehabilitation Services at Chapel Allerton and St James’s Hospitals.

    Steps in the Rehabilitation Process

    Rehabilitation begins as soon as a stroke occurs. The following steps illustrate the range of rehabilitation processes that need to occur after a stroke, but need not necessarily occur in this particular order:

    Individuals who may have further potential for recovery can be referred to the Community Rehabilitation Unit (CRU) at St Mary’s Hospital in Armley. This is an interdisciplinary rehabilitation service for patients who are medically stable and who have been living in the community for at least six weeks. The CRU can offer outpatient therapies, botulinum toxin treatment and short, goal-focused inpatient admissions. Please discuss the referral with your consultant and contact Dr Rory O’Connor at the CRU.

    NICE Stroke rehabilitation pathway can be found at:

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    28. Treatment of Spasticity

    Spasticity is commonly associated with upper motor neurone conditions. It manifests as an increased tonic stretch reflex resulting in velocity- and length-dependent hypertonia due to abnormal spinal processing of proprioceptive input. It can lead to pain and contractures and interfere with rehabilitation.   Spasticity is made worse by cold, pain, poor positioning, anxiety, urinary tract infections, skin breakdown and constipation. These should be managed before considering drugs treatments.   Spasticity should not limit the use of strength training.  Baclofen is commonly used to treat spasticity, but may interfere with rehabilitation by reducing trunk control.

    Botulinum Toxin treatment for spasticity
    There is more evidence on the effectiveness of botulinum toxin in spasticity than for other drugs.   It is relatively safe but has to be injected into the muscle and is expensive.   The cost depends on the preparation but can be up to £300 per treatment session. In patients with disabling or symptomatic spasticity, botulinum toxin should be considered to reduce tone and/or improve range of joint movement (B).   This should be planned with realistic aims and objectives which are clearly communicated to patients and carers.  It should be used as part of a rehabilitation programme involving physiotherapy, occupational therapy and orthotics, which may include serial casting.  Only staff trained in its use should administer botulinum toxin. 
    If you think increased muscle tone is affecting (a) recovery of limb movement or (b) the person's overall rehabilitation program, please refer to Dr Rory O’Connor after discussing with your team.
    Systemically acting drugs
    Drugs used in stroke spasticity include, Baclofen, Dantrolene, Tizanidine and Clonazepam.  There is reasonable evidence for the efficacy of these drugs on limb stiffness (B).  It is important to consider targeted treatments for spasticity such as Botulinum toxin before any systemic antispasticity treatments are used.  Systemic treatments can cause unwanted muscle weakness and increase disability

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    29.  Risk of recurrence and prognosis

    Following a stroke:

    Patients with PACI more commonly have early recurrent events than other ischaemic subtypes.  
    Following a TIA:

    Death after first stroke

    Type of stroke

    Case fatality (%) i.e. proportion of patients who die in the period of time


    30 days

    1 year

    All strokes



    All ischaemic strokes















    All strokes due to bleeding



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    30. Palliative care

    Many patients admitted with stroke will die.  Features associated with a poor prognosis include:

    It is impossible to predict with certainty what the likely outcome will be for individual patients.   Significant comorbidity will worsen the prognosis.  How the clinical picture evolves with time may give a better indication of likely outcome. The decision about moving from active treatment to a palliative care focus is complex and depends on patient views, carer and family views and the feelings of all staff involved. This includes decisions around the area of artificial feeding and fluids.

    Patients are often not able to speak for themselves and make their wishes known (lack capacity).  In these cases, it is always worth checking if supported conversation or use of other media, improve communication abilities. In some cases this is not possible so the views of next of kin are especially important.  Where there are no friends or relations, then and independent mental capacity advocate (IMCA) should be requested.  This is a new system put in place from October 2007 as part of the Mental Capacity Act 2005.  Their role is to assess the situation from a standpoint outside the MDT and they can challenge recommendations made, in the way that a family member could do.

    In all cases where the patient lacks medicolegal capacity to decide, and the decision is that life prolonging treatment would not be in the patient’s best interests, a second opinion is required.  In difficult cases or where there are divergent opinions within families or between families and professionals a second opinion should also be sought.  Where the issue cannot be resolved it is appropriate to involve line managers and possibly the Trust solicitors. Decisions are not necessarily absolute and treatment can move from palliation to active treatment or vice versa.

