Stroke + soalan

1. STROKE &
CEREBROVASCULAR
ACCIDENT
MOHD HANAFI RAMLEE

2. Definition
• Transient Ischaemic Attack (TIA) – an acute focal
neurological deficit resulting from cerebrovascular
disease with resolution of signs and symptoms
within 24 hours.
• Reversible Ischaemic Neurological Deficit (RIND) –
attack lasting longer than 24 hours but with
complete clearance of signs and symptoms within 7
days.
• Completed Stroke – neurological deficit lasts longer
than 7 days.

3. HOW YOU GIVE THE
DIAGNOSIS?
• The diagnosis should provide answers to the following
questions:
• 1. What is the neurological deficit?
• 2. Where is the lesion?
• 3. What is the lesion?
• 4. Why has the lesion occurred?
• 5. What are the potential complications and prognosis?

4. What Artery Involved?
• Aphasia (dominant hemisphere)
• Hemiparesis / plegia
• Hemisensory loss/disturbance
• Homonymous hemianopia
• Parietal lobe dysfunction, e.g. astereognosis, agraphaesthesia,
impaired two-point discrimination, sensory and visual
inattention, left-right dissociation and acalculia

5. What Artery Involved?
• Weakness of lower limb more than upper limb

6. What Artery Involved?
• Homonymous hemianopia
• Cortical blindness
• Ataxia
• Dizziness or vertigo
• Dysarthria
• Diplopia
• Dysphagia
• Horner’s syndrome
• Hemiparesis or hemisensory loss contralateral to the cranial
nerves palsy
• Cerebellar signs

7. SO… BASIC IS
IMPORTANT!!!!!!!!

8. Brain Blood Supply Features:
• High oxygen requirement.
• Brain 2% of body weight - 15% of cardiac output
• 20% of total body oxygen.
• Continuous oxygen requirement
• Few minutes of ischemia - irreversible injury.
• Neurons - Predominantly aerobic.
• Sensitive areas:
• Adults -Hippocampus,
3,5th & 6th layer of cortex,
Purkinje cells.
Border zone (watershed areas)
• Brain stem nuclei in infants.

9. Anatomy – Stroke.

10. Brodman’s Cortical Map:

11. Frontal[f*ck–motor]Lobe Functions:
• High level cognitive functions. i.e reasoning, abstraction,
concentration
• Storage of information – memory
• Control of voluntary eye movement
• Motor control of speech in the dominant hemisphere.
• Motor Cortex – Motor control of the contralateral side of
the body
• Urinary continence
• Emotion and personality

12. Parietal[p-sx–sensory]Lobe Functions:
• Sensory cortex – sensory input is interpreted to define
size, weight, texture and consistency (contralateral)
• Sensation is localised, and modalities of touch, pressure
and position are identified.
• Awareness of the parts of body
• Non-dominant – processes visuospatial information and
• controls spatial orientation
• Dominant is involved in ideomotor praxis (ability to
perform learned motor tasks

13. Temporal[t-telinga]Lobe Functions:
• Primary auditory receptive areas
• In dominant ability to comprehend speech
(wernicke’s) – reception
• Interpretive area – area at the junction of the
temporal, parietal and occipital lobes.
• Plays an important role in visual, auditory and
olfactory perception
• Important role in learning; memory and
emotional affect.

14. Occipital[O-optic]Lobe Functions:
• Primary visual cortex
• Visual association areas
• Visual perception
• Some visual reflexes (i.e. visual
fixation)
• Involuntary smooth eye movement

15. Diencephalon Functions:
• Brain Stem:
• Midbrain, Pons & Medulla
• 10 of the 12 ranial nerves arise from the brainstem
(ipsilateral signs)
• Cortical pathway decussation contralateral signs.
• Some major functions: eye movement, swallowing,
breathing, blood pressure, heat beat, consciousness
• Cerebellum:
• movement – Balance & coordination

16. Motor & Sensory Cortex:

17. Diencephalon & Brain stem:

18. Cranial Nerves:

19. Stroke Types:
• Clinical
• Transient Ischemic Attack –TIA resolve <24h
• Evolving stroke – increasing >24h. – Thromb.
• Recurrent / multiple stroke – sec. factors.
• Completed stroke – no change… embolic.
• Pathological
• Focal / Global
• Ischemic & hemorrhagic (chronic/acute)
• Venous infarcts. (young, infections)

20. Common Types and Incidence:
• Infarction: Incidence 80% - mortality 20%
• 50% - Thrombotic – atherosclerosis
• Large-vessel 30% (carotid, middle cerebral)
• Small vessel 20% (lacunar stroke)
• 30% Embolic (heart dis / atherosclerosis)
• Young, rapid, extensive.
• Venous thromboembolism (rare)
• Hemorrhage: Incidence 20% - mortality 80%
• Berry aneurysm, Microaneurysm, Atheroma.
• Intracerebral or subarachnoid.

