Stroke

Acute stroke (Brain attack)

Based on ABC of strokeUpdated on 10th March 2003

based on RCP guidelines (2002/feb)

WHO definition

Clinical syndrome typified by rapidlydeveoloping signs of local or globaldisturbance of cerebral functions, lastingmore than 24hrs or leading to death

withno apparent causes other than of

vascularorigin

Introduction Stoke: sudden neurological deficit of

presumed vascular origin It’s a syndrome rather than a single disease Acute stroke is now a treatable condition

that deserves specialised attention A senior clinician should review all pts with

presumed stroke (class B recommendation) Drug Rx and specialised care both influence

survival and recovary

Assesing the patient Pts should be assessed at hospital

immediately after stroke Hyperacute treatments such as thrombolysis

must be administered within 3-6 hrs Stroke is a clinical diagnosis, but imaging is

required to differentiate between ischemic and primary intracerebral h’age

Following can be used to diagnose and predict prognosis Eivdence of motor, sensory or cortical

dysfunction Hemianopia

Pathophysiology For practical purposes – 2 types of stroke

(after excluding SAH) Ischaemic: 85% 1ry h’age: 15%

H’ge causes direct neuronal injury and pressure effect causes adjacent ischemia

1ry ischaemia results from atheroembolic occlusion or embolism

Usual sources of emboli are LA in pts with AF or LV in MI/LVF

Pathophysiology Vessel occlusion from atherosclerosis

Typically in internal carotid just above carotid bifurcation

If form small vessel – small vessel disease deep wihin the brain

Ischaemia causes direct neuronal injury from Lack of oxygenation Lack of nutritional support Cascade of neurochemical events that lead to

spreading damage Ischaemia may be reversible if reperfusion is obtained

quickly (3-6hrs) Chemical injuries may be interrupted by various

neuroprotective drugs (unproved in humans)

Symptoms and signs of stroke

Anterior circulation strokes Unilateral weakness Unilateral sensory loss or inattention Isolated dysarthria Dysphasia Vision

Homonymous hemianopia Monocular blindness Visual inattention

Symptoms and signs of stroke Posterior circulation strokes

Isolated homonymous hemianopea Diplopia and disconjugate eyes Nausea and vomiting Unilateral or bilateral weakness and/or sensory

loss No specific signs

Dysphagia Incontinence Loss of consciousness

Characteristics of subtypes of stroke

Lacunar PACI TACI Post

Signs Motor or sensory only

2 of the following: motor or sensory, cortical, hemianopia

All of: motor or sensorycortical, hemianopea

Hemianopia, brainstem, cerebellar

%dead at 1yr

10 20 60 20

%depend at 1 yr

25 30 35 20

Anterior cerebral stroke Ant cerebral artery gives a branch called ‘recurrent artery of

Huebner’ immediately after its origin If present it contributes to the supply of internal capsule Two ant cerebral arteries are joined together by ant

communicating artery Ant cerebral artery occlusions are rare If there is no recurrent artery

Face, arm will not be affected Entire leg area of the cortex is destroyed So it causes flaccid paralysis of the leg with cortical sensory loss

If there is recurrent artery & block occurs proximal to its origin

Ant internal capsule will also be affected UMN Facial weakness, spastic arms and useless flaccid leg The arm has good potential for recovary, because the cortical

control is there But the leg has no potential for recovary as the cortical control is

lost

Anterior cerebral stroke Perforating artery occlusion

If the recurrent artery Huebner is present and occluded weakness of face & arm will be present

Even if the dominant hemisphere is affected dysphasia will not occur, because the cortex is spared

Terminal branch occlusion Terminal vessels supply mainly the cortex

controlling the legs, so the motor & sensory function will be affected

Pt may not walk at all Less severe intellectual & sphincte

involvement than with main trunck occlusion

Anterior cerebral stroke Because of the affection of precentral gyrus

Incontinence of urine is common – when there is desire to pass they cannot control

Incontinence with flaccid leg weakness can mimick cauda equinal lesion

But the reflexes will return and plantar will be upgoing with time

Considerable memory and intellectual deficits may be there

If there is evidence of weakness of other leg also (ie, that the lesion is not strictly unilateral) a parasagital tumor should be excluded

Vascular occclusions affecting hemispheres should not produce B/L signs

Middle cerebral artery occlusion Massive infarction of the bulk of hemisphere There is considerable cerebral oedema

