Download Stroke Guidelines - West Coast District Health Board

Stroke Guidelines
CONTENTS
1 Document Management ...................................................................................................... 4
1.1 Manual Authorisation .................................................................................................... 4
1.2 Staff Familiarity with Document..................................................................................... 4
1.3 Distribution of Documents ............................................................................................. 4
1.4 Amendments to Previous Issue .................................................................................... 4
1.5 Amendments to Future Issue will be documented here Amendments ........................... 4
2 Organisation of Stroke Services .......................................................................................... 5
2.1 Acute Stroke Admission Policy ..................................................................................... 5
2.2 Discharge Planning – Medical Ward ............................................................................. 6
2.2.1 Referral guidelines for ongoing rehabilitation .......................................................... 6
2.2.2 Driving Guidelines .................................................................................................. 9
3 Acute Management of Stroke ............................................................................................ 11
3.1 Thrombolysis Protocol ................................................................................................ 11
3.1.1 Inclusions: ............................................................................................................ 11
3.1.2 Exclusions and Precautions: ................................................................................ 11
3.1.3 Medical Assessment Protocol Instructions ........................................................... 12
3.1.4 ALTEPLASE for Acute Ischaemic Stroke ............................................................. 13
3.1.5 NURSING PROTOCOL ........................................................................................ 15
3.2 Acute BP management first 7 Days after stroke .......................................................... 19
3.2.1 BP Monitoring....................................................................................................... 20
3.2.2 Antihypertensive medication for Secondary Prevention after stroke or TIA........... 21
3.2.3 Hypotension ......................................................................................................... 21
3.3 Malignant Cerebral Oedema / Hemicraniectomy Guideline ......................................... 22
3.3.1 “Malignant Infarction” Guideline ............................................................................ 22
3.3.2 Malignant Infarction Guideline Procedures: .......................................................... 23
3.4 Acute Management of Intracerebral Haemorrhage ..................................................... 24
3.5 Intracerebral Haemorrhage whilst on warfarin: Reversal of the warfarin related
coagulopathy .................................................................................................................... 24
4 Inpatient Care ................................................................................................................... 26
4.1 The Acute Stroke Swallow Screen for dysphagia trained nurses ................................ 26
4.2 Communication for patients with disability following stroke ......................................... 29
4.3 Hydration Guideline .................................................................................................... 29
4.3.1 Guideline for hydration after acute stroke ............................................................. 29
4.4 Nutrition Guideline ...................................................................................................... 30
4.4.1 Guidelines ............................................................................................................ 30
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Stroke Guidelines
4.4.2 All Patients ........................................................................................................... 30
4.4.3 Patients receiving ongoing dietetic input............................................................... 31
4.4.4 Patients receiving enteral feeding......................................................................... 31
4.4.5 Decision to institute enteral feeding ...................................................................... 31
4.5 Diabetes Guidelines.................................................................................................... 32
4.5.1 Guideline for Hyperglycaemia after Acute Stroke ................................................. 32
4.5.2 General Recommendations: ................................................................................. 32
4.5.3 Management of Patients with Known Diabetes or Documented Hyperglycaemia . 32
4.5.4 All Diabetic Patients Post Stroke .......................................................................... 32
4.5.5 Insulin Requiring Diabetes.................................................................................... 33
4.5.6 Type 2 Diabetes ................................................................................................... 33
4.5.7 Type 2 Diabetes on Diabetic Diet Alone or Antidiabetic Agents ............................ 34
4.5.8 Patients with Raised Blood Sugar on Admission .................................................. 34
4.6 Transferring Patient from Bed to Chair Guidelines ...................................................... 35
4.6.1 Transferring Checklist .......................................................................................... 35
4.7 Management of the Hemiplegic Upper Limb ............................................................... 35
4.7.1 Assessment of the Hemiplegic Upper Limb .......................................................... 36
4.7.2 Pain ...................................................................................................................... 36
4.7.3 Positioning ........................................................................................................... 37
4.7.4 Sensation ............................................................................................................. 38
4.7.5 Shoulder Subluxation ........................................................................................... 38
4.7.6 Oedema ............................................................................................................... 38
4.7.7 Spasticity.............................................................................................................. 39
4.7.8 Splinting ............................................................................................................... 39
4.7.9 FES ...................................................................................................................... 40
4.7.10 Strapping ............................................................................................................ 40
4.8 DVT / PE Prophylaxis Guideline ................................................................................. 41
4.8.1 Venous Thromboembolism Prevention in Stroke Patients .................................... 41
4.8.2 Guidelines for the prevention of Venous Thromboembolism................................. 41
4.9 Urinary Incontinence ................................................................................................... 43
4.9.1 Stroke Continence Protocols ................................................................................ 43
4.9.2 Urinary Incontinence Assessment Source: Dunedin Acute Stroke Unit................. 43
4.10 Formal Family Meeting Guidelines ............................................................................ 50
4.10.1 Purpose.............................................................................................................. 50
4.10.2 Introduction ........................................................................................................ 50
4.10.3 Procedure .......................................................................................................... 50
4.11 Palliative Care .......................................................................................................... 52
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5 Transient Ischaemic Attack (TIA) Guidelines ..................................................................... 53
5.1 Acute Management in the ED /Medical Ward.............................................................. 53
5.1.1 Transient Ischaemic Attack (TIA) Acute Management in the ED/Medical Ward .... 53
5.1.2 Transient Ischaemic Attack (TIA) Acute Management In the ED / AMAU / ASU
Guidelines ..................................................................................................................... 54
6 Secondary Prevention Guideline ....................................................................................... 60
6.1 Secondary Prevention after Stroke ............................................................................. 60
6.2 Antiplatelet Therapy .................................................................................................... 61
6.3 Anticoagulation ........................................................................................................... 61
6.4 Carotid Endarterectomy .............................................................................................. 61
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Stroke Guidelines
1 Document Management
1.1 Manual Authorisation
This manual has been through a review process and achieved signoff from
• Stroke Physician General Medicine.
1.2 Staff Familiarity with Document
Staff are expected to become familiar with the contents of this manual. And keep up to date
with additions and amendments. The information in this manual applies to all staff who work
as part of the stroke services offered within the West Coast District Health Boards, these
areas of practice include Emergency Department, the Critical Care Unit, Medical and ATR
ward. Evidence of familiarity is recorded in Induction Documentation and stored in the
employees file.
1.3 Distribution of Documents
This Manual is available electronically on the intranet under WCDHB Policies and
Procedures. Controlled hard copies will be made available for the Emergency Department,
the Medical Ward and the Critical Care Unit.
1.4 Amendments to Previous Issue
This is the first issue of the West Coast DHB Stroke Guidelines manual. With permission
from the original source, this manual has been largely adapted from Canterbury DHB Stroke
Guidelines Issue Five- July 2014. Any amendments have been made in accordance with the
New Zealand Clinical Guidelines for Stroke Management 2010. They are explained in more
detail in that document, which can be accessed online www.stroke.org.nz/resources/.
Readers are encouraged to refer to the New Zealand Stroke Guidelines for more information
1.5 Amendments to Future Issue will be documented here Amendments
Date
Signature
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2 Organisation of Stroke Services
2.1 Acute Stroke Admission Policy
Acute Stroke admissions are admitted to the only Medical Ward or critical care unit at
Greymouth Hospital. In the case that a patient is admitted the Buller Hospital with a potential
diagnosis of acute stroke, all patients should be transferred the Greymouth Hospital for
further assessment and treatment unless clinically indicated by senior medical staff.
The Medical ward will take any patient admitted to hospital with a diagnosis of an acute
stroke. This will include strokes of all severities, including those with a devastating stroke
and who may be dying. The individual cases requiring thrombolysis treatment are to be
admitted to CCU for the duration of this treatment and/or longer.
NB: TIAs (by definition are non-disabling) may not necessarily need inpatient admission.
However they require URGENT investigations and secondary prevention instituted (Refer to
Section 8: TIA Acute Management in the ED/Morice).
In general patients admitted following acute stroke will be admitted under a General Medicine
Physician. If they require specialised neurological assessment, they should be reviewed by
the on call RMO and/or physician and if requiring specialist input, contact the on call Acute
Neurology Registrar on duty at CDHB.
For example:
• patients with progressive or unstable stroke deficits
• younger patients with large strokes who may be at risk of deterioration due to
progressive brain swelling
• patients where the diagnosis or aetiology of stroke is uncertain or unusual kind,
including younger patients without traditional vascular risk factors.
The following two clinical pathways are commenced in ED
• Thrombolysis pathway (document to be complete)
• Acute Stroke Clinical Pathway (document to be completed)
Stroke patients admitted under general medical physicians will be reviewed daily on the ward
round. If a patient requires ongoing inpatient care and treatment they will remain under the
medical physicians care for this period of time, until deemed medically stable for transfer to
rehabilitation services, to long term residential care or discharged home.
The first point of contact is the physician in which the patient is being admitted under. If Dr to
Dr contact is requested, the RMO caring for the patient is required to make contact with the
physician the patient is admitted under or secondly the physician on call. Contact the front
reception regarding these contact details. It may be appropriate to contact the Acute
Neurology Registrar at CDHB, depending on the patient’s presentation ie, if the patient is
younger, with a complex or atypical stroke.
Principles
• All stroke patients regardless of types and severity are admitted to the only medical
ward.
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•
•
Patients who are dying from their acute stroke should remain in the medical ward for
palliative care (short term).
Patients admitted because of a presumed stroke that subsequently have an
alternative diagnosis, should remain on the medical ward if appropriate for the
diagnosis, transferred out to the most appropriate specialist ward or discharged
home, as soon as possible.
Patients who develop a stroke whilst in hospital should also be reviewed on an individual
basis. For most (e.g. stroke on a surgical ward) it would be appropriate to shift the patient
into the medical ward when they are surgically stable. Those patients who have a stroke in
hospital for whom thrombolysis is considered should be referred to the on-call physician for
further discussion regarding this.
2.2 Discharge Planning – Medical Ward
Discharge planning should commence as soon as possible after admission to the medical
ward. In general, an estimation of the likely length of inpatient care required should be made
within the first 48-72 hours of hospital admission.
• If a further 4-5 days (or less) of hospital stay seems likely, then a plan for the patient
to be transferred to the only rehabilitation services available should be commenced.
The patient and family should receive stroke education, which is reinforced by written
information on discharge.
•
If a further 7-10 days (or longer of inpatient care) seems likely, then early referral for
rehabilitation services should be made. See referral guidelines for ongoing
rehabilitation following (2.2.1)
•
Discharge plans for patients who fall between these time estimates may be deferred
for a further 48-72 hours, then reviewed. However, it is recommended that a
rehabilitation specialist is involved early for these patients.
All patients will continue to have active multidisciplinary rehabilitation during their stay in the
medical ward and this will not be deferred because of an impending transfer to another
rehabilitation facility/service.
If a patient is not for active treatment and not for rehabilitation, a decision regarding palliation
and/or hospital level care placement may be necessary. These decisions are complex. They
will be made on an individual patient basis with involvement of the patient, the family and the
wider multidisciplinary team (which should include a Geriatrician if placement in a long term
care facility is likely). Generally, a period of observation on the medical ward will be required
before such a decision can be made.
2.2.1 Referral guidelines for ongoing rehabilitation
Key issues that are essential to know prior to making a decision about further rehabilitation
include:Type and severity of stroke and stroke related disabilities
• Progress since stroke ictus
•
Complications from stroke
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Medical Stability- medical stability is not a prerequisite for transferring a stroke patient to
rehabilitation services but some medical conditions are best managed under acute services.
Previous Level of Function
• What are main types and causes for their disabilities?
•
•
Severity of these disabilities?
Previous living arrangements?
What does the person want? What does the family/whanau or caregiver want? Where should
rehabilitation take place.
• Home - What is home like and who lives at home?
•
Inpatient Rehabilitation
These patients will still be dependent on others for self-cares and/or mobility. If not, they can
usually be managed in a community rehabilitation setting where available.
AGE:
• All stroke patients regardless of age should be considered and offered the opportunity
of rehabilitation. With the exception of those who are significantly disabled from the
stroke and those are have minor disabilities and do not require support or assistance
with mobility and self-cares. Each individual patient is to be assessed on an individual
basis.
2.2.1.1 Admission Policy for the Rehabilitation Service
Principles
Those patients who need further stroke rehabilitation will have been seen by and/or
discussed with the lead physician of the rehabilitation services prior to transfer.
Stroke patients will transfer to the rehabilitation service- IF but NOT limited to the following
criteria
• Are 65 years old or over and have a diagnosis of an acute stroke AND
•
They need ongoing inpatient rehabilitation AND
•
Their needs are best met in the rehabilitation unit.
Principles of the Rehabilitation Service
The rehabilitation services at Greymouth hospital aim to take all types and severity of
strokes. All patients, irrespective of their age, gender and severity of their stroke, have the
potential to benefit from a stroke rehabilitation approach. However the presence of
comorbidities or frailty may modify the decision as to potential for rehabilitation. Greymouth
hospital offers a general rehabilitation service and rehabilitation will be provided on an
individual patient to patient basis with the aim to rehabilitate the individual as close to
baseline as possible.
This includes:
• Acute stroke is the major determinant of current disability
• Acute stroke in previously independent healthy older person
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•
•
•
•
Acute stroke is not the major determinant of current disability
“frailty” factors and (diminished) functional reserves
Significant cognitive impairment
Multiple comorbidities
2.2.1.2 Admission Criteria For Brain Injury Rehabilitation Service (BIRS) Inpatients.
If a stroke patient is under the age of 65 years and would benefit from BIRS approach of
rehabilitation, the option is available for transfer to this service within the CDHB.
The following criteria need to be taken into consideration when considering a patient for
BIRS. The criteria’s are not absolutes and each patient is considered on their merits around
the appropriateness and beneficence of rehabilitation for their condition and where this
should take place. Due to geographical location of this service, a family meeting will be held
prior to acceptance into this service to ensure willingness from the patient and associated
family involved.
Inclusion Criteria
• BIRS accepts patients from 16-64 yrs.
• Patients must be deemed to benefit from inpatient rehabilitation.
• Patients must be able to engage in an active intensive inpatient rehabilitation
program.
• Patients must be medically stable which includes having completed their
investigations and interventions (to stop unnecessary interruptions and transport
between hospitals).
• The patient has a minimum of two impairments
• The patient or family must give consent to rehabilitation at BIRS which includes being
educated about BIRS.
Relative exclusion criteria:
• The patient is 65 yrs or older
• Medically unstable- includes patients requiring walled oxygen (BIRS has no walled
O2)
• Investigations and interventions are incomplete unless the intervention is deferred to
an agreed time after a period of rehabilitation.
• Medical conditions which, in spite of maximal medical therapy, are expected to recur
in the medium term resulting in ongoing impairment and disability thereby negating
the effects of rehabilitation.
• The assessment by IDTM considers that benefit from rehabilitation is negligible
whereupon recommendations will be made to the referrer.
• Low level of consciousness so that patient not able to interact in an intensive
rehabilitation program
• The patient’s condition is such that they are deemed to be better suited to a slow
stream rehabilitation facility
• Malignant conditions- although if life expectancy >6 months and it is thought that the
patient could get home to be with family, a short period of rehab may be considered.
