Acute Stroke Guideline

7/29/2019 Acute Stroke Guideline

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NHS FORTH VALLEYAcute Stroke Guideline

Date of First Issue 26/03/2012Approved 01/11/2011Current Issue Date 26/03/2012Review Date 26/03/2014Version Final: 2.08EQIA Yes / No DD / MM / YYYYAuthor / Contact Dr Anthony ByrneGroup Committee –Final Approval

Drug & Therapeutics Committee

This document can, on request, be made available in alternative formats

Version 2.08 13th

January 2012 Page 1 of 17 UNCONTROLLED WHEN PRINTED



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Consultation and Change Record

Contributing Authors: Dr. L. Fielden, Dr. A. Byrne, Dr. A. Grant, Dr. A. McKenzie,Mr. J. McCall

Consultation Process:

Distribution:

Change Record

Date Author Change Version



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FOREWORD

This guideline is intended to summarize treatment of acute stroke during the initial phases of diagnosis,investigation and management (i.e. the first few hours to days). They are to support non-specialist staff prior to the patient being admitted to the Stroke Unit.

More comprehensive guidelines exist and can be accessed online e.g. SIGN guideline 108, NICE.

This guidance is not intended to serve as a standard of medical care or be applicable in every situation.Decisions regarding the treatment of individual patients must be made by the clinician in light of thatpatient’s presenting clinical condition and with reference to current good medical practice.

Subarachnoid haemorrhage, subdural and extradural haemorrhage are not dealt with in this document asthey do not fall under the remit of stroke disease.

National Guidelines for further reference.

Scottish Intercollegiate Guidelines Network (SIGN)

• “SIGN 108: Management of patients with stroke or TIA: assessment, investigation, immediatemanagement and secondary prevention.” December 2008.URL - http://www.sign.ac.uk/pdf/sign108.pdf

National Institute for Clinical Excellence (NICE)

• “Stroke: National clinical guideline for diagnosis and initial management of acute stroke andtransient ischaemic attack (TIA).” July 2008.URL - http://guidance.nice.org.uk/nicemedia/live/12018/41363/41363.pdf

Where reference is made to drug therapy, further information on indications, cautions, contra-indications,side-effects and dosing can be obtained from the British National Formulary (BNF).

http://www.sign.ac.uk/pdf/sign108.pdf


http://guidance.nice.org.uk/nicemedia/live/12018/41363/41363.pdf






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Section 1: Acute Management of suspected Stroke

1.1 Acute Assessment

Airway Maintain airway. Airway obstruction is usually due to reduced conscious level or aspiration

in this setting. Consider simple airway opening manoeuvres, airways suction and insertion of an oropharyngeal or nasopharyngeal airway. Tracheal intubation if clinically appropriate.

Breathing Assess oxygen saturation and respiratory rate. Maintain oxygen saturations 94%-98%.

In patients at risk of hypercapnic respiratory failure the target is 88-92%. In such patientsobtain an arterial blood gas on oxygen therapy (NB: Do not perform arterial puncture if considering thrombolysis).

Circulation Assess blood pressure and pulse. Avoid wide fluctuations in blood pressure.

Commence IV fluids in hypovolaemic or drowsy patients and in those nil by mouth.If IV access cannot be obtained and central venous access is inappropriate, thensubcutaneous fluids can be used to maintain plasma osmolality. Avoid dextrose in the early post-stroke phase to avoid iatrogenic hyperglycaemia.

Disability Assess Glasgow Coma Scale. If GCS <13 consider emergency CT brain scan (see 1.4).

D (Dextrose) EXCLUDE HYPOGLYCAEMIA AS THE CAUSE OF NEUROLOGICAL DEFICIT

Check rapid blood glucose with finger-prick testing.If below 4.0 mmol -1 give repeated doses of 50ml 10% glucose solution until corrected. Reassess the neurological deficit once blood glucose is corrected. If the neurological deficitresolves rapidly, the neurological deficit is more likely hypoglycaemia induced rather thandue to stroke.

If nil by mouth and type I diabetic, commence insulin sliding scale (see section 2.1.6).

Monitor temperature. If temperature exceeds >37.5oC commence regular paracetamol.Intracerebral events may induce pyrexia, however, a possible infective source should beconsidered. Take cultures, identify source and commence antibiotics as appropriate(adapted from SIGN)

Exposure Full clinical assessment: History & Examination.

Cognitive Calculate an Abbreviated Mental Test (AMT)

Function (Age, Time, Recall address, Year, Place, Recognise 2 people, WW1, Monarch, PM, 20-1).

Note the presence or absence of delirium if possible (e.g. CAM score or 4AT).

1.2 Immediate investigations

• Obtain blood for FBC, U & E, LFT, CRP, glucose, cholesterol, ESR & clotting screen.

• Perform 12 lead ECG, in particular looking for the presence or absence of atrial fibrillation.

• Request Chest X-ray

• Request a CT brain scan (see section 1.4)



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1.3 Swallow Screen

• An appropriately trained member of staff should perform a water swallow test on the day of admission prior to any oral fluid, food or medication (NICE).

• If the patient is not sufficiently alert to cooperate, note this. Record test as ‘failed’.If failed, keep Nil By Mouth, commence intravenous fluids and arrange early Speech &Language Therapy Assessment. The patient remains at risk of aspiration.

•

The swallow test result must be recorded in the medical notes, regardless of outcome.

1.4 CT Brain imaging

Antiplatelet agents/Anticoagulants should be withheld while awaiting brain imaging.

Indications for Immediate Scanning:-

• Potential candidate for thrombolytic therapy (refer immediately to thrombolysis protocol)

• On anticoagulant therapy

• Known bleeding tendency

• Reduced level of consciousness (GCS <13, where level of consciousness diminished rather than

lone dysphasia) • Unexplained progressive or fluctuating symptoms

• Papilloedema, neck stiffness or fever

• Severe headache at onset of stroke symptoms

For all other stroke patients:

• Efforts should be made to scan the patient on the day of the admission if this can be done in-hours.

• If presenting out-of-hours and no ‘immediate indication’ (as above), a CT brain should berequested for the following morning by the admitting doctor.

• The requesting of a CT scan should be confirmed in the patient’s case notes to avoid duplicaterequesting.

• The result of the scan should be recorded in the patient’s case notes.

It is the responsibility of the person requesting the CT brain to ensure the report is reviewed andacted upon e.g. administering aspirin 300mg or neurosurgical discussion, as soon as possible.

1.5 Immediate Management Post-Imaging

If brain imaging has excluded an intracerebral haemorrhage or complicating structural CNS lesion (e.g.tumour, abscess);

• Prescribe aspirin 300mg stat immediately.

• If unable to swallow, prescribe rectally or by enteral tube. (SIGN)

• Aspirin 300mg should be prescribed for 14 days on the drug prescription sheet.

• If aspirin allergic/intolerant:Give a loading dose of clopidogrel 300mg then continue clopidogrel 75mg daily.

After initial workup in the Emergency Department, Acute Admissions Unit or Clinical Assessment Unitpatients with stroke or transient ischaemic attack (who require admission) should be transferred to theStroke Unit as per guidance in the Operational Service Guidelines.



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Section 2: Ischaemic Stroke Management

2.1 Pharmacological Therapy

2.1.1 Antiplatelet therapy

• Patients prescribed aspirin 300mg should continue on this for 14 days then change to clopidogrel

75mg for long term secondary prevention. (NICE update 2010).• Patients initially prescribed clopidogrel (300mg loading dose then 75mg daily) should continue on

the clopidogrel.

• Review any proton pump inhibitor (PPI) therapy. There is evidence that omeprazole/esomeprazolemay reduce the efficacy of clopidogrel:

- stop PPI if no longer indicated and no ongoing gastric protection required.

or

- change to lansoprazole if PPI specifically required or an H2 antagonist e.g. ranitidine.

• If unable to take clopidogrel for long term therapy, aspirin 75mg PLUS dipyridamole retard

200mg BD is the preferred option.• If both aspirin and clopidogrel intolerant, dipyridamole retard 200mg BD as a single agent can

be prescribed.

2.1.2 Anticoagulant therapy (warfarin or heparin)

• Anticoagulant therapy should not be used routinely in the acute ischaemic stroke setting (SIGN,NICE).

• The administration of anticoagulants is contraindicated during the first 24 hours after IVthrombolytic therapy.

• For patients in atrial fibrillation or with paroxysmal atrial fibrillation following stroke,anticoagulation with warfarin can be introduced early in patients with minor stroke or TIA (SIGN), butshould be deferred for two weeks after onset in those with major stroke (SIGN, NICE). Target INR is2.0-3.0. Antiplatelet therapy as in 2.1.1 should be used in the interim.

• Anticoagulation is not recommended for preventing recurrent stroke in patients with non-cardioembolic ischaemic stroke.

• In people with prosthetic heart valves who have disabling cerebral infarction and who are atsignificant risk of haemorrhagic transformation, anticoagulation treatment should be stopped for 1week and aspirin 300 mg substituted (NICE). Such patients should be discussed with the

cardiologist at the earliest opportunity.

• Patients with ischaemic stroke and symptomatic proximal deep vein thrombosis or pulmonaryembolism should receive anticoagulation treatment in preference to treatment with aspirin unlessthere are other contraindications to anticoagulation (NICE).

• People with haemorrhagic stroke and symptomatic deep vein thrombosis or pulmonary embolismshould have treatment to prevent the development of further pulmonary emboli. Each patient shouldbe considered on an individual basis. Treatment options include a caval filter or anticoagulation.

• New anticoagulant drugs are becoming available (direct thrombin inhibitors e.g. dabigatran or factor Xa inhibitors e.g. rivaroxaban). These agents should be used in line with NHS Forth Valley

formulary guidelines.



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2.1.3 Thromboprophylaxis

• The administration of anticoagulants is contraindicated during the first 24 hours after thrombolytic therapy.