Coma & eventual death If non dominant hemisphere

Severe dyspraxia or Denial of existance of the left side

If dominant hemisphere is affected Global dysphasia

Motor: Destroys both pyramidal & extrapyramidal

mechanisms producing flaccid weakness of face & arm with little or no chance of recovary

The leg cortex is spared, but rarely recovers significantly

Middle cerebral artery occlusion Hemianaesthesia & hemianopia are associated

with hemiparesis Devastating type of stroke

Minimal chance of recovary High chance of death due to cerebral odema,

unresponsive to steroids or osmotic agents It is similar to total occlusion of carotid artery

in the neck With cross circulation via ant communicating artery With normal vertebro basilar artery

The anastomoses could be so efficient that pt may not have any neurological deficits

Signs to be looked for

Conscious level Neurological signs BP HR/rhythm Heart murmurs Peripheral pulses Systemic signs of infection or

neoplasm

Death rate after stroke

30 days 1 year 5 years

Ischaemic stroke

10 23 52

ICH 52 62 70

SAH 45 48 52

Conditions that can mimick stroke

Diagnosis Diagnostic features

Decompression of previous stroke Evidence of infection such as urinary or respiratory tract; metabolic dist.

Cerebral neoplasm (1ry or 2ry) Less abrupt; 1ry tumor or 2ry (lung or breast CA)

SAH Recent head injury

Epileptic seizures Possible previous fits

Traumatic brain injury H/O trauma

migraine Less abrupt onset; followed by headache; young pt

Multiple sclerosis Less abrupt onset, possible previous epi

Cerebral abscess Infection

Investigations of stroke All should have a CTwithin 48hrs to

distiguish between ischaemic and h’gic stroke

Imaging should be urgent in Depressed conscious level, fluctuating

symptoms, papilloedema, neck stiffness, fever, severe headache, previous trauma, anticoagulant treatment or bleeding diathesis (B)

MRI is superior, because it also assess blood flow and perfusion of the brain/detect wether lesion is old or new and identify carotid stenosis

Imaging will also identify stroke mimicking conditions

But a low grade glioma could still be difficult to be differentiated from cerebral infarction

Investigations of stroke All patients

CT/MRI ECG CXR FBC Clotting screen SE/creatinine Plasma glucose

Investigations of stroke

Sub groups Carotid duplex scanning ECHO Thrombophilia screen Immunology screen Syphillis serology Cerebral angiography (Rarely)

Investigations – to what extent

Depends on several factors Likely degree of recovary Presence of obvious risk factors Age of the pt (younger pts likely to

have identifiable cause such as inflammatory or clotting dissorder)

Ix better be restricted to tests that will help in the management

Stroke unit Stroke unit should be centred in a hospital Should be staffed by

Multidisciplinary team with expertise in stroke care (A) Team should work to agreed protocols for common problems (A) Should provide educational programmes for staff, pts and carers

Stroke unit trialist’s collobaration Stroke units compared to alternatives showed reduction in odds ration for

death recorded at follow up (OR 0.86) Odds ratio of death, instituitionalised care and death or dependency were

significantly less Outcomes were independent of age, gender and stroke severity and

appeared to be better in stroke units based in a geographincally discrete ward

No increase in hospital stay in stroke unit In a study where patients were randomly assigned to stroke unit care,

general wards with stroke team support, or domiciliary stroke care, mortality and institutionalisation rates at one year were lower in patients who received care on the stroke ward

The benefits of stroke unit care have been shown to persist at 10 years after initial stroke

Early supported discharge from hospital to a specialist rehabilitation team providing care at home is feasible for selected pts (A)

If the pt can transfer from bed to chair, can be sent home and equally effective specialised multidisciplinary care could be given at home (A)

Patients should only be managed at home if acute assessment guidelines can be adhered to and the services organised for home are flexible, and part of a specialist stroke service (A)

The guidelines do allow for the management of some patients in the community, particularly those with transient ischaemia attacks (TIAs) and strokes with good recovery

The consensus was that these patients could be managed at home provided they had access to a neurovascular clinic within two weeks (C)

More than one TIA within a short period (crescendo TIA) requires admission to hospital (C)

The guidelines are not prescriptive in defining a short period but the authors consider that recurrent TIAs within one week merit admission

The guidelines recommend that families are involved in the decision making process and have input into future plans for the patient (C)

Caring for a stroke patient can be very difficult & emotional distress is seen in 55% of caregivers at six months after stroke

Caregivers are more likely to be depressed if the patients are severely dependent or emotionally distressed themselves