• Life-expectancy is <6 months.
• Patients referred merely for placement - BIRS is not a placement agency.
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•
Patients who would benefit from but are not able to access 6 weeks post-discharge
therapy at Christchurch Hospital due to resourcing constraints.
Relative exclusion/low priority
• Multiple comorbidities of such a nature that benefit from intensive rehabilitation is
significantly affected
Significant drug and alcohol abuse which is thought to impact on the patient willingness and
ability to persevere with rehabilitation as well as cognitive recovery
2.2.2 Driving Guidelines
Patient must be given driving advice prior to discharge by the Medical Staff or delegated to
Occupational Therapist or authorized Nursing Staff. There should be documentation of this
advice in the clinical notes and in the discharge letter. It is good practice that the patient be
given a copy of this advice in writing [driving advice form – see appendix].
IT IS ESSENTIAL THAT ADVICE GIVEN TO PATIENT IS CONSISTENT
Where there is doubt about fitness to drive in terms of residual disability in any area, a
referral for driving assessment should be made to the Greymouth Driving assessors or to
the driver assessment occupational therapists at Burwood Hospital. It may be more
appropriate for the general practitioner to make this referral in a review 1 month following the
event.
1. Stroke
a) Class 1 or Class 6 licence and/or a D, F, R, T or W licence endorsement in relation to
vehicles less than 4500kg GLW or GCW
• An individual should not drive until such time as clinical recovery is complete, with no
significant residual disability likely to compromise safety. This period should not be
less than 1 month from the event
• Permanent homonymous hemianopia is contraindication to ongoing driving. If the
extent of visual field deficit is uncertain referral to the Opthalmology department for
visual field mapping is appropriate.
• Epilepsy associated with stroke should be managed as per the LTSA “Medical
aspects of fitness to drive” guidelines.
b) Class 2, 3, 4, or 5 licence and/or a P, V, I, or O licence endorsement.
• A cerebrovascular event is usually considered a permanent contraindication to
ongoing driving with such licences.
• Under some circumstances it may be possible to grant a licence with conditions. If
there has been full and complete recovery with no suggestion of recurrence over a
period of 3 years an application can be made to the Director of the LTSA with a
supporting specialist physician or neurologists report.
2. Transient Ischaemic Attacks (TIAs)
a) Class 1 or Class 6 licence and/or a D, F, R, T or W licence endorsement in relation to
vehicles less than 4500kg GLW or GCW
• Individuals should not drive for at least 1 month following a single attack
• Individuals should not drive for at least 3 months following stabilisation of recurrent
attacks.
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b) Class 2, 3, 4, or 5 licence and/or a P, V, I, or O licence endorsement.
• Individuals should not drive for at least 6 month following a single attack subject to the
cause being investigated and satisfactorily treated.
• Individuals, who have multiple transient ischaemic attacks that impair consciousness
or awareness, cause vertigo, or cause visual disturbance, should not drive.
In some circumstances following multiple ischaemic attacks it may be possible to grant a
license with conditions. If there has been no attack for 12 months an application can be
made to the Director of the LTSA with a supporting specialist physician or neurologists report
These guidelines are an abridged version of those in the “Medical aspects of fitness to
drive” guidelines from the Land Transport and Safety Authority. If there is any doubt
then these guidelines should be consulted.
http://www.nzta.govt.nz/resources/medical-aspects/docs/medical-aspects.pdf
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3 Acute Management of Stroke
3.1 Thrombolysis Protocol
3.1.1 Inclusions:
• Acute management of ischemic stroke in patients with the following
parameters:
• Within 3.5 hours after onset of symptoms,
• After clinical diagnosis via CT scan.
• Patient is > 18 years and < 85 years
• Patient must NOT have woken from sleep with symptoms UNLESS able to
clearly state the time of going to sleep and time of waking and is less
than 3.5 hours.
3.1.2 Exclusions and Precautions:
• Severe stroke as assessed clinically (NIHSS>25) and/or by appropriate imaging
techniques.
• Minor stroke where symptoms are rapidly improving (NIHSS).
• Seizure prior to administration of alteplase*.
• Presentation suggestive of subarachnoid haemorrhage, even if CT normal.
•
Presumed septic embolus.
•
Stroke or serious head trauma in previous 3 months*.
•
Major surgery or internal injury (including MI, organ biopsy) within 30 days*.
•
GI or urinary tract haemorrhage within 21 days*.
•
Arterial puncture at non-compressible site within 7 days*.
•
History of intracranial haemorrhage, aneurysm, arterio-venous malformation, cancer.
•
History of other neurological disorder causing significant disability / may confound
assessment.
•
Pregnancy, lactation, or parturition within 30 days.
•
Other serious, advanced, or terminal illness, or any other condition that would impose
a significant hazard to the patient if IV alteplase were initiated.
•
Blood pressure >185 systolic or >110 diastolic on repeated measurements.
•
Known hereditary or acquired haemorrhagic diathesis, e.g., APTT or PT greater than
normal.
•
Warfarin therapy with an INR of >1.5, dabigatran treatment within 12 hours or TT
>75s. Dual antiplatelet therapy with aspirin plus clopidogrel/ticagrelor is a warning but
not an absolute contraindication.
•
•
Baseline glucose<2.8 or >22.0 mmol/L*.
Platelets <100 109/L or Hct <0.25.
*warnings, not absolute contraindications.
Note: Order to give Alteplase must be given by General Physician.
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3.1.3 Medical Assessment Protocol Instructions
3.1.3.1 Registered Medical Officer/Registrar Instructions
‘TIME IS BRAIN ’
Call received from ED triage: ambulance pre-hospital notification of suspected acute stroke.
1 Confirm basic inclusion criteria: likely stroke within 3.5h of onset.
Notify Clinical Nurse Manager/ Duty Nurse Manager of possible stroke thrombolysis
Record symptom onset time.
2 Confirm that immediate CT scan has been arranged on arrival, including immediate
transportation to scanner. Confirm that urgent CBC has been sent (& INR if on warfarin).
3 Proceed to ED to meet patient on arrival for Thrombolysis screening assessment.
4 Notify CCU nurse of possible acute stroke patient who may need admission to CCU and
possible Alteplase infusion.
5 Proceed to CT scanning for clinical assessment.
a) Follow Acute Stroke Register Form WCDHB/ Stroke Thrombolysis Pathway- To be
completed.
b) History: DIAGNOSIS of stroke, ONSET TIME, check-list of inclusion & exclusion
criteria for Alteplase.
6 Examination
a) Confirm findings are those of a STROKE.
b) Quantify deficits to enable NIHSS score calculation use Stroke Register form:
• consciousness, commands (gesture if aphasic), speech
• gaze palsy, hemianopia
• power face, arms and legs bilaterally
• incoordination (esp. if suspect post. circulation lesion)
• hemisensory abnormality
• neglect / inattention
6 CT scan review- must be interpreted by a radiology registrar, a radiologist or a neurologist.
Record time CT interpreted. See CT exclusion criteria below.
7 Obtain Blood count and glucose results (INR if warfarin).
8 PAGE MEDICAL PHYSICIAN ON CALL THROUGH HOSPITAL OPERATOR
• Discuss clinical presentation and finding with the on call physician and if agree
to thrombolysis continue to next step.
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9 Treat with Alteplase:
a) Consent from patient or next of kin (written consent is desirable but not mandatory)
b) Transfer patient to CCU for Alteplase bolus and infusion- This is ONLY to be
administered in CCU. Use dose-calculation table. Prescribe on drug chart. RMO
should be present when giving the IV bolus and is to attend until infusion is
commenced.
10 If patient is NOT treated with Alteplase:
a) Proceed with admission under general medical physician to the medical ward
unless medical unstable and requiring closer observation then consider admission to
CCU. DO NOT send the patient back to ED unless essential for patient safety.
b) Notify Clincal Nurse Manager/Duty Nurse manager and Critical Care Nurse that the
alteplase infusion is not to proceed.
3.1.3.2 CT Exclusions Criteria
• Likely aetiology other than acute brain ischemia; haemorrhage
• Early signs of major infarction (sulcal effacement, mass effect, oedema/hypodensity
darker than white-matter, possible haemorrhage).
• ‘Subtle’ early signs eg ‘grey-white differentiation’ do not exclude from treatment within
3 hours but may be a caution between 3 and 4.5 hours of stroke onset if extensive in
nature.
3.1.4 ALTEPLASE for Acute Ischaemic Stroke
• Actilyse 10mg per vial
• Actilyse 50mg per vial
Dose:
The dose is 0.9mg/kg (maximum of 90mg) given as:
1. 10% of the total dose as a bolus over 1 minute.
2. Remaining 90% as an infusion over 60 minutes via buretrol primed with saline.
Note: Do NOT exceed a 90mg dose due to increased risk of intracranial bleeding.
Note: No other anticoagulant or antiplatelet medication to be given for 24 hours
Patient
Weight
(kg)
Total
dose @
0.9mg/kg
(mg)
40
41
42
43
44
45
46
47
36
36.9
37.8
38.7
39.6
40.5
41.4
42.3
Vol of 1mg/ml
alteplase
10%
90%
Bolus
infusion
(ml)
(ml)
3.6
32.4
3.7
33.2
3.8
34
3.9
34.8
4
35.6
4.1
36.4
4.1
37.3
4.2
38.1
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Patient
weight
(kg)
Total
dose @
0.9mg/kg
(mg)
70
71
72
73
74
75
76
77
63
63.9
64.8
65.7
66.6
67.5
68.4
69.3
Vol. of 1mg/ml
alteplase
10%
90%
Bolus
Infustion
(ml)
(ml)
6.3
56.7
6.4
57.5
6.5
58.3
6.6
59.1
6.7
59.9
6.8
60.7
6.8
61.6
6.9
62.4
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48
49
50
51
52
53
54
55
56
57
58
59
60
61
62
63
64
65
66
67
68
69
43.2
44.1
45
45.9
46.8
47.7
48.6
49.5
50.4
51.3
52.2
53.1
54
54.9
55.8
56.7
57.6
58.5
59.4
60.3
61.2
62.1
4.3
4.4
4.5
4.6
4.7
4.8
4.9
5
5
5.1
5.2
5.3
5.4
5.5
5.6
5.7
5.8
5.9
5.9
6
6.1
6.2
38.9
39.7
40.5
41.3
42.1
42.9
43.7
44.5
45.4
46.2
47
47.8
48.6
49.4
50.2
51
51.8
52.6
53.5
54.3
55.1
56
78
79
80
81
82
83
84
85
86
87
88
89
90
91
92
93
94
95
96
97
98
99
100+
70.2
71.1
72
72.9
73.8
74.7
75.6
76.5
77.4
78.3
79.2
80.1
81
81.9
82.8
83.7
84.6
85.5
86.4
87.3
88.2
89.1
90
7
7.1
7.2
7.3
7.4
7.5
7.6
7.7
7.7
7.8
7.9
8
8.1
8.2
8.3
8.4
8.5
8.6
8.6
8.7
8.8
8.9
9
63.2
64
64.8
65.6
66.4
67.2
68
68.8
69.7
70.5
71.3
72.1
72.9
73.7
74.5
75.2
76.1
76.9
77.8
78.6
79.4
80.2
81
Administration:
Step
1
2
Action
Determine dosing according to patient weight (refer Table 1).
Reconstitute each vile with water for injection using the following ratios:
- 10mg : 10ml water
- 50mg : 50ml water
Notes: If using the transfer device supplied with Actilyse®, it should be inserted into the
diluent vial first since the alteplase vials are under partial vacuum.
DO NOT use the vial if the vacuum is not present.
3
Mixing should be accomplished by gentle swirling and slow inversion. Do NOT shake.
4
Slight foaming upon reconstitution is normal – Allow to settle.
Bolus IV Injection of 10%
5
A separate IV cannula should be used to administer the alteplase.
6
Draw up 10% of the total dose (refer Table 1) and administer as a bolus IV injection
over 1 minute.
Infusion of Remaining 90%
7
The remaining 90% of the dose should be administered as an infusion using a
volumetric pump via a buretol over 60 minutes. Prime the buretol and IV giving set with
100ml bag of saline, leaving only 10ml of saline in the buretrol to prevent air entering
the IV line once the actilyse is place into the buretrol. (refer Table 1).
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Note: In line filters should NOT be used due to potential for the drug to bind to the filter.
3.1.5 NURSING PROTOCOL
3.1.5.1 Neurological Observation and Monitoring during and after Atleplase Infusion
• Full neurological observations, including Glasgow Coma Score, pupils and limb
strength (using coma record form) and pulse, temperature, BP, respiratory rate and
oxygen saturation for the first 48 hours as below:
o Every 15 minutes
 2 hours
o Every 30 minutes
 4 hours
o Hourly
 4 hours
o 2 hourly
 12 hours
o 4 hourly if stable
 until medical team review
• Monitor for intracranial haemorrhage and other potential bleeding sites.
3.1.5.2 Reportable observations and Possible Complications:
• Hypertension ≥ 185/110.
• Hypotension (systolic BP ≤ 110).
• Symptomatic intracranial haemorrhage (up to 10% of patients).
• Neurological deterioration (assume = bleed until proved otherwise).
• Bleeding: into GI tract, urogenital tract, the skin, nose bleed and superficial bleeding
from punctures or damaged vessels.
• Further embolism.
• Hypotension.
• Nausea and/or vomiting.
• Fevers.
• Allergic reactions. They may appear as: rash, urticaria, bronchospasm, angioedema,
hypotension, shock etc. Protect airway and treat as per anaphylaxis.
3.1.5.3 Further Assessments of Patient
• Continue to monitor blood pressure for up to 24 hours following treatment.
• Observe / test all body waste for suggestion of occult bleeding.
• Check potential bleeding sites (i.e. wounds, IV access, puncture sites)
Note: onset of abdominal pain may indicate retroperitoneal bleeding.
• Minimise physical handling of the patient to prevent bruising/bleeding:
o strict bed rest for the first 24hrs
o safety precautions to prevent falls
o do not use razor blade for shaving
• Minimise invasive procedures:
• Avoid IDUC placement during alteplase infusion and at least 30 minutes after
infusion.
• Avoid NGT placement for 24h after infusion, if possible.
• Leave a dedicated IVL in situ for blood taking, if possible.
• If venepuncture is required, apply direct pressure to puncture site for 20 minutes.
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3.1.5.4 Management of adverse effects:
Management of Bleeding Complications
Bleeding should be considered as the likely cause of neurological worsening after use of
alteplase until CT is available.
Emergency CT required
For any life-threatening haemorrhagic complication, including ICH:
1) Discontinue ongoing infusion alteplase.
2) Obtain blood samples for coagulation tests (FBC, APTT/INR, fibrinogen) and
cross-match if transfusions are needed.
3) Emergency imaging investigation.
4) Obtain surgical consultation, as necessary (surgery is usually delayed until the
fibrinolytic state is corrected).
5) Consider other interventions that may be useful, such as transfusion,
cryoprecipitate, and platelets (e.g. 6-8 U of cryoprecipitate or fresh frozen plasma,
and 6-8 U of platelets).
6) Mechanical compression should be applied to bleeding sites, when possible.