    A systematic approach has been shown to improve the process of caring for those needing palliative treatment.  In those who have difficult to control symptoms, or other issues arising in the terminal phase of the illness, refer to the hospital specialist palliative care service.

    Some patients are not in the terminal phase of their illness but may have multiple comorbid conditions and are frail.  Frailty is an increasingly recognised (but still variably defined) syndrome encompassing loss of physical and cognitive function with severely reduced physiological reserve to respond to new stressors.  Acute admission is an opportunity to identify frail adults and start advance care planning.  A good way of identifying such patients is to ask yourself “would I be surprised if this person did not survive the next year?”

    This should lead to open discussion with the patient (and usually carers) about the problems and this allows ongoing dialogue about preferences for place of care and dying which should continue into primary care.  It should also prompt a review of clinical priorities and goals, with relief of symptoms becoming more important and acute invasive interventions less useful. 

    A good resource is the gold standards framework organisation

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    31. Stroke research at LTHT

    There are always studies recruiting stroke patients at LTHT.  These are very varied ranging from hyperacute treatment to secondary prevention and from stroke genetics to rehabilitation.

    Clinical trials aim in providing solid answers in areas where there is lack of evidence or evidence is scarce. On top of that, a clinical trial can offer the patient the chance to be on better monitored environment whilst future patients might get better treatment based on his/her participation.

    Details are available on the research section of this site ( 
    The Stroke Research Team may be contacted in their office on 22938


Record: 1165

Where possible/relevant we have given important references and website addresses are also mentioned for those seeking further information. These are not exhaustive. The guidelines also consider the LTHT local prescribing policies, which may differ from those in other parts of the UK. Where some expensive drugs have minimal benefit over cheaper alternatives we have tended towards financial prudence as resources may be of greater benefit if directed into other modes of treatment or service provision.

Clinical condition:


Target patient group: All patients having had a stroke
Target professional group(s): Secondary Care Doctors
Secondary Care Nurses
Allied Health Professionals
Adapted from:

Evidence base


[1] Royal College of Physicians Sentinel Stroke National Audit Programme (SSNAP). Is stroke care improving? Second SSNAP Annual Report prepared on behalf of the Intercollegiate Stroke Working Party November 2015. 

[2] Feigin VL, et al. (2013). Global and regional burden of stroke during 1990-2010: findings from the Global Burden of Disease Study 2010. Lancet 383: 245-255 

[3] Royal College of Physicians Sentinel Stroke National Audit Programme (SSNAP). National clinical audit annual results portfolio March 2015-April 2016. Available:

[4] Fullerton HJ, Wu YW, Zhao S, Johnston SC (2003). Risk of stroke in children: ethnic and gender disparities. Neurology 61: 189-194.

[5] Office for National Statistics. (2016). Deaths registered in England and Wales: 2015. http:// bit. ly/2h7Om7P 

[6] Adamson J, Beswick A, Ebrahim S (2004). Is stroke the most common cause of disability? Journal of Stroke and Cerebrovascular Diseases 13:171-177.

[7] Omer S, et al. Cost of stroke in the United Kingdom. Age and Ageing, Volume 38, Issue 1, 1 January 2009, Pages 27–32,

