Dr. Takdir Setiawan MSc, Sp.

S


Bagian Saraf
RSUD Ambarawa
Kab. Semarang

2
Definisi Stroke
Stroke adalah gangguan fungsional otak fokal
maupun global yang terjadi secara akut, berasal dari
gangguan aliran darah otak. Termasuk di sini
perdarahan subarachnoid, perdarahan intraserebral
dan iskemik atau infark serebri. Tidak termasuk disini
gangguan peredaran darah otak sepintas, tumor otak,
infeksi atau stroke sekunder karena trauma (WHO,
1986)
3
4
Risk Factors for Stroke
Non-Modifiable
Risk Factors for Stroke
Age
Sex
Race/ethnicity
Family history

Modifiable Risk Factors for
Stroke
6

Hypertension
Diabetes
Smoking
Hyperlipidemia
Carotid stenosis
Atrial fibrillation
5
Perbedaan klinis
Anamnesis
Gejala Perdarahan Infark
Onset
Saat onset
Warning
Nyeri Kepala
Kejang
Muntah
Kesadaran
Mendadak
Sedang aktif
- -
+ + +
+
+
+ + +
Mendadak
Istirahat
+ + (TIA)
+/-
-
-
+/-
6
Perbedaan klinis
Tanda-tanda
Tanda-tanda Perdarahan Infark
Bradikardi
Udem papil
Kaku kuduk
Tanda
Kernig
Brudzinski
++(dari
permulaan)
sering +
+
+++
+++
+/-
-
-
-
-
7
SCORE SIRIRAJ
S= kesadaran
0=CM
1= somnolen
2= sopor/koma
M= Muntah
0=tidak ada
1= ada
N= nyeri kepala
0= tidak ada
1= ada
D= Diastolik
A=Ateroma
0= tidak ada
1=salahsatu atau lebih: DM, angina,
penyakit pembuluh darah

Score SSS >1:
perdarahan
supratentorial
Score SSS< -1: Infark
serebri
Score SSS -1 s/d 1:
meragukan
(2,5xS)+ (2xM)+ (2xN)+ (0,1D)- (3xA)- 12
PERBEDAAN STROKE
HEMORAGIK DAN ISKEMIK
VARI ABEL PI S PSA TROMBOSI S EMBOLI
Usia 40-60 Tidak tentu 40-70 Semua umur
Onset Akut (dtk/mnt) Akut (mnt/jam) Bertahap Akut
Saat Aktiitas Aktivitas Bangun tidur Tidak tentu
Sakit kepala ++ ++++ - -
Muntah ++ ++++ - -
Prodromal - - TI A+++ -
Kesadaran/Hernia
si Otak
Cepat koma Variasi dapat
koma/normal
Normal/ ringan
hari ke 3-5
Normal/sedang
hari 3-5
Kaku Kuduk ++jarang ++++selalu - -
Kelumpuhan Cepat hemiplegi
(mnt/jam)
Variasi Bertahap Mendadak berat
Afasia/Tanda
Kortikal
- - Sering Sering
Arterial Sindrom - Kadang Selalu Selalu
Kejang/Rigiditas Sering+++ Kadang++ J arang Kadang
PERBEDAAN STROKE HEMORAGI K DAN I SKEMI K
VARI ABEL PI S PSA TROMBOSI S EMBOLI
Reflek Patologis Segera Variasi Lambat Lambat
Hipertensi Selalu + Variasi Kadang
N/Hipotensi
J arang
J antung Hipertrofi LV Variasi N Aritmia, AF,
I nfark miokard,
asma kardial,
angina pektoris
Riwayat Hipertensi - Hipotensi/
Diabetes/
Dehidrasi
LP/LCS N/darah++ Darah++++ J ernih J ernih
Bruit Arteri - - - Sering
X Foto Shift pineal++ - Calcifikasi -
CT scan Hiperderns Hiperderns Hipoderns Hipodens
Optalmoskop Retinopati HT Sub hyaloid Silver wire N
Arteriografi Shift Aneurisma,
AVM
Oklusi/stenosis Oklusi/ stenosis
Doppler N N Aliran lambat Aliran lambat
Hematology N N Hematokrit/
Diabetes/
hiperlipidemia
N
Kejadiannya antara : 70-85%
Klasifikasi :
Stroke iskemik
1. TIA (transient ischemic attack) : < 24 jam
2. RIND (Reversible Ischemic Neurological Deficits)
normal antara 7 hari s/d < 3 minggu
3. Stroke in evolution : stroke semakin berat
4. Stroke complete : defisit neurologis menetap