21. Stroke location and incidence:
Cause %
Clinical
presentation
30day
mort(%) Pathogenesis
Cerebral
infarction
85 Slowly / sudden
evolving signs and
symptoms
15-45 Cerebral
hypoperfusion
Embolism
Thrombosis
Intracerebral
hemaemorrha
ge
10 Sudden onset of
stroke with raised
intracranial
pressure
80 Rupture of micro-
aneurysm or arteriole
Subarachnoid
haemorrhage
5 Sudden headache
with meningism
45 Rupture of saccular
aneurysm on circle of
Willis

22. Clinical Categories:
• Global Ischemia.
• Hypoxemic encephalopathy
• Hypotension, hypoxemia, anemia.
• Focal Ischemia.
• Obstruction to blood supply to focal
area.
• Thrombosis, embolism or hemorrhage.

23. GLOBAL ISCHAEMIA

24. Global Ischemia:
• Etiology:
• Impaired blood supply - Lung & Heart disorders.
• Impaired O2 carrying – Anemia/Blood dis.
• Impaired O2 utilization – Cyanide poisoning.
• Morphology:
• 3rd, 5th and 6th layers of the cortex, hippocampus and in the
Purkinje cells in the cerebellum
• Laminar necrosis, Hippocampus, Purkinje cells.
• Border zone infarcts – “Watershed”
• Sickle shaped band of necrosis on cortex.
• Clinical Features:
• Mild transient confusion state to
• Severe irreversible brain death. Flat EEG, Vegetative state. Coma.

25. Morphology in Global Ischemia
1. Watershed zone
(Acute - ACA-MCA)
2. Laminar necrosis -
(chronic- short penetrating
arteries)
3. Sommer sector of
hippocampus.
4. Purkinje cells of
cerebellum.

26. Watershed/Boundary zone infarcts:
Carotid thrombosis

27. Lamellar necrosis in global ischemia.
Chronic

28. Local infarction:
Cell death ~
6min
central infarct
area or umbra,
surrounded by
a penumbra of
ischemic tissue
that may
recover

29. Infarct Pathogenesis:
• Reduced blood supply – hypoxia/anoxia.
• Altered metabolism  Na/K pump block.
• Glutamate receptor act.  calcium influx.
• ischemic injury – Red neuron, vacuolation.
• cell death, karyorrhexis.
• Inflammation – edema.
• Macrophages - > 5d.
• Liquifaction cavity – >1wk
• Glial proliferation – >1wk. (astrocytes)
Hours
1-day
3-day
1 wk.
>4wk

30. Infarct Stages:
• Immediate – <24 hours
• No Change gross, micro  Na/K loss, Ca+ influx.
• Acute stage – < 1week
• Oedema, loss of grey/white matter border.
• Inflammation, Red neurons, necrosis, neutrophils
• Intermediate stage – 1- 4 weeks.
• Clear demarcation, soft friable tissue, cysts
• Macrophages, liquifactive necrosis
• Late stage – > 4 weeks.
• Removal of tissue by macrophages
• Fluid filled cysts with dark grey margin (gliosis)
• Gliosis – proliferation of glia at periphery.

31. FOCAL ISCHAEMIA

32. Brain Stem Stroke:CommonPattern
• Pure Motor - Weakness of face and limbs on one side of the
body without abnormalities of higher brain function,
sensation, or vision (MCA/ACA)
• Pure Sensory - Decreased sensation of face and limbs on one
side of the body without abnormalities of higher brain
function, motor function, or vision (PCA).

34. MCA [mostcommon]Features:
• Paralysis of the contralateral
face, arm and leg
• Sensory impairment over the
contralateral face, arm & leg
• Homonymous hemi or
quadrantonopia
• Paralysis of gaze to the
opposite side
• Aphasia (dominant) and
dysarthria [broca/wernicke]
• Penetrating - contralateral
hemiplegia/paresis, slurred
speech.
• Impaired spatial perception

35. MCA stroke.

37. MCA stroke.
Wikipedia: GNU Free Documentation license

38. MCA stroke.
Wikipedia: GNU Free Documentation license

39. ACA stroke.
• Paralysis of contralateral foot and
leg
• Sensory loss over toes, foot and
leg
• Impairment of gait and stance
• Abulia (slowness and prolonged
delays to perform acts)
• Flat affect, lack of spontaneity,
slowness, distractibility
• Cognitive impairment, such as
perseveration and amnesia
• Urinary incontinence
Wikipedia: GNU Free Documentation license

41. PCA stroke.
Peripheral (cortical)
• Homonymous hemianopia
• Memory deficits
• Perseveration
• Several visual deficits (cortical blindness,
lack of depth perception, hallucinations)
Central (penetrating)
• Thalamus - contralateral sensory loss,
spontaneous pain, mild hemi
• Cerebral peduncle - CN III palsy with
contralateral hemiplegia
• Brain stem - CN palsies, nystagmus,
pupillary abnormalities
Wikipedia: GNU Free Documentation license