Approved By

Trust Clinical Guidelines Group

Document history

LHP version 2.0

Related information

32. Glossary (version historical)

ACE- angiotensin converting enzyme inhibitor; used to treat blood pressure and heart failure
ACE-3.  Cognitive score aka ‘Addenbrooks’ with score out of 100. Better for picking up frontal lobe dysfunction and vascular dementia
Activity limitation
- loss or decrease in an individual’s ability to execute a task
e.g. unable to dress because of arm weakness
Agnosia is an inability to interpret sensations despite having normal sensory input and there are a number of types which can be described in various ways.  Here is one way:
1.            Agnosias involving the external environment e.g. the patient who cannot find their way back from the toilet on the ward despite many attempts.
2.            Agnosias involving body self image. Patients who have proprioceptive loss and inattention may have altered self image. The most severe example is anosagnosia where the person denies having had a stroke despite obvious deficits.
3.            Agnosias involving the interface between body and environment e.g. tactile agnosia where a patient can feel an object in the hand but cannot decide what it is, or proprioceptive agnosia where the patient ignores or neglects the affected side. 
Allodynia- abnormal perception of a non-noxious stimulus and pain
AMTS-abbreviated mental test score out of 10. 7 pr more is normal in those over 65
Aneurysm- an abnormally enlarged/widened  artery which may rupture
Anton’s syndrome is cortical blindness due to bilateral occipital cortical damage
Apathy/abulia/akinetic mutism.  These are terms in a scale of severity in disorders of initiation, purposeful movement, drive and responsiveness ranging from mild (apathy) to profound (akinetic mutism).  They may occur following damage to the frontal lobes or basal ganglia most commonly.
Apraxia is an inability to carry out learned functional movements in the absence of gross motor impairment e.g. despite having normal power, the person may be unable to sequence movements to be able to use a toothbrush.
ARB- angiotensin receptor blocker drug used to treat hypertension and heart failure
Atherosclerosis- thickening of an artery wall due to build up of lipid rich plaque
AVM is an artero-venous  malformation, usually congenital, and may result in cerebral haemorrhage
Balint’s syndrome- deficit in perceiving the whole visual field, fixating on objects and placing limbs visually
Bell’s palsy- lower motor neurone facial nerve lesion
Buccal- relating to the mouth
Cardioembolism- fragment (usually of clot) from the heart causing blockage in the downstream circulation
CAA- cerebral amyloid angiopathy.  Condition affecting older people with genetic component. May result in cerebral bleeds
CCB- calcium channel blocker e.g. amlodipine
CCF- congestive i.e. biventricular cardiac failure
CDU-Clinical Decision Unit
CEA- carotid endarterectomy
CVD- cerebrovascular disease
Delirium- acute confusion with poor concentration/attention and disturbed behaviour and sleep cycle. May exhibit carphology (grasping at things not there) or flocculation (picking at clothes etc)
Dementia- chronic cognitive impairment
Detrusor instability- over activity of bladder muscles causing urgency and sometimes incontinence
DH- department of health
Diathesis- tendency or predisposition
DVLA- driver and vehicle licensing agency
Dysphasia means an impairment of language ability. 96% of the population have the speech centre in the left hemisphere.  It takes 2 main forms; expressive (aka Broca’s, non fluent) and receptive (aka Wernicke’s, fluent), though in practice most patients have a component of each.  Impaired reading (dyslexia) and writing (dysgraphia) are frequent accompanying features.  This impairment can be devastating psychologically and up to 50% of affected patients become depressed.
Dysarthria means slurred speech usually as a consequence of reduced coordination in tongue and/or face muscles.
Dysphagia- difficulty swallowing. ~45% have it in first 24 hours after stroke and worst for liquids
Dysphonia means hoarse voice and occurs due to altered laryngeal muscle control.
Endarterectomy- surgery to core out and remove narrowing in an artery to restore blood flow and reduce embolisation
GMC- general medical council
Health condition
- effect of an illness on an organ or system altering its normal anatomy or physiology
e.g. osteoarthritis or ischaemic heart disease
Hemianaesthesia is the loss of sensation (pain, light touch and position sense) down one side of the body.  Poor thumb finding, for example, has been shown to have an adverse effect on rehab recovery.
Hemicraniectomy- surgical decompression of swollen hemisphere by removing portion of the overlying skull
Hemiplegia is loss of motor power in one half of the body resulting in paralysis.  Impaired movement or partial paralysis is termed hemiparesis.
After stroke, even if power is normal, fine movements may be impaired e.g. a clumsy hand.
Homonymous hemianopia means loss of the nasal field of vision in one eye and the temporal field in the other eye.  Patients are aware of the visual loss and often compensate for it by moving their eyes or head.
HRT- hormone replacement therapy
Hyperacusis- increased perception
- loss of a normal bodily function
e.g. weakness of arm after stroke or urinary incontinence
IPC- intermittent pneumatic compression
LMWH- low molecular weight heparin e.g. tinzaprin, dalteparin, enoxaparin
LSS- Leeds Stroke Service
MI- myocardial infarction
MMSE- mini mental state examination. Useful cognitive screen out of 30.  26 or more is normal.
NAO- national audit office
NASCET- north american surgical carotid endarterectomy trial
NOAC- novel oral anticoagulant drugs (dabigatran, rivaroxaban and apixaban)
NNT- number needed to treat to benefit one person with an intervention
NSAID- non steroidal anti-inflammatory drug
OCP-oral contraceptive pill
Ophthalmoplegia- abnormality of eye movement control after stroke usually due to damage to cranial nerves 3, 4 or 6
Papilloedema- swelling of optic disc due to raised intracranial pressure
Parenteral- not given via the gastrointestinal tract e.g. intravenous
Participation restriction
- loss of an individual’s involvement in a life situations
e.g. unable to return to work and act as the family’s breadwinner
Using these terms emphasises the individual’s role in society and position in the community as the benchmark against which recovery from a stroke is judged. Disability is an overarching phrase that encompasses impairments, activity limitations and participation restrictions. Disability is, however, profoundly affected by the individual’s environment and the support they receive from their family or carers. The International Classification of Functioning, Disability and Health (ICF) provides a framework for these concepts (WHO 2001).
PE- pulmonary embolism
Postural hypotension- drop in blood pressure standing which may results in dizziness and falls
Proprioception- body position sense
Prostatism- urinary symptoms caused by enlargement of the prostate gland (benign or malignant)
Ptosis- drooping eyelid
PV- plasma viscosity
RCT- randomised controlled trial
Rankin score (modified)- score for measuring dependence
RBS-Referral Bureau Service
Sensory inattention means an inability to attend to information presented on the affected side. This can be visual, auditory or tactile.  Remember, it is not possible to assess for visual inattention by confrontation testing if the patient also has a hemianopia.  Patients may ignore things when presented on the affected side.  They may bump into things on the affected side when walking or using a wheelchair.  They are usually unaware of the deficit and so do not compensate well.  However, recovery of lateralised attention problems does occur.
Spondylosis- degenerative joint damage in the spine
Stenosis- narrowing (of an artery)
Stereotypical- fixed unvarying form
TENS- transcutaneous electrical nerve stimulator
Thrombosis- clot
TIA- transient ischaemic attack
Thrombophilia- abnormal tendency to form blood clots
TWOC- trial without (urinary) catheter
Vasculitis- inflammation of blood vessels often due to autoimmune mechanism
Vena cava filter- device inserted to catch clots and prevent PE
Visual agnosia means inability to make sense of visual inputs so that objects may be seen but not recognised.  An example of this is prosopagnosia; an inability to recognise faces.
VTE- venous thromboembolism, Pulmonary (usually) emboli.