Note: As alteplase has a short half-life and minimal effects on blood coagulation,
replacement of coagulation factors is generally not required.
3.1.5.5 Blood Pressure Management
Monitor BP during first 24 hours after alteplase treatment.
• q15 min for 2 h, q30 min for 4 h, q1h for 4 h, q2h for 12 h, then q4h
If Systolic BP is 180-230mmHg or Diastolic BP 105-120mmHg (≥2 recordings; 5-10min
apart):
• Give IV labetalol 10mg over 1-2 minutes.
• The dose may be repeated or doubled every 10-20 minutes up to a total dose of
150mg.
• Monitor BP every 15 minutes during labetalol treatment and observe for development
of hypotension.
If Systolic BP >230 or Diastolic BP 121-140mmHg:
• Treat with repeated doses of IV labetalol, as above, every 10 minutes up to a total
dose of 150mg.
• If no satisfactory response, infuse sodium nitroprusside (0.5- 10ug/kg per minute)*.
If Diastolic BP >140 for 2 or more recordings 5-10 minutes apart:
• Infuse sodium nitroprusside (0.5-10ug/kg per minute).*
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3.1.5.6
Alteplase Record in Acute Ischaemic Stroke
Time of Stroke Onset
(24hr clock) __________________
Date of Stroke Onset
_____________________
Time of Arrival to Emergency
(24hr clock) __________________
Time of CT head
(24hr clock) _____________________
Candidate for alteplase (refer to Alteplase protocol for management)
 YES
 NO reason:
If Yes
 YES  NO
Informed consent obtained for alteplase?
Time (24hr clock) _________________
Highest pre alteplase BP recording
_______/______
Time of start of alteplase administration (24hr clock)
Laboratory Results
Date: ____/____/_____
Time: _________________
APTT:
INR (if on warfarin):
Glucose:
Pregnancy Test
Weight ______________Kg  Estimated
Alteplase Dose
0.9mg/kg dose
(max dose 90mg)
 Measured (please tick)
Doctor’s signature:
Name:
Date
/Time
Volume given
(1mg/ml)
Signatures
10% of total dose given as IV bolus
dose over 1 minute
Remaining 90% infused over 60
minutes
NB Prescription and Administration must also be recorded on the Adult
Medication Chart
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Alteplase Record in Acute Ischaemic Stroke- COPY ONLY
Place bradma here:
Stroke Guidelines
3.1.5.7 Mechanism of action:
Alteplase is a recombinant human tissue-type plasminogen activator. It is relatively inactive
in the general circulation and its main effects are exerted when bound to a fibrin clot. Once
bound to fibrin it is activated and causes the conversion of plasminogen to plasmin resulting
in the dissolution of the clot.
It is cleared rapidly from the body with approximately 80% removed from circulation 10
minutes after the infusion is terminated.
Drug interactions:
Medications
Warfarin
Dabigatran
Platelet aggregation
inhibitors (eg
aspirin, clopidogrel,
ticagrelor)
Heparins (including
enoxaparin)
Rivaroxaban
ACE-Inhibitors
Interaction
Increased risk of bleeding prior to, during, or after alteplase therapy
Increased risk of bleeding prior to, during, or after alteplase therapy
Increased risk of bleeding prior to, during, or after alteplase therapy
Increased risk of bleeding prior to, during, or after alteplase therapy
Increased risk of bleeding prior to, during, or after alteplase therapy
Increased risk of an anaphylactoid reaction with concurrent use
Storage:
Store below 25oC. Protect from light.
The reconstituted solution can be kept for up to 24 hours in a refrigerator and up to 8 hours
at temperatures up to a maximum of 25°C. However, from a microbiological point of view the
product should be used immediately after reconstitution.
List of excipients:
L-arginine, phosphoric acid, polysorbate 80, gentamicin (a trace residue from the
manufacturing process).
References:
CDHB Blue Book (December 2013) Acute Management of Ischemic Stroke.
Waitemata District health Board. Alteplase-Acute Ischaemic Stroke. February 2010
th
Notes on Injectable Drugs 6 Ed. 2010
British National Formulary 68th Ed. Published September 2014
ACTILYSE Datasheet (Last updated 14/9/2012). Available from www.medsafe.govt.nz
Alteplase profile. Available from www.nzf.org.nz. Accessed 15/10/2014
th
Stockleys Drug Interactions 7 Ed. Pharmaceutical Press
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3.2 Acute BP management first 7 Days after stroke
Note: for patients receiving alteplase refer to the Alteplase guideline
NZ Stroke Guideline: “There is no evidence from randomised controlled trials to guide
management of blood pressure in the first week after a stroke. A cautious approach should
be taken toward the treatment of arterial hypertension in the acute stage.”
Patients with known hypertension, taking regular antihypertensive medication should
continue their usual medications when the patient is able to take them p.o. (or has an
NGT placed for another reason), as long as BP > 130-140 systolic / symptomatic
hypotension is avoided.
Hypotension is a common problem in those hospitalised with stroke and may result in
extension of an ischaemic stroke. Hypotension should be avoided and the underlying cause
treated (section 3.2.3).
New antihypertensive treatment for secondary prevention of stroke can be introduced 7-14
days following acute stroke (see page 26, section 3.2.2).
New antihypertensive agents should be AVOIDED in the acute phase unless:
• Ischaemic Stroke: systolic blood pressure > 220 mm Hg or
diastolic blood pressure > 120 mm Hg
•
Intracerebral haemorrhage: systolic blood pressure > 180 mm Hg or
diastolic blood pressure > 105 mm Hg
Acute antihypertensive protocol – ischaemic stroke:
• In the exceptional circumstances where acute blood pressure lowering is required,
use oral antihypertensive medications if possible, unless BP elevation is extreme (eg
>240/130: see IV protocol below).
Oral / NGT antihypertensives:
• labetalol 100-200mg qid po/NGT is preferred in the acute stage: it has a short
duration of action and minimal effect on cerebral blood vessels.
• If beta-blockers contraindicated (eg severe asthma / COPD) then consider: felodipine
2.5mg; or cilazapril 0.5mg initial dose then 2.5-5mg daily.
• Sublingual nifedipine should be avoided.
Acute antihypertensive protocol – intracerebral haemorrhage
• Intravenous antihypertensive treatment (see below) is recommended to ensure rapid
reduction of BP to safer levels below 180/105. There is evidence that reducing
systolic BP to 140mmHg is safe and results in a reduction in ICH progression, with
weaker evidence to support an improvement in clinical outcomes.
• Conversion to po/NGT regimen as above can be usually made after 24hrs.
Intravenous antihypertensive protocol
If SBP is 180-230mmHg or DBP 105-120mmHg
(≥2 recordings; 5-10min apart):
• Give IV labetalol 10mg over 1-2 minutes
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•
The dose may be repeated or doubled every 10-20 minutes up to a total dose of
150mg
Monitor BP every 15 minutes during labetalol treatment and observe for development of
hypotension.
If SBP >230 or DBP 121-140mmHg:
• Treat with repeated doses of IV labetalol, as above, every 10 minutes up to a total
dose of 150mg
• If no satisfactory response, infuse sodium nitroprusside (0.5-10ug/kg per minute)* or
glyceryl trinitrate (GTN)**
If DBP >140 for 2 or more recordings 5-10 minutes apart:
• Infuse sodium nitroprusside (0.5-10ug/kg per minute).*
* Continuous arterial monitoring of BP is advised (in ICU) if nitroprusside is used. The risk of
bleeding from arterial puncture should be weighed against the possibility of missing dramatic
changes in pressure during infusion.
** GTN infusion: as per CDHB cardiology guidelines – 50mg in 250ml 0.9% Saline. Start at
3ml/hour and titrate in 3ml/h steps every 5 minutes. Do not use for more than 24 hours.
Other options include:
IV hydralazine
• 5-10mg IV dose, repeat q20-30 minutes
•
Continuous infusion (diluted in 0.9% Saline)
•
0.2-0.3mg/min initially, usual maintenance 0.05-0.15mg/min
•
GTN patch
•
Clonidine patch (note: clonidine usually takes >24h to take effect)
3.2.1 BP Monitoring
Day 1: BP measurement QID
• If SBP > 200 or DBP > 115 (ICH: > 180 / 105) increase BP measurement to q2h
• Advise medical team if SBP > 220 or DBP > 120 (ischaemia) or BP > 180 / 105 (ICH)
on 2 successive readings
Day 2: BP measurement QID
• for stable patients with BP > 120 / 70 and BP < 180 / 105
• More frequent BP measurements is required for patients outside these BP limits
• Medical team notification as above
Day 3+: BP Measurement reduced to BD
• for stable patients with BP > 120 / 70 and BP < 180 / 105 (Lying and standing where
applicable).
• More frequent BP measurement is required for patients outside these BP limits
• Medical team notification as above
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3.2.2 Antihypertensive medication for Secondary Prevention after stroke or TIA
NZ Stroke Guideline:
“Bloodpressure
pressure--lowering
loweringtreatment
treatmentisisrecommended
recommendedfor
forall
allpeople
peopleafter
afterstroke
strokeor
ortransient
transient
Blood
ischaemic attack unless the person has symptomatic hypotension.
For all people presenting with an acute stroke or transient ischaemic attack, lowering blood
pressure reduces the risk of a recurrent stroke and other major vascular events, irrespective
irrespective
of the
person’s
baseline
blood
pressure [PROGRESS
trial]
of
the person’s
baseline
blood
pressure
[PROGRESS
trial]
Theoptimal
optimaltime
timetotostart
startblood
bloodpressure
pressure––lowering
loweringtreatment
treatmentisisnot
notknown,
known,but
butititisis
The
usually
advisable
to wait
7 –an
14 acute
days after
an acute stroke
usually advisable
to wait
7 – 14 days
after
stroke
The combination of an angiotensin-converting enzyme inhibitor and a diuretic is of
proven benefit in preventing recurrent vascular events. This benefit is seen irrespective of the
the patient’s
baseline
blood
pressure,
including
patients
considered
tonormotensive.
be normotensive.
patient’s
baseline
blood
pressure,
including
patients
considered
to be
There is
There is insufficient
to determine
a beneficial
effect isto
specific
to this
insufficient
evidenceevidence
to determine
whether awhether
beneficial
effect is specific
this combination
of
combination of antihypertensive
drugs
whether
other blood pressure-lowering
drugs
are
antihypertensive
drugs or whether
otherorblood
pressure-lowering
drugs are equally
effective.”
equally effective.”
•
Cilazapril 0.5mg daily is recommended as a starting dose (unless ACE inhibitors are
contraindicated). A documented plan is required to titrate the dose appropriately
over time to 2.5-5mg daily followed by introduction of a thiazide diuretic, such as
bendrofluazide 2.5mg daily. Other equivalent antihypertensive agents can be
substituted for cilazapril/bendrofluazide when appropriate for individual patients.
•
This medication is additional to any previous antihypertensive therapy the patient had
been taking at the time of stroke.
•
Dose titration takes TIME so will need to be managed by the GP or by stroke
rehabilitation physicians. A clearly documented plan is required on the discharge
summary.
•
It may be appropriate to defer decisions regarding appropriate long-term
antihypertensive therapy for patients presenting with major severely disabling stroke,
particularly when the patient is to be transferred to another inpatient facility within 714 days of stroke onset.
•
Patients with severe bilateral carotid stenoses should not have intensification of
antihypertensive therapy until the symptomatic carotid lesion has been repaired.
3.2.3 Hypotension
Avoid symptomatic hypotension. All patients should have SBP maintained >100-110.
Some patients (eg those with severe bilateral carotid stenosis or carotid occlusion) may be
symptomatic at “normal” levels of BP. Consider the possibility of exacerbation of stroke
symptoms due to inadequate BP in any patient with progression or fluctuation of symptoms.
Suggested management considerations:
•
Assess hydration status and correct dehydration
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•
•
•
•
•
•
•
•
Withdraw hypotensive medications
Lie patient flat if hypotensive
ECG +/- TNT to assess for AF, other arrhythmia, MI or myocardial ischaemia
Treat CHF, if present
Assess for blood-loss, particularly if taking aspirin or warfarin
Assess for sepsis
Consider bilateral full-length compression stockings
Medications to elevate BP could be considered in rare cases, eg if symptoms are
fluctuating while a patient is waiting for carotid intervention.
3.3 Malignant Cerebral Oedema / Hemicraniectomy Guideline
3.3.1 “Malignant Infarction” Guideline
Early identification of patients at risk of “malignant infarction”
• Early identification of these patients is to allow close monitoring and multidisciplinary
specialist involvement in patient care. It does not imply the need for or
appropriateness of any specific medical or surgical intervention.
Discussion with patients or families of any specific intervention for treatment of
cerebral oedema must be left to the specialist team who is offering that treatment
when deemed appropriate.
Criteria for close neurological monitoring and a preliminary neurosurgical opinion
a) Age =<60 years
b) Premorbid functioning fully independent, no major medical comorbidities
c) Clinical features of a large anterior circulation ischaemic stroke.
•
Usually will have complete hemiplegia, hemisensory deficit, neglect and/or dysphasia,
and may have gaze deviation and/or visual field deficits.
•
Any reduction in level of consciousness due to anterior circulation ischaemic stroke
Note: Young patients with large MCA stroke who are alert at admission are at risk of
deterioration in the next 24-72 hours. A reduction in GCS by 2 points that is sustained
for more than 2-3 hours is an indication for urgent specialist opinion.
d) Imaging Criteria:
• Imaging evidence of >50% of MCA territory infarction plus
• signs of significant mass effect
Note: if patient meets clinical criteria a), b) and c) at admission, but not imaging criteria, then
repeat CT scan is indicated if any clinical deterioration occurs, or at 24 hours.
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3.3.2 Malignant Infarction Guideline Procedures:
•
•
•
Physician/ RMO to consult with neurosurgical registrar at CDHB regarding the
patients clinical details.
If agreed the patient is a candidate for intervention and treatment, consider urgent
transfer and admission to Ward 28 NPCU at CPH under “malignant infarction”
guideline.
If requiring further information regarding ‘malignant infarction” guidelines please see
CDHB Stroke Guidelines.
Neurological deterioration:
Deterioration in level of consciousness: eg drop in GCS by 2 or more points that is sustained
for more than 2-3 hours or New brainstem or cranial nerve signs (eg Unilateral Pupil
enlargement >=2mm from baseline)
• Urgent medical review then urgent CT head – results are communicated to Neurology
Consultant.
• Neurology consultant determines whether urgent Neurosurgical opinion is required.
Guidelines for urgent Neurosurgical opinion regarding hemicraniectomy
• Clinical deterioration to loss of consciousness or new brainstem/CN signs suggesting
coning
and/or
•
Imaging shows space-occupying MCA infarction with midline shift and compression of
the lateral ventricles &/or basal cisterns; enlargement of contralateral lateral ventricle
is of particular concern
Medical management of brain swelling due to infarction:
Indication:
•
Patient has lesser neurological deterioration and does not (yet) meet criteria for
Hemicraniectomy. Definitive decision regarding Hemicraniectomy is recommended
within 24-48h of stroke onset.