42. Posterior Cerebral Artery
• Visual disturbances
• contralateral homonymous
hemianopsia
• (central vision is often spared)
• L. Hemi: lesions alexia
• (with or without agraphia)
• Bilateral lesions: cortical
blindness
• patients unaware they cannot see
• (Anton's syndrome)
• Memory impairment if temporal
lobe is affected ~
• Proximal occlusion
• contralateral hemisensory
loss,
• spontaneous pain and
dysesthesia if thalamus
affected
• (thalamic pain syndrome)
• contralateral severe proximal
chorea
• (hemiballism) ~

45. Haemorrhagic - Arterial embolus
Embolic stroke: sudden, pin point hemorrhages over a triangular area.

46. Infarct with Punctate hemorrhage

47. Cerebral Infarction - Late

48. Cerebral Infarction - Late

49. Hypertensive CVD
• Intraerebral/Subarachnoid Hemorrhage
• Microaneurysm hemorrhages – Basal ganglia.
Putamen(60%), thalamus, ventricles.
• Berry aneurysm hemorrhages – subarachnoid.
• Chronic Hypertension: (dementia)
• Slit hemorrhages. Microhemorrhages heal as slit with
pigment.
• Lacunar infarcts: Brain stem - pale infarcts. A.sclerosis
• Hypertensive encephalopathy-Malignant.
• Headache, confusion, vomiting – Raised ICP.

51. Central PontineHemorrhage- Herniation

52. Subarachnoid Hemorrhage:

53. Ruptured Berry Aneurism

54. Fusiform
atherosclerotic
aneurysm

55. Saccular(berry) Aneurysm:

58. Intracerebral Hemorrhage:

59. Lacunar Infarct in pons

60. Left(Dominant)HemisphereStroke:Clinical
• Aphasia
• Right hemiparesis
• Right-sided sensory loss
• Right visual field defect
• Poor right conjugate gaze
• Dysarthria
• Difficulty reading, writing, or
calculating
Diagnosis: Recent cerebral infarction in left MCA distribution.
Left cerebral hemisphere shows swelling with compression of the lateral ventricle
mainly in the frontal area, due to recent infarct in the Middle Cerebral Artery (MCA)
distribution. The brain in the MCA area shows discoloration of the cortex and also
blurring between the cortex and white matter.

61. Right(Non-dominant)-HemisphereStroke:
• Defect of left visual field
• Extinction of left-sided
stimuli
• Left hemiparesis
• Left-sided sensory loss
• Left visual field defect
• Poor left conjugate gaze
• Dysarthria
• Spatial disorientation

62. CNS AV Malformations:
• Many types:
• AV Malformation *
• Cavernous angioma
• Telangiectasia
• Venous angioma
• Cause of Seizure disorders
& hemorrhage.
• Most common congenital
vascular malformation.
• Typically located in the
outer cerebral cortex
underlying white matter.

64. Pathological Review:
• Stroke: Ischemic / Thrombotic / Hemorrhagic
• Acute neurological deficit - Clinical
• Cerebro Vascular Accident – Pathology.
• Etiology: Thrombosis, Embolism, Hemorrhage.
• Risk factors: AS, Hypertension, Smoking.
• Global – Systemic Hypoxia – Watershed & lamellar infarct
• Focal – Basal ganglia, Putamen, Int. capsule (MCA)
• Pathogenesis: Infarction  Liquifaction necrosis  Cyst formation
with peripheral gliosis. (loss of neural function)
• Hypertension & CVA:
• Atherosclerosis - Thrombosis
• Haemorrhage (Intra/subarachnoid),
• chronic benign: Lacunar infarcts & slit hemorrhages.
• Hypertensive Encephalopathy,

65. Stroke – Risk Factors
• Modifiable
• Hypertension
• Tobacco use
• Excess Alcohol
• Hx of TIA’s
• Heart Disease
• Diabetes Mellitus
• Hypercoagulopathy
• Pregnancy, cancer, etc.
• Sickle Cell and
increased RBC
• Hx of carotid Bruit
• Unmodifiable
• Age
• Gender
• Race
• Previous CVA
• Heredity

67. Stroke – Signs and Symptoms
• Ischemic
• Carotid Circulation
• Unilateral paralysis (opposite side)
• Numbness (opposite side)
• Language disturbance
• Aphasia – difficult comprehension, nonsense, difficult reading/writing
• Dysarthria – slurred speech, abnormal pronunciation.
• Visual disturbance (opposite side)
• Monocular blindness (same side)

68. Stroke – Signs and Symptoms
• Ischemic
• Vertebrobasilar Circulation
• Vertigo
• Visual disturbance
• Both eyes simultaneously
• Diplopia
• Ocular palsy – inability to move to one side
• Dysconjugate gaze – asynchronous movement
• Paralysis
• Numbness
• Dysarthria
• Ataxia

69. Stroke – Signs and Symptoms
• Hemorrhagic
• Subarachnoid hemorrhage
• Sudden severe HA
• Transient LOC
• Nausea/Vomiting
• Neck pain
• Intolerance of noise/light
• AMS
• Intracerebral hemorrhage
• Focal sx w/ LOC, N/V

70. History
• Detailed history from relative or friend or patient if he is able
to speak.
• Rapidity of onset – sudden onset of a focal neurological
deficit.
• Time course of symptoms – maximum deficit over seconds or
minutes before starting to improve.
• Headache, coma at onset and vomiting at onset are more
common in haemorrhage but also occur with infarction.
• Sudden onset of severe generalised headache associated with
neck stiffness – subarachnoid haemorrhage.
• Specific record should be made about the presence of vascular
risk factors.