-
Apoptotic
Cell Death
Necrotic
Cell Death
Ischemic
Injury
Aterosklerosis merupakan respon normal
terjadinya injury pada sel endotel arteri
Proses pembentukan plak aterosklerotik
berlangsung lama, mulai usia dini sampai lanjut
Manisfestasi klinisnya terjadi secara akut dan
cenderung pada satu waktu akibat hancur /
terlepasnya plak secara tiba-tiba.
1. Vaskuler : Proses aterosklerosis
2. Perubahan biokimia / kimia seluler
Ada 2 proses pada stroke iskemik :
Multiple faktor risiko Aterotrombosis
MI, myocardial infarction.
Adapted from Yusuf S, et al. Circulation. 2001;104:2746-2753.
Drouet L. Cerebrovasc Dis. 2002;13(suppl 1):1-6.
Lifestyle
Smoking
Diet
Lack of exercise
Genetic Traits
Gender
PlA2
Generalized
Disorders
Age
Obesity
Systemic
Conditions
Hypertension
Hyperlipidemia
Diabetes
Hypercoagulable
states
Homocysteinemia
Atherothrombotic
Manifestations
(MI, stroke,
vascular death)
Inflammation
Elevated CRP
CD40 Ligand, IL-6
Prothrombotic factors (F I and II)
Fibrinogen
Local Factors
Blood flow patterns
Shear stress
Vessel diameter
Arterial wall structure
% arterial stenosis
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Pembentukan Plak Aterosklerotik
1. Akumulasi lipoprotein pd tunika
intima
2. Stres oksidatif
3. Aktivasi Citokine 4. Penetrasi Monocyte
5. Migrasi makrofag foam cell 6. Muscle Cell Smooth
7. Akumulasi matriks ekstraseluler 8. Kalsifikasi dan
fibrosis
Penyebab sumbatan
Sumbatan aliran darah oleh ateroma, emboli, trombus
(Aterosklerosis)
A small clot may break off from a larger thrombus and be carried to other places
in the bloodstream. When the embolus reaches an artery too narrow to pass
through and becomes lodged, blood flow distal to the fragment ceases, resulting
in infarction of distal brain tissue due to lack of nutrients and oxygen.
As a cause of stroke, embolism accounts for approximately 32% of cases.
Cerebral Embolism Formation
HCT Scan Stroke Infark
Cerebral Infarct - 1 Week
Cerebral Infarct - 2 Weeks
Brain: Haemorrhagic infarct.
22
Oleh karena ruptur aneurisma, angioma, lesi
aterosklerotik
23
Definition (ICH) :
Intracerebral
hemorrhage (ICH)
results from the
rupture of an
intracerebral vessel
leading to the
development of a
hematoma in the
substance of the
brain.
HYPERTENSION
OTHER
AV-MALFORMATION
ANEURYSM
Other causes: bleeding into tumor, hypocoagulable state,
hemorrhagic infarction, iatrogenic, and trauma
INTRACEREBRAL HEMORRHAGE
NON TRAUMATIC
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Primary and Secondary
Causes of Intracerebral Hemorrhage
Primary Secondary
Hypertension
Amyloid angiopathy

Aneurysms
Arteriovenous
malformations
Neoplasms
Trauma
Anticoagulation
Use of thrombolytics
Hemorrhagic conversion
of ischemic stroke