• Anti-embolic stockings are not recommended for thromboprophylaxis after stroke (CLOTS-1 andCLOTS-2 trials).

• Consider a thromboprophylactic dose of low molecular weight heparin if:

• haemorrhagic stroke excluded

AND

• risk of haemorrhagic transformation or bleeding into another site is assessed to be low

AND

• the patient is at high risk of VTE (such as major restriction of mobility, previous history of venous thromboembolism, dehydration or significant co-morbidities e.g. malignant disease).

• There can be difficulty with treatment as those who are immobile due to large cerebral infarcts are atrisk of VTE but are also at highest risk of haemorrhagic transformation of the infarct. Decisions need

to be made on an individual patient basis.

• Regularly review the need for thromboprophylaxis (both the need to commence therapy or todiscontinue therapy when no longer appropriate).

2.1.4 Antihypertensive therapy (acute phase)

Do not lower blood pressure routinely in acute stroke (SIGN)

• There is no evidence of benefit in treating hypertension in ischaemic stroke acutely and there issome evidence suggesting potential harm.

Avoid fluctuations in blood pressure• If able to swallow and no other contra-indication continue any usual blood pressure medication,

unless there is good evidence that the patient has not been complying with anti-hypertensivemedication pre-admission.

Consider lowering BP acutely only with the following serious concomitant medical issues (NICE)

• Hypertensive encephalopathy

• Hypertensive nephropathy

• Hypertensive cardiac failure/myocardial infarction

• Aortic dissection

• Pre-eclampsia or eclampsia

• Intracerebral haemorrhage with systolic blood pressure ≥ 200 mmHg

or • The patient may be considered for blood pressure lowering medication if a potential candidate for

thrombolysis and BP is >185/110, however, this is at the discretion of the on-call stroke specialist.



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2.1.5 Statins

• A statin should be prescribed to patients who have had an ischaemic stroke, irrespectiveof cholesterol level. Cholesterol level should still be checked on admission.

• Patients with ischaemic stroke on prior statin therapy should continue treatment, via a nasogastrictube, if necessary.

• SIGN recommends using simvastatin 40mg or atorvastatin 80mg based on the Heart Protection

Study (HPS) and SPARCL trial respectively.• Patients not currently prescribed a statin would usually receive simvastatin 40mg. Following clinical

risk assessment by a stroke consultant atorvastatin 80mg may be recommended.

• Statin therapy following haemorrhagic stroke is not recommended routinely unless the risk of further ischaemic vascular events outweighs the risk of further haemorrhage.

2.1.6 Hyperglycaemia/Diabetes treatment

Hyperglycaemia in stroke

• Diabetic patients on insulin who are unable to swallow (or in whom there is concern about ability tomaintain adequate oral intake) should be commenced on an IV sliding scale insulin regimen.

•

Care should be taken not to cause hypoglycaemia with such regimes and a glucose of 7mmol/l is acceptable as the minimum level. The insulin dosing for the sliding scale mayhave to be adjusted to avoid glucose levels below this.

• Routine use of intravenous insulin regimens to lower blood glucose in patients with ‘moderate’hyperglycaemia after acute stroke is not recommended as there is no trial evidence yet of benefitand a significant demonstrated risk of inducing hypoglycaemia.

• Advice should be sought from the diabetic specialist team if there is continued concern aboutglycaemic control.

• A random glucose >6.0mmol/l should be further assessed to exclude or confirm a diagnosis of impaired glucose tolerance or diabetes.

Hypoglycaemia in stroke

•

Hypoglycaemia should be avoided and a blood glucose minimum of 7mmol/l is acceptable.• Hypoglycaemia should be managed as per the usual local protocol.



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2.2 Further investigation

2.2.1 Further brain imaging

• Consider if there is an otherwise UNEXPLAINED DETERIORATION in the patient’s condition (toexclude hydrocephalus, haemorrhagic transformation of infarct) and when repeat imaging willinfluence further management.

• Clinical deterioration following stroke may be related to intercurrent infection so this must beconsidered.

• Routine follow up scanning is required after THROMBOLYTIC THERAPY for acute ischaemicstroke. This should usually be performed around 24 hours from treatment but can be done at anappropriate time earlier or later if treated out-of-hours. Emergency scanning following thrombolysisshould be done if there is a neurological deterioration raising suspicion of intracerebralhaemorrhage. See thrombolysis protocols.

• Further imaging with CT angiogram, MRI or MR angiogram may be required and should bediscussed with a consultant.

2.2.2 Carotid artery imaging

• Request urgent carotid duplex scan for all patients with non-disabling ischaemic stroke syndromeor TIA in the carotid territory who are potential candidates for carotid surgery (SIGN).

2.2.3 Echocardiogram

• Echocardiography is not recommended for all patients with ischaemic stroke (SIGN).

• Echocardiogram should be considered for patientso where clinical findings or baseline investigations (e.g. abnormal ECG) suggest cardiac

disease.o with cryptogenic stroke.

• Hypertension without ECG abnormality is not an indication for echocardiogram.

• Enter as much information on the request card as possible to allow appropriate vetting of therequest (e.g. ECG findings, presence of murmurs etc).

• If a patient has had a recent echocardiogram prior to their stroke, a repeat echo may not beappropriate.

• The routine use of echocardiography with contrast media for further evaluation of patients followingstroke or TIA is not recommended. This should only be requested after discussion with acardiologist.

2.2.4 Cardiac Rhythm Monitoring

• Cardiac rhythm monitoring (24/48/72 hour ECG tapes) may be appropriate to investigate for paroxysmal atrial fibrillation in patients with sinus rhythm on admission ECG.

• This should be requested on discussion with a consultant.



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Section 3: Primary Intracerebral Haemorrhage

3.1 Initial Management

Following brain imaging confirming intracerebral haemorrhage

• All antiplatelets/anticoagulants should be discontinued.

•

A baseline full blood count and clotting screen is required (if not already done).• Clotting levels in those receiving anticoagulation treatment (and have an elevated INR) should be

returned to normal as soon as possible. The haematoma seen on the CT is a “snapshot” image andwill often continue to expand following the CT scan. Discuss with the on-call haematologist theappropriate treatment to give. This will usually be a combination of prothrombin complex andintravenous vitamin K. (NICE).

While routine surgical evacuation by craniotomy is not recommended for supratentorial primaryintracerebral haematoma, early neurosurgical discussion may still be required in individual circumstances.This may include younger patients with haemorrhage and subsequent pressure effects or those with verysuperficial haemorrhage. If there is doubt about appropriateness, then discussion should take place inorder that patients do not miss out on appropriate intervention.

Blood Pressure Management

• Consider acute management of hypertension in intracerebral haemorrhage if systolic bloodpressure >200mmHg. Lowering by no more than 20% in the first 24 hours may be advisable.Intravenous labetolol or glyceryl trinirate may be options.Evidence in this area is inconclusive.

Clinical Observation

• Regular clinical observation should be made including neuro-obs and Glasgow Coma Scale. Thisshould be done at least hourly for the first 24-48 hours.

• A deterioration may indicate haematoma expansion or a re-bleed. Further CT imaging may beappropriate, particularly where neurosurgery has indicated they may accept the patient in the eventof a clinical deterioration.

Patients with Prosthetic Heart Valves

• Patients with cerebral haemorrhage and a prosthetic heart valve should also be discussed withcardiology, particularly those who need long term anticoagulation due to the valve.

• Patients anticoagulated solely due to atrial fibrillation who have a cerebral haemorrhage shouldusually have their anticoagulation fully reversed.

Statin Therapy

• Statin therapy after haemorrhagic stroke is not recommended routinely unless the risk of further ischaemic vascular events outweighs the risk of further haemorrhage (SIGN).

Subarachnoid haemorrhage and subdural and extradural haemorrhage are managed differentlyfrom primary intracerebral haemorrhage and are not covered in this guidance.



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Section 4: Post-stroke Dysphagia

4.0 Swallowing Impairment

• An early swallow screen should be performed by an appropriately trained member of staff on theday of admission prior to any oral fluid, food or medication (NICE).

• The swallow test result must be recorded in the medical notes, regardless of outcome.

• Oropharyngeal dysphagia can result in serious complications such as aspiration pneumonia,undernutrition, dehydration and missed medication.

• Early placement of a nasogastric feeding tube should be considered in patients identified as unableto take adequate food or medication due to a low conscious level and/or the presence of dysphagia(SIGN). This would usually be a decision made once the patient is in the Stroke Unit

• Aspiration +/- radiological evidence of pneumonia• Aspiration is a risk of stroke and associated with poor outcome.• Risk reduction - sit up and mobilise as soon as possible (NICE, SIGN)• Treat for aspiration pneumonia as per the local antibiotic guidelines.

The presence of a nasogastric tube does not prevent aspiration of saliva or reflux of NG feed andaspiration. Attending staff should remain alert to the possibility of aspiration after placement.

4.1 Screening for Swallowing Difficulties and Referral to SLT.

If the patient is drowsy and unable to sit upright for 15 minutes, it is NOT SAFE to carry out a Water Swallow Test, (see flow chart below).

• document decision not to screen and why

• patient should remain Nil by Mouth with IV hydration

• monitor conscious level

Attempt to re-screen every 12 hours



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Water Swallow Test - Part 1

Give patient 3 x 5 ml teaspoons of water, one at a time. Observe closely and record results below.

If the answer is YES at any time STOP screening.

Maintain Nil By Mouth and repeat full Water Swallow Test every 12 hours over 2 days.

First Test

SecondTest

+ 12 HRS.

Third Test+ 24 HRS.

Fourth Test+ 36 HRS.Does the patient show signs of any of the

following?

YES NO YES NO YES NO YES NO

• coughing

• choking

• (increased) breathlessness

• change in voice quality (hoarse and/or wet/gurgly)

If the answer is NO throughout this section continue to Part 2.