71. Examination
General Examination
• BP – should be taken in both arms.
• Stroke may cause an acute rise in BP and therefore
hypertension should not be diagnosed in the first few days
after a stroke unless left ventricular hypertrophy of fundal
changes are present.
• Pulse – for arrhythmias particularly atrial fibrillation.
• Peripheral pulses.
• Auscultation for a carotid bruit.
• Heart – for valvular heart disease especially mitral stenosis.
• Neck stiffness – subarachnoid haemorrhage or meningitis.
• Identify the anatomical localization of the lesion and record
the degree of disability.

72. OXFORDSHIRE COMMUNITY STROKE
PROJECT CLASSIFICATION
OCSP

76. Causes of ischaemic stroke

77. Causes of ischaemic stroke 2

78. Causes of ischaemic stroke 3

79. Causes of intracranial
haemorrhage

80. Subarachnoid haemorrhage
• Initial headache or coma – sudden rise in intracranial pressure.
• Focal symptoms if aneurysm ruptures into underlying brain.
• Cerebral vasospasm causes delayed cerebral infarction 4-14
days after onset in 30% of patients.
• Recurrent haemorrhage and hydrocephalus are other
complications.

81. Intracerebral Haemorrhage
• Sudden rupture of microaneurysms caused by hypertensive
vascular disease.
• Characteristically occurs in the basal ganglia, pons and
cerebellum.
• Elderly patients – cerebral amyloid angiopathy, a degenerative
disorder affecting the walls of the artey – subcortical
haematomas.
• Cryptic av malformations are suspect especially in younger
patients < 40 yrs and when the haemotoma is Lobar (frontal,
temporal, parieto-occipital).

82. Investigations
Confirm the diagnosis
CT Scan
 To establish the site, size and pathological diagnosis by
showing infarction or haemorrhage.
 To exclude other conditions that may mimic stroke like
subdural haematoma, intracranial tumour.

83. (a) There is doubt about the diagnosis.
(b) Symptoms progress or fluctuate.
(c) Conscious level is depressed or patient is in coma.
(d) If thrombolytic therapy or anticoagulant treatment is
considered.
(e) Neck stiffness is present.
(f) Has severe headache.
(g) Deteriorates unexpectedly.
(h) Haemorrhage can be seen within a few minutes as an area of
increased attenuation.
(i) Infarction as a low density lesion which conforms to a
vascular territory usually wedge shaped.
(j) It is not immediately visible on CT but in most patients
becomes apparent in 4-7 days.
Y CT Scan?

87. MRI Scan
• Posterior circulation strokes are more readily identified than
by CT.

88. General Investigations
• identify conditions which may predispose towards premature
cerebrovasculardisease.
• Full blood count – polycythemia, thrombocytopoenia.
• Blood glucose – diabetes mellitus.
• Serum lipids – hypercholesterolemia.
• Blood cultures – SBE.

89. General Investigations II
• HIV screen – AIDS.
• Syphilis serology – VDRL.
• Clotting Screen.
• Thrombophilia Screen – Protein C, Protein S, Antithrombin III.
• Anticardolipin antibodies – SLE.
• Lumbar Puncture – subarachnoid haemorrhage.

90. DD Stroke
• Differential Diagnosis of Stroke
• Head/Cervical trauma
• Meningitis/encephalitis
• Hypertensive encephalopathy
• Intracranial mass
• Tumor
• Sub/epi dural hematoma
• Todd’s paralysis
• Migraine w/ neuro sx
• Metabolic
• Hyper/hypo glycemia
• Post arrest ischemia
• Drug OD

91. Differential Diagnosis
• Space occupying lesion
• 5% of people with stroke like symptoms have a subdural
haematoma, tumour or cerebral abscess.
• Distinction is readily made on CT or MRI.
• If there is any doubt repeat the scan after 6 weeks.

92. Differential Diagnosis II
• Multiple sclerosis
• May present with hemiparesis, sensory impairment or
brainstem symptoms that mimic stroke.
• Symptoms occur gradually over a few days.
• Hypoglycaemia
• May cause hemiparesis.
• Migraine

93. Complications I
• Cerebral oedema
•Should be suspected in a patient
with a large infarct or haemorrhage
experiences a lucid interval of 24-48
hours and then shows a decline in
consciousness.

94. Complication II
• Haemorrhagic transformation
• Can occur as a result of thrombolysis.
• Pneumonia
• In patients with swallowing difficulties as a result of aspiration.
• Pressure sores
• Develop rapidly and may be exacerbated because of
incontinence.
• Oedema of Weak Limbs
• Is common and has a partially autonomic basis.