•
Patient has been determined as being permanently ineligible for Hemicraniectomy
or
Mannitol
•
1g/kg/day (generally for no more than 24 hours )
•
bolus 0.5g/kg over 20 minutes
•
repeat doses usually 0.25g/kg
•
serum osmolality should be tested at 24 hours and maintained <315mosmol/l
•
If medical treatment for brain swelling is required for >24 hours, other options could
be considered, including: Glycerol (NG); Frusemide 40-80mg IV; Hypertonic saline.
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3.4 Acute Management of Intracerebral Haemorrhage
Many aspects of acute management of intracerebral haemorrhage (ICH) are similar to
ischaemic stroke, particularly the benefit of stroke unit care, maintenance of homeostasis
and early rehabilitation. There are some important differences however:
• Avoid aspirin, heparins and thrombolytic agents.
• Full coagulation screen is required urgently.
• If taking oral anticoagulants, this is a life-threatening emergency and immediate
action to reverse the anticoagulant effect is required (if this is possible). See Reversal
of the Warfarin related coagulopathy below.
Acute blood pressure management: the threshold for considering use of IV antihypertensive
agents in the acute phase of stroke is lower in patients with ICH (>180/105) compared with
ischaemic stroke (>220/120). More aggressive BP lowering to systolic BP <140mmHg is
associated with reduced expansion of ICH. See Acute BP management first 7 days after
stroke, Section 3.2.
Neurosurgical referral should be considered for potentially life-threatening ICH in previously
neurologically well patients who have cerebellar ICH or superficial supratentorial ICH.
Please consult with physician/ on-call physician and/or Neuro registrar at CDHB. See Blue
Book Section 18.3.5 re investigations
3.5 Intracerebral Haemorrhage whilst on warfarin: Reversal of the warfarin
related coagulopathy
Background
• ICH whilst taking warfarin is life threatening medical emergency with a mortality of
between 43-70% at 30 days.
•
Initial ICH volume and further haemorrhagic expansion are both independent
predictors of mortality
•
ICH volume is not maximal at the outset but can continue to increase for several
hours or up to 24-48 hours if taking warfarin.
•
Most warfarin related ICHs occur with the INR within the “therapeutic” range.
•
Warfarin causes functional deficiencies of several different clotting factors which need
immediate replacement in the setting of ICH whilst taking warfarin.
Reversal Guidelines
• Any patient with both (1) an acute intracerebral haemorrhage and (2) taking warfarin
should have immediate intravenous reversal of the coagulopathy. This includes
•
Stop warfarin
•
Give Vitamin K 5-10 mg intravenously immediately
•
Give Prothrombin complex concentrate (PCC) 50 units / kg intravenously
immediately
• Give Fresh Frozen Plasma (FFP- 150-300ml) (1-2 units)
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Notes:
•
Vitamin K takes 6-24 hours to be effective
•
Prothrombin complex concentrate (PCC) rapidly reverses the coagulopathy within 15
minutes. It is accessed by either
o Following “life threatening bleed on warfarin” protocol in Emergency
Department (warfarin reversal pack to accompany patient to CT scanner from
ED).
o contacting New Zealand Blood Service Doctor on call.
•
If PCC is NOT available, vitamin K (as above) and larger doses of FFP can be given
(at a dose of 15-30ml/kg) but produces suboptimal anticoagulation reversal.
Monitoring
• INR is not useful for monitoring the effectiveness of clotting factor replacement. It is
only useful for monitoring warfarin use in steady state situations.
•
Monitoring should be done immediately after treatment using a coagulation screen
(INR, APPT, Thrombin time and fibrinogen). If still abnormal, more coagulation
factors should be given immediately.
•
If normal recheck in 4-6 hours (reflecting shortest half life of factor VII and vitamin K
onset of action).
•
If normal again, then recheck at 24 hours, or sooner if patient clinically unstable.
•
The risk of thrombotic events during this short term reversal appears very low, even in
patients with prosthetic heart valves.
Oral thrombin inhibitors (Dabigatran) related ICH
Like warfarin related ICH, these patients need urgent reversal of the coagulopathy. See
notes in Blue Book Section 14.8.5 (CDHB Haematology) for dabigatran reversal.
Longer term management
This requires an individual assessment of the risks and benefits of restarting warfarin or not.
Most should not restart warfarin, but it is dependent on indications for anticoagulation,
location and severity of bleed, comorbidities, age and concurrent medications.
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4 Inpatient Care
4.1 The Acute Stroke Swallow Screen for dysphagia trained nurses
Purpose
Suspected or confirmed acute stroke patients should be kept NBM until they receive
Acute Stroke Swallow Screen by a Speech and Language Therapist or by a certified
dysphagia trained nurses or completed by RMO/Registrar. If completed in ED/Medical
ward by an RMO/’Registrar the finding must be clearly documented in the clinical notes. If a
patient has no swallowing issues identified on the screen, they may receive their normal diet.
If issues are identified then the patient will remain NBM until formal assessment by SLT.
This aims to:
• To improve early identification of dysphagia and aspiration risk.
• To reduce inappropriate referrals to SLT.
• To meet New Zealand Guidelines for Management of Stroke regarding swallowing
• To ensure a safe and high quality service that is consistently delivered to patients with
acute stroke and their family/whānau.
Speech-Language Therapist’s Role
To assess patients who
• have an abnormal result on the
screen,
• meet the exclusion criteria within the
WCDHB Nurse Dysphagia
Screening policy,
•  are currently being managed by
SLT services.
 To organise and implement
instrumental/diagnostic assessment of
swallowing, e.g. videofluoroscopy.
Nurse’s Role
 To screen all new patients admitted
with an acute stroke as per WCDHB Nurse
Dysphagia Screening policy.
 To provide initial training session for
nurses as per WCDHB Nurse Dysphagia
Screening policy.
 To complete initial training and
competency requirements as per WCDHB
Nurse Dysphagia Screening policy.
 To provide annual refresher training
sessions for nursing staff already trained in
Acute Stroke Swallow Screen to maintain
their competencies.
 Nursing staff to maintain competency
as per WCDHB Nurse Dysphagia
Screening policy.
NOTE: Only Nurses who are trained to
assess using the Dysphagia Screening
Policy can assess any patient.
 Any communication issues identified
during the screen to be referred to SLT as
per usual referral procedures.
 To provide management of those
patients identified as presenting with
dysphagia or aspiration risk, as per
departmental dysphagia protocols.
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At present the implementation of a WCDHB Dysphagia Screening Policy is being piloted and
trailed. Selected Nurses within the Medical Ward are receiving competency based education
and training. As the tool is still within the trail phase, once completed the tool and Dysphagia
Screening Policy has been finalised and a copy of the tool will be inserted on the page
below.
NOTE: Only Nurses who are trained to assess using the Dysphagia Screening Policy
can assess any patient
For further information on the Acute Stroke Swallow Screen and/or training please refer to
the WCDHB Nurse Dysphagia Screening policy.
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4.2 Communication for patients with disability following stroke
Patients admitted to Greymouth Hospital with suspected communication disability following
stroke will be referred to the Speech-Language Therapy service. The patient should have
initial contact and a management plan in place within 48 hours.
The management plan will include:
• Information about diagnosis
•
Strategies for effective communication with staff and family
•
Written information will be provided about the communication disorder.
•
Ideally training for staff in supportive communication strategies for successful
communication with patients post stroke will be provided.
Communication diagnosis following stroke are:
Aphasia: (also known as dysphasia). Aphasia is a language condition that affects one or all
of the modalities of speech, writing, reading and auditory comprehension of language.
“Aphasia” is the internationally preferred term for researchers and consumers affected by the
condition.
It can be classified into fluent and non-fluent types of aphasia.
Non-fluent aphasias are; Broca’s aphasia, trans-cortical motor aphasia and anomia.
Fluent aphasias are; Wernicke’s aphasia, trans-cortical sensory aphasia and conduction
aphasia.
Aphasia can present in a range of severities and has ongoing social consequences for
participation in life events and wellbeing for patients and families.
For more information about best practice guidelines in the rehabilitation of aphasia please
refer to: www.aphasiapathway.com.au
Apraxia: Apraxia of speech is a motor speech disorder that affects the initiation and
sequencing of speech sounds. A person may have reduced dysdiadochokinesia and exhibit
more difficulty with longer words and phrases. It often co-occurs with aphasia and can be
present with people who present with non-verbal communication.
Dysarthria: Is a motor-speech disorder that affected the muscles involved in speech
production. It may present in a number of ways and is characterised by slurred speech.
Speech intelligibility is affected but literacy is usually preserved.
There are a range of classifications of dysarthria: flaccid, spastic, ataxia, hyperkinetic,
hypokinetic, unilateral upper motor neuron and mixed
4.3 Hydration Guideline
4.3.1 Guideline for hydration after acute stroke
Dehydration is a common and avoidable problem after acute stroke. Patients are frequently
unable to eat or drink adequately or are made ‘Nil by mouth (NBM)’. Dehydration can result
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in discomfort, hypotension and decreased cerebral perfusion. Avoidance of both dehydration
and hypotension are associated with improved patient outcomes after stroke
•
All patients who are NBM [or have limited oral intake] after acute stroke should either
be prescribed parenteral fluids or have nasogastric tube (NGT) placement to allow
feeding, if they are not being managed in a palliative manner.
•
For parenteral fluids, subcutaneous administration should be considered if there is
no other indication for IV cannulation. An IV line in a paretic arm can result in an
oedematous limb, and an IV line in a non-affected arm can result in a patient having
two ‘non-functional’ arms. Both of these problems are avoided by using the
subcutaneous route administered over the trunk area.
•
In general, 2 litres of fluid per day is required (Total fluid volume per 24hrs = 30-40
mls/kg body weight), however caution is needed for patients with congestive heart
failure or raised intracranial pressure
•
Prescription of parenteral fluids must be tailored to individual patient needs. Particular
care is required when the patient is NBM or has very low oral intake and therefore
reliant on parenteral fluid replacement for all of their hydration needs.
o Exclusive use of hypotonic dextrose-saline or 5% dextrose can result in
hyponatraemia
o Exclusive use of normal saline can result in volume overload or
hypernatraemia
o The patient’s daily oral fluid intake should be recorded
•
Hyperglycaemia is associated with poor outcome after stroke and, as a general
recommendation; direct intravenous administration of glucose-containing fluids should
be avoided when possible. Normal saline will generally be the intravenous fluid of
choice, but cannot be used as the only source of hydration (as above)
•
If glucose-containing fluids (dextrose-saline or 5% dextrose) are required, to maintain
correct fluid and electrolyte balance, the subcutaneous route of administration is
recommended when possible.
•
If patients remain NBM longer than 48-72 hours, NGT placement to allow full
hydration and nutrition if appropriate should be considered. This should be a TEAM
decision to ensure all relevant issues are addressed
4.4 Nutrition Guideline
4.4.1 Guidelines
Nutrition Guidelines for Acute stroke patient
4.4.2 All Patients
1. Patients are to be weighed within 24 hours of admission (where appropriate) and on
discharge from the acute medical/ Rehabilitation ward.
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2. Monitoring of oral intake should occur for all patients, with food charts kept for those with
marginal intake.
3. Serum glucose, CRP, creatinine, and electrolytes
4.4.3 Patients receiving ongoing dietetic input
1. Twice weekly weigh.
2. Weekly biochemistry as indicated.
3. Albumin, urea, pre-albumin if requested.
4.4.4 Patients receiving enteral feeding
1. Twice weekly weigh.
2. Food and fluid charts to be kept during transition periods.
3. Magnesium, phosphate, potassium, calcium, glucose and sodium for patients suspected to
be at risk of re-feeding syndrome. If results are subnormal, correction is required. Clarifying
the most appropriate way of correcting these, will require discussion between dietitian and
medical staff prior to commencing feeding.
4. All patients who are at risk of re-feeding syndrome should be given thiamine and a
multivitamin prior to commencing feeding.
4.4.5 Decision to institute enteral feeding
This is a complex decision that requires input from all MDT members. Decisions should be
tailored to individual needs and circumstances.
In general:
• Enteral feeding will not normally be considered within 48 hours of stroke onset for
purely nutrition requirements (but could be considered if there were a need for
NGT placement for other reasons, eg essential oral medications).
•
If patient remains NBM for longer than 48-72 hours, then discussion needs to begin
with the patient, their family and the team about all the relevant issues. These include
patient preferences, prognosis, dysphagia, nutrition/hydration and other issues.
Other factors to consider include (but may not be limited to):
• Previous nutritional status
• Ability to participate in rehabilitation (active rehab may require nutritional support)
• Trends of improvement in swallowing / oral nutrition intake
• Prognosis: ‘comfort’ vs ‘active’ care issues
• Importance of oral medications (eg some anticonvulsants) requiring NGT
• Patient preference
• Logistical concerns – ease of NGT placement / maintenance
• Discharge / placement plans
Gastrostomy (usually PEG) tube placement
• should be considered only when long-term nutritional support is required
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4.5 Diabetes Guidelines
4.5.1 Guideline for Hyperglycaemia after Acute Stroke
There is an association between hyperglycaemia and poor outcome after stroke. At present
there is a paucity of information on hyperglycaemia interventions, thus there is insufficient
evidence to support aggressive treatment of hyperglycaemia for all patients after stroke.
Stroke may represent the first clinical presentation of diabetes or impaired glucose tolerance.
Current NZ recommendations suggest that management of stroke patients with
hyperglycaemia should be “the same as for other medical patients”. However, management
of hyperglycaemia and diabetes after stroke is sometimes complicated, for example due to
reduced dietary intake when patients are made ‘Nil by Mouth’ (NBM), or by the use of
nasogastric feeding. European stroke guidelines recommend maintenance of BSL
<10mmol/L, American (ASA) guidelines recommend intervention if BSL>16.7mmol/L.
The aim of these guidelines is to encourage a consistent approach to management of
hyperglycaemia and diabetes after stroke.
4.5.2 General Recommendations:
• All patients who are NBM (or have limited oral intake) after acute stroke should either
be prescribed parenteral fluids for hydration or have nasogastric tube (NGT)
placement to allow feeding.
• Normal saline will generally be the parenteral fluid of choice, unless as part of a
dextrose plus insulin infusion protocol.
• If patients remain NBM longer than 24-48 hours, NGT placement to allow feeding
and full hydration should be considered.
• Goal BSL 4-10 mmol/l premeal (ideally 4-7 mmol/l). Post prandial < 15 mmol/l
(ideally around 10mmol/l Hypoglycaemia should be avoided.
4.5.3 Management of Patients with Known Diabetes or Documented Hyperglycaemia
BSL Measurement
• Measure BSL two hourly from 0800-2200 (or pre and 2 hours post meal if eating
meals), and four hourly if stable from 2200 to 0800 over the first 24 hours.
• If stable, BSLs can then be checked four times daily, prior to meals if the patient is
eating.
If however, BSLs are unstable, and/or insulin boluses, or intravenous insulin are required,
more frequent BSL monitoring (two hourly or more) will be necessary.
4.5.4 All Diabetic Patients Post Stroke
Oral Antidiabetic Agents
• Stop sulphonylureas and Acarbose unless patient is on usual diet.
• Continue metformin and/or Thiazolidinediones (eg Rosiglitazone and Pioglitazone), if
the patient is usually on them and if there are no other contraindications.