Water Swallow Test - Part 2

Give glass with 50 ml. water to patient and observe drinking. Record observations below. First Test Second Test

+ 12 HRS.Third Test+ 24 HRS.

Fourth Test+ 36 HRS.

Does the patient show signs of any of thefollowing? YES NO YES NO YES NO YES NO

• coughing

• choking

• (increased) breathlessness• change in voice quality (hoarse and/or

wet/gurgly)

Results

Staff signature: Staff signature: Staff signature: Staff signature:

Outcome of Water SwallowTests Ward/ Date Ward/ Date Ward/ Date Ward/ Date

PASS ( NO throughout Part I and II)

FAIL ( YES at any time)

Patients PASSING the Water Swallow Test should progress to oral feeding under observation as per flow chart overleaf

Patients FAILING the Water Swallow Test should be re-tested as per the chart overleaf or be referred on to SLTas appropriate

To make a referral to SLT please phone:

Speech & Language Therapy Dept., Forth Valley Royal Hospital: Ext. 66591 (01324 566591)

This checklist is not designed to screen patients who have complex intra-oral or head and neck surgery, or tracheostomy. In those

cases please use existing ward protocols or refer directly to SLT. (Review Date May 2006)



Guidelines for Referral to Speech and Language Therapy (SLT) for Assessment of OropharyngealSwallowing Function.

NO

•Keep Nil By Mouth. • Implement and maintain full oral hygiene• Consider intravenous hydration.• Refer to dietitian if still NBM after 48hrs.

• Repeat screening on a 12 hourly basis.

Can the patient: -• be seated upright (in bed or chair?)

• remain alert and awake for atleast 15 minutes?

YES

Is the mouth clean?

YES

Begin and maintain full oral hygiene.

Refer to SLT on completion of checklist overleaf

Give glass with 50 ml. water to patientand observe drinking

• Does the patient:-- cough?- choke?- become (more) breathless?

• Does the voice quality- change on the sound “ah”?- become hoarse or “wet”?

• Record results on checklist

NO

NO

Give 1 x 5 ml teaspoon of cold water

• Does the patient:-- fail to swallow?- cough?- choke?- become (more) breathless?

• Does the voice quality- change on the sound “ah”?- become hoarse or “wet”?

• Repeat twice (total = x 3 times)

• Record results on checklist

YES

• Keep Nil By Mouth.

• Maintain full oral hygiene.

•

Consider intravenous hydration.• Refer to dietitian.

• Repeat screening on 12 hourlybasis

• Commence oral feeding – free diet and fluids• Carefully supervise first meal and observe eating/drinking over 2 days• Ensure patient is fully upright and alert when eating/drinking• If patient is noted to cough, choke, experience voice changes asabove, reports difficulties, or develops a moist chest, refer to SLT

• Consider putting patient Nil By Mouth, particularly if chest infection develops

The above guidelines do not apply to the following groups of patients who may be referred directly to SLT: -• Patient is reported to have one or more of the following –

- a history of more than one otherwise unexplained chest infection- aspiration on barium swallow or other similar radiological procedure- evidence of aspiration (suspected infiltrate) on plain chest x-ray.

• Patient has rapid and/or poorly co-ordinated respiration (may be on ventilation) and is experiencing swallowing difficulties.

• Patient is reporting oropharyngeal swallowing difficulties (food “sticking” in mouth or throat, for example).• Patient has a known swallow problem (e.g., requiring modified diet) but is reported to be experiencing new problems.

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Section 5: Transient Ischaemic Attack (TIA)

The symptoms of a TIA usually resolve within minutes or a few hours at most, and anyone with continuingneurological signs when first assessed should be assumed to have had a stroke.

1. Take History and Perform Examination

2. Is this likely to be a vascular event?• Was the event of sudden onset? y Are the symptoms focal (attributable to a single vascular territory)?

• Unilateral weakness and/or sensory disturbance of face, arm, leg or a contiguous combination

• Dysphasia y Visual Field Defect y Diplopia y Does the patient have vascular risk factors? Stroke – a clinical syndrome of rapidly developing symptoms and/or signs of focal neurological dysfunction lasting

more than 24 hours with no apparent cause other than of vascular origin

TIA - transient episodes of focal cerebral dysfunction or transient monocular dysfunction during which symptoms lastless than 24 hours and are presumed to be of vascular origin.

Patients with LOSS OF CONSCIOUSNESS should NOT be referred to this clinicBlackouts, faints, seizures & dizziness should be admitted or referred to other clinics as appropriate

3. Are symptoms/signs still present?

• YES – Admit & treat as stroke • NO - Continue risk assessment

4. Risk Assessment

ABCD2

Score1

– Age / Blood pressure / Clinical symptoms / Duration / Diabetes Age 60 years or over = 1, under 60 years = 0 BP Systolic BP>140 or Diastolic BP>90=1, other values=0

Clinical Unilateral weakness (face/arm/leg) = 2 OR Speech disturbance only = 1 OR Other impairment = 0

Duration >60 min = 2, 10 to 59 min =1, <10 min = 0 Diabetes Yes = 1, No = 0

Risk of Recurrence at IntervalScore Risk Group

2 days 7 days 90 days

0 to 3 Low 1.0% 1.2% 3.1%

4 to 5 Medium 4.1% 5.9% 9.8%

6 to 7 High 8.1% 11.7% 17.8%

Other Factors considered High Risk: y More than 1 event in 7 days y Atrial Fibrillation yOn anticoagulantsy Prosthetic Heart Valve y TIA plus neck pain suggesting arterial dissection

5. Action Plan“Office Hours” - 0900h to 1600h Monday to Friday

Contact TIA MOBILE 01324 567691 Complete Referral Form Bloods2

ECG CXR3

“Out of Hours” - 1600h to 0900h AND all day Saturday & Sunday

ABCD2 score ≥ 4 or Other High Risk Factor ABCD2 score < 4 and no High Risk Factors ADMIT & arrange tests below Bloods

2ECG CXR

3

Complete referral & leave at A&E reception

Complete referral form & leave at ED reception

Bloods2

ECG CXR3 Start appropriate secondary prevention

CT Brain scan – next day Give Driving Advice (see below)

Carotid Doppler & Echo (if indicated per protocol) – next day Advise call 999 if further symptoms pending review

Start appropriate secondary preventionIf diagnostic doubt, significant abnormality found on basic tests,

or significant co-morbidity, then use clinical judgement &

admission may be appropriate

6. Other InformationImmediate Secondary Prevention Drug Regime

Aspirin 300mg STAT followed by 75mg daily(If true aspirin intolerance, Clopidogrel 300mg STAT followed by 75mg daily)

Drugs to be dispensed from the Emergency Department or Clinical Assessment UnitOther drug therapy (other antiplatelets, statins, anti-hypertensives etc.) will be started after clinic review

TIA TRIAGE MOBILE – 01324 567691 PAGE 1684

Patients with stroke, TIA or amaurosis fugax must not drive for at least one month4

Document that advice given. If patient drives against advice, will not be covered by insurance company

1. Johnston SC et al. Validation and refinement of scores to predict very early stroke risk after transient ischaemic attack. Lancet 2007;369:283-922. SIGN 108.Section 4.5 – U&E’s, random glucose, random cholesterol, FBC, ESR. Other blood tests as clinically indicated.

3. CXR for all who are admitted, all smokers and all with another clear indication (unless a CXR has recently been performed).Other patients will be assessed at clinic and a chest x-ray performed if necessary.

4. DVLA guidelines can be found online at http://www.dvla.gov.uk/media/pdf/medical/aagv1.pdf



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Section 6: Special circumstances

6.1 Malignant MCA syndrome

• Following proximal middle cerebral artery (MCA) occlusion, subsequent massive oedema of infarcted tissue can result in a progressive increase in intracranial pressure, coning and death.

• For individuals aged up to 60 years who suffer an acute MCA territory ischaemic stroke

complicated by massive cerebral oedema, surgical decompression by hemicraniectomy cansignificantly reduce mortality if performed within 48 hours of stroke onset (SIGN).

• Patients ≤60 yr showing neurological deterioration after major MCA infarction should be discussedwith the neurosurgical team at the Department of Surgical Neurosciences, Edinburgh WesternGeneral Hospital.

• Intravenous mannitol and/or corticosteroids have no effect on outcome and are not recommended.

6.2 Posterior Circulation Infarct or Haemorrhage

• Patients presenting with a significant posterior circulation stroke should be discussed with asenior and may merit discussion with the Stroke team at Edinburgh Western GeneralHospital regarding temporary transfer even if there is no immediate neurosurgical issue attime of presentation.

• Local oedema within the posterior fossa following significant cerebellar infarction with local masseffect or mass effect from haemorrhage can result in occlusion of the 4th ventricle and obstructivehydrocephalus with coning.

• Events can proceed rapidly with rapid and catastrophic deterioration. Close observation of suchpatients is required including neuro-observation (including Glasgow Coma Scale) at least hourly for the first 48 hours.

• Basilar artery occlusion can also cause significant morbidity and mortality.

•

It may be advisable for patients to be monitored in a neurological centre with immediate access toneurosurgical decompressive facilities for 48 hours following onset, even if signs of hydrocephalusare not yet evident.

6.3 Cerebral Venous Sinus Thrombosis (CVT)

Cerebral venous thrombosis is a rare cause of stroke, accounting for 0.5% of all strokes per annum.Diagnosing cerebral venous thrombosis is difficult and CVT are often assumed to be ischaemic infarcts.Clinical symptoms are very variable and non-specific. CT appearances can be subtly different and other imaging such as MR or CT venography may be required. The aetiology is often multifactorial andunderlying thrombophilias are found in 22% of patients (SIGN).

• Patients with CVT should be discussed with a stroke specialist either locally or at the WesternGeneral Hospital, Edinburgh.

