Paulus Sugianto

Dept. of Neurology
Dr. Soetomo General Hospital/ Faculty of Medicine Airlangga University
 WORLD STROKE DAY
29th October 2015

Theme ‘I am Woman’.

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 Stroke is the first leading cause of
disability
Stroke is the third leading cause of death

67% of stroke is ischemic type

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Definition
 Ischemia :
Lack of circulating blood deprives the
neurons of oxygen and nourishment
 Hemorrhage :
Extravascular release of blood causes
damage by cutting off connecting pathways,
resulting in local or generalized pressure
injury

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 EPIDEMIOLOGY
 Indonesia :
 Riskesdas 2007 : Stroke prevalence 8.2/1000
population
 Stroke Registri 2012-2013 (Yudiarto et al., 2014)
 Stroke is the first leading cause of death in Indonesia
(15,4%)
 Ischemic stroke 67.1% and haemorrhagic stroke 32.9%.
 Major risk factor : hypertension, DM and dyslipidemia
 Prevalence :
 18-44 yrs old : 0,8%
 >65 yrs : 8,1%
 80 th : 1 of 3 will be prone to stroke.

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 STROKEStroke
RISKbased
FACTORS
on
Underlying Disease and Stroke type.
1,9
2,2
1,1 Stroke sebelumnya
1,5
1,3 0,3 2
TIA
11,2 29,4
Peripheral Arterial
10,2 Disease
3,1
1 Hipertensi

Dislipidemia

Hypertension Diabetes Mellitus

71,9 Atrial Fibrilation

Angina Pektoris

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Stroke Registri 2012-2013
 Acute Ischemic Injury
 45% due to Macroscopic View :
trombus formation/ Arterial Occlusion
thrombosis. Atherosclerotic Plaque

 20% due to emboli

& global ischemic/
hypotension.

 35% unknown.
A. Plaque.
B. Plaque with platelet-fibrin emboli.
Hickey, J. V., 2003 C. Plaque with occlusive thrombus
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Etiology Acute Ischemic Injury
 The most common : atherosclerosis.

Endothelial injury Thrombosis

Platelet adhesion Ulcerasi

Coagulation Calcification

Thrombus Intraplaque haemorrhage

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 Another Etiology of
Vascular Occlusion
 Hypercoagulation.
 Fibromuscular displasia.
 Arteritis (giant cell and Takayasu)
 Rupture of blood vessel

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Lacunar Infarct
 Insidens : 10-30% of all stroke.
 Deep Profundal artery.
 Most frequent :
 Putamen.
 Pallidum.
 Pons.
 Thalamus
 Caudate nucleus.
 Internal capsule.

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Lacunar Infarct
Chronic hypertension

Small arteriole lengthening & weaving

Sub-intimal dissection & microaneurysm

Occlusion due to microthrombi

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Embolic Stroke
 Source of emboli may come from many
sources which are far from the affected side:
 Sclerotic plaque on carotid artery.
 Heart with atrial fibrillation, patent for ovale.
 Hypokinetic left ventricle.
 Bacterial colonization, tumour/ metastatic
process, foreign body.
 Air embolic, water & blood embolic could
because by invasive prosedure of surgery.

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Embolic Stroke
 Two most common sources of emboli :
 Left sided cardiac chambers
 Artery to artery stroke: as in detachment of a
thrombus from ICA at the site of a plaque
 Many embolic strokes become
“haemorrhagic”

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“Hypotensive Stroke”
 Abrupt drop in blood pressure.