Use of PRN Insulin
Novorapid insulin boluses, usual dose 10-20% of total daily insulin dose, may be used if BSL
is greater than 15mmol/L up to two hourly. More frequent BSL monitoring (two hourly or
more) will then be required. If patients are requiring repeated doses, the diabetes regimen
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should be reviewed and intra-venous insulin may need to be considered. Liaison with the
Diabetes team is recommended.
4.5.5 Insulin Requiring Diabetes
NBM
Use twice daily Protaphane, with total daily dose to equal half of usual (premorbid) daily
insulin requirements.
Additional boluses of Novorapid, of around 10-20% of total daily insulin dose may be
required if BSL> 15mmol/L.
The daily insulin dose can then be titrated up or down depending on blood sugar recordings,
aiming to keep blood sugars between 4 and 10mmol/L.
Enteral feeding
This is a complex situation, particularly when feeding is commenced.
Liaison with the Diabetes team is recommended. Factors to be considered include
stability/reliability of the feeding tube, rate, timing and frequency of feeding.
Twice daily Protaphane as for NBM patients to cover basal insulin requirements could be
considered. Novorapid boluses could be used to cover feeding regimen.
Intra-venous insulin infusions may be suitable for unstable patients.
Impaired oral intake
Use twice daily Protaphane with total daily dose to equal half of usual (premorbid) daily
insulin requirements, plus Novorapid after food varied to match intake. For example: Daily
Novorapid dose to equal half of total daily premorbid insulin. Divide this dose by three and
give post meal in proportion to oral intake eg:
None of meal eaten  Do not give Novorapid
Half of meal eaten  Give half of Novorapid dose
Entire meal eaten  Give total Novorapid dose.
(For example if usual premorbid Protaphane dose is 36units, give 9 units of Protaphane
twice daily, plus 6 units of Novorapid after a meal, if the entire meal is eaten).
Normal Diet
Give usual insulin dose and antidiabetic agents if no contraindications.
Top up Novorapid may be required if blood glucose > 15mmol/L.
4.5.6 Type 2 Diabetes
On Maximal Oral Antidiabetic Agents Plus Nocturnal Protaphane
See guidelines for All Diabetic Patients Post Stroke (section 4.4.4)
NBM
Give half of nocturnal Protaphane dose twice daily
Enteral Feeding
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Give a total daily dose of insulin that is one and a half times the usual nocturnal Protaphane
dose. Give half of this total dose twice daily. (The total insulin dose is greater than premorbid
dose to cover the withdrawal of sulphonylureas.)
Novorapid boluses could be used to cover feeding regimen. Intra-venous insulin infusions
may be suitable for unstable patients.
Liaison with the diabetes team is advised
Impaired oral intake
Give one and a half times nocturnal Protaphane dose divided by two, twice daily.
Novorapid boluses may be required after meals as per other insulin requiring patients and for
blood sugars > 15mmol/L.
Normal Diet
Give usual insulin and oral antidiabetic agents
4.5.7 Type 2 Diabetes on Diabetic Diet Alone or Antidiabetic Agents
See guidelines above for All Diabetic Patients Post Stroke for instructions regarding
antidiabetic agents (section 4.4.4)
NBM
See guidelines above for all diabetic patients post-stroke
Enteral Feeding
Insulin may be required. Consider use of Novorapid for BSL > 15mmol/L. Liaison with the
diabetes team is advised.
Impaired oral intake
If blood sugars are greater than 15mmol/L Novorapid may be used. Liaison with the diabetes
team is advised
Normal Diet
Prescribe usual oral antidiabetic agents.
4.5.8 Patients with Raised Blood Sugar on Admission
Not Previously Diagnosed with Diabetes
• Patients with non-fasting blood glucose of >11.1mmols/L or fasting blood glucose of
>7.0mmols/L may have undiagnosed diabetes and/or be at risk of poor outcome after
stroke.
• Although HbA1C is not a diagnostic test for diabetes, it may help to differentiate
temporary stress hyperglycaemia from undiagnosed diabetes.
• If glucose is initially high (>/= 12mmol/L) and remains high and/or HbA1C is >8%
consider treating with insulin during the acute post-stroke period as per insulin
requiring diabetes.
• Liaison with the Diabetes team is recommended
These guidelines are a recommendation only. Patients with unstable blood sugars may be best
managed with intra – venous insulin infusions (see Blue Book guidelines). Liaison with the
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diabetes team is recommended for most patients who have altered insulin requirements or
difficult blood glucose control
4.6 Transferring Patient from Bed to Chair Guidelines
4.6.1 Transferring Checklist
Checklist for transferring a patient with stroke
1. Is the person receiving alteplase?
YES - Must stay in bed for the first 24 hours
NO - Continue
LYING ON THE BED
2. Can they move the affected side? YES NO
3. Are they aware of the affected side? YES NO
SITTING ON THE BED
4. Can they straighten the affected knee? YES NO
5. Can they sit, with feet on the floor without help? YES NO
If ‘NO’ to any of the questions 2 – 5 hoist transfer until physiotherapy assessment and
recommendation is made
If ‘YES’ to all of the questions 2 – 5 try transferring the patient.
•
Make sure feet are flat on the floor and positioned under the knees
• Adjust the height of the bed to >90
 a t the hips a nd kne e s
• Use a transfer belt – do not hold under the armpit.
• Use a Montreal sling if the affected arm is floppy.
• Use two people for safety
• Prepare to brace the affected knee in case it gives way on standing.
• Transfer towards the unaffected side through 90 
4.7 Management of the Hemiplegic Upper Limb
Purpose
Consistent and evidence based interdisciplinary approach in the management of the
hemiplegic upper limb.
Scope
This document is to be used as a guide to facilitate management of the hemiplegic upper
limb throughout the West Coast District Health Board.
Those working in the West Coast District Health Board are to refer to this guideline as a
foundation for the management of the hemiplegic upper limb. Specific treatment techniques
and procedures should be client-centred and involve an interdisciplinary approach in decision
making.
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4.7.1 Assessment of the Hemiplegic Upper Limb
Assessments used in stroke rehabilitation should be valid and reliable measures. They can
be used to differentiate among subjects to predict outcomes, to quantify and evaluate
patients’ progress and the effectiveness of interventions. Assessments aid in providing timely
identification of risk factors, providing a logical basis for treatment, structuring goals and
prioritising clinician’s time and resources.
Action
1. Physiotherapist and Occupational Therapist select the appropriate assessment measure.
The therapist may use but is not limited to the following measures: Chedoke-McMaster
Stroke Assessment, Motor Assessment Scale, The Tardieu Scale (See next page)
2. The therapist documents the outcome of the selected measure and forms a treatment
plan.
Suggested Measures
Chedoke-McMaster Stroke Assessment
The Chedoke-McMaster Stroke Assessment has been shown to have good reliability and
validity. It consists of two parts, a Physical Impairment Inventory and a Disability Inventory.
The Physical Impairment Inventory is divided up into six dimensions which include measures
of shoulder pain, postural control, the arm, the hand, the leg, the foot. Each dimension is
measured on a seven point scale which correlates to seven stages of motor recovery. The
Disability Inventory is designed to measure clinically significant changes in physical disability
and is divided into the Gross Motor Function Index and the Walking Index.
Motor Assessment Scale
The Motor Assessment Scale is a measure of motor impairment and mobility based on a
format of functional task observation. It consists of eight tasks including supine to side lying
onto the intact side, supine to sitting on the side of the bed, balanced sitting, sitting to
standing, walking, upper arm function, hand movements and advanced hand activities. Each
item is scored on a seven point scale. The Motor Assessment Scales has been documented
to have good validity and reliability.
The Tardieu Scale
The Tardieu Scale should be used to measure spasticity clinically. The affected limbs are
passively moved through range as slowly as possible (V1) and as quickly as possible (V3).
The quality of the muscle reaction to stretch (X) is measured at each velocity and the angle
of the muscle reaction (Y) is also recorded. The Tardieu Scale is a more accurate tool to
measure spasticity in upper and lower limb muscles compared with the Ashworth scale as
velocity of stretch is altered to identify the presence of spasticity and also the presence of
contracture. Ideally tone assessment using the Tardieu scale should be completed and
reviewed at the same time of day.
4.7.2 Pain
Pain is a common problem following stroke and can limit an individual’s ability to participate
in ongoing therapy causing further problems in relation to recovery. People who have had a
stroke may experience pain of several types including mechanical, central post stroke pain
and pain from pre morbid disease such as osteoarthritis. Most pain is mechanical, arising
from reduced mobility, poor alignment and poor integrity of the glenohumeral joint.
Hemiplegic shoulder pain tends to be less common in the acute stages of stroke but
increases over time due to secondary biomechanical changes.
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Action
Pain should be assessed regularly by all staff.
Pain location and intensity should be documented in the notes using the Visual Analogue
Scale as a standard baseline assessment.
1. Pain should be prevented by the following:
a. Education of staff and carers about correct handling and positioning of the
hemiplegic arm.
b. Avoiding the use of overhead arm slings, which encourage uncontrolled abduction
2. People with stroke who have musculoskeletal pain should be:
a. Assessed by specialist therapists for potential alleviation through exercise, passive
movement, improved seating or other procedures.
b. Prescribed appropriate analgesics where non-pharmacological treatments are
ineffective
3. For established shoulder pain:
a. Simple interventions should be used first (eg analgesia, non-steroidal antiinflammatory)
b. If simple measures do not work, the treatment option of high-intensity
transcutaneous electrical nerve stimulation (TENS) may be considered post the acute
phase but not restricted to this.
4. People with stroke who have central post stroke pain:
a. Neuropathic pain may respond to tricyclic antidepressants (eg amitriptyline) or
anticonvulsants (eg gabapentin)
b. People with intractable pain should be referred to a specialist pain service as soon
as possible
4.7.3 Positioning
Positioning of people who have had a stroke and provision of appropriate seating may
prevent the development of contractures, abnormal tone, pain, skin breakdown and
respiratory complications. Staff should position people, whether lying or sitting, to minimise
the risk of complications such as aspiration, respiratory complications, shoulder pain, and
contractures.
Action
1. Educate staff and carers of correct handling and positioning of hemiplegic arm.
2. Positioning charts placed above person’s bed if appropriate following assessment by
physiotherapist or occupational therapist.
3. Staff should attempt to maintain external rotation, abduction, and flexion of hemiplegic
shoulder.
4. Shoulder should not be passively moved beyond 90 degrees of flexion and abduction
unless the scapula is upwardly rotated and the humerus is laterally rotated.
5. Upper limb must be handled carefully during functional activities to prevent pain.
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4.7.4 Sensation
Impaired sensation affects people following a stroke. Sensation plays an important role in the
execution of skilled fine motor tasks, activities of daily living and mobility. Altered sensation
affects sensory feedback in the sensory-motor loop therefore increasing recovery times.
Sensory information that can be affected includes: touch, pain, temperature, superficial
pressure, vibration, proprioception and presence of sensory inattention.
Action
1. Assess changes in sensation and record findings in notes.
2. Educate staff and carers in the role that sensation plays in rehabilitation.
3. Sensory re-education as appropriate.
4.7.5 Shoulder Subluxation
Shoulder subluxation after stroke is a significant problem. The reported incidence of post
stroke shoulder subluxation is high (up to 80%) and may contribute to impaired function and
shoulder pain (Linn et al 1999). Weakness of the muscles surrounding the shoulder results in
prolonged stretching of the joint capsule, causing capsule damage and subluxation (Faghri et
al 1994). A recent Cochrane systematic review found that there is limited evidence in
prevention of shoulder subluxation. Supportive devices can provide immediate effect in
reducing subluxation in the shoulder that is already subluxed (Ada 2005).
Action
1. Staff will monitor the hemiplegic upper limb and will inform the team if subluxation occurs.
2. If shoulder subluxation is noted by any staff member an assessment should be completed,
including but not limited to: history of previous shoulder impairments, palpation, sensation,
cognition, pain, range of motion and x-ray.
3. If shoulder subluxation is identified management techniques can include but are not limited
to: shoulder strapping, lap tray, arm trough, triangular/collar & cuff sling, positioning in bed
and education to staff and carers on appropriate handling techniques.
4. It is recommended the above supportive devices should be applied as soon as the patient
is allowed in an upright position.
4.7.6 Oedema
Following a stroke, people with a hemiplegic upper limb are at risk of developing oedema
due to immobility. Oedema has implications on function, skin integrity, pain, circulation and
aesthetics.
Action
1. All staff will monitor the hemiplegic upper limb for oedema.
2. If oedema is noted by any staff member it will be brought to the attention of the relevant
staff for management. The therapist will consider the following factors: positioning, 24 hour
management, type of oedema, history, differential diagnosis, implications for concurrent
treatments, impact on function, daily routines, pain and presentation.
3. The interdisciplinary team will initiate techniques to manage oedema and prevent further
oedema from occurring (See Appendix below)
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Management Techniques for Oedema
Management techniques: positioning, pressure garments, passive/active assisted/active
range of movement exercises, electrical stimulation
4.7.7 Spasticity
Spasticity is defined as a motor disorder characterised by a velocity dependent increase in
resistance to passive stretch of muscles with hyperactive muscle stretch reflexes (Lance
1980). Spasticity typically presents as flexor tone of the upper limb. The scapula retracts and
depresses, internally rotates and adducts the shoulder, flexes the elbow, pronates the
forearm and flexes the wrist and hand. Spasticity limits shoulder abduction, flexion and
external rotation.
Spasticity and shoulder pain are related. Therefore range of motion should be monitored and
maintained as much as possible to help reduce development of hemiplegic shoulder pain. It
is now known that spasticity (i.e., hyperactive stretch reflexes) is not a major determinant of
activity limitations. Interventions to reduce spasticity may be considered if the level of
spasticity interferes with activity or the ability to provide care to those with stroke (Van Kuijk
et al 2002).
Action
1. If the person has spasticity, complete the appropriate spasticity scale. If the person has
decreased tone consider preventative management techniques.
2. The therapist will provide positioning and supports as indicated by assessment.
3. Spasticity should be monitored and regularly re-assessed using the selected scale.
4.7.8 Splinting
Splints are sometimes used as a means of intervention to reduce spasticity and prevent
contracture after stroke. Clinical aims for splinting adults following stroke include: reduction of
spasticity, reduction in pain, improvement of functional movement, prevention of contracture,
prevention of overstretching and oedema. While there is limited published evidence to either
support or refute the effectiveness of hand splinting for adults following stroke, one recent
randomised study suggested it should not be routine practice for most patients with hand
weakness soon after stroke (Lannin 2007).
Action
1. If a splint is indicated a physiotherapist or occupational therapist will conduct an
assessment of the upper limb.
2. In the assessment process the therapist will take the following factors into consideration:
oedema, sensation, skin integrity, presentation, positioning, tolerance, biomechanical
changes, other impairments, daily routines, function, removability, compliance, dynamic
splint versus static splint, carers/family and goal of splinting.
3. The therapist will also assess and document in the notes all precautions prior to splinting.
If any precautions are identified the therapist will document reason for proceeding with
splinting ( See section 4.6.8.1 below)
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4. If the therapist and the interdisciplinary team agree that splinting will benefit the person the
therapist will use clinical judgement to choose the material, design and goal of the splint.