  1. Stroke is a medical emergency with around 130,000 new cases per year (100,000 first ever strokes and 30,000 recurrent events) in the UK [1].
  2. The overall annual incidence of first-ever stroke is about 2 / 1000 population, but this rises exponentially with age to around 20 / 1000 over the age of 85, though overall incidence rates fell 19% from 1990 t0 2010 [2].
  3. About 25% of patients are aged < 65 years. In the UK (excluding Scotland) the average age for a man to have a stroke is 71 and for a woman is 76 [3]
  4. There are over 400 Childhood strokes per year in the UK, 50% occurring between ages 1-10 and around a quarter occur in those under the age of 1 [4].
  5. Stroke is the fourth commonest cause of death in the UK [5], though rates fell by almost half in the period from 1990 to 2010 [2]
  6. Stroke is the commonest cause of severe, acquired adult neurological disability [2], [6].
  7. The cost of stroke in the UK has been estimated at £8.9BN per year including treatment costs and loss of productivity with direct care health and social care costs accounting for over 50% of this; 5% of total UK NHS costs [7]
  8. Detailed guidance about stroke care and the evidence base on which they are based are contained in the National Clinical Guidelines for Stroke (NCGS) which were updated most recently in 2016. These can be found at:
  9. The management of stroke often involves complex ethical decisions about feeding, communication and palliative care. These decisions are not easily covered by guidelines though there is guidance provided by the General Medical Council (GMC). These can be found at:
  10. The Department of Health National Stroke Strategy, which included the FAST campaign, ran from November 2007 to November 2017. Further useful information can be found at The Stroke Association:
  11. Stroke is considered a sentinel conditionin the NHS Long Term Plan (2019) with clear milestone plans for specialist hyperacute, acute and rehabilitation care, and a modernisation of the workforce. The Long Term Plan can be found at:



Recommendations have been graded based on the strength of evidence available:

Level of evidence


Grade of recommendation





At least 1 RCT



Well-designed case control study



Well-designed quasi-experiment



Descriptive study



Expert reports


Local consensus

Clinical experience


Section 1:

Atypical presentations of stroke.  Lancet Neurol 2011; 10: 550–60
ROSIER. Lancet Neurology 2005; 4: 727-34