95. Complication III
• Anxiety and Depression
• Common reactions to stroke but
depression may have an organic basis
related to damage of the frontal and
limbic systems.
• Emotional Lability
• Precipitated by minor emotional stimuli.

96. Management I
• Has the following aims
• Confirmation of the diagnosis,
anatomical site of the lesion, pathology
and aetiology.
• Acute care.
• Rehabilitation of persistent disability
and handicap.
• Prevention of recurrence.

97. Management II
Acute Care
Treatment aims
• Prevent progression of present event.
• Prevent immediate complication.
• Prevent the development of subsequent events.
• To rehabilitate the patient.

98. Management III
General Measures
• Around the edge of the infarct, ischaemic tissue is at risk, but is
potentially recoverable.
• This must be protected by ensuring a good supply of glucose
and oxygen.
• Maintain hydration, oxygenation and blood pressure.

99. Specific Measures
MedicalTreatment
Anticoagulation
• Patient with high risk of developing deep vein
thrombosis.
• Thromboembolic stroke - started as soon as
possible, except in large infarcts where it may
be wise to delay anticoagulation for 2 weeks.
• Stroke in a patient with myocardial infarct -
due to mural thrombus.
• Stroke in evolution.
Exclude a haemorrhage by doing a CT scan first.

100. Medical Treatment II
Antiplatelet Agents
• Especially in TIA.
Thrombolysis
• I/V thrombolysis espcially recombinant tissue plasminogen
activator rTPA to be given only within the first 3 hours after
onset to those patients who have not developed CT
abnormalities especially in patients with basilar artery
occlusion.
• Risk – haemorrhage.

101. Hypertension
• Treated cautiously in acute stroke.
• A reduction in blood pressure may lower cerebral blood flow in
the regions surrounding the infarct below a critical level at
which further ischaemic brain damage will occur.
• Mild to moderate elevations in BP – no treatment unless they
are maintained for several days after admission.

102. • If stroke associated with hypertensive encephalopathy or if
diastolic BP is persistently above 120 mm Hg.
• The BP should be lowered cautiously using oral agents.
• Sudden precipitious fall in BP should be avoided.
Hypertension II

103. Medical Treatment
CalciumAntagonist
• Nimodipine prevents ischaemic brain damage and reduces
the number of patients remaining disabled after
subarachnoid haemorrhage.
• Prescribed as soon as diagnosis is made (within 12 hours).

104. Neurosurgery
• Should be considered in subaracnoid and intracerebral
haemorrhage.
• Evacuation of cerebellar haematoma.
• Evacuation of supratentorial haematomas should only be
considered in younger patients with superficial cortical
haematomas causing mass effect with a deteriorating level of
conciousness.

105. Nursing Care and
Rehabilitation
• Physiotherapy, proper positioning and early mobilization –
prevent pressure sores.
• Support stockings – prevent deep vein thrombosis and
pulmonary embolism.
• Swallowing difficulties.
• Lead to silent aspiration – aspiration pneuomonia.
•Nasogastric tube feeding.
• Percutanious endoscopic gastrostomy.

106. Rehabilitation
• Physiotherapy, occupational therapy, speech therapy and
psychology input – multidisciplinary stroke rehabilitation
team.
• Home visit by occupational therapist to plan adaptations to
home before discharge.

107. Secondary Preventation
• Control hypertension and diabetes mellitus.
• Correct lipid abnormality.
• Stop cigarette smoking.
• Stop thrombogenic drugs e.g. oral contraceptives.

108. • Give platlet antiaggregation drugs to reduce the rate of
reinfarction.
• Low dose aspirin (75 mg – 150 mg), if
patient allergic or has gastrointestinal
side effects give ticlopidine. Regular
blood tests because of a small risk of
neutropoenia.
• Remove or treat embolic source (long term anticoagulation in
atrial fibrillation).
• Treat inflammatory or vascular inflammatory diseases.
Secondary Preventation II

109. • Carotid Endarterectomy – preventing stroke in symptomatic
patients with recent TIA and stroke and severe stenosis of the
internal carotid artery (at least 70%).
Secondary Preventation III

110. Chain of Survival Stroke
• Stroke Chain of Survival
• Detection
• Early sx recognition
• Dispatch
• Prompt EMS response
• Delivery
• Transport, approp, prehospital care, prearrival notification
• Door
• ER Triage
• Data
• ER evaluation incl, CT, etc.
• Decision
• Appropriate therapies
• Drug/Therapy

111. Detect & Dispatch
• Detection: Early Recognition
• Public education of Stroke sx
• Early access to medical care
• Dispatch: Early EMS and PDI’s
• Caller triage
• EMD recognition of Stroke sx

112. How to detect?
• Delivery:
• Pre-hospital Transport and
Management
How we scale the pre-
hospital management of the
patient?