5. The person/carer/staff will receive education by the therapist regarding splint wearing
schedules, splint care and cleaning, and monitoring of skin integration.
4.7.8.1 Precautions to Splinting
Precautions include but are not limited to: uncontrolled intracranial pressure, heterotrophic
ossification, poor skin condition, oedema, sensory impairment, acute inflammation, vascular
impairment, behavioural impairment, concomitant fracture, cognitive impairment, severe soft
tissue injury, uncontrolled epilepsy, medically unstable condition, medical procedures
requiring access to limb.
4.7.9 FES
Functional Electrical Stimulation (FES) includes superficial application of electrodes to
specific motor points in order to stimulate peripheral nerves and muscle fibres. It can be used
to increase motor activity/control, reduce spasticity, improve range of motion and prevention
of shoulder subluxation following stroke (Ada and Foongchomcheay 2002).
Contraindications for FES
People who have a Pacemaker or other electrical stimulator, areas with PVD (more likely to
create skin breakdown), excessive adipose tissue in area of stimulation, areas of neoplasm,
internal fixation (where metal is within the area of electrode placement, or where there is a
strong electrical stimulus), people who are unable to give adequate feedback, pregnancy –
do not apply on trunk areas, over thoracic region and carotid sinus.
FES can also be used to increase pain free range of external rotation (Price and Pandyan
2000). If indicated FES should be initiated as soon as possible following a stroke.
Action
1. The physiotherapist or occupational therapist will complete an assessment of the upper
limb and identify whether FES is indicated for that person. See Appendix 4 for list of
Contraindications.
2. If indicated electrodes will be placed over posterior deltoid and supraspinatus muscles at
appropriate parameters for shoulder subluxation.
3. Treatment with FES should be continued until the patient has adequate control of the
glenohumeral joint.
4.7.10 Strapping
Recent literature suggests that shoulder strapping has potential to reduce the incidence and
or severity of shoulder pain however studies are limited. The theories behind the benefits of
shoulder strapping include: mechanical alignment, stimulation of flaccid muscles and
proprioceptive input. In addition, strapping can act as a reminder to carers and staff of the
extra care needed with handling which can increase the number of pain-free days (Griffin &
Bernhardt 2006).
Action
1. Shoulder assessment completed by the physiotherapist or occupational therapist.
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2. If the therapist deems strapping would be beneficial based on clinical reasoning and
evidence based practice the therapist will perform the appropriate strapping technique.
3. The therapist will monitor the person’s progress and reaction if any to the strapping.
4. Education to staff and carers will be provided in regards to the care and monitoring of the
strapping.
4.8 DVT / PE Prophylaxis Guideline
4.8.1 Venous Thromboembolism Prevention in Stroke Patients
Background:
• Deep venous thrombosis (DVT) and pulmonary Thromboembolism (PTE) are
recognised complications following a stroke.
• Pulmonary embolism is detected in 0.8% of acute stroke patients within the first 14
days.1 Mortality from PE may be as high as 50%2 but fatal PE is rare within the first
week following stroke.3
• In rehabilitation settings, symptomatic DVT’s occur in 10-15% of patients and deaths
from pulmonary emboli occur in approximately 2%.
• The risk of developing venous thromboembolism is higher in patients who are
immobile with a paralysis of the leg. Those who are very immobile such as those who
are bed-ridden or wheelchair bound are at greatest risk.
• A variety of agents have been shown to be effective in the prevention of DVT and
PTE in other (non-stroke) high risk patients including post-operative patients. These
include Aspirin, unfractionated (standard) Heparin subcutaneously, low molecular
weight Heparin (LMWH) sub-cut, low dose Warfarin, graduated compression
stockings (GCS) and intermittent pneumatic compression (IPC) devices.
• In acute stroke patients, prevention of DVT/PTE with anticoagulants is complicated by
the risk of haemorrhagic transformation of the new cerebral infarct. Such
haemorrhagic transformation can increase both morbidity and/or mortality. This risk of
haemorrhagic transformation reduces over time (first 1-2 weeks). Thus for any
intervention, the risks and potential benefits need to be carefully weighed up.
• The ideal timing for starting of anticoagulants for DVT prophylaxis after stroke is not
known.
• Graduated compression stockings have been shown to be ineffective in prevention of
DVT and PE after stroke
• Intermittent pneumatic compression (IPC) in immobile patients has been shown to
reduce DVT after stroke with a trend to increased 30-day survival and no increase in
falls with injury. However, there are logistical difficulties with implementation of this
treatment, including some concerns that rehabilitation efforts might be impeded.
4.8.2 Guidelines for the prevention of Venous Thromboembolism
All stroke patients:
• Early mobilisation and optimal hydration should be maintained from the outset.
• Graduated compression stockings should not be used routinely for DVT prevention
after stroke.
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For patients with ischaemic stroke only:
Aspirin 150 – 300mg per day should be given unless contra – indicated (lower aspirin doses
have not been studied specifically with regard to DVT prophylaxis following stroke).
Prophylactic anticoagulation should not be routinely administered for deep vein thrombosis
prophylaxis immediately after stroke, because of the risk of haemorrhagic transformation
within an infarct.
Prophylactic anticoagulation or intermittent pneumatic compression devices may be
considered after the first 2 or 3 days of stroke in immobilised people with additional high risk
factors for DVT/PE such as:
• intolerant of aspirin
•
unable to lift each leg off the bed
•
past history of DVT or PE
•
morbid obesity
•
known history of inherited Thrombophilia
For immobile patients, a decision regarding the plan to use or not use anticoagulants for DVT
prophylaxis should be documented in the patient’s notes by 7 days after stroke onset.
If anticoagulants are to be used for DVT prophylaxis after stroke, the recommended regimen
is:
• enoxaparin 40mg daily sc (with dose adjustments for renal impairment, Fu =0.7)
•
aspirin should be continued
The optimal duration of anticoagulant therapy for DVT prophylaxis is not known. Pulmonary
embolism is a very important cause of death after stroke between weeks 2 and 4
For patients with Intracerebral Haemorrhage
The best evidence available supports use of intermittent pneumatic compression devices for
DVT/PE prophylaxis for immobile patients with ICH. The benefit from this treatment appears
greatest for patients who are unable to raise both legs off the bed or have other high-risk
features for DVT/PE.
Anticoagulants are generally contraindicated after an acute ICH. There may be some
circumstances when the benefits of anticoagulation are considered to outweigh the risks.
Risks of further or worsened intracerebral bleeding are higher early after the bleed, and with
lobar bleeds.
DVT prophylaxis after ICH
• Anticoagulants are generally not recommended for most ICH patients as the risk is
likely to outweigh any benefit
• Pneumatic compression stockings should be used for immobile patients with ICH,
particularly those who are unable to raise both legs independently off the bed or have
other high-risk factors for DVT/PE.
The role of DVT monitoring with ultrasound to guide treatment is not established
These guidelines apply to prevention of DVT / PTE only. Treatment of established
venous thromboembolism requires careful analysis of the benefit to risk ratio in each
individual patient. Temporary IVC filter placement can be considered in patients with
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significant DVT burden who are considered at high risk of haemorrhage if
anticoagulated
4.9 Urinary Incontinence
4.9.1 Stroke Continence Protocols
Vision
Bladder continence identified and managed in stroke from acute admission through
rehabilitation.
Scope
All clinical staff, patients and patient’s families.
Background
Urinary incontinence (U.I.) is common following stroke (reportedly 32-79% of patients – preexisting for some). (Williams, Perry and Watkins, 2010) Bowel function is also often affected,
especially constipation which is related particularly to functional ability/immobility.
Background Policy Statements
1. Urinary incontinence is not an indication for an indwelling catheter (IDC). Patients
should not have an IDC inserted in the first 48 hours unless indicated to relieve
retention.
2. Bladder and bowel incontinence should be identified and managed in the acute phase
of stroke by high levels of nursing care. (see associated documents)
3. Intermittent catheterisation where indicated.
Associated documents:
1. Intermittent catheterisation protocol
2. Urinary Assessment (Dunedin’s by permission)
3. Interventions based on U.I. types and to promote urinary continence
Definitions
Retention = >500mls on bladder scanner
4.9.2 Urinary Incontinence Assessment Source: Dunedin Acute Stroke Unit
Urinary Incontinence Assessment
Three commonest causes of post-acute stroke urinary incontinence (UI) are
• Detrusor instability
• Functional: Impaired communication secondary to cognitive or language deficits
• Overflow incontinence
Step 1: History.
Take an adequate history from patient and or family, and staff. Include pre-stroke status, and
a history of bowel function. As an aid to guiding the questions, below are listed the common
symptoms of urinary incontinence. Keep in mind that there may be more than one cause of
urinary incontinence.
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Stress UI
Involuntary leakage on effort, sneezing or
coughing.
a. Leakage with cough, sneeze, physical
activity.
b. UI in small amounts (drops, spurts).
c. No nocturia or UI at night.
d. UI without sensation of urine loss.
Urge UI
Involuntary leakage accompanied by or
preceded by urgency
a. Strong, uncontrolled urge prior to UI.
b. Mod/large volume of urine loss (gush).
c. Frequency of urination.
d. Nocturia > 2 times.
e. Enuresis
Overflow UI
Functional UI
Inability to maintain continence because of
impairments
a. Mobility or manual dexterity impairments
b. Lack of toilet or toilet substitute
c. Restraints
d. Sedative, hypnotic, CNS depressant, diuretic,
anticholinergic, alpha-adrenergic antagonist.
e. Depression, delirium, dementia.
f. Language impairment.
g. Pain.
a. Difficulty starting urine stream.
b. Weak or intermittent stream (dribbles).
c. Post-void dribbling.
d. Prolonged voiding.
e. Feeling of fullness after voiding.
f. Voiding small amounts often or dribbling
with changes in position.
Step 2: Simple tests
• Record results of a dip stick test of the urine
• Send urine for C&S
• PR examination
• Measure post void bladder volume
Step 3: Management Stress
UI
Urge UI
•
•
Overflow UI
•
•
•
•
•
•
•
Q2h toileting
Pelvic floor exercise
Q2h toileting
If not progressing consider medication;
Oxybutynin 2.5 mg bd
Functional UI
Acute retention – IDC
Large residual – consider
Terazosin
Intermittent catheterisation if
appropriate
Address constipation
Regularise bowel function
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•
•
•
•
Address any correctable impairments
Communication aids
Easy access clothing
Frequency/volume chart
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Normal Bladder Function
Bladder (detrusor) and urethral functions are coordinated for the storage and emptying of
urine (Borrie 1998). This involves areas of the central nervous system and multiple peripheral
nervous systems as listed below:
1. Sympathetic nervous system relaxes the detrusor muscle while internal urethral
sphincter control is maintained by sympathetic alpha-adrenoreceptors
2. Parasympathetic acetylcholine receptors mediate detrusor contracture.
3. Somatic (voluntary) nervous system innervates the pelvic floor muscles, including the
external urethral sphincter.
4. The micturition centre in the brainstem (pons) monitors when the bladder is filling and
controls the sacral reflex when bladder filling reaches a certain level.
5. The micturition centre in the frontal lobes provides conscious input to the pontine
micturition centre allowing the inhibition of urination until the time of voluntary control.
Normally, we are unaware of bladder fullness until a capacity of about 300 cc is reached. The
need to void is then inhibited or controlled by the frontal lobes.
Urinary Dysfunction
40-60% of people admitted to hospital after a stroke can have problems with urinary
incontinence, with 25% of stroke survivors still having problems on hospital discharge, and
15% remaining incontinent after one year (Barrett 2001). Not all the studies excluded people
with pre-morbid incontinence, however.
1. The most frequently occurring voiding abnormalities associated with a stroke have
been identified as
•
urinary frequency,
•
urge incontinence and
•
urinary retention (Marinkovic and Badlani 2001).
2. Urinary tract infection is not uncommon in stroke patients.
Urinary Incontinence is a strong predictor of poor functional recovery, discharge to
long-term care, and limited resumption of social participation (Dumoulin et al. 2007). While
there are problems with attributing better stroke outcome to improvements in continence, it is
possible that recovery from incontinence may improve morale and self esteem and therefore
speed overall stroke recovery (Barer 1989; Patel 2001).
Conversely, stroke outcome is better in those stroke survivors who remain continent or
regain continence (Barer 1989). Improvement is common over time (Marinkovic 2001), which
suggests that problems with continence may be transient in some stroke survivors, and/or
amenable to intervention.
Mechanisms most commonly responsible for urinary incontinence
Gelber et al. (1993) suggested that three mechanisms were responsible for incontinence
post stroke (van Kuijk et al. 2001). These included:
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•
•
•
Detrusor hyper-reflexia with urge incontinence and bladder hyper-reflexia from
disrupted neuromicturition pathways (frontal lobe or pontine micturition centers)
(Nazarko 2003, Fader & Craggs 2003).
Incomplete bladder emptying with overflow incontinence and bladder hypo-reflexia
from concurrent neuropathy or from the concurrent medications, such as diuretics
(Fader & Craggs 2003).
Incontinence from stroke-related motor, cognitive and language deficits, despite
normal bladder function
Detrusor Hyperreflexia
Cortical and subcortical strokes generally result in an unstable or hyper-reactive detrusor
(Borrie 1998). Borrie (1998) has noted that unstable detrusor contractions occur with little
warning and result in symptoms of urinary urge incontinence. The bladder volume at which
this occurs can be variable but it is usually lower than the volume at which a person with a
normally functioning bladder would normally have a strong urge to void (Borrie 1998). He
comments that detrusor hyper-reflexia is not inevitable following a stroke. It has been noted
that urinary incontinence is more common with larger strokes with a greater number of
accompanying deficits and is closely associated with bowel incontinence, dysphagia and
overall functional level, all markers of more severe strokes.
Urinary Retention
1. Urinary retention is common following an acute stroke (21-47%).
2. Potential contributing factors include difficulty with communication, mobility and
decreased consciousness.
3. Other contributing factors may be a hyper-reflexic bladder, as seen in diabetic
neuropathy, or an obstruction such as prostatic hypertrophy.
4. Occasionally urinary retention will persist in very severe stroke patients, often in
patients with embolic strokes with no previous warnings.
Other Factors Contributing to Post-Stroke Incontinence
Stroke results in a number of factors which can affect continence, but which are often
overlooked:
1. Communication difficulties, particularly an inability to communicate voiding needs,
either due to aphasia, dysarthria or confusion/cognitive impairments.
2. Mobility problems, such as hemiplegia make some patients dependent on caregivers
to void in a socially appropriate manner. Lack of caregiver support may also make it
difficult to toilet the stroke patients quickly enough.
3. Post stroke depression and confusion may result in a failure to communicate the need
for assistance.
4. Medications, such as diuretics can increase the frequency of the need to void; others
can increase confusion, while still others such as anti hypertensives may affect the
autonomic nervous system leading to retention.
Risk Factors for Urinary Incontinence (Nazarko 2003, Brittain et al. 1999, Jorgensen et al.
2005).
1. Severe strokes have a higher incidence of urinary incontinence.
2. Premorbid history of urinary incontinence, i.e comorbidities.
3. Motor weakness and mobility difficulties, including ataxia.
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4.
5.
6.
7.