Angiopati Amiloid Serebral
Penyebab tersering ketiga perdarahan
intraserebral setelah hipertensi arterial dan
aneurisma adalah angiopati amiloid, yaitu
sekitar 10% dari seluruh perdarahan
intraserebral spontan. Kelainan angiopati
amiloid ini khas yaitu terbentuknya deposit
fibril amiloid pada tunika media dan tunika
intima pada arteria kecil dan sedang.
Perdarahan terjadi akibat robeknya dinding
pembuluh yang lemah atau mikroaneurisma
(Kazui et al., 1997; Qureshi et al., 2001).
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Klasifikasi
Perdarahan Subarakhnoid
Perdarahan Intraserebral
Perdarahan intrakranial non spesifik dan
yang lain misalnya perdarahan ekstradural
atau epidural non traumatik; perdarahan atau
hematoma subdural non traumatik dan
perdarahan intrakranial nonspesifik
WHO ICD-NA, 1987
INTRACEREBRAL HEMORRHAGE
Intraventricular Hemorrhage:
HCTS
10/ 9/07
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Gejala Klinis
Onset sewaktu aktivitas
Penurunan kesadaran, 2/3 koma
Nyeri kepala dan muntah sebagai tanda
peningkatan TIK
Kejang jarang
32
Anamnesis
History
Onset:
usually during daytime activity, with progressive (ie,
minute to hours) development:
Alteration in level of consciousness (appr 50%)
Nausea and vomiting (appr 40-50%)
Headache (appr 40%
Seizure (appr 6-7%)
Focal neurological deficit
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Px Fisik
Physical: Clinical manifestations of ICH are determined
by the size and location of hemorrhage, but may include
the following:
Hypertension, fever, or cardiac arrhythmia
Nuchal rigidity
Subhyaloid retinal hemorrhages
Altered level of consciousness
Anisocoria
Focal neurological deficits
34
Imaging studies
CT scan
Hyperdense signal intensity
Hematoma volume (cc)
Perihematomal edema and displacement of tissue
with herniation
MRI
Vessel imaging
CT angiography: AVMs, vasculitis, and other
arteriopathies
MR angiography
35
S A H
Subarachnoid Hemorrhage:
37
Tanda & gejala SAH
Nyeri kepala berat, acut
Penurunan kesadaran sementara/lama
Kejang
Nausea & vomitus
Defisit neurologic focal (hemiparese,disfasia)
Funduscopi : papiledema/vitreous haemorrhage
Reactive hypertension
Pyrexia
Meningismus
(Lindsay,1997)

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Penggolongan SAH
Derajat I :
asimtomatik/sakit kepala minimal/kaku kuduk
Derajat II :
hanya sakit kepala lebih hebat dan kaku kuduk
Derajat III :
Mengantuk/bingung, mungkin dengan hemiparesis ringan
Derajat IV :
Stupor dalam, mungkin disertai hemiparesis sedang-berat,
Reaksi awal deserebrasi
Derajat V :
Koma Dalam
Hunt dan Hess
Greenberg,2001
SAH The case you could miss
(Sokransky 2001)
Well-appearing patient
with previous
headaches

Presents with a
sudden headache that
is now better
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Cerebral vasospasm

42
Haemorrhage
Increase
Intracranial press
Influks Ca
+

Necrosis
Neuron
Global ischemic
Release
Vasoconstrictor agen
Effects of blood
toxic
Influks Ca
+

Vasospasme
Focal Ischemic
Serotonin, Prostaglandin,
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Vasospasme Process on Haemorrhage
vasoconstrictor agens & blood componen release
Influks Ca
+

smooth muscle
vasculer
stronge
Vasospasme

Ischemic + deficit neurologic
Lumen
vasculer
Vasospasme
What is cerebral vasospasm?
Classically described based on the
angiographic appearance of narrowed
arteries in one of several settings:
Subarachnoid hemorrhage (usually, but not
always, aneurysmal SAH)
SAH from other causes seems less likely to be
associated with arterial narrowing
Ruptured AVM causing SAH
Perimesencephalic SAH
Traumatic SAH
45
Insuffisiensi brain function which suplaied by
vasospasm artery
Local vasospasm around hematome at intact
arteri (unrupture)
Probable local vasospasm around central of
haemorrhage change into diffuse vasospasm