113. CINCINNATI STROKE SCALE

114. CINCINNATI STROKE SCALE
• Identifies patients with strokes.
• It evaluates three major physical
findings.
•Facial droop
•Motor arm weakness
•Speech abnormalities

115. CSS - Facial Droop
• Have the patient show their teeth or
smile.
• Normal – both sides of the face move
equally well
• Abnormal – one side of the face does
not move as well as the other side

118. Arm Drift
• Have the patient close his/her eyes and
hold both arms out.
• Normal – both arms move the same way,
or both arms do not move at all.
• Abnormal – one arm does not move or
one arm drifts down compared to the
other arm.
Other findings such as pronator grip, may
be helpful

121. Speech
• Have the patient say “You can’t teach
an old dog new tricks.” –
“Perlambagaan Malaysia”
• Normal – patient uses correct words
with no slurring.
• Abnormal – patient slurs words, uses
inappropriate words, or is unable to
speak

122. “You can’t teach an old
dog new tricks.”

124. Cincinnati Prehospital
Stroke Scale
• Patients with 1 of these 3 findings -as a
new event - have a 72% probability of an
ischemic stroke.
• If all 3 findings are present the probability
of an acute stroke is more than 85%
• Immediately contact medical control and
the destination ED and provide prearrival
notification.

125. Stroke – Management
In Review:
Prehospital Critical Actions
• Assess and support cardiorespiratory function
• Assess and support blood glucose
• Assess and support oxygenation and ventilation
• Assess neurologic function
• Determine precise time of symptom onset
• Determine essential medical information
• Provide rapid emergent transport to ED
• Notify ED that a possible stroke patient is en route

126. Stroke - Management
• Door: ER Triage
• Stroke evaluation targets for stroke patients who are thrombolytic
candidates
Door-to–doctor first sees patient …….………… 10 min
Door-to–CT completed …….………………….. 25 min
Door-to–CT read ...…………..………………… 45 min
Door-to–fibrinolytic therapy starts …………….. 60 min
Neurologic expertise available* …..…………… 15 min
Neurosurgical expertise available* …………… 2 hours
Admitted to monitored bed ..……...…………… 3 hours
*By phone or in person

127. Stroke - Management
• Data: ER Evaluation and Management
• Assessment Goal: in first 10 minutes
• Assess ABCs, vital signs
• Provide oxygen by nasal cannula
• Obtain IV access; obtain blood samples (CBC, ’lytes, coagulation
studies)
• Obtain 12-lead ECG, check rhythm, place on monitor
• Check blood sugar; treat if indicated
• Alert Stroke Team: neurologist, radiologist, CT technician
• Perform general neurologic screening assessment

128. Stroke - Management
Assessment Goal: in first 25 minutes
• Review patient history
• Establish symptom onset (<6 hours required for fibrinolytics)
• Perform physical examination
• Perform neurologic exam
• Determine level of consciousness (Glasgow Coma Scale)
• Determine level of stroke severity (NIHSS or Hunt and Hess Scale)
• Order urgent non-contrast CT scan/angiogram if non-hemorrhage
(door-to–CT scan performed: goal <25 min from arrival)
• Read CT scan (door-to–CT read: goal <45 min from arrival)
• Perform lateral cervical spine x-ray (if patient comatose/trauma
history)

129. Stroke - Management
• ER Diagnostic Studies
• CT scan – done w/in 25 mins, read w/in 45 mins
• r/o hemorrhage
• Often normal early in ischemic stroke
• Lumbar puncture
• EKG
• Changes may be caused by or cause of stroke
• MRA (Magnetic Resonance Angiography)
• Cerebral Angiography

130. Hypodense area:
• Ischemic area with
edema, swelling
• Indicates >3 hours old
• No fibrinolytics!

131. (White areas indicate
hyperdensity = blood)
Large left frontal
intracerebral
hemorrhage.
Intraventricular
bleeding
is also present
No fibrinolytics!

132. Acute
subarachnoid
hemorrhage
Diffuse areas of white
(hyperdense) images
Blood visible in
ventricles
and multiple areas on
surface of brain

133. Stroke - Management
• Decision: Specific Therapies
• General Care
• ABC’s, O2
• IV w/ BSS
• Treat hypotension
• Avoid over-hydration
• Monitor input/output
• Normalize BGL
• Manage Elevated BP?

134. Stroke - Management
• Indications for Antihypertensive therapy
In general:
• Consider: absolute level of BP?
• If BP: >185/>110 mm Hg = fibrinolytic therapy contraindicated
• Consider: other than BP, is patient candidate for fibrinolytics?
• If patient is candidate for fibrinolytics: treat initial
BP >185/>110 mm Hg
• Consider: response to initial efforts to lower BP in ED?
• If treatment brings BP down to <185/110 mm Hg: give fibrinolytics
• Consider: ischemic vs hemorrhagic stroke?
• Treat BP in the 180-230/110-140 mm Hg range the same
• The obvious: no fibrinolytics for hemorrhagic stroke

135. Stroke - Management
• Decision: Specific Therapies (cont.)
• Management of Seizures
• Benzodiazepines
• Long-acting anticonvulsants
• Management of Increased ICP
• Maintain PaCO2 30mm Hg
• Mannitol/Diuretics
• Barbiturates
• Neurosurgical decompression

136. Stroke - Management
• Drugs: Thrombolytic Therapy
• Fibrinolytic Therapy Checklist Ischemic Stroke
Candidates for Neurointerventional Therapy
 Age 18 years or older
 Acute signs and symptoms of CVA <6 hours onset.
 No contraindications.