The stroke team must be alert to recognising carer stress and helping carers in this difficult situation (B)

Disseminating information about the nature of stroke and on relevant local and national services improves patient and carer knowledge (A)

Introduction of stroke family support workers increases the quality of life

Emergency management

Within the 1st hour after cerebral ischaemia, part of the brain is under threat of death

The densly ischaemic area will inevitably die, but there is also tissue that could be salvaged

At this stage oxygenation, haemodynamic and metabolic factors are crucial

Management Restore vascular anatomy

Thrombolysis Angioplasty/stent Antiplatelets/anticoagulants

Stop ischaemic neurones dying Prevent complications

DVT MI Infection

Seccondary prevention

Emergency management The emergency managemet of stroke requires

Medical stabilisation Assesment of factors that may lead to complications

Swallowing hydration

It is important to keep physiological variables such as hydration,

temperature, nutrition, and oxygenation within normal range

in the acute phase of stroke (C) Thrombolysis may be considered Stroke units are associated with better outcome

Early Rx of ischemic stroke General care Specific Rx: thrombolysis, anticoagulants,

antiplatelets, neuroprotective agents Emergency aproach Stroke unit care Treatment of complications Treatment of co-morbidity Rehabilitation

Swallowing and feeding Dysphagia in ~35%

Unrecognised in mild stroke But associated with poor outcome

Aspiration Pnuemonia Poor nutrition

Presence of gag reflex is a poor guide and therefor formal assesment is essential

Fluids are more difficult to swallow than solids They should be fed through NG or percutaneous endoscopic feeding

tube Most pts will not need enteral feeding beyond a few weeks However when and how optimally to feed dysphagic pts is yet to be

determined Dysphagia Mx involves:

Initial swallow screen Diet modification Compensatory swallowing techniques

-reduces aspiration pneumonia

Malnutrition is also common and is seen in 30% of patients one week after stroke

Routine oral or enteral protein supplementation improves nutritional indices but there is no evidence that it affects outcome

In the dysphagic patient, enteral nutrition can be supplied by either nasogastric tube or percutaneous endoscopic gastrostomy

There is some evidence that percutaneous endoscopic gastrostomy feeding is superior to nasogastric feeding,36 but its insertion requires an invasive procedure.

Questions concerning the most effective nutritional route as well as the timing of nutritional intervention after stroke are being addressed in a large randomised controlled trial, the FOOD trial

Information is available at http://www.dcn.ed.ac.uk/food.

Communication and speech Stroke can affect communication and speech

in a variety of ways, including impaired motor speech production (dysarthria) impaired language skills (dysphasia) Impaired planning and execution of motor speech

(articulatory dyspraxia) Deficits can be subtle and every patient with a

communication difficulty needs to be assessed by a speech and language therapist

Speech therapy input is effective at improving communication, with short, intensive courses of speech therapy lasting 4–8 weeks proving most beneficial

Acute treatment of stroke Asprin: in most patients

2 large trials (160-300mg/d by PO/NG/ Rectum) started within 48hrs of stroke, reduces subsequent death and disability

NNT- 77 (reducing risk by reducing reinfarction) For 1000 pts –

12 avoid death and dependency Risk of h’age minimal (1-2/1000) Early asprin is beneficial

In a study where patients were randomly assigned to stroke unit care, general wards with stroke team support, or Patients with acute ischaemic stroke should receive aspirin

(160–300 mg) as soon as possible after stroke if a diagnosis of haemorrhage is considered unlikely (A)

But CT/MRI is essential before asprin But if CT is not availble and ischaemic stroke is highly suspected

may give asprin

IST(International Stroke Trial) and CAST (Chinese acute stroke trial) combined 40,000 pts Significant decrease in death and

dependency at 6/12 if asprin is given immediately

13 more pts alive per 1000 Rxed Increase in ICH – 2 per 1000 Reduction in recurrence - 7 per 1000

Acute treatment of stroke Heparin (conventional or LMWH)

Trials did not show any improved outcome. But useful certain groups of pts

Prophylactic: Previous venous thromboembolism Morbid obesity

Therapeutic: Carotid artery dissection Embolic, recurrent transient ischaemic

attacks

Anticoagulation has no net benefit Decreases recurrent ischaemic stroke (9

per 1000 Rxed) and pulmonary emboli (4 per 1000 Rxed)