 Affected area located at the end of an

arterial territory  Hence the term
“watershed or boundary zone infarct”

 10% of ischemic stroke is hypotensive

stroke, 40% of which occurs in patient with
carotid artery stenosis/ occlusion

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Watershed infarcts (Hypotensive Stroke)

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CBF & Ischemic Thresholds
 Normal CBF  50-
60 cc/100 g/minute
 Varies in different
regions of the brain

 CBF 20-30 cc /100

g/ min  Loss of
electrical activity

 CBF 10 cc/100g/min
 Neuronal death
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CEREBRAL BLOOD FLOW
 Depend on neuronal activity.
 High activity  CBF 
 Low activity  CBF 
 Autoregulation CBF :
 Normal : MABP 50-150 mmHg.
 Hypertension : MABP   more sensitif to
hypotension.
 Oxygen treatment :
 Normal : vasoconstriction
 Ischemic area : vasodilatation  CBF 
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Ischemic Penumbra
Ischemic core & Peri-infarct zone

 Glutamate & K+ extracellular

as Multiple focus

Spontaneous Wave Depolarization

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Conditions influencing progression
and extent of ischemic injury
 Rate & duration of the Ischemic event
 Collateral circulation in the involved
area of the brain
 Systemic circulation & arterial blood
pressure
 Coagulation abnormalities
 Temperature
 Glucose

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SIGN & SYMPTOMS
 F : Face
 A : Arm
 S : Speech
 T : Time  Onset : First Abnormal Time
(FAT)  to Last Normal Time (LNT)

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SIGN & SYMPTOMS
SUDDEN :
 numbness or weakness in the Face, Arm, or leg,
especially on one side of the body
 confusion, trouble Speaking, or difficulty
understanding speech.
 trouble seeing in one or both eyes.
 trouble walking, dizziness, loss of balance, or lack of
coordination
 severe headache with no known cause Contralateral
conjugate gaze paresis.

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 SIGN & SYMPTOMS
 Contralateral conjugate gaze
paresis.
 Downward deviation of eyes.
 Small sluggish pupil
 Vertigo
 Dysarthria, dysphagia
 Forgetfullness
 Contralateral homonymous
hemianopsia, small reactive pupil.
 Hyperthermia.

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SIRIRAJ STROKE SCORE
Formula :
(2.5 * consciousness) + (2 * vomiting) + (2 *
headache) + (0.1* DBP) – (3 * atheroma) – 12 =
Consciousness point : Diagnosis
Alert : 0 >1 cerebral haemorrage 90. 0%
Drowsy and stupor : 1
Semicoma and coma : 2

Vomiting/ headache within 2 hrs

No 0
Yes 1

Atheroma(diabetic history, angina,

claudication)
None 0
Yes ≥1
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Laboratory
 Full blood count.
 Random blood sugar(Class I; Level of Evidence B),
 Electrolyte : K, Na, Cl
 RFT
 LFT
 Oxygen saturation.
 INR/ Protrombin time, Activated partial thromboplastin
time,
 Cardiac ischemia marker,
 Alkohol saturation in the blood
 Electrocardiogram (ECG)

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Laboratory & Radiology
 Thorax foto(Class IIb; LoE: B)
 Head CT or MRI + MRA (Class I; LoE: A).
 CT perfusion and MRI perfusion or diffusion
 to see core and penumbra damage
(Class IIb; Level of Evidence B).
 EEG (Elektroencephalography) if the
patient get seizure.

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 Head CT Scan without contrast
Ischaemia Haemorrhage

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 CT Scan & MRI
Head CT Scan Head DW-MRI

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 Management :
 Assess and manage ABCs
 Cardiac monitoring should be performed for at least the
first 24 hours (Class I; Level of Evidence B) for AF and
arrythmias.
 Supplemental oxygen should be provided to maintain
O2 saturation >94% (Class I; LoE: C).
 Establish IV access per local protocol
 Determine blood glucose and treat accordingly
 Determine time of symptom onset or last known normal
 Triage and rapidly transport patient to nearest most
appropriate stroke hospital
 Notify hospital of pending stroke patient arrival
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Management
 the benefit of routine prehospital blood
pressure intervention is not proven;
 consultation with medical control may
assist in making treatment decisions
regarding patients with extreme
hypertension (systolic blood pressure
≥220 mm Hg)

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Management : specific (r-tPA)
 Onset of symptoms <3 hours before beginning
treatment (Class I; LoE: A)
 Onset of symptoms <4,5 hours before
beginning treatment (Class I; LoE: B).
 Intra-arterial fibrinolysis :
 carefully selected patients with major
ischemic strokes
 <6 hours’ duration caused by occlusions of
the MCA
 not candidates for iv r-tPA (Class I; LoE B).

