STROKE

dr. Randy V. Alfons

Ambon,5 maret 2018
Apa itu stroke ???
• Stroke menurut WHO adalah gangguan peredaran darah
otak yang bersifat fokal atau global, yang berlangsung
cepat, lebih dari 24 jam, dan dapat menyebabkan kematian,
serta tanpa ditemukan penyebab lain selain gangguan
vaskular.

Aliah et al., 2003

 Klasifikasi dan Epidemiologi
• Berdasarkan patologi :
• Stroke iskemik (87 %)
• Serangan stroke sepintas -- TIA (15 %)
• Trombosis serebri
• Emboli serebri
• Stroke hemoragik/perdarahan
• Perdarahan intra serebral (10 %)
• Perdarahan sub araknoid (3 %)

Misbach, 2011; Liebeskind, 2015

 Klasifikasi dan Epidemiologi
• Berdasarkan waktu kejadian
• Transient Ischemic Attack (TIA)
• Reversible Ischemic Neurologic Deficit (RIND)
• Stroke In Evolution (SIE) / Progressing Stroke
• Completed stroke

• Berdasarkan lokasi lesi

• Sistem karotis
• Sistem vertebrobasilar

Goetz, 2007
 Klasifikasi dan Epidemiologi
• Data CDC di USA lebih dari 795.000 orang
terkena stroke per tahun.
• 610.000 stroke baru
• 185.000 stroke rekuren
• 1 dari 14 pasien meninggal karena stroke.
• Laki-laki 25 % lebih sering dibanding wanita.

Townsend et al., 2015; Hall et al., 2012

Klasifikasi dan Epidemiologi

• Laki- laki >> wanita

• Insiden laki laki : 62.8 per 100.000 26.3%
meninggal
• Insiden wanita : 59 per 100.000 39.2%
meninggal
• Usia
• 95 % terjadi pada usia lebih dari 45 tahun
• 34 % berusia kurang dari 65 tahun

Liebeskind et al., 2013; Jauch, 2013

 Faktor Risiko
• Hipertensi (54 %)
• Diabetes Melitus (20 %)
• Fibrilasi atrium (20 %)
• Kolesterol
• Kontrasepsi (1.5%)
• Merokok (66 %), alkohol &
obat terlarang (12,8 %)
• Penggunaan antikoagulan atau
antiagregasi
• Penyakit anemia sel sabit (24
%)
• Patent Foramen Ovale
• Genetik dan riwayat keluarga
• Usia, jenis kelamin, ras
tertentu
• Riwayat stroke sebelumnya
Misbach, 2011; Go et al 2012
Stroke
Stroke is undoubtedly one of the most
devastating events experienced by
humans
“Many stroke victims would rather die
than live without their dignity and quality
of life”
Bahle, J. (1998).

8
Key Message

Stroke is an Emergency
Act Fast

*6 Million Neurons a Minute are lost

Time is Brain
Dr. Lownie

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Basic Neuro-anatomy

10
THE BRAIN IS DIVIDED INTO 3 MAJOR AREAS

1. Cerebrum

2. Brain stem

3. Cerebellum

11
THE CEREBRUM IS COMPOSED OF FOUR LOBES

Each lobe has many functions

12
13
 THE BRAIN STEM HAS 3 MAJOR DIVISIONS

1. Midbrain
2. Pons
3. Medulla

14
 THE CEREBELLUM

www.injuryprevention.ca 15
The Carotid Arteries
Anterior & middle Anterior & middle
cerebral arteries cerebral arteries