But 9 per 1000 increase in ICH But it has definitive place in 2ry

prevention Immediate anticoagulation in AF is not

advised RCP guidelines: start anticoagulation

14d after the acute event (A) There is evidence for acute

anticoagulation in the specific stroke syndrome of cerebral venous thrombosis

Acute treatment of stroke Thrombolysis

Standard acute Rx in USA, Australia and most european countries

Type of drug and timing important NINDS trial: Alteplase (tPA) within 3 hrs

increases the chances of near complete recovary (NNT-7)

3-4x increase in ICH 20% reduction in death and dependency Rx after 6 hrs less effective (NNT-12) Complications: intra or extracranial h’age

Acute treatment of stroke Contra indications to thrombolysis:

Seizure at onset Pre Rx BP >185/110 Major infarct on CT Previous ICH Recent MI Recent or intended surgery Use of anticoagulants

Acute treatment of stroke Withhold antihypertensives for 10 days Indications for early Rx of high BP

Evidence of pre existing HBP Documented previous HT:clinic recors etc Evidence of target organ damage

Hypertensive retinopathy, LVH on ECG

Evidence of hypertensive emergancy HT encephalopathy LVF

BP is very high SBP >220-240 DBP >120

Complications of stroke Hyperglycaemia** Hypertension** Fever** Infarct extension

or bleeding Cerebral oedema Herniation coning

Aspiration Pneumonia UTI Cardiac

dysrrhythmia Recurrence DVT PE

Mood disorders are common after stroke and difficult to diagnose due to speech problems

Crying after minimal provocation is common, may be due to emotionalism and may be treated by fluexetine (A)

Pain after stroke varies in type, origin and modes of treatment Some related to stroke damage – neuropathic

or central pain (responds to tricyclics) Mechanical pain due to immobility or

exacerbation of pre-existing osteoarthritis Shoulder pain is seen in 30% Rx should begin with simple analgesia and

proper handling techniques

Venous thrombolism Is common after stroke and studies using

radiolabelled fibrinogen leg scanning suggest that deep vein thrombosis occurs in up to 50% of patients with hemiplegia

The guidelines recommend that aspirin (75–300 mg daily) should be used (A) (in non-haemorrhagic strokes)

Compression stockings should be applied to patients with weak or paralysed legs (A)

The final recommendation on the length of stocking to be used awaits results from the on-going CLOTs trial.

Spasticity Spasticity is a motor disorder characterised by a velocity

dependent increase in tonic stretch reflexes It may lead to secondary complications such as muscle and

joint contractures Management requires several coordinated interventions

including physiotherapy, drug treatment, and patient education

Physiotherapy using isokinetic strength training can improve strength and gait velocity without increasing spasticity

Drug therapy with either baclofen or tinzanadine as an adjunct to physiotherapy has been shown to reduce spasticity

In patients with disabling or symptomatically distressing symptoms, botulinum toxin is safe and effective & can be targeted to individual muscles

The guidelines indicate that spasticity should be treated if causing symptoms, though functional benefit is uncertain (B)

Mx of increased IC pressure Elevate head by 30 degrees Avoid or correct aggravating factors

Hypoxia hyperglycemia

Moderate fluid restriction Avoid hyperosmolar fluids eg: dextrose Osmotic agents: eg: manitol; as indicated Hyperventillation IV barbiturates NO STEROIDS Neuroprotective agents are not proved to be

effective

Rehabilitation Aims

Restore function Reduce the effects of stroke on pt and theirs

carers Regain independence and maximise ability in all

activities of daily living Should start early during recovery Once pt is medically stable, should be

transferred to a stroke rehabilitation unit Formal rehabilitation at a centre reduces

death, disability and hospital stay (NNT-12)

A physiotherapist with expertise in neurodisability should coordinate treatment to improve movement performance of patients with stroke (C)

The effectiveness of motor and strength rehabilitation is being underpinned by new evidence based

Progressive resistive exercise studies have also been shown to improve gait, strength, activity, and mood

There is some evidence that increased intensity of therapist input improves outcome but some patients cannot tolerate intense therapist input

The guidelines recommend that patients receive as much as they find tolerable and at least every working day (B)

It is vital that patients have the opportunity to practise rehabilitation tasks

The need for special equipment such as a wheelchair or adapted cutlery should be assessed on an individual basis as review by an occupational therapist with specialist knowledge in neurological disability can significantly reduce disability and handicap (B)

The provision of hoists or adaptation of the home environment may prevent the patient going to institutional care

Secondary prevention

Should start shortly after admission, except BP control

All pts should be offered Life style guidance Stop smoking Reduce saturated fat, alcohol and salt Asprin for life