Altered level of consciousness.
Cognitive impairment
Depression
Elderly (Marinkovic and Badlani 2001).
Gariballa (2003) found that patients with urinary incontinence at admission tended to be
more undernourished and dehydrated, more impaired, at greater risk for infective
complications and older then patients without urinary incontinence.
Course of Urinary Incontinence
Brooks (2004) has noted that a stroke may exacerbate existing stress incontinence, a
problem more common in women. Urinary incontinence was reported among 17% (n=213) of
non-institutionalised post stroke survivors, an average of nine years post stroke, compared to
7% of control subjects without stroke (Jorgensen et al. 2005) (OR = 2.8, 95% CI 1.5-5.2).
Incontinence post stroke often resolves without treatment in eight weeks (Borrie et al. 1986,
Brocklehurst et al. 1985).
Urinary Tract Infection
1. UTI is the most common medical complication in stroke rehabilitation.
2. Risk factors include use of beta-blockers and high post-void residuals.
Urinary tract infections (UTI) are the most commonly encountered medical complication
associated with stroke rehabilitation (Roth et al. 2001). Although age greater than 65, male
sex, a history of prior stroke, stroke syndrome, use of β-Blocker or antidepressants and a
post void residual (PVR) of 150 ml or more have been reported as risk factors for the
development of UTIs, Dromerick and Edwards (2003) only found an increased risk of UTI to
be associated with β-Blocker use (OR = 4.01, 95% CI 1.26-14.59) and PVR ≥ 150 ml (OR =
3.97, 95% CI 1.24- 9.53) among 120 stroke patients admitted to a rehabilitation service.
Post-Void Residual Urine Testing
1. PVR is able to determine if bladder emptying is complete.
2. PVR > 150 cc is generally regarded as abnormal.
3. Increased PVRs increases the risk of urinary tract infections.
Borrie (1998) notes that “A true void residual (PVR) urine test is critical to determine if
bladder emptying is complete... although in/out catherisation is the gold standard for
determining the PVR urine, portable bladder ultrasound is practical, noninvasive and costeffective (Chan 1993). A sterile culture from the catheter specimen would rule out urinary
tract infection. Two consecutive residual urines of greater than 150ml suggest a significant
degree of incomplete bladder emptying, and physical outlet obstruction should be ruled out
by urology assessment with cystoscopy. There is no consensus as to what residual urine
volume is definitively abnormal (Grosshans et al. 1993). Most would regard greater than 150
ml abnormal, but is depends to some degree on the volume of urine voided before
catheterisation.”
Diagnosis of Bladder Dysfunction
1. Detrusor instability or hyper-reflexia with urge incontinence.
2. Stress incontinence.
3. Overflow incontinence with incomplete emptying.
4. Mixed types of incontinence.
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5. Functional incontinence, due to non-urinary factors.
6. Iatrogenic incontinence, due to drugs or restraints.
The intervention used to manage urinary incontinence largely depends on the patient’s
history and type of incontinence. Due to the absence of strong evidence regarding treatment
efficacy, Borrie (1998) has suggested using a stepwise approach, with behavioural
interventions used as first line treatments followed by pharmacological and surgical
interventions. This approach highlights the fact that patients should always be treated with
the least invasive intervention option.
There are few randomised controlled trials evaluating the efficacy of bladder management to
treat urinary incontinence post stroke, although the issue has been studied in other patient
populations. The choice will often be dictated by the stroke patient’s type of incontinence.
Behavioural Interventions for Incontinence
1. Scheduled voiding q 2-4 hours
2. Fluid restriction
Dumoulin et al. (2005) conducted a systematic review investigating the benefits of
behavioural therapies used to treat urinary incontinence. The study included only four
randomised controlled trials, a single cohort study and recommendations from three clinical
practice guidelines. This study found limited evidence for the reduction of urinary
incontinence in male stroke patients using combination treatment including bladder retraining
with urge suppression and pelvic floor exercises. The authors concluded that although there
is increasing recognition of the benefits of using behavioral approaches as treatment for
stroke patients with a high occurrence of continual urinary incontinence, the evidence
remains very limited for specific treatments used for stroke survivors with urinary
incontinence.
Bladder Training
Scheduled voiding programs follow a set schedule of voiding every 2-4 hours regardless of
whether the patient “needs to go” because post stroke cortical awareness of bladder fullness
is often reduced (Borrie 1998).
Initiation of toileting in response to urgency, while shown to promote continence, often does
not provide enough time to void especially when mobility is limited. Bladder training allows for
lengthening of the voiding interval as the patient becomes consistently dry (Burgio and
Paurgio 1986, Borrie 1998). However, Duncan et al. (2005) suggest that there is no evidence
for or against a scheduled voiding program. These authors recommend an individualised
bladder training program and the use of prompted voiding for incontinent stroke patients.
Pelvic Floor Exercises are designed to strengthen the pelvic floor muscles through
repeated contraction and relaxation of specific muscle groups. Although these exercises
were originally developed to manage stress incontinence, rapid contractions have also been
found to help patients suppress the “urgency wave” of the relax bladder contraction (Borrie
1998).
Fluid Intake
The total measurable fluid intake should be approximately 1500 – 1800 ml per 24 hours. The
use of intravenous fluids or a feeding tube may result in fluid loads greater than 2000 ml per
day, which will in turn compromise bladder continence (Borrie 1998).
Pharmacological Interventions for Incontinence
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1. Pharmacological treatment will depend on the cause of the stroke.
2. The vast majority of bladder incontinence is due to detrusor hyper-reflexia due to
central loss of inhibition.
3. Drugs with anticholinergic actions are recommended in these cases, i.e Oxybutynin.
4. For overflow incontinence due to detrusor inactivity, a cholinergic such as Bethanecol
is recommended.
5. For overflow incontinence due to outlet obstruction, an alpha-adrenergic blocker may
be recommended.
Drug therapy should be considered an adjunct to behavioural therapy and should only be
used when behavioural interventions are either inappropriate or have had an adequate trial.
The side effects of anticholinergic medications are often underestimated, particularly in the
post-stroke population. Therefore, the goal of pharmacological therapy should be to use the
lowest dose to achieve the optimal effect with the fewest side effects (Borrie 1998).
Post stroke detrusor hyper-reflexia treated with drugs with various degrees of anticholinergic
medications. These medications include, oxybutynin, propantheline and imipramine. These
drugs should be started at a low dose and increased gradually over days, if not weeks.
Propantheline supposedly does not cross the blood-brain barrier, with a theoretical
advantage over other drugs which can lead to confusion. Tolterodine is another
anticholinergic which is said to have less influence on salivary gland function and therefore
less likely to lead to dry mouth as a complication. (Note that Tolterodine is not a subsidised
drug in NZ).
Borrie (1998) has also noted that for patients with poor detrusor contracture, Bethanechol
may improve detrusor contracity (Sonda et al. 1979). It serves as an adjunct to intermittent
catherisation. Bethanechol is discontinued if residual urines do not diminish, there is
excessive sweating, asthmatic attacks, congestive heart failure and abdominal cramps.
Catheters for Bladder Dysfunction
1. Catheters for bladder dysfunction should always be seen as a treatment of last resort.
2. Intermittent catheterisation is the preferred option in urinary incontinence with
overflow incontinence.
3. An indwelling catheter should be limited to those patients with intractable urinary
retention, continuous wetness (+/- skin breakdown) and those who have need of
monitoring.
Intermittent catheterisation is the preferred management option for patients suffering from
urinary retention with overflow incontinence. The combined voided and residual volume
should not exceed 500 ml. and the frequency of catheterisation should be monitored and
adjusted if the residual volume changes. Long-term in-dwelling catheters are associated with
several risks, such as chronic urinary bacteruria and bladder stones, and should only be
used if intermittent catheterisation is impractical.
Gresham et al. (1995) noted that “use of indwelling catheters should be limited to patients
with incontinence due to urinary retention that cannot be otherwise treated, severely impaired
patients with skin breakdown, in whom frequent bed or clothing changes would be difficult or
painful and in patients in whom incontinence interferes with monitoring of fluid and electrolyte
balance.” Brocklehurst et al. (1985) noted that 40% of patients regain continence during the
first two weeks. The use of a catheter will inhibit that process. Again catheterisation should
be reserved for exceptional circumstances (Nazarko 2003).
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Bjork et al. (1984), Sabanthan et al. (1985) and Wareen et al. (1982) observed the chronic
use of indwelling catheters increases the risk of bacteria and urinary tract infection.
Moreover, it has been shown that more than three-quarters of persons catheterised for three
months or more will develop inflammatory bladder wall changes. While bacteraemia can be
identified by urine culture, treatment with antibiotics should be reserved for those patients
with symptomatic urinary tract infections.
4.10 Formal Family Meeting Guidelines
4.10.1 Purpose
To ensure that Family Meetings within General Medicine and Stroke are organised,
facilitated, supported and documented in a manner that enhances quality care and service
provision.
4.10.2 Introduction
Individual members of the MDT often meet informally with patients and families during a
patients stay in hospital, however these guidelines refer to Family Meetings which are
formally arranged and include the patient, their family or support people, and all relevant
members of the MDT.
Family meetings provide an opportunity to enhance the quality of care provided to patients at
Christchurch Hospital. They are an ideal avenue to inform, deliberate, clarify and set goals
for future care, based on discussions between health professionals and the patient and
family. Adequate preparation, skilled facilitation and accurate documentation can improve the
effectiveness of family meetings, while maintaining the patient’s sense of autonomy.
Different family meetings have different roles/agendas, which may include;
 Diagnostic and treatment issues
 Patient and/or family compliance issues
 Patient/family conflict relating to hospital admission
 Discharge planning – especially complex issues around discharge needs
4.10.3 Procedure
Planning
The decision that a family meeting is required can be made by the interdisciplinary team, an
individual staff member, or the patient/family. A good time for this to be communicated with
the team is at the morning board meeting.
Once the decision has been made for a family meeting, the facilitator for the meeting needs
to be established.
The facilitator meets with the patient to ensure they understand the purpose of the family
meeting, to get their consent for the meeting, and to clarify who should be invited to attend.
The patient is given the choice of whether they wish to attend or not, provided their physical
health or cognitive status is adequate. Where the patient is unable to be involved in this
process, the next of kin (or nominated contact), Enduring Power of Attorney or closest family
member will be consulted.
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The facilitator (or his/her nominee) must then arrange a date, time and venue for the family
meeting, and ensure that all members of the family meeting are aware of the details for the
meeting. The details of the meeting must also be clearly recorded in the patient’s clinical file.
Format
All members of the MDT who are attending the meeting should meet briefly before the
meeting to clarify the key issues to be discussed and to decide on the expected outcome of
the meeting.
It is the responsibility of the Facilitator to:
• Facilitate introductions of all present.
• Establish a timeframe for the meeting.
• Make it clear that questions can be raised at any time.
• Ensure that support is available for the patient where/when needed (eg. Mental
Health Worker, Maori Health Worker).
• Ensure the meeting is a safe, empowering and culturally appropriate forum.
• Check in with the patient and family at regular intervals throughout the meeting to
ensure they have a clear understanding of what is being discussed.
• Define the purpose of the meeting
• Ensure that after the introductions etc, the Medical Officer in charge of the patient’s
case summarises medical treatment, diagnosis, results of tests and ongoing
management of the patient’s case.
• Ensure each discipline outlines their assessment of the patient’s situation with
ongoing explanations and general discussion. If a relevant team member is not
available, a written handover may be read by the facilitator.
• Ensure the opportunity for the patient and family members to ask questions and/or
discuss any concerns.
• At the end of the meeting, sum up the key points of discussion and ensure all present
clearly understand the
• outcome/plan/information given. If relevant, tasks yet to be completed by the patient,
family and MDT should be clearly summarised and specified timeframes set.
When the outcome of the meeting is for residential care for the patient (rest home, dementia
care or hospital level care), the social worker may stay behind with the family after the other
MDT members have left the meeting to provide the patient and family with the information
they need and to complete necessary paperwork.
If the meeting has been especially complex or upsetting for the family, an appropriate health
professional may stay after the meeting has finished to provide support.
Documentation
The facilitator of the meeting is responsible for documenting the meeting in the clinical file.
This should be done as soon as possible following the meeting.
When the facilitator is not the Medical Officer, the Medical Officer must summarise the
medical outcome of the meeting in the clinical file, in addition to the summary that the
facilitator has documented.
The documentation must:
• State the name and designation of all those present at the meeting
• Include the date and time of the meeting.
• Be written in a manner that is clear, neat and legible.
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•
•
Summarise the information shared, issues raised, concerns of the patient/family and
recommendations made by the MDT.
Clearly summarise the outcome of the meeting, including (where appropriate),
medical treatment plan, discharge destination, referrals to be made, supports to be
put in place on discharge etc.
Things which may make family meetings go more smoothly:
• Know your role and be clear in what you want to communicate.
• Keep the language non-medical and free of jargon.
• Do not use ambiguous words which may confuse or mislead the patient and family.
• Be supportive of the patient and family and aware of their feelings.
• Ensure that the cultural needs of the patient and family are met and include
interpreters and cultural supports where required/requested.
• Be optimistic but realistic.
• Be supportive of your colleagues and work as a team, respecting other disciplines
skills.
• Be flexible in the way the meeting runs, as some information comes up unexpectedly.
• Respect the patient, talk to them, with the family listening (as opposed to the reverse).
4.11 Palliative Care
Palliative Care
An accurate assessment of prognostic risk factors or imminent death should be made for
patients with severe stroke or those who are deteriorating. Patients with stroke who are
dying, their families and caregivers should have access to specialist palliative care teams as
needed, and have care that is consistent with the principles and philosophies of palliative
care. (Palliative care subcommittee, 2007)
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5 Transient Ischaemic Attack (TIA) Guidelines
5.1 Acute Management in the ED /Medical Ward
5.1.1 Transient Ischaemic Attack (TIA) Acute Management in the ED/Medical Ward
NB Please refer to accompanying guidelines for more detailed information
regarding each step.
Step 1:
Diagnosis
Is it a TIA?
No
Alternative Diagnosis!
Yes
Step 2: ABCD2 risk
assessment
3 or less (low early stroke risk)
4 -7 (high early stroke risk)
Step 3: Investigations and
Risk Factors
Essential Investigations
+
(tick)
Yes
No
N/A
Urgent impatient investigations if ABCD2 score 4 -7
•
•
CT Head
US Carotids if
indicated
Step 4: Secondary
Prevention
Antiplatelet agent: Clopidogrel
plus aspirin for first 3 weeks
after TIA then Clopidogrel or
Aspirin monotherapy
Yes
No
N/A
Steps 5 & 6: Lifestyle &
Yes
No
General Advice
Smoking cessation
Alcohol consumption
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N/A
Warfarin or Dabigatran if atrial
fibrillation
Antihypertensive agent
Cholesterol lowering Rx
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Dietary advice
Exercise
Information phamplet
Driving advice
Step 7: Discharge Arrangements
Step 1 to 6 complete
ALL investigations completed as
impatient if ABCD2 score 4-7
Incomplete investigations requested as
outpatient if ABCD2 score 3 or less
Follow up with GP arranged
O/P Clinic
Yes
No
5.1.2 Transient Ischaemic Attack (TIA) Acute Management In the ED / AMAU / ASU
Guidelines
STEP 1
Diagnosis – are you confident it was a TIA?