Effects of Vasospasme
Cerebral Blood Flow
Regional cerebral blood flow in health people :50-
70 mL/min per 100 mg
Symptoms of cerebral ischemia: < 20 mL/min
per 100 mg
Structure damage and neuronal death: flow <
15mL/min per 100 mg

NEUROPROTEKTAN
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Citicholine
Mechanism (neuronal)
Increase choline formation and alter degradation phosphatydilcholine
Increase glucose uptake, asetilkholine, prevention lipid radical
Increase glutation
Decrease lipid peroxida
Na/K ATPase modulation
Mechanism (vascular)
Increase CBF
Increase O2 consumtion
Decrease vasculer resistance

(Perdossi, 2004)
49
Piracetam
Mechanism (neuronal)
Repair cell membran fluidity
Repair neurotransmission
Stimulation adenylate kinase
Mechanism (vascular)
Increase eritrocyte deformability
Decrease platelet hyperagregation
Repair microcirculation

(Perdossi, 2004)
Mekanisme Kerja Ganda Piracetam
Piracetam

mengurangi alir masuk Kalsium yang tidak normal ke dalam neuron & sel otot
polos pembuluh darah. Oleh karena itu, Piracetam

mempengaruhi sistem saraf dan sistem
serebrovaskuler, dimana Piracetam memiliki efek sitoprotektif dan fungsional
Melindungi Sel Memperbaiki Fungsi
Jaringan
Neuron
Piracetam
Jaringan
Serebrovaskuler
Meningkatkan Aliran Darah
Otak
Efek Sitoprotektif Dalam
Pembuluh Darah Otak
HIPERTENSI
Hipertensi
Hipertensi
Akut
Kronis
Pemb.drh kecil Spasme
Ensefalopati
hipertensif
Pemb drh kecil
Pemb drh sedang
Lipohialinosis
Mikro
aneurisma
Trombosis
PIS
Infark
lakunar
Aterosklerosis
TIA,trombosis,
Emboli serebri
Faktor resiko lain
DM,hiperlipidemi
pecah
MANAJEMEN
54
Management
Medical Management
Surgical Management
55
Tatalaksana Perdarahan Intraserebral
1. Pencegahan & penanganan tekanan intrakranial yg
meningkat :
- mengatur posisi kepala penderita
- osmoterapi
- hiperventilasi yang dpt dilaksanakan sesuai fasilitas &
kondisi penderita
2. Mengontrol peningkatan tekanan darah
3. Mencari dan mengobati penyebab
4. Pemberian neuroprotektan
5. Tindakan pembedahan
6. Pencegahan dan penanganan komplikasi sistemik
56
Management
In emergency Room
ABC rules
BP continuous monitoring
Continuous ECG monitoring
O2 pulse oxymetry
2 IV lines (norma saline only)
Blood (CBC, SMAC, RBS, PTT, INR)
Save 6 ml of blood
Facilitate transfer to the operating room or ICU

57
57
Hasil optimal terapi Stroke perdarahan
sampai 96 jam setelah onset
Puncak vasospasme antara hari ke 5-10)

58
58
Acute stroke care-General management (Ischemic
Stroke)
The mainstay of acute treatment (A,B,C)
Treatment and stabilisation of general condition
Specific therapy
Recanalisation of a vessel occlusion
Preventive of mecanism leading to neuronal death in
the ischhemic brain
Early secondary prevention
Early rehabilitation
Prophylaxis and treatment of complications

(Lamsudin, 2004)
59
59
Blood pressure
There are adequately sized randomized , controlled
study guiding BP mangement
Elevated BP (sistolic>200mmHg or diastolic
>110mmHg0 may tolerated in the acute phase
Avoid and treat hypotension or drastic reduction BP
BP may be lowered if cardiac condition require it
Acute stroke care-General management
(Lamsudin, 2004)
60
60
Blood pressure (BP)
Indications for immediate AH therapy in acute
stroke
Intracerebral haemorrhage
Cardic failure
Acute coronary syndrome
Aortic dissection
Hypertensive enchephalophaty