R Internal carotid L Internal carotid

Common carotid a Common carotid a

R subclavian a L subclavian a
ANTERIOR
VIEW
Aorta 16
Vertebral-basilar Arteries

Posterior cerebral a’s

Basilar a

R Vertebral a L. Vertebral a

R subclavian a L subclavian a
POSTERIOR
VIEW

Aorta 17
Anterior and middle cerebral a’s Post communicating a

Post cerebral a

Basilar a

Internal Carotid

Vertebral a

Common carotid

Subclavian a
Aorta 18
 CIRCLE OF WILLIS
Anterior
Communicating
artery

Anterior C.
artery
Internal
Post. Communicating carotids
artery

Posterior C.
artery

Basilar C. artery

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CIRCULATION WITHIN THE LOBES OF THE BRAIN IS OFTEN
SUPPLIED BY
MORE THAN ONE CEREBRAL ARTERY
E.g.. ACA and MCA to the frontal lobe

20
Generally, the Anterior Cerebral Artery (ACA) runs between the
left and right hemispheres of the brain within the great
longitudinal fissure.

Longitudinal
fissure

21
 Generally, the Middle Cerebral Artery (MCA) runs on the lateral
side of the 2 hemispheres and portions of the ventral (bottom) side
of the lobes.

22
Generally, the Posterior Cerebral Artery (PCA)
is located on the bottom of the brain.

23
POSTERIOR CEREBRAL ARTERY

Note the ventral location of this artery

24
DEFICITS IN A PATIENT WITH A STROKE CAN BE EXPLANED BY:

1. AREAS OF THE BRAIN

2. CIRCULATION OF THE BRAIN
3. AND/OR A COMBINATION OF BOTH

25
 A STROKE IN
FRONTAL LOBE

BLOOD SUPPLIED
BY ACA AND MCA

THIS PATIENT MAY EXPERIENCE:

• Contralateral paralysis or paresis of face, arm, leg

• Difficulty expressing language “ stuttering, using wrong word,

articulation, repeating word(s)”
(BROCA’SAPHASIA)

• Urinary incontinence

• Personality changes and emotional lability

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FRONTAL LOBE CONTINUED

IMPORTANT STRUCTURES

Controls ability to express language

27
 FRONTAL LOBE CONTINUED
IMPORTANT STRUCTURES

Primary motor strip

Control of muscle movement

28
 “ Homunculus”

DEFINITION : A figurative representation of the body map encoded in the

primary motor cortex ( strip )
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 A STROKE IN
PARIETAL LOBE

BLOOD SUPPLIED BY
ACA, MCA, PCA

THIS PATIENT MAY EXPERIENCE

• Sensory deficit – loss of sensation i.e. pain, pressure, touch

• Neglect – patient does not recognize a body part

• Denial of deficits (often with neglect)

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 PARIETAL LOBE CONTINUED

Parietal lobe

The primary sensory cortex (strip) of the parietal lobe

is arranged in the same topographic scheme
as the motor strip in the frontal lobe. 31
 A STROKE IN
TEMPORAL LOBE

BLOOD SUPPLIED
BY MCA AND PCA

THIS PATIENT MAY EXPERIENCE

• Severe communication problem : loss of comprehension of spoken language

( Receptive Aphasia also called Wernicke’s Aphasia)

• Memory loss or disturbances in memory

• Aggressiveness

32
Note location of Wernicke’s Area

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 A STROKE IN
OCCIPITAL LOBE

BLOOD SUPPLIED BY MCA

AND PCA

THIS PATIENT MAY EXPERIENCE

VISUAL DISTURBANCES
• Types of blindness- total or hemianopsia’s

• Loss of recognition of objects when shown them

• Hallucinations

34
 IF A STROKE IN
CEREBELLUM
BLOOD SUPPLIED BY
VERTEBROBASILAR
ARTERIES

PATIENT MAY EXPERIENCE

• A gait that looks similar to an inebriated person

• Poor balance

• Complaints of dizziness, light headedness, “floating”

35
 BLOOD SUPPLIED BY VERTEBROBASILAR AND PCA

A STROKE IN THE BRAIN STEM

The signs and symptoms depend on the location of the stroke in the 3
areas of the brain stem

Mid brain
Pons
Medulla
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 A STROKE IN THE MEDULLA

• dysphagia
• cardiac, respiratory, blood pressure difficulties
• limb weakness

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 A STROKE IN THE PONS
Respiratory function can be effected and
often this stroke is so severe that
the patient may die.