Stroke secondary prevention

Introduction

A second stroke will not necessarily be of the same type as the initial event

Pts with previous stroke commonly suffer other vascular events like MI

Effective 2ry prevention depends on attention to all modifiable risk factors and treating the cuase of initial stroke

Four questions should be answered

Is it acute cerebrovascular disease Is it ischaemic or Haemorrhagic Cardioembolic or vascular

aetiology Anterior or posterior circulation

Is it acute CVA

Key features are Focal neurological deficit Sudden onset Absence of an alternative explanation

Exclude stroke mimicking conditions

Ischaemic or haemorrhagic History or examination cannot reliably distinguish A small bleed can produce transient symptoms Imaging is essential H’age is immediately apparent on CT, but over

few weeks it becomes indistinguishable from infarction

Small bleeds may be missed after one week MRI has a greater sensitivity for brain stem,

cerebellar and small ischaemic strokes Can also identify h’gic stroke and remains

diagnostic long after signs have disappeared

Sub cortical h’age with TIA D0 and D8

Correct imaging techniques

Symp <1h

Symp >1h onset<2w

Symp>1hronset>2w

Abrupt onset, typical CVA

Image only if anticoagulation proposed

CT MRI

Insidious onset suspicious of tumor

NA CT with contrast

CT contrast

Insidious onset suggestive of multiple sclerosis

NA MRI MRI

Cardioembolic or vascular aetiology 25% are due to embolism from heart or

major vessels Embolic stroke can affect any vascular

territory Certain features should prompt search

for embolic source TOE is justified if the results are

unequivocal or index of suspicion is high

Embolic causes of stroke found on echo MS LAH (>4cm) Dyskinetic or akinetic LV Severe global LV dysfunction Valvular vegetation LA/LV thrombi MV calcification Calcific aortic valve or stenosis

predispose to embolism but may not justify anticoagulation

Justification for echo AF HF MI within 3/12 ECG abnormalities

MI IHD BBB

Heart murmur Peripheral embolism Clinical events in >2

territories R & L hemisphere Ant & post circulation

>/= cotical events (in same territory) unless severe carotid disease

Anterior or posterior circulation Ant circulation (Carotids)

Cerebral hemispheres Post circulation (Vertebro basillar)

supplies the Brain stem Cerebellum Occipital lobe

If ant circulation stroke Carotid doppler to decide on

endarterectomy

Risk of recurrence after stroke or TIA

Stroke: 8% per year

TIA 8% risk of stroke in the first month 5% risk of stroke a year thereafter 5% risk of MI a year

Modifiable risk factors for stroke HBP Smoking DM Diet: high salt &

fat, low K & vitamins

Excess alcohol

Morbid obesity Low physical

exercise Low temperature Cholesterol

concentrations – atleast in pts with CAD

Management of risk factors

Smoking: Important correctable risk factors Risk returns to that of a non smoker

within 3-5 yrs of cessation

Management of risk factors Blood pressure

Immediate reduction may be deleterious Long term risk is inversely related to BP

achieved HT should be treated 1 or 2 weeks after the

stroke Rx reduces

Recurrence of fatal and non fatal stroke by 28% Pts at high risk of further stroke derive greatest

benefit (eg: elederly) Target BP recommended by British

Hypertension Society is <140/85

BP threshold for Rx

PROGRESS study: Pts with history of stroke or TIA were treated

with antihypertensives irrespective of baseline BP

Pts treated with Perindropril and indapamide had a reduction in BP of 12/5

And reduced stroke risk of 43% There were similar reductions in

hypertensives and non-hypertensives HOPE study

32% relative risk reduction in 1ry and 2ry stroke prevention in 9297 high risk pts with ramipril

Base line BP was 139/79 Reduction in BP was only 3.8/2.8 Efficacy of ACEI may explained by anti-

inflammatory effect and plaque stabilization

Management of risk factors Role of cholesterol – contraversial But statins reduce risk of stroke in

pts with CAD Use of statins after a athersclerotic

stroke or TIA probably reduces recurrent events and IHD

Since stroke pts are high risk pts cost Rx may be justified

Heart protection study Over 20,000 pts with high risk of vascular

disease aged 40-80 There were 1820 pts with history of non

disabling stroke or TIA All were randomised to simvastatin 40mg/d or

placebo for 5 years, independent of baseline cholesterol

Simvastatin pts showed highly significant 25% reduction in incidence rate of 1st stroke