Acute stroke care-General management
(Lamsudin, 2004)
61
MEDICAL MANAGEMENT OF ICH
(Pouratian 2003)
Cardiopulmonary optimization ( Airway, Breathing, Circulation,skin,
seizures)
Reversing coagulation defects (coagulopathies and platelet disorders)
Blood pressure control (Labetolol & nicardipine IV, nitroprusside not
often used brain edema).
ICP reduction:
- Ventriculostomy as therapeutic means of reducing ICP
- Head-of-bed elevated at 30
0
, patients neck in neutral position
maximize venous outflow.
- Minimize agitation: sedatives
- Hyperosmolar fluids (mannitol, hypertonic saline)
- Hyperventilation used only as temporary measures
- Barbiturate-induced coma : rarely
- Vasogenic edema with mass effect: corticosteroids (controversial)
Ultra-early hemostatic therapy:
- Antifibrinolytic tranexamic acid, aprotinin, activated recombinant
factor VII (rFVIIa)
BLOOD PRESSURE MANAGEMENT
IN ICH (Broderick 1999)
- If SBP > 230 mm Hg or DBP > 140 mm Hg on 2 readings 5
minutes apart nitroprusside 0.5-10 g/kg/min.
- If SBP is 180-230 mm Hg, DBP 105-140 mm Hg, or mean
arterial BP 130 mm Hg on 2 readings 20 minutes apart
labetolol, esmolol, enalapril, or other smaller doses of
titrabble IV medications eg diltiazem, lisinopril, or verapamil.
- If SBP is < 180 mm Hg and DBP < 105 mm Hg, defer
antihypertensive therapy.
- If ICP monitoring is available, cerebral perfusion pressure
should be kept at > 70 mm Hg.

Labetolol: 5-100 mg/h by intermittent bolus doses of 10-40 mg or continuous drip (2-8 mg/min).
Esmolol: 500 g/kg as a load, maintenance use, 50-200 g/kg/min.
Hydralazine: 10-20 mg Q 4-6 h
Enalapril: 0.625-1.2 mg Q 6 h as needed.
MANAGEMENT OF ELEVATED
ICP (Broderick 1999)
Osmotherapy:
- Mannitol 20% (0.25-0.5 g/kg every 4 h), for only 5 d.
- Furosemide (10 mg Q 2-8 h) simultaneously with mannitol.
- Serum osmolality 310 mOsm/L, measured 2 X daily.
No steroid
Hyperventilation:
- Reduction of pCO2 to 35-30 mm Hg, by raising ventilation rate
at constant tidal volume (12-14 mL/kg), lowers ICP 25%-30%.
Muscle relaxants:
- Neuromuscular paralysis in combination with adequate
sedation can reduce elevated ICP.
- Vecuronium or pancuronium, with only minor histamine
liberation and ganglion-blocking effects are preferred.
Pemilihan terapi untuk Stroke
Pemilihan cairan sebaiknya berdasarkan atas status
hidrasi pasien, konsentrasi elektrolit,dan kelainan
metabolik yang ada
The American Heart Association sudah menganjurkan
normal saline 50 ml/jam selama jam-jam pertama dari
stroke iskemik akut. Metabolisme anaerobik yang
dipicu oleh iskemia mengakibatkan asidosis laktat dan
meninggikan PCO2 jaringan(tidak harus asidosis laktat
sistemik),hal inilah yang menyebabkan banyak dokter
enggan memakai RL selama fase akut stroke, kedua
osmolaritas RL 273 dianggap hipotonik bila dibanding
plasma (normal 285 + 5 mOsm/L)
Iyan Darmawan,md 2008
Pemilhan terapi cairan untuk stroke
Ringer asetat (acetad ringer)
Merupakan alternative yang lebih baik dari pada ringer laktat
dan normal saline .RL dan AR berbeda pada sumber bikarbonat
LR mengandung 28 mmol laktat per liter sedangkan AR 28
mmol asetat. Berbeda dengan laktat, yang metabolismenya
terjadi terutama di dalam hati, asetat dimetabolisme terbanyak
dalam otot dan sebagian kecil dalam ginjal dan jantung.