Diagnosis of TIA can be problematic. Diagnosis in primary care and ED is likely to only be
50-60% accurate. Diagnosis of TIA is more likely to be correct if
•
Abrupt onset of symptoms – with neurological deficit maximal at onset
•
Focal loss of brain or monocular function – that is typical for TIA, ie. consistent
with vascular cause and territory. (see below)
•
Rapid recovery occurs – most TIAs resolve within minutes and 60-70% within 1
hour. If symptoms /signs persist then assume likely acute stroke
TIA Symptoms (ref 1)
Typical of TIA
Consistent with TIA
(only if typical symptoms are
also present but not diagnostic if
in isolation)
Dysarthria (23%)
Confusion (exclude dysphasia)
Unilateral altered sensation
(35%)
Ataxia (12%)
Impaired or lost consciousness
Dysphasia (18%) – name pen,
watch
Vertigo (5%)
Non specific dizziness
Monocular Blindness (18%)
Diplopia (5%)
Light headed, faint or syncope
Unilateral weakness
face/arm/leg (50%)
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Not Typical of TIA
(if occur in isolation – without
typical symptoms)
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Hemianopia (5%) – assess
visual fields
Dysphagia (1%)
Bilateral sensory symptoms
Dyspraxia – copy diagram,
draw, clock
Drop attacks
Bilateral blurred vision
Incontinence
(%) = frequency reported in Oxfordshire Community Stroke Project (ref 2)
Differential diagnosis (in order of frequency as seen in primary care) includes
• Migraine aura (+ headache)
• Syncope
•
“Funny turns”
• Labyrinthine disorders (isolated vertigo + secondary nausea & ataxia)
• Partial (focal) epileptic seizures
• Drop attacks
•
Hyperventilation.
STEP 2: Assess Risk = risk of stroke within the next 7 days – use ABCD2 score (ref 3)
ABCD2 items
Value
Age: > 60yrs
1
< 60yrs
0
BP: > 140/90
1
< 140/90
0
Patient Score
/1
/1
Clinical Features
Unilat. weakness
2
Or Speech affected
1
Or Other neuro symptoms
0
/2
Duration of TIA
> 60 mins
2
10 - 59 mins
1
< 10 mins
0
/2
Diabetes
Present
1
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Absent
0
ABCD2 Total Score:
/7
Stroke Risk Assessment
ABCD2 Score
0-3
4-5
6-7
2 Day Risk
1%
4.1%
8.1%
7 Day Risk
1.2%
5.9%
11.7%
90 Day Risk
3.1%
8.1%
17.8%
Low Risk Scores: 0-3, or greater than 7 days from symptom onset
May be discharged from the ED /Medical ward with management plan and outpatient
investigations organised.
Requires:
• OP investigations
• Immediate institution of secondary prevention measures
• Lifestyle & general advice
• GP follow-up
•
High Risk Scores: 4-7, within 7 days of symptom onset
Require:
• Immediate investigations (CT, carotid US etc) and initiation of secondary prevention
management before discharge
Patients require inpatient management unless appropriate investigations can be arranged
within the following timeframes:
• CT Head same day prior to discharge
• Carotid Ultrasound within 48 hours (weekdays) or 72 hours (weekends)
• Urgent Outpatient options include referral to Neurology TIA clinic or GP investigations
according to Health Pathways and Begin Early Aggressive Therapy (BEAT)
All patients should have all appropriate medical treatments initiated at the point of first
medical contact and prior to discharge to GP care.
Guidelines for selection of patients for carotid ultrasound as below
STEP 3: Investigations and Vascular Risk Factors
For all patients (ref 4)
Investigations
Done Norm AbN Vascular Risk Factors
Yes
No UnK
ECG
Hypertension
FBC
Diabetes
ESR
Cholesterol
U&Es
Smoking- Past
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Creatinine
Glucose
Smoking- Current
Atrial Fibrillation (any)
Alcohol excess (> 4-6)
Other investigations that may be required
CT Scan
•
Brain imaging with CT or MRI is recommended for all people with TIA
• Same day imaging for high risk patients (as defined above)
•
If low risk should be done within 7 days
• If TIA is fully recovered it is reasonable to give aspirin while awaiting scan.
Carotid Ultrasound Scan
Patients should meet the following criteria (presence or absence of bruits should not alter
decision)
• Anterior (carotid) territory TIA (ie. NOT VBI or posterior circulation event)
• Fit for surgery and with life expectancy >2-3 years
• Priority for scan and surgery is urgent (surgery within 1-2 weeks) because of risk of
early stroke – high risk TIAs should have this as an inpatient eg. those with ABCD2
scores 4-7 (usually those with any weakness or speech disturbance)
Symptomatic carotid artery stenosis greater than 50% requires urgent referral to vascular
surgery or neurosurgery departments for consideration of carotid endarterectomy (as
inpatient for ABCD2 scores 4-7)
STEP 4: Secondary Prevention
Antiplatelet agents:
•
Clopidogrel plus aspirin appears to reduce early stroke recurrence when initiated
within the first 24 hours of symptom onset and continued for 3 weeks. Combination
therapy of aspirin and clopidogrel is not indicated for long-term vascular secondary
prevention due to increased bleeding risk.
Clopidogrel monotherapy is as effective as combined Aspirin and Dipyridamole and is better
tolerated (ref 5) - 300mg stat, then 75 mg daily. It has a modest additional benefit compared
with Aspirin alone.
•
•
•
•
•
Dipyridamole 150mg bd and Aspirin 75-100 mg daily is an alternative treatment
option, equally as effective as Clopidogrel. Start Dipyridamole at low dose (e.g.150
mg nocte for 1 week) and titrate upwards to 150 mg twice daily to reduce the adverse
effect of headache. Advice that the headache may resolve after some days may aid
compliance.
Aspirin – montherapy may be a reasonable treatment for some patients.
300mg stat and 75 – 150mg daily for first event, preferably after CT scan
If CT scan delay > 12-24 hrs it is reasonable to start aspirin while waiting
Consider 300mg daily for recurrent events in case of aspirin resistance
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Warfarin
Only if in AF or other cardiac source of emboli identified (ref 4)
•
•
•
•
•
•
Not recommended if in sinus rhythm even if recurrent TIAs on aspirin
Every person with TIA and AF (paroxysmal or sustained) unless contraindicated. The
benefit of anticoagulation for secondary prevention of cardioembolic TIA far
outweighs the risk of haemorrhage for most people.
CT head scan must be done first to exclude haemorrhage or other pathology
Target INR of 2.5 (range 2-3) is recommended. Higher ratios indicated for mechanical
heart valves or antiphospholipid syndrome.
It is reasonable to initiate warfarin 48 hours after a cardioembolic TIA or minor stroke
Potential risk and benefits must be discussed with patient and this documented
Dabigatran is available as an alternative to warfarin for patients with atrial fibrillation (ref 6).
The usual dose is 150 mg BD PO. This drug should be used with caution in the elderly. If it is
given, a lower dose of 110 mg BD PO is recommended for patients over 80 years of age.
Dabigatran should not be used for patients with severe renal impairment (CrCl< 30 mL/min).
Before using Dabigatran, refer to Section 14.9.1 (Haematology) in The Blue Book
Antihypertensive agents
Blood pressure-lowering treatment is recommended for all people after stroke or TIA unless
the person has symptomatic hypotension (ref 4).
Do not lower BP rapidly. The best evidence for reduction in stroke incidence is using a
combination of and ACE inhibitor and a diuretic. (See section 3.2.2)
Cholesterol lowering therapy
A statin is recommended for most people after TIA
Atorvastatin 80 mg and simvastatin 40 mg daily reduce the risk of recurrent stroke or
vascular disease. Atorvastatin 80 mg is recommended for patients with LDL cholesterol > 2.6
mmol/l. (ref 7)Lower doses may be required, depending on patient tolerability, frailty, LDL <
2.6 mmol/L
•
•
•
•
Benefit occurs even in those with normal or low baseline cholesterol
Optimal levels include total cholesterol < 4 and LDL <2.5
At least 2-year life expectancy is required for patients to gain significant stroke
prevention benefit from statin treatment.
Patients with low HDL, high triglycerides and clinical features of the metabolic
syndrome may be better treated with other therapies for correction of the lipid
disorder and require further assessment.
STEP 5: lifestyle advice
•
•
•
Smoking cessation if current smoker
Reducing alcohol consumption if excessive (>4-6 units/day).
Moderate exercise is recommended
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If BMI > 25-30 then lifestyle change & diet advice is required
STEP 6: Other general advice
•
Information – TIA leaflet or stroke foundation (0800 STROKE, www.stroke.org.nz)
•
Driving Advice
Document driving status and that advice is given.
- Private licence; single TIA = no driving for 1 month, multiple TIA = 3 months
- Vocational Licence; single TIA = no driving 6 months, multiple = permanent
STEP 7: Discharge arrangements
Low risk patients (ABCD2 score < 3) can be discharged either after Physician review or with
follow up arranged with Physician or GP within 1-2 weeks if:
•
•
•
All essential investigations arranged completed or only awaiting OP CT scan and
A management plan has been initiated (must address all points) and
Follow up arranged
High risk patients (ABCD2 score 4-7 or multiple TIAs within last week) should remain as
inpatient until;
• All investigations completed
•
A management plan has been initiated (must address all points) and
•
Follow up arranged
• Note: patients may be discharged prior to Carotid US only if a guaranteed urgent US
appointment is arranged within 48h (72h weekends) and a plan to immediately
follow-up the US result is in place.
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6 Secondary Prevention Guideline
6.1 Secondary Prevention after Stroke
Patients who have had a stroke remain at an increased risk of a further stroke (about 10-12%
per annum), and of other vascular events (about 7% per annum). The risk of a further stroke
is highest early after stroke. Therefore there should be a high priority given to secondary
prevention.
Lifestyle
All people with stroke or transient ischaemic attack should be given appropriate advice on
lifestyle factors such as not smoking, regular exercise, diet, achieving a satisfactory weight,
reducing the use of added salt.
Cigarette smoking
Cigarette smoking should be discontinued.
Alcohol consumption
Excessive alcohol consumption should be discontinued. Mild to moderate use of alcohol (1 –
2 standard drinks per day) is associated with reduction in stroke rates.
Physical Activity
Moderate exercise (30 – 60minutes of brisk walking, jogging, cycling, or other aerobic activity
at least 3 times per week) is generally recommended. A patient’s comorbidities and
functional state need to be taken into consideration when developing an exercise program.
Body Weight
People who have a body mass index (BMI) > 25 (especially those with BMI > 30) should
commence graduated lifestyle change aimed at weight reduction.
Reduction in blood pressure
• A blood pressure lowering treatment is recommended for all people after stroke or
transient ischaemic attack unless the person has symptomatic hypotension.
•
The optimal time to start blood pressure – lowering treatment is not known, but it is
usually advisable to wait 7-14 days after an acute stroke.[see separate blood
pressure protocol Section 3.2].
The benefit of anti-hypertensive treatment is seen irrespective of the patient’s baseline blood
pressure, including patients considered to be normotensive Canterbury DHB CDHB Stroke
Treatment of diabetes mellitus
Diet, oral hypoglycaemics and insulin should be prescribed as needed to control diabetes.
Intensive treatment of both type 1 and type 2 diabetes mellitus can reduce microvascular
complications such as retinopathy, nephropathy and neuropathy, but it has not been
conclusively shown to reduce the risk of macrovascular complications including stroke.
Lipid – modifying treatment
Treatment with a 3-hydroxy-3-methyl-coenzyme A (HMG-CoA) reductase inhibitor (statin) is
recommended for most people following ischaemic stroke or transient ischaemic attack.
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Total cholesterol levels fall within the first 7 – 10 days after stroke so lipids should be
checked at time of stroke or 6 – 8 weeks after the stroke.
6.2 Antiplatelet Therapy
This is described in Section 6 Secondary prevention after TIA. Clopidogrel monotherapy is
considered the firstline antiplatelet therapy for stroke secondary prevention. Combination of
Dipyridamole and Aspirin is an alternative firstline option, but there are compliance problems
related to number of tablets and headache. Aspirin monatherapy may be appropriate for
some patients.
6.3 Anticoagulation
Anticoagulation with warfarin or dabigatran should be started in every person with
cardioembolic ischaemic stroke or transient ischaemic attack due to atrial fibrillation
(paroxysmal or permanent), unless contraindicated. Anticoagulation with warfarin is required
for people with prosthetic heart valves and should be considered for mitral valve disease or
myocardial infarction within the preceding 3 months. This is further discussed in Section 6.1,
Secondary prevention after TIA
- For patients with contraindications to anticoagulation, aspirin is recommended although it is
much less effective than warfarin in secondary prevention for patients with atrial fibrillation.
- Anticoagulation should not be started until intracranial haemorrhage has been excluded by
brain imaging.
The optimal timing of anticoagulation after stroke is not certain. Anticoagulation is usually
started after 14 days. It may be started earlier in people with minor strokes IF intracerebral
haemorrhage has been excluded AND if there is a high risk of early recurrent stroke, such as
a recent full-thickness anterior myocardial infarct or prosthetic heart valve. In general, it is
preferable to commence anticoagulation prior to discharge from hospital.
6.4 Carotid Endarterectomy
Carotid endarterectomy is recommended for patients with symptomatic severe (50-99%)
stenosis of the proximal internal carotid artery All patients who may benefit from carotid
endarterectomy should be discussed with the vascular surgical team on an urgent basis.
Carotid ultrasound findings may need to be verified by CT angiography.
Comments:• The term ‘symptomatic’ applies to patients who have had a previous transient
ischaemic attack or non-disabling stroke in the territory of that artery. Carotid
endarterectomy is not recommended in these patients if the ischaemic event was
likely to have been due to cardiogenic embolism, if the stroke resulted in serious
permanent disabilities, or if important medical comorbidities exist. If in doubt,
discuss with vascular surgical team urgently
•
Carotid Endarterectomy should be performed only by specialist surgeons who can
demonstrate a complication rate (stroke or death within 30 days) of ≤7%
•
Maximum benefit of carotid endarterectomy is achieved when the procedure is
performed within 2 weeks of the symptomatic event.
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•
Risk factors that increase the likelihood of benefit from surgery include male sex,
increasing age up to 79 years, hemispheric rather than retinal symptoms, plaque
surface irregularity and coexistent intracranial atherosclerotic disease.
•
Carotid endarterectomy is not recommended for patients with symptomatic
proximal internal carotid artery stenosis
•
less than 50% severity or
•
severe stenosis demonstrating “trickle flow” on duplex scanning
•
Routine carotid endarterectomy is not recommended for unselected patients with
asymptomatic
Carotid stenosis
• Angioplasty and stenting of the internal carotid artery has been shown to have
worse results (death or stroke) than carotid endarterectomy
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CDHB
Reference:
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Issued:
Review Date:
CDHB Stroke Guidelines
Fifth issue
Dr Bopitiya
September 2015
March 2016
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Stroke Guidelines
Document Owner: Stroke Physician General Medicine
WCDHB, Version 1, Issued 1/9/2015
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