Appendix 3 .uk



LEEDS TEACHING HOSPITALS TRUST

eClinical Guidelines Template

|Stroke Management Guidelines |

|Guideline Detail |

|Ownership: Leeds Teaching Hospitals NHS Trust |

|Publication date: November 2014 |

|Next Review date : July 2022 |

|Status : Current |

|Summary |

|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. |

|Aims |

| |

|The information contained in this document is designed to help non-specialists to manage stroke patients to a high standard. As they are guidelines, they serve to guide|

|but should not deviate from patient-centred care and should interpreted in conjunction with the patient’s wishes or those of caregivers and relatives. They are based on|

|current evidence and agreed good practice but should also be interpreted in the context of the resources available. The medical guidelines are designed to be used in |

|tandem with the multidisciplinary acute stroke care documents. They are consistent with the National Clinical Guidelines for Stroke (2015) and NICE guidance but expand |

|on certain areas not covered within other documents. |

|Objectives |

|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. |

|Background |

| |

|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]. |

| |

|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]. |

| |

|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] |

| |

|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]. |

| |

|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] |

| |

|Stroke is the commonest cause of severe, acquired adult neurological disability [2], [6]. |

| |

|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] |

| |

|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: |

| |

|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: |

| |

|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: |

| |

| |

|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: |

| |

| |

| |

|References |

| |

|[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,  |

|Contents |

| |

|Section |

| |

|Making a diagnosis of stroke |

|Decision to admit |

|Clinical assessment |

|Pathology |

|TIA and Stroke mimics |

|Investigations |

|Acute phase management- BP, Temperature, Blood glucose |

|Acute phase management – parenteral fluids |

|Early neurological deterioration |

|Intracerebral haemorrhage |

|Antiplatelets in stroke and TIA |

|Thrombolysis in acute ischaemic stroke |

|Swallow assessment |

|Decision to start enteral feeding |

|Decision to insert Percutaneous Endoscopic Gastrostomy (PEG) |

|Anticoagulation following stroke |

|Hypertension management in secondary prevention of stroke |

|Cholesterol and stroke |

|Carotid Surgery |

|Stroke in Pregnancy |

|Venous thromboembolism prevention |

|Secondary prevention - lifestyle |

|Driving after TIA and stroke |

|Epilepsy after stroke |

|Pain after stroke |

|Skin Care |

|Rehabilitation |

|Treatment of spasticity |

|Risk of recurrence and prognosis |

|Palliative care |

|Stroke research at LTHT |

|Glossary (historical) |

| |

| |

|Diagnosis |

| |

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

1. 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).

2. 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.

3. Patients with a ‘stroke mimic’, a disorder that looks like stroke or TIA, but is due to another underlying condition (see section 4)

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

[pic]

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

07786250793 or bleep 2621

2. Decision to Admit

 

STROKE

• 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

• 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 | |Point(s) |

|Age |>=60 |1 |

|BP |SBP >= 140mmHg |1 |

| |OR | |

| |DBP >= 90mmHg | |

|Clinical Features of TIA |Unilateral weakness without speech |2 |

| |impairment | |

| |OR | |

| |Speech impairment without unilateral |1 |

| |weakness | |

|Duration |>= 60 minutes |2 |

| |10 – 59 minutes |1 |

| |0-9 minutes |0 |

|Diabetes Mellitus | |1 |

| | | |

|Total ABCD 2 score | |0-7 |

The LTHT TIA pathway

[pic]

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.

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

[pic]

• Cerebral haemorrhage

[pic]

• 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 

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 |

|Seizure |20 |History of seizure, LOC, previous stroke, witness account |

|Syncope |15 |LOC, low BP, arrhythmia |

|Sepsis |12 |Fever, changes in level of consciousness |

|Functional |9 |Stressors / triggers, no anatomical deficit, changing examination, |

|Migraine |9 |History of migraine / tendency, fortification spectra, headache |

|Brain tumour |7 |Slow onset of symptoms, seizure at onset |

|Metabolic |6 |Low sugars, change in level of consciousness, asterixis |

|Neurpathy |4 |Sensory pattern (glove / stocking), absent reflexes, |

|Peripheral vestibular disorder |4 |Positional vertigo, head thrust +ve, fatigable nystagmus |

|Dementia |3 |Progressive cognitive declune |

|Subdural haematoma |2 |Trauma, headache, fluctuating signs, on an OAC |

|Drugs and alcohol |2 |Changes in level of consciousness, myoclonus, asterixis |

|Transient Global Amnesia |2 |Isolated memory impairment with functional preservation |

|Other |6 |- |

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).

Radiology

• 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.

Cardiology

• 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:

▪ age180/110 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:

o GCS 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).

Oxygen

• All patients should have pulse oximetry measured at the time of initial assessment. If oxygen saturation 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

Non-neurological

• Sepsis

• Metabolic - Electrolyte disturbance, hypoglycaemia, dehydration

• Adverse drug reaction

• Hypoxaemia – pneumonia, PE, heart failure, bronchospasm

• Hypercapnoea

• Myocardial infarction

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

|Features |Finding |Points |

|GCS |3-4 |2 |

| |5-12 |1 |

| |13-15 |0 |

|Age |>= 80 |1 |

| |= 30mL |1 |

| |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

Laboratory

* Oral anticoagulation INR >1.7

* Heparin administration within 48 hours

* Platelet count 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.

A. PCSK9 Inhibitors (NICE Technology appraisal guidance TA393 and TA 394) – PCSK9 Inhibitors

• 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.

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.

B. Other medication

• 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.

C. 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)

• 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.

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:

• 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).

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

Lancet2004;363:915

20. Stroke in Pregnancy

• 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:

o Pregnancy is associated with an increased risk of both ischaemic and haemorrhagic stroke, the majority occurring in the third trimester or puerperium.

o Stroke accounts for more than 12% of all maternal deaths. 

o 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.

o Investigation should proceed as in the non-pregnant state, with special consideration of the pregnancy-specific causes outlined.

 

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.

o Graduated pressure stockings have been shown NOT to result in any reduction in proximal DVT in the recently published CLOTS trial 1.

o 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.

o 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 ................
................

In order to avoid copyright disputes, this page is only a partial summary.

Google Online Preview   Download