Section 2:
Stroke Unit Trialists Collaboration. Organised inpatient (stroke unit) care for stroke. Cochrane Stroke Group. Cochrane database of systematic reviews. Issue 2, 2002.
Langhorne P et al. Services for helping acute stroke patients avoid hospital admission. Cochrane Stroke Group. Cochrane database of systematic reviews. Issue 2, 2002.
Rothwell et al. ABCD2 score. Lancet 2007; 369: 283-92
NICE Guidance CG68 Initial diagnosis and management of TIA and stroke

Section 3:
Bamford, Sandercock, Dennis, Burn, Warlow. Classification and natural history of clinically identifiable subtypes of cerebral infarction. Lancet 1991; 337: 1521- 6.
OCSP. Bamford et al. Lancet 1991; 337:1521-6

Section 5:
Nadarajan V,Perry RJ, Johnson J, et al. Pract Neurol 2014;14:23–31

Section 6:
Warlow et al. Lancet 2003;362:1211-1224


Section 7:
Gray et al. Age and Ageing 2004; 33: 71-7.

Ivey et al. Cerebrovascular diseases 2006; 22: 368-71.

Kernan et al. Arch.Int.Medicine 2005; 165: 227-33.

Cossacs.  Lancet Neurol 2010; published online July 12. DOI:10.1016/S1474-4422(10)70163-0

CHHIPS. Lancet Neurol 2009;8: 48–56.

Interact 2. N Engl J Med 2013;368:2355-65.

ENCHANTED. Stroke 2017;48(7):1877-1883


Section 9:
Neurological complications of acute ischaemic stroke.  Lancet Neurology 2011; 10: 357-71

Medical complications following stroke Lancet Neurology 2010; 9: 105–18

Section 10:
Huttner et al.  Stroke 2006/37/1465-70

Aguilar-Maria-I et al. Treatment of warfarin-associated intracerebral haemorrhage: literature review and expert opinion. Mayo Clinic proceedings 2007/82/82-92

BCSH guideline on oral anticoagulation. Baglin et al, Br.J.Haematology 2006; 132: 277. 

STITCH. Mendelow et al. Lancet.2005; 365: 387-97.

STITCH 2  The Lancet, 2013; 382: 397 – 408

Lancet Neurology 2012/11/720. Excellent review

Section 11:
Gubitz G, Sandercock P, Counsell C. Antiplatelet therapy for acute ischaemic stroke. Cochrane Stroke Group. Cochrane database of systematic reviews. Issue 2, 2002

Dual antiplatelet therapy wih aspirin and clopidogrel for acute high risk transient ischaemic attack and minor ischaemic stroke: a clinical practice guideline. BMJ 2018; 363

Section 12:
Wardlaw et al. Thrombolysis for acute ischaemic stroke. Cochrane Stroke Group.  Cochrane database of systematic reviews. Issue 2, 2002.

Pooled analysis of ATLANTIS, ECASS and NINDS. Lancet. 2004; 363: 768-74.

SITS-MOST. Lancet. 2007; 369: 275-82

ECASS 3. NEJM 2008; 359: 1317-29.

LTHT guidelines for Thrombolysis in Acute Ischaemic Stroke are at:

NICE Guidance TA264 Alteplase for the treatment of acute ischaemic stroke

Section 14:
NICE guideline enteral nutrition in adults, Feb 2006

FOOD trial Lancet 2005/365/764-72

Smyth JA et al. The NEWT guidelines for administration of medication to patients with enteral feeding tubes or swallowing difficulties. North East Wales NHS Trust 2010. ISBN: 978-0955251511

Section 15:
FOOD trial Lancet 2005/365/764-72


Section 16:
Pisters R et al. A novel, user-friendly score (HAS-BLED) to assess one-year risk of major bleeding in atrial fibrillation patients: The Euro Heart Survey. Chest 2010; 138:1093-100.

NICE 2014 CG180: The management of AF.