• Anticoagulation appears to be safe following cerebral venous thrombosis (despite the presence of associated secondary haemorrhage on scanning) and may be associated with an improvement inmortality and outcome (SIGN)

• Treatment with IV unfractionated heparin or low molecular weight heparin followed by warfarin should be considered in patients with cerebral venous sinus thrombosis (SIGN, NICE).

• Long term treatment with warfarin (INR range 2.0-3.0) for 6-12 months is recommended (SIGN)



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6.4 Extra-cranial Cervical Arterial Dissection

Extracranial cervical arterial dissection is an uncommon cause of stroke, accounting for 2.5% of allstrokes and 5-22% of strokes in young people (<45 years). The incidence of carotid artery dissection is twoto three per 100,000 per year. Aetiologies include chiropractic neck manipulations & other neck trauma andarteriopathies such as fibromuscular dysplasia and cystic medial necrosis.

• The most likely cause of stroke in cervical artery dissection is embolism from the dissection flap.

• It is important to be aware of the possibility of intracranial extension of the dissection resultingin subarachnoid haemorrhage. This diagnosis should be excluded in the usual way if symptomsare suggestive prior to initiating treatment with antiplatelets or anticoagulation. (SIGN)

• In patients with extracranial cervical arterial dissection consider treatment with either anticoagulationfor three to six months or antiplatelet agents (SIGN, NICE).



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Appendix 1: Oxford Classification of Stroke

Total Anterior Circulation Stroke (TACS)-carries poorer prognosis

All of the below: Weakness +/- sensory deficit of at least 2 out of 3 of

face, arm and leg Homonymous visual field defect Higher cortical dysfunction e.g. dysphasia, dyspraxia

Partial Anterior Circulation Stroke (PACS) 2 out of 3 criteria from TACS criteria

OR

Isolated dysphasia or other cortical dysfunction

OR

Motor/sensory deficit more restricted than a LACSe.g. single limb, hand only.

Lacunar stroke (LACS) Pure motor (commonest) or pure sensory deficitaffecting contiguously 2 out of 3 of face, arm andleg, or a sensorimotor stroke (basal ganglia or internal capsule)

OR

Ataxic hemiparesis (cerebellar-type ataxia withipsilateral pyramidal signs – internal capsule or pons)

OR

Dysarthria plus clumsy hand

OR

Acute onset movement disorders (hemichorea,hemiballismus – basal ganglia)

Lacunar syndromes should not affect higher cortical function

Posterior Circulation Stroke (POCS) Include

Isolated homonymous hemianopia Isolated cerebellar stroke Disorders of conjugate eye movement Cranial nerve deficit with contralateral motor or

sensory deficit Bilateral motor/sensory symptoms



Version 2.1.5 October 2012

Name:

DoB:

Address:

CHI:

CLINICAL GUIDANCE & DOCUMENTATION FOR

THROMBOLYSIS IN ACUTE ISCHAEMIC STROKE

This should be filed as part of the patient’s case record.

This document is intended to guide a clinician to administer intravenous thrombolysis for acute ischaemic

stroke. The pathway attempts to identify patients who are appropriate for treatment and facilitate treatmentin as short a time interval as possible.

Much of the information, such as timing of symptoms, arrival and treatment and clinical information onsymptoms and severity is used for audit purposes to ensure safety and effectiveness of service, andcomparison with other centres. These are a national audit (NHS Quality Improvement Scotland) and aninternational audit (SITS-ISTR, Safe Implementation of Thrombolysis in Stroke, International StrokeThrombolysis Register). The information is difficult to obtain retrospectively. Please fill out the paperwork ascompletely as possible, but without delay to treatment.

Additional guidance is available through the South Scotland Telestroke Project – see associated protocols.

This protocol is for guidance only and is not intended to serve as a standard of medical care or beapplicable in every situation. Decisions regarding the treatment of individual patients must be made by theclinician in light of that patient’s presenting clinical condition and with reference to current good medicalpractice.

Page 1 of 7




Name: DoB: CHI:

1. TRIAGE, INITIAL ASSESSMENT & ACTIONS

1(a) CLINICAL SUSPICION

Immediate clinical assessment indicates that this patient has symptoms suggestive of a stroke.

ROSIER Scale

Has there been loss of consciousness or syncope? Yes (-1) No (0)

Has there been seizure activity [see also exclusion criteria] Yes (-1) No (0)

Is there a NEW ACUTE onset [or on waking from sleep]

1. Asymmetric facial weakness Yes (+1) No (0)

2. Asymmetric arm weakness Yes (+1) No (0)

3. Asymmetric leg weakness Yes (+1) No (0)

4. Speech disturbance Yes (+1) No (0)

5. Visual field defect Yes (+1) No (0)

Total Score:______ (Range –2 to +5. Stroke is unlikely but not completely excluded if total score ≤0)

1(b) TIME CRITERIA A definite time of onset must be known. For patients waking from sleep with symptoms or being found withsymptoms, onset is taken as the last time they were seen without symptoms .

(a) Time of Symptom Onset: Date: ___ / ___ / ___ Time: ___ : ___ hrs

(b) Time of Arrival Date: ___ / ___ / ___ Time: ___ : ___ hrs

(c) Time of Initial Assessment Date: ___ / ___ / ___ Time: ___ : ___ hrs

If the patient has been transferred to hospital rapidly, thrombolytic therapy may be possible. Assessment and imagingmust be completed to allow the delivery of the initial dose within 3 hours (for selected cases within 4.5 hours – see page 7 ). If within this time frame, continue through the following steps.

1(c) IMMEDIATE ACTIONS

If the patient fulfils the above criteria, take the following steps as rapidly as possible. Where possible, tasksshould be undertaken simultaneously by members of the attending staff to minimise delay. In addition, usethe telestroke protocols for contacts during “out-of-hours” periods.

1. Check BM – if low, treat urgently and reassess neurology.2. Alert the Stroke Team (Ext 67691) and/or the on-call medical middle-grade doctor that there is a

patient potentially for stroke thrombolysis.3. Insert IV cannulae in both upper limbs4. Send blood for FBC, coagulation screen, glucose and U&E. Other bloods should be sent as

clinically indicated. Inform the laboratory that these are for a potential thrombolysis case as results

are needed as an emergency before treatment can be administered.5. Contact Duty CT radiologist/radiographer and request an immediate CT Brain scan.6. Check temperature, pulse, blood pressure, respiratory rate 7. Perform ECG 8. Review Exclusion Criteria 9. Contact “Flow Co-ordinator” and inform of potential need for Critical Care bed.

Critical Care medical staff should also be informed when necessary (if treatment proceeds).10. Unless absolutely indicated, DO NOT perform arterial puncture.

A CXR is not usually required before treatment and should not delay proceedings. It should be doneat earliest convenience as the situation allows.

TIME IS BRAINThe shorter the time to brain reperfusion,the greater the potential benefit and the lower the haemorrhagic risk from thrombolysis

Page 2 of 7 File with Admission Documents

Time Difference

(a) to (b) ___ h _____ m

(a) to (c) ___ h _____ m




Name: DoB: CHI:

2. EXCLUSION CRITERIA CHECKLIST

CONTRA-INDICATIONS, POTENTIAL CONTRA-INDICATIONS AND CAUTIONSCircle Yes, No or Not Known as appropriate

History suggestive of subarachnoid haemorrhage (even if CT normal) Yes No Not Known

Seizure at stroke onset Yes No Not Known

BP Systolic <90mmHg or >185mmHgor Diastolic <40mmHg or >110mmHg

Baseline BP = / Yes No Not Known

Defect in coagulationOn oral anticoagulant (e.g. warfarin) and INR≥1.4 On heparin (unless APTT within normal laboratory limits)Treatment with Low Molecular Weight Heparin or HeparinoidTreatment with a direct thrombin inhibitor Other known defect in clotting function/bleeding diathesis

Yes No Not Known

Platelet count < 100,000 or known defect in platelet function(patients on antiplatelet agents are eligible e.g. aspirin, clopidogrel, dipyridamole)

Yes No Not Known

BM <3.0 or >22 mmol/l Baseline BM = Yes No Not Known

Neurological symptoms rapidly improving, considered likely to resolve

completely within the next few hours (i.e. a transient ischaemic attack)

Yes No Not Known

Bacterial Endocarditis or Pericarditis Yes No Not Known

NIH Stroke Scale <5 (mild neurological deficit) or >25 (see page 6) Yes No Not Known

Or History of

Previous stroke plus diabetes Yes No Not Known

Previous intracranial haemorrhage, CNS vascular malformation, CNSneoplasm, spinal or cranial surgery, or haemorrhagic retinopathy

Yes No Not Known

Another stroke or head injury in the last 3 months Yes No Not Known

Surgery (including liver or renal biopsy, lumbar puncture or thoracocentesis) or significant trauma (e.g. major fall at time of stroke)within previous 14 days

Yes No Not Known

GI, urinary, respiratory or menstrual bleeding in the last 21 days Yes No Not Known Arterial puncture at a non-compressible site in the last 10 days Yes No Not Known

Patient is female and of childbearing potential (unless it is certain thatpregnancy not possible) or less than 10 days post-partum

Yes No Not Known

Severe liver disease (hepatic failure, cirrhosis, varices etc.) Yes No Not Known

Severe renal disease, including haemodialysis or peritoneal dialysis Yes No Not Known

Alcohol or drug intoxication, or history of significant drug abuse Yes No Not Known

Other pathology for which thrombolysis may present a significanthaemorrhagic risk e.g. pancreatitis, ulcerative GI disease

Yes No Not Known

Patient already dependent with activities of daily living prior to this strokeevent

Yes No Not Known

Other life-threatening illness (e.g. advanced cancer) likely to lead to deathwithin a few months

Yes No Not Known

Treatment with thrombolytic agent within the last 14 days Yes No Not Known

AGE – Actilyse (rt-PA) is licensed for use in ischaemic stroke for patients aged 18 to 80 years.However, treatment may also be administered in selected patients out with this age range,although this is outside the current European labelling (ESO 2008 guideline – Class III, Level C).Such treatment is at the discretion of the attending physician.