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Mechanism of Stroke
Feature Hemorrhage Ischemic
Preceding TIA No 30%

Onset With Activity Sedentary

Hypertension Usually Present Often Present

Clinical Course Rapidly Stepwise or

Progressive static
Signs of ICP Present Absent - later

CT Scan Presence of Normal or

blood subtle changes39
Stroke Iskemik
• Terhentinya aliran darah secara tiba tiba ke area di otak
sehingga menyebabkan gangguan neurologis.
• Menurut TOAST :
• Large-artery atherosclerosis
• Cardioembolism
• Small-vessel occlusion
• Stroke of other determined etiology
• Stroke of undetermined etiology

Adam et al., 1993

Stroke Hemoragik
• Stroke hemoragik terjadi jika pembuluh darah arteri di otak
mengalami ruptur atau pecah sehingga menyebabkan
peningkatan tekanan dan kerusakan terhadap sel otak.
• Faktor risiko utama adalah hipertensi, artriovenous
malformation, dan aneurisma.
• Proporsi stroke hemoragik di asia (Jepang dan Cina)
mencapai 38,7% - 39,4%.

Go et al., 2012; Liebenskind, 2015

 Stroke Hemoragik
• Waspada tanda dan gejala perdarahan sub araknoid :
• Nyeri kepala sangat hebat dan akut
• Tanda meningismus dengan kaku kuduk.
• Fotofobia dan nyeri gerak bola mata.
• Mual, muntah.
• Syncope.
• Perdarahan intraventrikel angka kematian
meningkat 2 kali lipat

Go et al., 2012; Liebenskind, 2015; Liebenskind, 2014

 Transient Ischemic Attack
(TIA)
• Serangan stroke dengan tanda dan gejala menghilang dalam
24 jam ≈ Mini Stroke.
• Penanganan ≈ stroke.
• ± 15 % stroke iskemik diawali dengan klinis TIA.

Risiko
stroke
5% 8% 12 % 17 %
Pada 48 Pada 1 pada 1 Pada 3
pasca TIA jam minggu bulan bulan
 Tanda dan Gejala

• Kelemahan lengan 77% • Gangguan sensorik 33 %

• Depresi 33 %
• Kelemahan tungkai 72 %
• Gangguan BAB 33 %
• Gangguan visual 60 %
• Neglect 28 %
• Kelemahan wajah 54 % • Gangguan kognitif 20 %
• Gangguan artikulasi 50 % • Penurunan kesadaran 19 %
• Gangguan BAK 45 % • Sakit kepala hebat 17 %
• Gangguan menelan 45 % • Dizziness 9%
• Afasia 33 %

Lawrance et al., 2001; Rowe, 2015; Engelter et al., 2016; Lerdal et al.,
2011; Leys et al., 2005
SEnyum GErakan bicaRA SEGERA !!
 Otak Kiri Otak Kanan
Logika Feeling
Orientasi detail Orientasi global
Fakta/realitas Imaginasi /fantasi
Kata dan bahasa Gambar dan simbol
Masa kini dan masa lalu Masa kini dan masa depan
Kalkulasi dan pengetahuan Filosofi dan religius
Persepsi pola Persepsi spasial
Nama objek Fungsi objek
Menyusun strategi/analitikal Kesempatan saat ini/kreatif
“Cari aman” Mengambil risiko
Mengerjakan secara urut Mengerjakan secara acak
 Atherosclerosis
From risk factors to endothelial injury & CVD

LDL-C BP Risk factors Diabetes Smoking Cardiac failure

Oxidative stress

Endothelial dysfunction

NO Local mediators Tissue ACE-Ang II

Endothelium Collagen growth Proteinolysis

PAI-1 VCAM,ICAM, cytokines
factors

Vascular injury &

Thrombosis Inflammation Vasocontraction Plaque rupture
remodeling

Adhesion molecules
CV Clinical events
VCAM: vascular cell adhesion molecule,
ICAM: intercellular adhesion molecule
PAI-1: plasminogen activator inhibitor 1
Gibbons GH. N Engl J Med 1994
 Normal Arterial Wall
(intima, Media, Adventitia)

