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)

Prevalence :

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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
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
1,5
1,3 0,3 2

Stroke sebelumnya

TIA

29,4

11,2
10,2

3,1

Peripheral Arterial
Disease
Hipertensi
Dislipidemia

Hypertension

Diabetes Mellitus

71,9

Atrial Fibrilation
Angina Pektoris

Stroke Registri 2012-2013

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Acute Ischemic Injury

45% due to
trombus formation/
thrombosis.

20% due to emboli

& global ischemic/
hypotension.

35% unknown.
Hickey, J. V., 2003

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Macroscopic View :
Arterial Occlusion
Atherosclerotic Plaque

A. Plaque.
B. Plaque with platelet-fibrin emboli.
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 5060 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
Ischemic area

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: vasoconstriction
: 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 :
Alert : 0
Drowsy and stupor : 1
Semicoma and coma : 2

Diagnosis
>1 cerebral haemorrage 90. 0%

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

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Haemorrhage

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CT Scan & MRI

Head CT Scan

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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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