Many of the above contra-indications are relative and after discussion with a stroke physicianexperienced in thrombolytic therapy, treatment may proceed despite their presence.

If there is significant doubt as to whether the patient is appropriate for thrombolysis,the default position is BEST USUAL CARE and do not give rt-PA





Name: DoB: CHI:

3. IMAGING CRITERIA Circle Yes or No as appropriate

Evidence of intracranial haemorrhage Yes No INITIAL

Evidence of structural CNS lesion which can mimic stroke(e.g. tumour, vascular malformation or abscess)

Yes No INITIAL

Evidence of well-established acute infarct likely to be older than 3 (4.5*) hours Yes No INITIAL

Large hypodensity on CT scan suggesting large infarct Yes No INITIAL

Answer to ALL of the above must be “No” to proceed with thrombolytic therapy

Scan reported by: ______________________________________ Designation: Consultant / SpR

Reported in: Radiology Dept. Via teleradiology

CT scan Performed Date: ___ / ___ / ___ Time: ___ : ___ hrs These times are included in

Reported Date: ___ / ___ / ___ Time: ___ : ___ hrs the SITS-ISTR audit

4. DISCUSSION WITH STROKE PHYSICIAN EXPERIENCED IN THROMBOLYTIC THERAPY

This patient meets the above criteria for thrombolysis for acute ischaemic stroke, and discussion took place

with Dr./Prof. _______________________ at ____________________Hospital (face-to-face / by

telephone / by telemedicine link*). The CT brain images were / were not viewed (in SRI / via teleradiology*)

by this consultant. Agreement was reached that this patient is eligible for thrombolytic therapy.

* Or an appropriately trained & experienced stroke physician is in attendance (* Delete as appropriate)

Signed: Print:

5. CONSENT / ASSENT Tick appropriate box

Discussion of potential risks and benefits should take place with the patient and/or next of kin.

Consent should be obtained from a capable patient (either verbal or written). If a patient is unable to giveinformed consent (e.g. due to dysphasia), then discussion should take place with their next of kin wherepossible. In such a case, or when there is no way to discuss with their next of kin in a timely manner,treatment is administered as an emergency treatment under the Adults With Incapacity Act 2000.

Consent obtained from patient

Assent from next-of-kin for an patient who cannot consent

Not possible to obtain either consent or assent

6. CONDITIONS Circle Yes or No as appropriate

1. Treatment will be given within 3 (4½*) hours of definite symptom onset Yes No INITIAL

2. Exclusion checklist has been completed with no contra-indications present or relative contra-indications which have been discussed and accepted

Yes No INITIAL

3. Brain imaging criteria have been met Yes No INITIAL

4. Discussion has taken place with a stroke physician experienced inthrombolytic therapy or such a physician in attendance

Yes No INITIAL

5. Consent/assent has been obtained Yes No INITIAL

6. Critical Care Bed is or will be available Yes No INITIAL

7. CONCLUSION Tick appropriate box

Is the patient to receive thrombolytic therapy? Yes No

Signed: Print: Designation:

Date: Time:

If YES, proceed to the Administration Protocol

If NO, document reason & proceed with BEST USUAL CARE





Name: DoB: CHI:

ADMINISTRATION PROTOCOL See Dosage Table

DELIVERY OF THROMBOLYSIS Ensure rt-PA prescribed on drug Kardex

NIHSS Score: _____ INITIAL

Actual Weight / Estimated Weight _____kg INITIAL

Total rt-PA dose – 0.9mg/kg body weight to a maximum dose of 90mg

Dose= weight(kg) _____ x 0.9 = _____mg See Dosage Table INITIAL

Administration is by a bolus IV injection (over 1 to 2 minutes) of 10% of the totaldose, followed by an IV infusion of the remaining 90% over 1 hour

Bolus Dose (10%): _____mg Infusion Dose (90%): _____mg

INITIAL

Bolus Dose Delivered at: Time: ___ : ___ hr on Date: ___ / ___ / ___

Infusion Started at: Time: ___ : ___ hr on Date: ___ / ___ / ___

INITIAL

INITIAL

OBSERVATION & FURTHER PROCEDURES

During infusion and for first 12 hours patient should have high dependency monitoring and nursing,with an EWS chart, following the “Nursing Protocol” for stroke thrombolysis

During the first 24 hours, the following procedures/treatments should be avoided:Urinary Catherterisation Central Venous Access Arterial PunctureNG Tube Insertion Aspirin or other anti-platelets

During the first 48 hours, the following procedures/treatments should be avoided:Intra-muscular injections Heparin / LMWH / Anticoagulants

A repeat CT Brain scan should be performed 24 to 36 hours from treatment

FOR MANAGEMENT OF COMPLICATIONS – SEE APPROPRIATE INSTRUCTION CARD

BASELINE BLOOD RESULTS (not all are necessary before treatment)

Na Hb APTT AST

K WCC APTT control ALT

Cl Platelets PT Bil

Urea MCV PT control T Prot

Creatinine Cholesterol INR Alb

Glucose CRP Alk Phos

ADDITIONAL NOTES

Signed: Print: Date:





Name: DoB: CHI:

NIH Stroke Scale – Serial RecordingsPre-

Treatment2 hour 24 hour 7 day

†

Date

Time

1a. Level of

Consciousness

0 = Alert; keenly responsive1 = Not alert; but rousable by minor stimulation

2 = Not alert; requires repeated stimulation to attend3 = Unresponsive; reflex movements only

1b. LOC Questions Ask patient the month

and their age

0 = Answers both questions correctly1 = Answers one question correctly2 = Answers neither question correctly

1c. LOC CommandsOpen & close eyesand grip & release withnon-paretic hand

0 = Performs both tasks correctly1 = Performs one task correctly2 = Performs neither task correctly

2. Best GazeHorizontal eye

movements only

0 = Normal1 = Partial gaze palsy2 = Forced Deviation not overcome by oculocephalic manoeuvre

3. Visual Fields

0 = Normal1 = Partial Hemianopia2 = Complete Hemianopia

3 = Bilateral Hemianopia (blind including cortical blindness)

4. Facial Palsy

0 = Normal1 = Minor paralysis (flattened nasolabial fold, asymmetry on smiling)

2 = Partial paralysis(total or near total paralysis of lower face) 3 = Complete paralysis of one or both sides (absence of facial

movement in the upper and lower face)

5. Motor Function -

Arm

0 = Normal; limb holds 90 (or 45) degrees for 10 seconds without drift

1 = Drift; limb holds 90 (or 45) degrees but drifts down before full 10

seconds but does not hit bed or other support 2 = Some effort against gravity 3 = No effort against gravity; limb falls 4 = No movementUN – Untestable; joint fused or amputated

R

L

6. Motor Function –

Leg

0 = Normal; leg holds 30 degree position for 5 seconds 1 = Drift; leg falls by end of 5 second period but does not hit bed

2 = Some effort against gravity 3 = No effort against gravity; limb falls 4 = No movementUN – Untestable; joint fused or amputated

R

L

7. Limb Ataxia Finger/nose & heel/shinboth sides. Ataxiadisproportionate toweakness only

0 = No ataxia or paralysed/comatose/does not understand 1 = Present in one limb2 = Present in two limbsUN = Untestable only if amputation or joint fusion

8. Sensory0 = Normal; no sensory loss 1 = Mild to moderate sensory loss: aware of touch2 = Severe to total sensory loss

9. Best Language

0 = No aphasia1 = Mild to moderate aphasia; loss of fluency or comprehension 2 = Severe aphasia; fragmented communication 3 = Mute, global aphasia;no useable speech or auditory comprehension

10. Dysarthria

0 = Normal1 = Mild to moderate dysarthria; slurring of words,

at worst can be understood with some difficulty

2 = Severe dysarthria unintelligible or unable to speak

(out of proportion to aphasia)

UN = Untestable due to intubation or other physical barrier

11. Extinction &Inattention

0 = No abnormality1 = Inattention or extinction to bilateral simultaneous stimulation

in one sensory modality

2 = Profound hemi-inattention to more than one modality

Total Score

Assessors Initials

* Time intervals as per SITS audit. Interval refers to time from completion of infusion. † 7 days post-treatment or discharge from hospital.





Criteria for Extended Time Window Thrombolytic Therapy (3 to 4½ hours from onset)

Following the ECASS-3 study1, benefits have been seen in selected patients treated beyond the previous 3 hour time

window for thrombolytic therapy. Recommendations taking this information into account are as follows;

Patients with acute ischaemic stroke who are eligible for treatment with rt-PA within 3 hoursshould be treated as recommended in existing guidelines. Although a longer time window for treatment with rt-PA has been formally tested, delays in evaluation and initiation of therapy

should be avoided because the opportunity for improvement is greater with earlier treatment.

Treatment with rt-PA should be administered to eligible patients who can be treated in thetime period 3 to 4.5 hours. The eligibility criteria for treatment in this period are similar tothose treated at earlier period with the additional exclusion criteria:

o Patients older than 80 yearso Patients taking oral anticoagulants, regardless of the INR o Patients with a baseline NIHSS>25o Patients with a history of both previous stroke and diabetes

Onset to treatment time should be minimised.

The use of rt-PA in the 3 to 4.5 hour time window remains unlicensed (September 2011)

All treatments should continue to be supervised by a physician appropriately trained andexperienced in the delivery of thrombolysis for acute ischaemic stroke.

Background Information - The ECASS-3 study1

was a multicentre, prospective, randomised, placebo-controlled

trial examining the efficacy and safety of thrombolysis with rt-PA in acute ischaemic stroke administered between 3and 4.5 hours of definite symptom onset. The trial used the same dosing regimen as described above. The trialexcluded patients older than 80 years, those with a baseline NIHSS>25, those taking oral anticoagulants (regardlessof INR value), and those with a history of stroke and diabetes mellitus. Otherwise, inclusion & exclusion criteria weresimilar to those in the American Heart Association Stroke Council 2007 guidelines for thrombolysis within 3 hours.

