This document discusses the management of stroke. It begins by defining stroke as a clinical syndrome caused by vascular issues leading to neurological deficits lasting more than 24 hours. It emphasizes the importance of specialized care in a stroke unit and assessing patients immediately to determine if they are eligible for time-sensitive treatments like thrombolysis. The main types of stroke are ischemic and hemorrhagic. Secondary prevention focuses on controlling risk factors like high blood pressure, smoking, diabetes, and atrial fibrillation through medications and lifestyle changes to reduce the risk of recurrent strokes.

2. MANAGEMENT OF STROKE
DR W.D.A.Patirana
MBBS.MD

3. WHO definition
Clinical syndrome typified by rapidly
deveoloping signs of local or global
disturbance of cerebral functions, lasting
more than 24hrs or leading to death with
no apparent causes other than of vascular
origin

4. 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

5. 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

6. 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

7. Characteristics of subtypes of
stroke
Lacunar PACI TACI Post
Signs Motor or
sensory
only
2 of the
following:
motor or
sensory,
cortical,
hemianop
ia
All of:
motor or
sensory
cortical,
hemian
opea
Hemian
opia,
brainste
m,
cerebell
ar
%dead at
1yr
10 20 60 20
%depend
at 1 yr
25 30 35 20

8. Signs to be looked for
• Conscious level
• Neurological signs
• BP
• HR/rhythm
• Heart murmurs
• Peripheral pulses
• Systemic signs of infection or neoplasm

9. Death rate after stroke
30 days 1 year 5 years
Ischaemic
stroke
10 23 52
ICH 52 62 70
SAH 45 48 52

10. 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

11. 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)

12. • 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

13. Investigations of stroke
• All patients
– CT/MRI
– ECG
– CXR
– FBC
– Clotting screen
– SE/creatinine
– Plasma glucose

14. Investigations of stroke
• Sub groups
– Carotid duplex scanning
– ECHO
– Thrombophilia screen
– Immunology screen
– Syphillis serology
– Cerebral angiography (Rarely)

15. 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

16. 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

17. 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
, 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

18. 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

19. 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
–

20. Swallowing and feeding
• Dysphagia in ~35%
– Unrecognised in mild stroke
– But associated with poor outcome
• Aspiration
• Pnuemonia
• Poor nutrition
• They should be fed through NG or percutaneous
endoscopic feeding tube
• Dysphagia Mx involves:
– Initial swallow screen
– Diet modification
– Compensatory swallowing techniques
-reduces aspiration pneumonia

21. Communication and speech
• can affect in a variety of ways, including
– impaired motor speech production (dysarthria)
– impaired language skills (dysphasia)
– Impaired planning and execution of motor speech (articulatory
dyspraxia)
• needs to be assessed by a speech and language
therapist

22. 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
- if a diagnosis of haemorrhage is considered CT/MRI is
essential before asprin
– But if CT is not availble and ischaemic stroke is highly suspected may
give asprin

23. • 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

24. • 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
– There is evidence for acute anticoagulation
in the specific stroke syndrome of cerebral
venous thrombosis

25. 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

26. 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

27. Acute treatment of stroke -- BP
• 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

28. Complications of stroke
• Hyperglycaemia**
• Hypertension**
• Fever**
• Infarct extension or
bleeding
• Cerebral oedema
• Herniation
• coning
• Aspiration
• Pneumonia
• UTI
• Cardiac dysrrhythmia
• Recurrence
• DVT
• PE

29. 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)

30. Summary of acute 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

31. STROKE SECONDARY
PREVENTION

32. 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

33. 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

34. 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

35. Management of risk factors
• Smoking:
– Important correctable risk factors
– Risk returns to that of a non smoker within 3-5
yrs of cessation

36. Alcohol and risk of stroke
• Protective effect with light to moderate
intake
• One drink a day – reduces stroke
• If more than one drink a day –risk
increases

37. Management of risk factors
• Blood pressure
– 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

38. • PROGRESS study:
– irrespective of baseline BP
– Pts treated with Perindropril and
indapamide had a reduction in BP of 12/5
– And reduced stroke risk of 43%
–
• 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-

39. 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

40. 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

41. 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

42. 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

43. Atrial fibrillation and stroke
• Over the age of 60 – 2-5% Have AF and
associated with a stroke rate of 4-5%
• Meta-analysis of warfarin in Non
rheumatic AF – 60-65% reduction in
stroke (INR 2-3)
• With asprin 20% reduction

44. Atrial fibrillation and stroke –
CHADS2 Scheme for risk assesment
• C – Congestive cardiac fairlure
1
• H – Hypertension 1
• A - Age >75 1
• D – Diabetes 1
• S – Past Stroke or TIA

45. Atrial fibrillation and stroke
• If patients aged 65-95 with AF
– Score 0 – risk is 1.9
– Score 6 –risk is 18.2
• Asprin is sufficient in patients with score 0
• Warfarin is the choice if score 1 or more
• Warfarin is under used, especially in
elderly (appropriate anticoagulation used
in only 30-60%)

46. contraindications to long term
warfarin
• GI bleeding
• Active peptic ulcer
• Frequent falls
• Alcohol misuse
• History of ICH
• Age by itself is not a contraindication

47. Anti platelet therapy
• Asprin
– 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

48. Carotid endarterectomy for symptomatic
carotid stenosis in elderly patients
• Efficacy of CEA in symptomatic carotid
stenosis >70% is well established
• Elderly – surgical risk is higher, but
benefits even greated
• NASCET Trial
– Absolute risk reduction is 28.9% in >75yrs
– 15.1% for 65-74yrs
– 9.7% for below 65yrs

49. THANK YOU