The benefits were seen across all age ranges and base line cholesterol levels

Management of risk factors

Diabetes: Confers substantial dissadvantage for

Survival Functioning outcome on pts with acute

stroke Plasma glucose should be normalised

early BP targets for diabetics are lower

BP targets for non diabetic and diabetic stroke pts

No DM DM

Titrate to DBP </=85 </=80

Optimal BP <140/85 <130/80

Suboptimal BP >/=150/90 >/=140/85

Management of risk factors Hyperhomocystenemia:

Linked to premature vascular disease Easily lowered with vitamin

supplements Folic acid Pyridoxine

Although value of lowering homocysteine level has not been proven, younger pts with high plasma homocysteine levels may benefit

Anti platelet & anticoagulation therapy Warfarin:

Pts with AF should receive warfarin if there are no CI – INR 2-3

Pts with other sources of cardiac embolism also benefit from warfarin

Pts with mechanical prosthetic valve require INR of 2.5-4.5

If warfarin is not suitable asprin 300mg daily should be given, but it’s a less effective alternative

Main contraindications to long term warfarin treatment

GI bleeding Active peptic ulcer Frequent falls Alcohol misuse History of ICH Age by itself is not a

contraindication

Anti platelet & anticoagulation therapy Asprin

All other pts should receive antiplatelet Rx as first line

Benefits of asprin conclusively proven ASA – initial dose of 300mg & followed by 75mg/d

Dipyridamol Dipyridamole MR 200mg BD has independent and

additive effect to low dose asprin in preventing stroke, but not coronary events or overall mortality

So routine addition of dipyridamol may be cost effective

Dipyridamol alone does not prevent cardiac events

Anti platelet & anticoagulation therapy

Clopidogrel: Inhibits ADP receptors Well tolerated and slightly more effective

than asprin Not cost effective as 1st line Rx So should be used in pts with true

intolerance to asprin (allergy or intractable side effects on low dose enteric coated asprin with or without antiulcer drugs)

There is no clear evidence for superiority of one antiplatelet agent over another or for combination antiplatelet therapy in cerebrovascular disease

But if a patient on one antiplatelet agent experiences a recurrent stroke then it is better to add a second antiplatelet agent

Treatment protocol

Carotid surgery Benefit from endarterctomy upto 12 months after

the event in pts with ipsilateral severe carotid stenosis

Surgical risk Operative mortality in pts with severe disease -- 1% Risk of death or disabling stroke <4% Risk of death or any stroke <7.5%

Surgical risk less in busy units Surgeons must quote their own risk, rather than

the trial results Any pt with carotid territory symptom should be

considered a potetial candidate and doppler USS should be done, if fit for surgery

Presence or absence of carotid bruit is irrelavent

Indications for carotid endarteractomy Surgery indicated

Carotid territory symp within 6/12 and ipsilateral 70-99% stenosis

Carotid territory symp within 12/12 & ipsilateral 80-99% stenosis

Surgery not indicated: Carotid territory symp and an ipsilateral

0-69% stenosis Complete occlusion of the carotid artery

Carotid angiogram tight stenosis of internal carotid

Before & after endarterectomy

Succesful surgery is not major surgery, so pts can leave hospital within 24hrs

Neither clinical nor USS surveilance prevents late stroke, so most pts are discharged from followup after 6/52

The operation should only be carried out by a specialist with a proved low complication rate (A)

Carotid surgery

Angioplasty indications:

Fibromuscular dysplasia Radiation injury Symp stenosis after carotid endartartectomy

advantages: Less hospital stay Less cranial N injury Less wound complications Less cardiovascular morbidity

Dissadvantage: Embolic stroke at the time of surgery Recurrent stenosis

Complex cases that may require hospital referral

case Possibel treatment

Recurrent stroke or TIA despite antiplatelet treatment

High dose ASA, addition of Dipyridamol substitution or addition of clopidegrel or sub or add of warfarin

Recurrent embolic events despite adequate warfarin

Consider adding low dose asprin

Recurrent non haemodynaemic symp from severe carotid stenosis or serious I/C stenosis despite antriplalet Rx

Consider warfarin

HT or inoperable severe carotid stenosis

Consider cerebral blood flow monitoring before anti HT

Summary of management of stroke Admit to stroke unit – improves survival

& dependency Immediate CT Leg stockings (CLOTS trial) Asprin 300mg stat and 75mg thereafter Avoid heparin Thrombolysis (Randamise) Relaxed about BP Nursing, swallowing and nutrition