821 patients were enrolled, 418 to the treatment group and 403 to the placebo group. 10% were treated 3 to 3.5 hoursfrom onset, 47% were treated 3.5 to 4 hours and 39% were treated 4 to 4.5 hours. Median time was 3 hours 59minutes.

Symptomatic intracranial haemorrhage was more common in patients treated with thrombolysis .By ECASS-3 definition, it was diagnosed in 10 patients treated with rt-PA (2.4%) and 1 patient with placebo (0.2%)[odds ratio 9.85, 95% CI 1.26 to 77.32, p=0.008]. By the NINDS

2definition, symptomatic intracranial haemorrhage

was diagnosed in 33 patients treated with rt-PA (7.9%) and 14 patients given placebo (3.5%) [odds ratio 2.38, 95% CI1.25 to 4.52, p=0.006].

A favourable outcome was more common in patients treated with thrombolysis than placebo.The frequency of the primary efficacy outcome in ECASS-3 (defined as modified Rankin Scale score of 0 to 1 at 90days after treatment) was significantly greater with rt-PA (52.4%) than with placebo (45.2%) [OR 1.34, 95% CI 1.02 to1.76; risk ratio 1.16, 95% CI 1.01 to 1.34; p=0.04].

The mortality between treatment and placebo groups did not differ significantly.90-day mortality in the group treated with rt-PA was 7.7% compared to 8.4% in the placebo group (p=0.68).

Treatment Benefit is strongly time dependent.The number needed to treat (NNT) to gain one more favourable outcome is 2 with treatment within 90 minutes, fallingto 7 when treated within 3 hours, falling to 14 when treated between 3 and 4.5 hours. This has been consistentlyshown in other analyses

3.

This study, along with analysis of the “Safe Implementation of Thrombolysis in Stroke – International Stroke TreatmentRegistry 3 to 4.5 hour study” (SITS-ISTR 3 to 4.5 hour)

4, and other studies has lead to recommendations from the

American Heart Association / American Stroke Association (AHA/ASA)5, the European Stroke Organisation (ESO)

6,

and the Scottish Intercollegiate Guideline Network (SIGN)7which can be summarised as above.

1. Hacke W et al. Thrombolysis with alteplase 3 to 4.5 hours after acute ischaemic stroke. N Engl J Med. 2008;359:1317-13292. The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. Tissue plasminogen activator for acute ischemic stroke. N Engl J Med . 1995;333:1581 –1587.3. Hacke W et al. Association of outcome with early stroke treatment: pooled analysis of ATLANTIS, ECASS and NINDS rt-PA stroke trials. Lancet 2004;363:768-744. Wahlgren N et al. SITS Investigators. Thrombolysis with alteplase 3-4.5 hours after acute ischaemic stroke (SITS-ISTR): an observational study. Lancet . 2008;372:1303-13095. del Zoppo GJ et al. Expansion of the time window for treatment of acute ischaemic stroke with intravenous tissue plasminogen activator. Stroke. 2009;40:2945-29486. ESO. Guidelines for Management of Ischaemic Stroke and Transient Ischaemic Attack 2008. URL http://www.eso-stroke.org/pdf/ESO%20Guidelines_update_Jan_2009.pdf 7. Scottish Intercollegiate Guidelines Network. Management of patients with Stroke or TIA. December 2008. ISBN 978 1 905813 40 7. www.sign.ac.uk




v 2.01 FINAL March 2011

THROMBOLYSIS FOR ACUTE ISCHAEMIC STROKEHow to administer rt-PA

Equipment

Actilyse –

Two 50mg bottles (only one needed if patient 54kg or less) Syringe for initial bolus – 5ml or 10ml syringe

Syringes for infusion – Two 50ml luer-lock type

Syringe driver capable of taking 50ml syringe

Labels, needles, giving set etc.

How to administer

Open the actilyse vials only when the decision has been made totreat the patient.

Dissolve the drug using the solution within the pack. If two vials needed, dissolve both bottles simultaneously to save time.

Use the Dosing Chart to select the appropriate dose of Actilyse for the patient

Solution concentration should be 1mg/ml

Draw up the Bolus Dose a 5ml or 10ml syringe and administer intravenouslyover 2-3 minutes.

Draw up the first Infusion Dose in a 50ml syringe, insert in the syringe driver

and prime the infusion line. Set the Syringe driver to the appropriate infusion rate and start the infusion as

soon as possible after the bolus has been given

If a second syringe is needed (patients 64kg and above), have this drawn upand ready before the first syringe has finished.

Swap syringes as soon as the first has gone through.

The infusion rate for the second syringe is the same as for the first.

If two bottles of Actilyse are needed, then it is easier to use one bottle for theBolus dose and second Infusion syringe, and the other full 50ml bottle for the

first infusion syringe.

If during the infusion there is suspicion of an adverse reaction then stop theinfusion immediately e.g.

- Haemorrhage - Anaphylaxis - Oral/lingual angioedema

Follow the appropriate algorithm to treat the adverse reaction.

Remember that haemorrhage and oral/lingual angioedema can occur hours

after the treatment has been completed.



v 2.01 FINAL March 2011

THROMBOLYSIS FOR ACUTE ISCHAEMIC STROKErt-PA Dosage Table

WeightTotal Dose

(mg)Bolus Dose

(mg)Infusion Dose

(mg)

Infusion Administration(50ml Syringes, 1mg/ml concentration)

kg st lb 1st Syringe 2nd SyringeInfusion Rate*

(ml/hr)

40 6 4 36.0 3.6 32.4 32.4 N/A 32.4

42 6 8 37.8 3.8 34.0 34.0 N/A 34.0

44 6 13 39.6 4.0 35.6 35.6 N/A 35.6

46 7 3 41.4 4.1 37.3 37.3 N/A 37.3

48 7 8 43.2 4.3 38.9 38.9 N/A 38.9

50 7 12 45.0 4.5 40.5 40.5 N/A 40.5

52 8 2 46.8 4.7 42.1 42.1 N/A 42.1

54 8 7 48.6 4.9 43.7 43.7 N/A 43.7

56 8 11 50.4 5.0 45.4 45.4 N/A 45.4

58 9 2 52.2 5.2 47.0 47.0 N/A 47.0

60 9 6 54.0 5.4 48.6 48.6 N/A 48.6

62 9 11 55.8 5.6 50.2 50.2 N/A 50.2

64 10 1 57.6 5.8 51.8 50.0 1.8 51.8

66 10 5 59.4 5.9 53.5 50.0 3.5 53.5

68 10 10 61.2 6.1 55.1 50.0 5.1 55.1

70 11 0 63.0 6.3 56.7 50.0 6.7 56.7

72 11 5 64.8 6.5 58.3 50.0 8.3 58.374 11 9 66.6 6.7 59.9 50.0 9.9 59.9

76 11 13 68.4 6.8 61.6 50.0 11.6 61.6

78 12 4 70.2 7.0 63.2 50.0 13.2 63.2

80 12 8 72.0 7.2 64.8 50.0 14.8 64.8

82 12 13 73.8 7.4 66.4 50.0 16.4 66.4

84 13 3 75.6 7.6 68.0 50.0 18.0 68.0

86 13 8 77.4 7.7 69.7 50.0 19.7 69.7

88 13 12 79.2 7.9 71.3 50.0 21.3 71.3

90 14 2 81.0 8.1 72.9 50.0 22.9 72.9

92 14 7 82.8 8.3 74.5 50.0 24.5 74.5

94 14 11 84.6 8.5 76.1 50.0 26.1 76.1

96 15 2 86.4 8.6 77.8 50.0 27.8 77.8

98 15 6 88.2 8.8 79.4 50.0 29.4 79.4

100+ 15 10 90.0 9.0 81.0 50.0 31.0 81.0

* Infusion rate is the same for both the first and second syringes.

The above table has been checked by the Pharmacy Department and ratified as correct.



Adapted from Lothian University Hospitals NHS Trust Nursing Protocol for the IST-3 trial v1.02 FINAL March 2011

THROMBOLYSIS FOR ACUTE ISCHAEMIC STROKENURSING PROTOCOL

ACTION RATIONALE

Ensure that the bed space is appropriately

equipped with oxygen, suction, drip stand,O2 saturation monitor, cardiac monitor andmanual sphygmomanometer

The patient needs close monitoring for aminimum of 24 hours.

Patients receiving thrombolysis can deterioratequickly, therefore it is essential that they aremonitored closely and emergency equipmentneeds to be accessible.

Record a full set of baseline neurologicalobservations and vital signs. Document andreport any unusual observations

Baseline observations are necessary and areuseful in detecting any deterioration during or post treatment

Following administration of the treatment, vitalsigns and GCS need to be monitored asfollows:

Every 15 minutes for 2 hours (using amanual BP cuff)

Every 30 minutes for the next 6 hours

Hourly for a further 6 hours

4 hourly for the next 36 hours

If there is any cause for concern, review, report,document and increase observation frequencyaccordingly

Close observation of vital signs and the GCS isessential to detect any deterioration in the

patient’s condition as early as possible.Deterioration may be due to an intracranial or extracranial haemorrhage.

Manual BP cuffs are recommended sincemechanical cuffs, when used frequently inpatients receiving thrombolytics, can causesevere bruising and bleeding.