137. Stroke - Management
Contraindications for Interventional Therapy
Absolute
 Evidence of intracranial hemorrhage on non-contrast head CT
 Patient with early infarct signs on CT scan.
Relative
 Recent (w/in 2 mo’s) cranial or spinal surgery, trauma, or injury
 Known bleeding disorder and/or risk of bleeding including:
- Current anticoagulant therapy, prothrombin time >15 sec.
- Heparin within 48 hrs of admission, PTT elevated
- Platelet count <100,000/mm
 Active internal bleeding w/in the previous 10 days
 Known or suspected pregnancy
 History of stroke w/in past 6 weeks

138. Stroke - Management
Contraindications for Interventional Therapy (cont.)
Relative
 Patient comatose
 >85 years old
 Diabetic hemorrhagic retinopathy or other opthalmic
hemorrhagic disorder
 Advanced liver or kidney disease
 Other pathology with a propensity for bleeding
 Infectiouse endocarditis
 Severe EKG disturbance, uncontrolled angina or acute MI

139. Stroke - Management
• Thrombolytic Agents
• TPA
• NINDS trial
• Streptokinase
• VEGGIE trial
• Anticoagulant Therapy
• Heparin
• ASA/Warfarin/Ticlodipine

140. Stroke - Management
• Management of Hemorrhagic Stroke
• Subarachnoid
• Neurosurgical intervention
• Nimodipine
• Intracerebral
• Management of ICP
• Neurosurgical decompression
• Cerebellar
• Surgical evacuation
• Often associated with good outcome
• Lobar
• Surgical evacuation

141. 14
1

142. THE END

143. If they come to you
with stroke, what
investigation what
you like to do?

145. QUIZ ON
STROKE
MOHD HANAFI RAMLEE

146. ANSWER
GILIR2 TAU

147. QUESTION 1
On the history of a patient with suspected or known stroke, what
should you ask about?

148. ANSWER 1
 Ask about the presenting symptoms of stroke
initially, for example
1. Unilateral weakness or clumsiness
2. Difficulty understanding or expressing spoken
language
3. Altered sensation unilaterally
4. Partial or complete loss of vision in one eye

149. ANSWER 1
 Questions to focus on the causes of stroke
1. Atherosclerosis, e.g. enquire about vascular risk factors (smoking,
DM, hyperlipids, PVDs, etc…)
2. History of heart disease, e.g. recent myocardial infarction, history
of AF requiring anticoagulation, palpitations
3. History of hypertension (lacunar infarcts due to arteriosclerosis of
small penetrating arteries of the brain)
4. Migraine
5. Manipulation of neck (precipitating cause for dissection of carotid
artery or vertebral artery)
6. Any recent cessation of anticoagulation
7. Family history of stroke
8. History of connective tissue disease (e.g. SLE, vasculitis, etc…)

150. ANSWER 1
1. History of connective tissue disease (e.g. SLE, vasculitis, etc…)
 Medication history, esp. those that increase risk of stroke include
oral contraceptives, some antihypertensives
 Ask about alcohol consumption and recent falls (may have caused
an intracranial haemorrhage)
 Enquire about premorbid as well as the current level of
independence and mobility
 If patient is incapacitated, ask about social support available at
home
 Don’t forget to screen for depression

151. QUESTION 2
On examination, what features should you be looking for?

152. ANSWER 2
A complete examination of the neurological and cardiovascular systems is essential
 Check the fundi for evidence of emboli, hypertensive changes, diabetic changes
and ischaemic neuropathy
 Test the visual fields for homonymous hemianopia
 Listen for bruit over the carotids and orbits (commonly heard in the side
opposite the carotid occlusion, due to increased contralateral flow)
 Decide whether patient is in AF
 Assess BP and test for postural drop
 Listen for murmurs (e.g. AS, infective endocarditis, rheumatic heart disease or
prosthetic valve)
 Note presence of electronic pace maker and assess whether it’s working
 Perform peripheral vascular examination
 Look for complications, e.g. pressure sores, limb contractures and disuse
atrophy of the paralysed limbs
 See if patient has a percutaneous gastrostomy (PEG) feeding tube inserted and,
if present, inspect for cellulitis or pus around the insertion site

153. QUESTION 3
What clinical features are suggestive of a carotid arterial stroke?

154. ANSWER 3
 Transient aphasia
 Ipsilateral amaurosis fugax
 Contralateral hemiplegia/monoplegia
 Contralateral hemi or monoparesis
 Carotid bruits (a/w >50% stenosis)

155. QUESTION 4
What clinical features are suggestive of vertebrobasilar insufficiency?

156. ANSWER 4
All the Ds
 Dizziness (vertigo and ataxia)
 Diplopia +/- blindness
 Dysphagia
 Dysarthria
 ‘Demi-anaesthesia’ – ipsilateral face, contralateral limb
 Quadraparesis – indicates basilar artery involvement