Intima:
Endothelium
Internal elastic laminae

Media:
Smooth muscle cell
Lumen
Collagen proteins

External elastic laminae

Endothelial dysfunction in atherosclerosis
(Early changes)

up-regulation of endothelial
adhesion molecules

Leucocyte migration into the arterial wall

Penetration of lipoproteins

greater permeability of the

endothelium

Leucocyte adhesion
Lipid core formation (fatty streak)
in atherosclerosis

Platelets’ adhesion and coagulation

Migration of smooth muscle cells

Foam cells formation

T cells activation

Adhesion and penetration of

leucocytes
Formation of atherosclerotic plaque
(death & rupture of foam cells in fatty streak)

Formation of necrotic core

Accumulation of macrophages

Formation of fibrous cap

Rupture of plaque and thrombus formation (supsequent luminal
occlusion)

Intravascular thrombus

Lipid layer

Thrombus inside the plaque

 Progression of atherosclerosis
Threshold
Decades Years-Months Months-Days
Healthy Subclinical Symptomatic

Intima
Lumen
Media

Plaque

Threshold

Thrombus
Intima
Lumen
Media

Plaque

HEALTH POLICY PRIMARY PREVENTION SECONDARY PREVENTION

Diet and lifestyle changes Drug treatment Aggressive drug therapy
Pathophysiology of Stroke

Brain injury
Due to:

• Vascular occlusion or hemodynamic disturbances from intracranial or extracranial

vascular injury (stenosis, splitting, vasculitis)

• Interruption of cerebral blood flow

• Neuronic death (infarct) when self regulation of blood flow and collateral
circulation are insufficient

Results to:
• Functional body disorders which are controlled by the damaged part of the brain
 Pathophysiology of ischemic stroke
Neuronal disturbances
• Decreased energy supply to the cerebral
parenchyma with simultaneous decrease in Ο2,
Glucose and ATP production (25% of normal levels in
the central area, 50-70% in Penumbra)
• Anaerobic glycolysis and metabolic acidosis
• Release of excitative aminoacids (glutamino-acid)
and inflammatory mediators in extracellular space,
decreased energy production, ions and water
intracellular entrance, increase of catabolic enzymes
and free radicals,
• neuron cells oedema, cellular membrane injury and
cytolysis
• Disturbance of regional blood flow autoregulation
(regional vasodilation) and as a consequence it’s
absolute dependency from systemic BP (thus
when BP reduces, ischemia worsens)
• Angiogenic oedema around the ischemic area
because of blood-brain barrier destruction
(endothelial cell connections, 1-4 days after
ischemia), may cause compressive effect and
necrotic area expansion
 Pathophysiology of ischemic stroke
• Large hemispheric strokes (10-20% in the total of ischemic strokes) are due to middle
cerebral artery occlusion

• Several mechanisms contribute to ischemic stroke evolution, the main being the clot
expansion

•Other possible mechanisms during the first 48-72 h after ischemic stroke initiation are:

- cerebral oedema development and space occupational action,

- metabolic disturbances like hyperglycemia, hyponatremia,
- hemorrhagic transformation,
- fever (infection) aggravating ischemic neuron metabolism
 B
Normal A

C
 Ischemic infarct: Frequently, up to 50%, there is delay in CT
imaging within 48 h

“Normal CT” at admission of an Large infarct in the area of middle brain artery
ischemic stroke with left hemiparesis| causing compressive effect, 48h after admission
 Hemorrhagic Stroke