Immediately report any signs of bleeding or deterioration in the patients condition to the

senior nurse and the medical team looking after the patient

To ensure that every effort can be made to

prevent serious bleeding or other complications

Avoid giving IM injections for 48 hours fromtime of treatment administration

IM injections can cause bleeding at the injectionsite in patients who have received thrombolytictherapy

Avoid giving heparin or warfarin. Refer to thedoctor in charge before commencing anyanticoagulant therapy. Do not give aspirinuntil post treatment CT scan results areavailable

Anticoagulants are contraindicated in patientswho have received thrombolysis due to theincreased risk of bleeding

Avoid: urinary catheterisation (until at least 30minutes after infusion has finished); passing anasogastric tube (for 24 hours). Check withmedical staff if this is required

Carrying out these procedures can causebleeding

Should haemorrhage be diagnosed please sendsamples for urgent FBC, clotting screen andGroup & SaveRefer to the appropriate protocol for extracranialor intracranial haemorrhage

These results can enable an abnormality to bedetected and early treatment initiated



Adapted from Lothian University Hospitals NHS Trust Nursing Protocol for the IST-3 trial v1.02 FINAL March 2011

THROMBOLYSIS FOR ACUTE ISCHAEMIC STROKE – NURSING PROTOCOL

ACTION RATIONALE

Blood pressure is to be maintained between110/60 and 240/120mmHgIf BP outside these parameters call theappropriate doctor.

To maintain adequate cerebral perfusionpressure to perfuse the brain, but reduce therisk of intracerebral bleeding due tohypertension

Signs of raised intracranial pressure or intracranial bleeding:

unequal pupils

sudden drop in GCS

onset of drowsiness

onset of nausea, vomiting, sometimesphotophobia

Rising BP and falling pulse

To diagnose if there has been a further intracranial event and seek urgent assistance

In the event of a sudden drop in GCS or change

in vital signs an urgent medical review isessential.

Early detection and intervention can minimise

complications. An urgent CT scan can bearranged to help detect complications of treatment

If temperature is elevated above 370C, treatwith PR or PO paracetamol 1g 4 hourly. Reportany sustained pyrexia

Increased temperature is detrimental torecovery in patients who have suffered brainattacks

Consider an anaphylactoid reaction if thepatient develops rash, urticaria, bronchospasm,angioedema, and hypotensionStop rt-PA infusion obtain immediate medical

assistance

Anaphylaxis is a rare but life-threateningcomplication.

Ensure thrombolytic drug is prescribed on drugchart

According to NHS Forth Valley policy all drugsshould be prescribed

If unsure seek helpREMEMBER “TIME IS BRAIN”

Early intervention can limit complications



Adapted from Lothian University Hospitals NHS Trust Protocol v1.01 FINAL March 2011

THROMBOLYSIS FOR ACUTE ISCHAEMIC STROKENursing Pathway Summary

Preparation for patient arrival

Minimum Equipment required: Supplementary Oxygen O2 Saturation Monitor Suction

Manual sphygmomanometer

Syringe pump

Drip stands

On arrival of patient

Record basic observations on chart GCS Pulse Blood pressure O2 saturation

Thrombolytic Therapy

Where thrombolytic therapy has not been given: Initial bolus of thrombolytic to be given over 1-2 minutes by doctor Remainder of treatment to be given over 1 hour via syringe driver

Observation of Vital Signs & GCS

Every 15 minutes for 2 hours

Every 30 minutes for next 6 hours

Every hour for a further 6 hours

Every 4 hours for next 36 hours

IF THERE ARE ANY SIGNS OF BLEEDING OR THE PATIENT DETERIORATES IN ANY WAY,IMMEDIATELY CONTACT THE RESPONSIBLE MEDICAL TEAM

Post – treatment interventions

In the 24 hours post treatment avoid the following to minimise the risk of haemorrhage: Urinary catheterisation Nasogastric tube Central venous cannulation Arterial punctureThe procedures may be necessary but should be discussed with medical team

Avoid intra-muscular injections for 48 hours

Avoid anticoagulant therapy

Do not give aspirin until post-treatment CT results available

Consider paracetamol for pyrexia

Unless there are problems which require emergency brain imaging (see below), a CT brain scanshould be requested the day after treatment. This would normally be during working hours at atime most approximate to 24 hours post-treatment.

If progress is uncomplicated, patient will likely be ready to step down to ward-level care after 24 hours

Outcomes following thrombolysis

Comparing treatment with thrombolysis to “best usual therapy” (aspirin and supportive care) in anappropriate population of patients with acute ischaemic stroke:

There is a 1-in-10 greater chance of living independently after treatment with thrombolysis(50% compared to 41%)

There is no excess of deaths following thrombolysis (18% for both groups)

There is a higher risk of intracranial haemorrhage following thrombolysis(approx. 1-in-20 compared to 1-in-100)

There is also a small risk of extracranial haemorrhage or allergic reaction

Appropriately selected patients are more likely to benefit from thrombolysis than to come to harm



Adapted from Lothian University Hospitals NHS Trust Protocol v1.01 FINAL March 2011

HROMBOLYSIS FOR ACUTE ISCHAEMIC STROKE – NURSING SUMMARY

THROMBOLYSIS FOR ACUTE ISCHAEMIC STROKE – NURSING SUMMARY

Potential Complication – Extracranial Haemorrhage see appropriate protocol

Potential bleeding sites include (list not exhaustive): Arterial & venous puncture sites GI tract Urinary tract Retroperitoneum

Occult injuries sustained if fell/collapsed at onset of stroke Suspect if -

Clinical signs of hypovolaemic shock – tachycardia, fall in blood pressure, peripheral shutdown Evidence of blood loss such as melaena or haematuria

Stop rt-PA infusion immediately

Use mechanical compression to control bleeding if possible

Check coagulation screen (PT, APTT, fibrinogen) and full blood count

Send blood for “Group & Save” or cross-match depending on the situation

Support circulation with intravenous fluids or blood transfusion as appropriate

Discuss case & test results with haematologist

Transfusion of fresh frozen plasma, cryoprecipitate and platelets may be necessary, depending onresult of coagulation screen and advice of haematologist

For severe life-threatening haemorrhage, a fibrinolytic inhibitor should be given immediatelye.g. tranexamic acid 1g IV over 15 minutes repeated every 8 hours as necessary1

Delay any surgery until the fibrinolytic state is corrected

Potential Complication – Intracranial Haemorrhage see appropriate protocol

Suspect if - Neurological deterioration New Headache Fall in conscious level Seizure Nausea or vomiting

Stop rt-PA infusion immediately Arrange an urgent CT brain scan


Send blood for “Group & Save”

Support circulation with intravenous fluids if necessary


Correct fibrinolytic state as advised

If intracranial bleeding confirmed, discuss possibility of evacuating haematoma with neurosurgeonsat Western General Hospital, Edinburgh

If no intracranial haemorrhage is found on CT (or insufficient to explain symptoms), look for other causes of the deterioration

Potential Complication – Anaphylaxis see appropriate protocol

Suspect if patient develops

Rash Urticaria Bronchospasm Angioedema Hypotension Shock

Stop rt-PA infusion

Urgent medical assessment – Airway, Breathing, Circulation, Disability, Exposure

High flow oxygen

Adrenaline 1:1000 solution 0.5ml IM (repeat if necessary)

Antihistamine – Chlorphenamine 10-20mg IV slowly

Hydrocortisone 100-200mg IV slowly, IV Fluid challenge, Salbutamol nebs



Adapted from Lothian University Hospitals NHS Trust Protocol v1.03 FINAL September 2011

THROMBOLYSIS FOR ACUTE ISCHAEMIC STROKEManagement of Suspected Intracranial Haemorrhage

Suspect intracranial haemorrhage if:

Neurological deterioration New Headache Fall in conscious level

Seizure Nausea or vomiting

Standard Management


Arrange an urgent CT brain scan


Send blood for “Group & Save”

Support circulation with intravenous fluids if necessary


Correct fibrinolytic state as advised

If intracranial bleeding confirmed, discuss possibility of evacuating haematoma with neurosurgeonsat Western General Hospital, Edinburgh

If no intracranial haemorrhage is found on CT (or insufficient to explain symptoms), look for other causes of the deterioration

Blood products are supplied by the Blood Transfusion laboratory once sanctioned by ahaematologist. Tranexamic acid is stored in cupboards in the Emergency Department, Critical CareUnit, theatres, ward 6, ward 7 & the emergency drug cupboard in FVRH

Other Information

The manufacturers of rt-PA, Boehringer Ingelheim1 suggest that in potentially dangerous haemorrhage, inparticular cerebral haemorrhage, the fibrinolytic therapy must be discontinued. Their advice is that mostpatients can then be managed with volume replacement. It is rarely necessary to replace the clotting

factors because of the short half-life of the drug and the minimal effect on the systemic coagulation factors.In those who fail to respond, transfusion of cryoprecipitate, fresh frozen plasma and platelets should beconsidered: seek the advice of your local haematologist. Antifibrinolytics (e.g. tranexamic acid) aresometimes used, but the benefits are unclear.

Clozel et al2 looked into the use of aprotinin as an antidote for rt-PA. In their small animal study they foundthat aprotinin immediately stopped thrombolysis, but the duration of this effect was dose dependent.However, this is now an unlicensed use for aprotinin and it is not stocked in Forth Valley. A study lookinginto intracranial haemorrhage after coronary thrombolysis3 found that the exact mechanisms behind thehaemorrhage were unclear. Their patients had received rt-PA and heparin and it was suggested thatexcessive prolongation of the APTT and elevated fibrin degradation products may have contributed to theoccurrence of intracranial haemorrhage. Hypofibrinogenemia was not a uniform finding. The British Society

of Haematology produced a consensus report in 1995 on guidelines for the use of thrombolysis. For severe life threatening bleeding they suggest a fibrinolytic inhibitor such as aprotinin (see above) or tranexamic acid and replacement of clotting factors depending upon the results of a coagulation screen.4

References

1. Boehringer Ingelheim. Summary of product characteristics for Alteplase2. Clozel JP, Banken L, Roux S. Aprotinin: an antidote for recombinant tissue-type plasminogen

activator (rt-PA) active in vivo. J Am Coll Cardiol . 1990 Aug;16(2):507-10.3. Kase CS, Pessin MS, Zivin JA et al. Intracranial haemorrhage after coronary thrombolysis with

tissue plasminogen activator. Am J Med . 1992 Apr;92(4):384-904. Ludlam CA, Bennet B, Fox KAA, Lowe GDO, Reid AW. Guidelines for the use of thrombolytic

therapy. Blood Coagulation and Fibrinolysis. 1995;6:273-285



Adapted from Lothian University Hospitals NHS Trust Protocol v1.03 FINAL September 2011

THROMBOLYSIS FOR ACUTE ISCHAEMIC STROKEManagement of Suspected Extracranial Haemorrhage

Suspect extracranial haemorrhage if:

Clinical signs of hypovolaemic shock – tachycardia, fall in blood pressure, peripheral shutdown etc.