157. QUESTION 5
What clinical features are suggestive of a middle cerebral artery
stroke?

158. ANSWER 5
 Contralateral hemiplegia, hemiparesis, homonymous hemianopia
 UMN face, arm > leg, eyes deviated to side of lesion
 Aphasia (if dominant lobe)
1. Expressive dysphasia, arm + leg involvement – anterior MCA
2. Receptive dysphasia, visual fields defects – posterior MCA
 If non-dominant – speech + comprehension intact

159. QUESTION 6
What clinical features are suggestive of a posterior cerebral artery
stroke?

160. ANSWER 6
 Homonymous hemianopia (complete)
 Cortical blindness
 Hemisensory loss
 Ipsilateral III nerve palsy

161. QUESTION 7
What clinical features are suggestive of an anterior cerebral artery
stroke?

162. ANSWER 7
 Contralateral monoplegia (UMN)
 Confusion, behaviour disturbance
 Grasp reflex
 Urinary incontinence

163. QUESTION 8
What clinical features are suggestive of a lacunar syndrome?

164. ANSWER 8
 Clumsy hand/dysarthria syndrome – lesion in mid pons
 Leg paresis + ataxia – pons or internal capsule
 Pure sensory stroke – usually thalamic
 Pure motor stroke (arm>leg) - pons or internal capsule

165. QUESTION 9
What investigations would you perform in a stroke patient? – MAINLY
TO DIAGNOSE ANY STROKE….

166. ANSWER 9
CT or MRI of the head, looking for ischaemic infarcts, haemorrhage, or
mass lesions

167. QUESTION 10
What investigations would you perform in a stroke patient? MAINLY
TO FIND THE CAUSE OF STROKE

168. ANSWER 10
 Doppler scan of the carotid arteries – if duplex scan suggest
significant carotid stenosis, esp. in patients <75, ask for results of
carotid angiography, carotid digital substraction angiography or MR
angiography
 If patient is in AF, ask for results of transoesophageal echo, looking
for thrombus or spontaneous atheromatous plaques in ascending
aorta and arch of aorta that may have contributed to stroke
 ECG for AMI and AF
 FBE, looking at Hb (to exclude polycythemia) and platelet count
(rarely, essential thrombocytopenia can contribute to stroke)
 ESR (to exclude an inflammatory arteritic/vasculitic process
 CXR (for cardiomegaly/neoplasm)
 Urea, creatinine and electrolytes

169. QUESTION 11
What investigations would you perform in a stroke patient?
MAINLY IN YOUNGER PATIENT?

170. QUESTION 11
 Drug screen, looking for narcotic agents
 Vasculitic screen (if there are features of vasculitis)
 Blood cultures and cardiac imaging if endocarditis is suspected
 Cardiac event monitor looking for paroxysmal AF and
 Thrombophilic screen

171. WHAT 3 SPECIFIC STRATEGIES IN THE
MANAGEMENT OF ACUTE STROKE THAT HAVE
BEEN PROVEN TO IMPROVE OUTCOMES?
The 3 main strategies are
 Administration of iv tissue plasminogen activator (tPA) within 3hrs
of stroke onset
 Giving aspirin (100mg) within first 48hrs of ischaemic stroke
 Managing patient in a stroke unit
Note that tPA and aspirin are never given before brain imaging to
exclude intracranial haemorrhage

172. WHAT ARE THE STRATEGIES FOR
SECONDARY PREVENTION OF
STROKE?
There are now at least 4 early strategies for secondary prevention in
improving long term outcomes after TIAs or stoke
 Antiplatelet therapy, e.g. aspirin, clopidogrel, aspirin with
dipyridamole
 Blood pressure lowering
 Warfarin (indicated for patients with AF)
 Carotid endarterectomy (indicated when stenosis >70%)
 Lipids lowering is the fifth strategy to consider

173. A PATIENT JUST HAD A STROKE, WHAT
CRITERIA DO YOU LOOK FOR TO SELECT THIS
PATIENT FOR REHAB.
1. Patients must be medically stable (i.e. no aspiration pneumonia,
AMI, DVT, etc…)
2. They have a functional disability
3. They have the intellectual capability to learn
4. There are defined goals to be achieved
5. There are non or minimal co-morbidities, e.g. recurrent stroke,
AMI, COAD, etc…
6. They are not clinically depressed (this can affect motivation to
rehabilitate)
7. They didn’t suffer from a dense stroke or ones that causes hemi-
neglect (e.g. a right hemisphere stroke)

174. WHAT ARE SOME OF THE COMMON
PREDICTORS OF POOR FUNCTIONAL
OUTCOME AFTER A STROKE?
 A dense stroke, a recurrent stroke, or a stroke resulting in hemi-
neglect
 Impairment of bladder and bowel function
 Depression or cognitive deficits
 Delayed acute medical care or delayed rehabilitation
 Co-morbidities and poor social support