Thachil J. The newer direct oral anticoagulants: a practical guide.  Clinical Medicine 2014; 14: 165-75.
Oral anticoagulants for prevention of stroke in atrial fibrillation: systematic review, network meta-analysis, and cost effectiveness analysis. BMJ 2017; 359
Section 17:
Hypertension in adults: diagnosis and management. NICE CG127, last updated November 2016

Pedelty L, Gorelick PB. Chronic management of blood pressure after stroke. Hypertension, 2004; 44: 1 – 5

Appleton JP, Sprigg N, Bath PM. Blood pressure management in acute stroke. Stroke and Vascular Neurology 2016; Volume 1, issue 2

Rothwell PM, Howard SC, Dolan E, O’Brien E, Dobson JE, Dahlof B, Sever PS, Poulter NR. Prognostic significance of visit-to-visit variability, maximu, systolic blood pressure, and episodic hypertension. Lancet 2010; 375: 895 - 905
Section 18:
MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20536 high risk individuals: a randomised placebo-controlled trial.  Heart Protection Study collaborative Group.  Lancet 2002; 360: 7-22.    

SPARCL. N Engl J Med 2006; 355:549-559
Royal College of Physicians. National Clinical Guideline for Stroke (Prepared by the Intercollegiate Stroke Working Party). Fifth Edition 2016.

NICE Guidance. Cardiovascular disease: risk assessment and reduction, including lipid modification. Clinical guideline [CG181] Published date: July 2014 Last updated: September 2016

Stroes ES, Thompson PD, Corsini A, et al. Statin-associated muscle symptoms: impact on statin therapy-European Atherosclerosis Society Consensus Panel Statement on Assessment, Aetiology and Management. Eur Heart J 2015; 36:1012-22.

A. K. Pandit  et al. High‐dose statin therapy and risk of intracerebral hemorrhage: a meta‐analysis. Acta Neurol Scand. 2016.

J. S. McKinney and W. J. Kostis. Statin Therapy and the Risk of Intracerebral Hemorrhage
A Meta-Analysis of 31 Randomized Controlled Trials. Stroke. 2012;43:2149-2156.

Section 19:
European Carotid Surgery Trial (ECST): interim results for symptomatic patient with severe (70 – 99%) or with mild (0 – 20%) carotid stenosis.  Lancet 1991; 337: 1235 – 43.

North American Symptomatic Carotid Endarterectomy Trial (NASCET) Collaboration.
Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis.  N Engl J Med 1991; 325 : 445 – 53.

Effect of carotid endarterectomy stratified by time from last event to randomisation.  Lancet  2004; 363: 915-24


Section 20:
Stroke in pregnancy and the puerperium. Treadwell et al. Postgrad Med J 2008;84:238–245. doi:10.1136/pgmj.2007.066167

Section 21:

CLOTS 1, Lancet 2009; 373: 1958-65
CLOTS 3, Lancet  2013; 382: 516-24

Section 22:

Chiuve SE et al. Primary prevention of stroke by healthy lifestyle. Circulation. 2008 Aug 26;118(9):947-54.

NICE Clinical Knowledge Summaries: Smoking cessation. Last revised March 2018. Available at .

Physical activity and exercise recommendations for stroke survivors: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2014 Aug;45(8):2532-53.

Section 24:
Rowan A.J. Epilepsy in older adults. Common morbidities influence development, treatment strategies, and expected outcomes. Geriatrics. 2005;60(12):30–32, 34

Brodie M.J., Kwan P. Epilepsy in elderly people. BMJ. 2005;331(7528):1317–1322.


Bladin C.F., Alexandrov A.V., Bellavance A., Bornstein N., Chambers B., Coté R., Lebrun L., Pirisi A., Norris J.W. Seizures after stroke: a prospective multicenter study. Arch. Neurol. 2000;57(11):1617–1622

Serafini A., Gigli G.L., Gregoraci G., Janes F., Cancelli I., Novello S., Valente M. Are early seizures predictive of epilepsy after a stroke? Results of a Population-Based Study. Neuroepidemiology. 2015;45(1):50–58

Rossi C., De Herdt V., Dequatre-Ponchelle N., Hénon H., Leys D., Cordonnier C. Incidence and predictors of late seizures in intracerebral hemorrhages. Stroke. 2013;44(6):1723–1725

Graham N.S., Crichton S., Koutroumanidis M., Wolfe C.D., Rudd A.G. Incidence and associations of poststroke epilepsy: the prospective South London Stroke Register. Stroke. 2013;44(3):605–611

Feely M. Drug treatment of epilepsy. BMJ 1999; 318: 106-9
Section 27:
NICE stroke rehabilitation guidance

Section 30:
Withholding and withdrawing life-prolonging medical treatment. BMA Books 1999.
End of life care. 2010, GMC, London.
 Mental Capacity Act
Palliative care for frail older people. Pal L, Manning L. Clinical Medicine 2014; 14: 292-5.



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