Admission CT of hemorrhagic stroke with Subdense appearance and severe compressive effect of
left hemiparesis and persistent headacne extented oedema around hematoma, 48h after admission
Tatalaksana Stroke iskemik
• Head up 300
• Mobilisasi bertahap jika hemodinamik stabil
• 02 1-2 lpm
• Pasang NGT untuk pemberian nutrisi
• Berikan cairan kristaloid 1500-2000 cc hindari
pemberian dekstrose dan salin
• Pantau kadar glukosa
• Nyeri kepala atau mual diberikan obat sesuai
kebutuhan,berikan anti hipertensi jika td
>220/120mmhg (pada 2x pengkuran selam 30 mnt/
pada gagal jantung kongestif, gagal ginjal dan infark
miokard akut)
Obat yang anti hipertensi direkomendasikan utk stroke
iskemik:
• Alfa bloker (terazosin,dexazosin)
• calcium chanel bloker (amlpdipin,diltiazem,nifedipin)
• ACE inhibitor (Captopril,lisinopril)
• Jika terjadi hipotensi (td <90/70mmhg) berikan NaCL
0.9% 250 cc selama 1 jam dilanjutkan 500cc selama 4
jam dan 500 cc selama 8 jam sampai target td minimal
tercapai jika belum berikan dopamin 2-20
ug/kgbb/menit sampai td >110mmhg
• Penurunan TD max 20%
Lanjt…
• jika kejang beri diazepam 5-20 mg iv pelan-pelan
selama 3 menit (max 100mg/hari) dilanjutkan
antikonvulsan p.o (fenitoin /karbamazepin). Jika
kejang mucul setelah 2 minggu beri antikonvulsan
jangka panjang.
• Jika terjadi peningkatan TIK berikan bolus manitol
iv 0,25-1 gr/kgbb/30 menit, jika dicurigai fenomena
rebound berikan 0,25 kg/bb selama 30 menit dalam
6 jam selama 3-5 hari. (sebagai alternatif dapat
diberika furosemid dan larutan hipertonik NaCL .
Tatalaksana stroke hemorhagik
• Harus dirawat di ICU jika volume hematoma >30ml,
perdarahan interventrikuler dengan hidrosefalus
dan KU yang memburuk.
• Terapi lain sama dengan stroke iskemik
• jika terjadi pngktn as.lambung : Antagonis H2
(ranitidin iv) ,PPI (OMZ iv),citoprotektor (sucralfate
syr).
• Jika ada komplikasi saluran nafas berikan antibiotik
broad spectrum (ceftriaxone/cefotaksim Inj)
Lanjt…
• Neuroprotektor kecuali yang bersifat vasodilator
• Tindakan bedah dengan pertimbangan: usia dan lokasi
perdarahan, pasien dengan KU kian buruk, perdarahan
serebelum >3 cm3, perdarahan lobaris, dan tanda
peningkatan TIK (Hipertensi, bradikardia,papil
edema,nyeri kepala, muntah proyektil).
• Perdarahan interventrikel disertai hidrosefalus : Vp-
Shunting
• Pada perdarahan subaraknoid : antagonis kalsium
(nimodipin), tindakan bedah (ligasi,ekstirpasi atau
gamma knife jika penyebabnya AVM (artery vena
malformation).
Lanjt…
Terapi lain :
• Fisioterapi
• Bladder training
• Terapi terhadap komplikasi
• Edukasi
Awareness (kesadaran)

• Stroke dapat terjadi pada semua orang dan usia.

• Kenali gejala stroke sebagai keadaan gawat darurat.
• Penyebab no 1 kecacatan, penyebab no 2 kematian.
• Stroke dapat diterapi.

Feigin et al.,
2015
Access (Ketersediaan)

• Kenali gejala stroke ------ segera ke rumah sakit.

• Akses perawatan unit stroke perbaikan 14 %
• Akses terapi trombolisis perbaikan 30 %
• Akses terapi “clot retrieval” perbaikan 50 %
• Akses rehabilitasi
• Akses pencegahan sekunder
Action (kepedulian)
• Bagikan informasi tentang gejala dini stroke.
• Kenali gejala stroke ------ segera ke rumah sakit.
• Tugas bersama tenaga medis dan masyarakat,
Thank you for your attention!