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Management : Antiplatelet
 Aspirin (initial dose: 325 mg) : within 24 to
48 hours after stroke onset is
recommended (Class I; LoE A).
 Clopidogrel for acute ischemic stroke is
not well established (Class IIb; LoE: C).
Further research testing is required.
 Other iv antiplatelet agents that inhibit the
glycoprotein IIb/IIIa receptor is not
recommended (Class III; LoE: B).

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Neuroprotectant
 No neuroprotectant has shown an
impressive outcome (Class III; LoA : A).
 Hyperbaric oxygen is not recommended
for treatment of patients with acute
ischemic stroke (Class III; LoE: B).
 Continuation of statin therapy during the
acute period is reasonable (Class IIa;
LoE: B).

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Brain Edema
 Head up 300.
 Hyperventilation.
 Osmotherapy.
 Surgical decompression.
 Prophylactic use of anticonvulsants is
not recommended (Class III; Level of
Evidence C).

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Hemorrhagic stroke
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Management : Hypertension
 If SBP is >200 mm Hg or MAP is >150 mm Hg  aggressive
reduction of BP with continuous i.v infusion, BP monitoring
every 5 min.
 If SBP is >180 mm Hg or MAP is >130 mm Hg and there is
the possibility of elevated ICP, then consider monitoring ICP
& reducing BP using intermittent or continuous i.v
medications while maintaining a CPP=60 mm Hg.
 If SBP is >180 mm Hg or MAP is >130 mm Hg and there is
not evidence of elevated ICP, then consider a modest
reduction of BP (eg, MAP of 110 mm Hg or target BP of
160/90 mm Hg) using intermittent or continuous i.v
medications to control BP and clinically reexamine the
patient every 15 min.
 If SBP is 150-220 mm Hg, acute lowering
of systolic BP to 140 mm Hg is probably safe
(Class IIa; LoE: B).
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Surgery
 For most patients with ICH, the usefulness of
surgery is uncertain (Class IIb; LoE: C).
 Ventricular drainage as treatment for
hydrocephalus is reasonable in patients with
decreased level of consciousness (Class IIa; LoE:
B).
 Cerebellar hemorrhage + :
 deteriorating neurologically or who have
 brainstem compression and/or
 hydrocephalus from ventricular obstruction
(Class I; LoE: B).

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Surgery
 Lobar clots >30 mL + within 1 cm of the
surface, evacuation of supratentorial ICH by
standard craniotomy might be considered
(Class IIb; LoE: B).
 Effectiveness of minimally invasive clot
evacuation utilizing either stereotactic or
endoscopic aspiration with or without
thrombolytic usage is uncertain (Class IIb;
LoE: B).
 Very early craniotomy may be harmful due to
increased risk of recurrent bleeding (Class III;
LoE: B).

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Prevention
 BP should be well controlled, particularly
for patients with ICH location typical of
hypertensive vasculopathy. (Class I,
Level A)

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 Summary
 Ischemic stroke 67.1% and haemorrhagic
stroke 32.9%.
 Trombus formation is the most common etiology
(45%).
 Embolic & global ischemic/ hypotensive contributes
to 20% of etiology.
 The use of r-tPA if onset of symptoms <3-4,5 hours
before beginning treatment.

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Summary
 Haemorrhage transformation occurs when
ischemic vessels ruptures & persistent
occlusion in proximal main artery is
reperfusioned
 The severity of ischemic injury depend on the
degree of obstruction & collateral circulation.
 Treatment is directed to prevent penumbra
becoming ischemic.
 Selective vulnerability of neuron to global
ischemia.
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Summary
 Management hypertension in ischaemic
stroke  haemorrhagic stroke.
 Glucose  normoglycemia is
recommended.
 Clinical seizures should be treated.
 The usefulness of surgery is uncertain
 Better management for supportive, specific
and rehabilitative treatment for better
outcome.

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