ANTI HT
Blood Pressure (BP) Management Protocol
in Acute Stroke
Antihypertensive treatment should await the
spontaneous decline in BP (within 1
st
to
10
th
days). If increased BP persist after 7-
10 days, start treatment.
Patients already on antihypertensive
medication prior to stroke, drugs should
be held or reduced for 7-10 days (except
B-blockers, should be gradually over 5-6
days)
Treat If:
1. BP is > 220/140 or MAP >130 mmHg
2. Malignant or hypertensive encephalopathy
3. Acute MI
4. Aortic dissection is suspected
5. BP is >180/100 and patient is for thrombolytic
therapy
6. 24 hours following thrombolytic therapy
(>185/110)
Blood Pressure (BP) Management Protocol in
Acute Stroke
The Following medications can be used, if needed:
Esmolol bolus (500 ug/kg IV)
Esmolol infusion (50-150 ug/kg/min) IV, (Body weight x 60 mg of
esmolol diluted in 100 ml of saline, in a rate of 5-15 ml/hour)
Labetalol infusion (15-35 ug/kg/ml) IV, (Body weight x 6 mg of
labetalol diluted in 100 ml of saline, in a rate of 15-35 ml/hour)
Labetalol 100-200 mg bid-tid. PO
Analaprilat 1,25-5 mg IV, 6 hourly
Lasix 20-40 mg iv tid-qid
Nicardipin 5 mg/hour IV
Clonidine 150-300 mg iv bolus (maximum of 750 mg per day)
Sodium nitroprusside 0,25-0,5 mg/kg/min
Avoid the use of calcium channel blockers and
sodium nitropusside as possible
Blood Pressure (BP) Management Protocol in
Acute Stroke
70
Guidelines for treating elevating Blood
Pressure in ICH (1)
1. If SBP is > 200mmHg or MAP >150mmHg, then
consider aggressive reduction of blood pressure with
intravenous infusion, with frequent blood presure
monitoring every 5 minutes.
2. If SBP is > 180mmHg or MAP > 130mmHg and there
is evidence of or suspicion of elevated ICP, then
consider monitoring ICP and reducing blood
pressure using intermittent or continuous
intravenous medications to keep cerebral blood flow
>60 to 80 mmHg

71
3. If SBP is > 180 mmHg or MAP > 130mmHg and there
is no evidence of or suspicion of elevated ICP, then
consider a modest reduction of blood pressure (eg,
MAP of 110 mmHg or target blood pressure of
160/90mmHg) using intrmittent or continuous
intravenous medications to control blood pressure,
and clinically reexamine the patient every 15 minutes.
Guidelines for treating elevating Blood
Pressure in ICH (2)
72
Pembedahan
Bukan tindakan rutin
GCS 7-10
Pemulihan fungsional tetap jelek
Dilakukan bila gagal mengendalikan
peningkatan TIK
Perdarahan serebeler sering dilakukan
pembedahan
73
Rekomendasi pembedahan pada perdarahan
intraserebral
(konsensus Nasional Pengelolaan Stroke di Indonesia)
Kandidat yang tidak dioperasi
1. Perdarahan dengan volume <10 cm
3
atau dgn defisit neurologis yg
minimal tidak dilakukan tindakan pembedahan
2. GCS <4. Tetapi penderita dgn GCS<4 dgn perdarahan serebelum dan
kompresi batang otak adalah kandidat operasi pada beberapa kasus

Kandidat yang dioperasi
1. Perdarahan serebelum dgn diameter >3 cm dgn deteriosasi atau
mengalami kompresi batang otak dan hidrosefalus akibat obstruksi
ventrikel
2. Perdarahan intraserebral karena lesi struktural (aneurisma, malformasi
arteriovenosa, angioma kavernosa, jika lesi terjangkau
3. Perdarahan lobar > 60 cm
3
dengan tanda-tanda peninggian tekanan
intrakranial akut dan ancaman herniasi