Evidence of blood loss such as melaena or haematuria

Standard Management


Use mechanical compression to control bleeding if possible


Send blood for “Group & Save” or cross-match depending on the situation

Support circulation with intravenous fluids or blood transfusion as appropriate


Transfusion of fresh frozen plasma, cryoprecipitate and platelets may be necessary, depending onresult of coagulation screen and advice of haematologist

For severe life-threatening haemorrhage, a fibrinolytic inhibitor should be given immediately

e.g. tranexamic acid 1g IV over 15 minutes repeated every 8 hours as necessary1

Delay any surgery until the fibrinolytic state is corrected

Blood products are supplied by the Blood Transfusion laboratory once sanctioned by ahaematologist. Tranexamic acid is stored in drug cupboards in the Emergency Department, CriticalCare Unit, theatres, ward 6, ward 7 & the emergency drug cupboard in FVRH.

Other Information

Major bleeding is an infrequent but important complication of giving thrombolysis for acute ischaemicstroke. There are no definitive guidelines on the management of thrombolysis related bleeding, but thefollowing points are a guide to managing such a patient in a safe and appropriate way.

The manufacturer, Boehringer Ingelheim2

suggest that in potentially dangerous extracranial haemorrhage,the fibrinolytic therapy must be discontinued. Their advice is that most patients can then be managed withvolume replacement. It is rarely necessary to replace the clotting factors because of the short half-life of thedrug and the minimal effect on the systemic coagulation factors. In those who fail to respond, transfusionof cryoprecipitate, fresh frozen plasma and platelets should be considered. Antifibrinolytics can be used,but the benefits are unclear.

Clozel et al3 looked into the use of aprotinin as an antidote for rt-PA. In their small animal study they foundthat aprotinin immediately stopped thrombolysis, but the duration of this effect was dose dependent.However, this is now an unlicensed use for aprotinin and it is not stocked in Forth Valley. A study lookinginto intracranial haemorrhage after coronary thrombolysis4 found that the exact mechanisms behind thehaemorrhage were unclear. Their patients had received rt-PA and heparin and it was suggested thatexcessive prolongation of the APTT and elevated fibrin degradation products may have contributed to theoccurrence of intracranial haemorrhage. Hypofibrinogenemia was not a uniform finding.

The British Society of Haematology produced a consensus report in 1995 on guidelines for the use of thrombolysis. For severe life threatening bleeding they suggest a fibrinolytic inhibitor such as aprotinin (seeabove) or tranexamic acid and replacement of clotting factors depending upon the results of a coagulationscreen.2

References

1. Ludlam CA, Bennet B, Fox KAA, Lowe GDO, Reid AW. Guidelines for the use of thrombolytic therapy. Blood Coagulationand Fibrinolysis. 1995;6:273-285

2. Boehringer Ingelheim. Summary of product characteristics for Alteplase3. Clozel JP, Banken L, Roux S. Aprotinin: an antidote for recombinant tissue-type plasminogen activator (rt-PA) active in

vivo. J Am Coll Cardiol . 1990 Aug;16(2):507-10.4. Kase CS, Pessin MS, Zivin JA et al. Intracranial haemorrhage after coronary thrombolysis with tissue plasminogen

activator. Am J Med . 1992 Apr;92(4):384-90



v2.02 FINAL March 2011

THROMBOLYSIS FOR ACUTE ISCHAEMIC STROKEManagement of Suspected Anaphylactic Reaction

Suspect anaphylactic reaction if:

Consider if any of the following develop: Rash Urticaria Bronchospasm

Angioedema

Hypotension

Shock

Treat as severe if: Airway compromise Clinical signs of shock

Treatment Algorithm for Anaphylactic Reactions Adapted from Resuscitation Council UK Guidance. 2008

Page 1 of 2

Suspected Anaphylactic Reaction

Airway, Breathing, Circulation, Disability, Exposure

Diagnosis - look for:• Acute onset of illness • Life-threatening Airway and/or Breathing and/or Circulation problems

1

• Any usually skin changes

High Flow Oxygen

Lie patient flat. Call for Help

ADRENALINE

1:1000 solution0.5ml (500 micrograms) IM

2

Monitor

Blood Pressure

ECG

O2 Saturation

Repeat in 5 minutes if no clinicalimprovement

STOP rt-PA INFUSION

AntihistamineCHLORPHENAMINE

10-20mg slow IV

IN ADDITION

For all severe or recurrent reactionsand patients with asthma give

HYDROCORTISONE 200mg slow IV

IV Fluid Challenge500 to 1000ml

Nebulised SALBUTAMOL may beused as an adjunctive measure if

bronchospasm is severe and doesnot respond to other treatment

1. Life Threatening Problems

Airway: Swelling, Hoarseness, Stridor Breathing: Rapid breathing, wheeze, fatigue, cyanosis, SpO2 < 92%, confusion Circulation: Pale, clamm , low blood ressure, faintness, drows /coma

2. Risk from anaphylaxis

outweighs risk of

haemorrhage from IM

injection. Therefore give

adrenaline as per usual

protocol

TONGUE ANGIOEDEMA

See additional notes

over page



v2.02 FINAL March 2011

FACIAL / TONGUE ANGIOEDEMA

Background: Angioedema of the tongue has been reported in occurring in patients receiving rt-PA

Cases series report a frequency of 1.3% to 5%1,2 (more frequently than in myocardial infarction)

It usually manifests as mild, transient hemifacial swelling starting in the tongue, usually contra-lateral to the ischaemic hemisphere, and resolves within 24hours1

Angioedema can develop hours after the rt-PA infusion is completed Combined observational data suggest severe, life-threatening airway compromise requiring

anaesthetic intervention is rare – 0.2 to 0.8% of all patients receiving rt-PA1,2,3 or 13% of thosedeveloping angioedema

Risk factors for developing angioedema are current use of ACE-inhibitors and involvement of theinsular/frontal cortex in the acute stroke

Treatment:

If ANY features of angioedema occur STOP THE INFUSION IMMEDIATLEY (if not already completed).

If not already in attendance, fast-page on-call MEDICAL MIDDLE GRADE

Contact on-call ANAESTHETIST

Commence treatment for anaphylaxis as aboveo High Flow oxygeno Chlorphenamine 10mg IVo Hydrocortisone 200mg IV

Consider NEBULISED ADRENALINE (5ml of 1:1000 solution driven by 100% oxygen)o ENSURE EYE PROTECTION with goggles/wet swabs or paper towelso Can be repeated 2-3 hourly as required

If no response to nebulised adrenaline within 5 minutes then giveIM ADRENALINE 500micrograms (0.5ml of 1:1000 solution)

o

Risks associated with anaphylaxis outweigh the risks of haemorrhage related to IM injectionduring or after thrombolytic therapy

Advanced airway management may be necessary if airway is significantly compromised, althoughthere are specific risks associated with stroke and thrombolytic therapy

o Airway haemorrhage due to trauma from intubation and thrombolysiso A drop in blood pressure due to rapid sequence induction may reduce cerebral perfusion

pressure and increase the volume of ischaemic brain

However, hypoxia due to airway compromise/loss will increase the risk of poor outcome

Ongoing treatment o Once stabilised transfer to HDU or ITU as appropriate (following stroke thrombolysis the

patient will normally be treated in HDU for first 24 hours).o Chlorphenamine 10mg IV tdso Hydrocortisone 100mg IV tdso Nebulised Adrenaline as required

1. Hill MD, et al. Hemi-orolingual angioedema and ACE inhibition after alteplase treatment of stroke. Neurology 2003; 60: 1525-15272. Hill MD, et al for the Canadian Alteplase for Stroke Effectiveness Study (CASES) Investigators. Thrombolysis for acute ischemic stroke:

results of the Canadian Alteplase for Stroke Effectiveness Study. Canadian Medical Association Journal 2005; 172:1307-13123. Engelter ST, et al. Life threatening orolingual angioedema during thrombolysis in acute ischemic stroke. Journal of Neurology 2005;

252:1167-1170

Page 2 of 2



CLOT-BUSTING TREATMENT FOR ACUTE STROKEPATIENT INFORMATION

FV Acute Stroke TeamMarch 2011

Standard Clot-Buster

You/your relative has had a stroke because an artery supplying blood to thebrain has been suddenly blocked by a clot.

The best treatment at present is to try unblocking this artery by injecting a“clot-busting” drug called Alteplase. The medical term f or “clot-busting” is thrombolysis.

The injection must be started within 4½ hours of the start of the stroke (for some groupsthis is limited to within 3 hours). Giving the treatment as soon as possible increases thechance of a good recovery and reduces the risk of problems because of the treatment.

This treatment gives a better chance of recovering fully from a stroke.

Above graphs are for treatment started within 3 hours of the start of stroke symptoms

A patient has a 1 in 10 greater chance of living independently after treatment with the clotbusting drug. (50% compared to 41%)

There is a higher chance of bleeding into the brain (1 in 20 with clot-busting compared to 1

in 100 without) or bleeding elsewhere immediately after the injection and a small risk of allergic reaction.

But, overall, patients are more likely to benefit from Alteplase than come to harm.

Clot-Busting Treatment

Independent 50%

Dependent32% Dead

18%

Standard Treatment

Independent 41%

Dependent41%

Dead18%



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