Dr. Takdir Setiawan MSc, Sp.

Bagian Saraf
RSUD Ambarawa
Kab. Semarang
 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)

2
3
 Risk Factors for Stroke

Non-Modifiable
Risk Factors for Stroke Modifiable Risk Factors for
•Age Stroke6
•Sex •
Hypertension
•Race/ethnicity
•Family history
•
Diabetes
•
Smoking
•
Hyperlipidemia
•
Carotid stenosis
•
Atrial fibrillation

4
 Perbedaan klinis
•
Anamnesis
Gejala Perdarahan Infark

•
Onset •
Mendadak •
Mendadak
•
Saat “onset” •
Sedang aktif •
Istirahat
•
Warning •
-- •
+ + (TIA)
•
Nyeri Kepala •
+++ •
+/-
•
Kejang •
+ •
-
•
Muntah •
+ •
-
•
Kesadaran •
+++ •
+/- 5
 Perbedaan klinis
•
Tanda-tanda

Tanda-tanda Perdarahan Infark

•
Bradikardi •
++(dari •
+/-
permulaan)
•
Udem papil •
-
•
sering +
•
Kaku kuduk •
-
•
+
•
Tanda Kernig •
-
•
+++
•
Brudzinski •
-
•
+++
6
 SCORE SIRIRAJ
(2,5xS)+ (2xM)+ (2xN)+ (0,1D)- (3xA)- 12
S= kesadaran
•
0=CM
•
1= somnolen
2= sopor/koma
•
Score SSS >1:
perdarahan
•

M= Muntah
•
0=tidak ada supratentorial
•
1= ada
N= nyeri kepala
•
Score SSS< -1: Infark
•

•
0= tidak ada
1= ada
serebri
D= Diastolik •
Score SSS -1 s/d 1:
A=Ateroma
•
0= tidak ada meragukan
•
1=salahsatu atau lebih: DM, angina,
penyakit pembuluh darah

7
 PERBEDAAN STROKE
HEMORAGIK DAN ISKEMIK

VARIABEL PIS PSA TROMBOSIS 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 - - TIA+++ -
Kesadaran/ Cepat koma Variasi dapat Normal/ ringan Normal/sedang
Herniasi Otak koma/normal hari ke 3-5 hari 3-5
Kaku Kuduk ++ jarang ++++ selalu - -
Kelumpuhan Cepat hemiplegi Variasi Bertahap Mendadak berat
(mnt/jam)
Afasia/Tanda - - Sering Sering
Kortikal
Arterial Sindrom - Kadang Selalu Selalu
Kejang/Rigiditas Sering+++ Kadang++ Jarang Kadang
 PERBEDAAN STROKE HEMORAGIK DAN ISKEMIK
VARIABEL PIS PSA TROMBOSIS EMBOLI
Reflek Patologis Segera Variasi Lambat Lambat

Hipertensi Selalu + Variasi Kadang Jarang

N/Hipotensi
Jantung Hipertrofi LV Variasi N Aritmia, AF,
Infark miokard,
Riwayat Hipertensi - Hipotensi/
asma kardial,
Diabetes/
angina pektoris
Dehidrasi
LP/LCS N/darah++ Darah++++ Jernih Jernih
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, Oklusi/stenosis Oklusi/ stenosis
AVM
Doppler N N Aliran lambat Aliran lambat
Hematology N N Hematokrit/ N
Diabetes/
hiperlipidemia
 Stroke iskemik
 Kejadiannya antara : 70-85%
 Klasifikasi :

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
 Ischemic
Injury
Apoptotic
Cell Death
Necrotic
Cell Death

-
Ada 2 proses pada stroke iskemik :
1. Vaskuler : Proses aterosklerosis
2. Perubahan biokimia / kimia seluler

 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.
 Multiple faktor risiko Aterotrombosis

Generalized Lifestyle
Disorders • Smoking
• Age • Diet
• Obesity • Lack of exercise

Systemic
Conditions
• Hypertension
Genetic Traits Atherothrombotic • Hyperlipidemia
• Gender Manifestations • Diabetes
• PlA2 • Hypercoagulable
(MI, stroke, states
vascular death) • Homocysteinemia

Inflammation
Local Factors
• Elevated CRP
• Blood flow patterns
• CD40 Ligand, IL-6
• Shear stress
• Prothrombotic factors (F I and II) • Vessel diameter
• Fibrinogen • Arterial wall structure
• % arterial stenosis
MI, myocardial infarction.
Adapted from Yusuf S, et al. Circulation. 2001;104:2746-2753.
Drouet L. Cerebrovasc Dis. 2002;13(suppl 1):1-6.
 Pembentukan Plak Aterosklerotik
1. Akumulasi lipoprotein pd 2. Stres oksidatif
tunika intima
3. Aktivasi Citokine 4. Penetrasi
Monocyte
5. Migrasi makrofag  foam 6.Muscle Cell
cell Smooth
7. Akumulasi matriks 8. Kalsifikasi dan
ekstraseluler fibrosis

15
Penyebab sumbatan

Sumbatan aliran darah oleh ateroma, emboli, trombus

(Aterosklerosis)
 Cerebral Embolism Formation

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.
HCT Scan Stroke Infark
Cerebral Infarct - 1 Week
Cerebral Infarct - 2 Weeks
Brain: Haemorrhagic infarct.
Oleh karena ruptur aneurisma, angioma, lesi aterosk
lerotik

22
 Definition (ICH) :
•
Intracerebral hemorr
hage (ICH) results fro
m the rupture of an in
tracerebral vessel lea
ding to the developm
ent of a hematoma in
the substance of the
brain.

23
 INTRACEREBRAL HEMORRHAGE
NON TRAUMATIC

HYPERTENSION

ANEURYSM

OTHER

AV-MALFORMATION
Other causes: bleeding into tumor, hypocoagulable state,
hemorrhagic infarction, iatrogenic, and trauma
 Primary and Secondary
Causes of Intracerebral Hemorrhage

Primary Secondary
•
Hypertension Aneurysms
•

•
Amyloid angiopathy Arteriovenous
•

malformations
Neoplasms
•

Trauma
•

Anticoagulation
•

Use of thrombolytics
•

Hemorrhagic conversion
•

of ischemic stroke
25
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).
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

27
INTRACEREBRAL HEMORRHAGE
Intraventricular Hemorrhage:
HCTS

10/ 9/07
 Gejala Klinis

•
Onset sewaktu aktivitas
•
Penurunan kesadaran, 2/3 koma
•
Nyeri kepala dan muntah sebagai tanda
peningkatan TIK
•
Kejang jarang

31
 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

32
 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

33
 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
34
SAH

35
Subarachnoid Hemorrhage:
 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)

37
 Penggolongan SAH
Hunt dan Hess

•
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

Greenberg,2001 38
 SAH – The case you could miss
(Sokransky 2001)

•
Well-appearing patient
with previous
headaches

•
Presents with a
sudden headache that
is now better
40
Cerebral vasospasm
 Haemorrhage
Effects of blood Release
Increase Vasoconstrictor agen
toxic Intracranial press Serotonin, Prostaglandin,

Global ischemic
Influks Ca+

Influks Ca+ Vasospasme

Necrosis
Focal Ischemic
Neuron

42
 Vasospasme Process on Haemorrhage

vasoconstrictor agens & blood componen release

Vasospasme

Influks Ca+ smooth muscle

vasculer

Lumen stronge
vasculer Vasospasme

Ischemic + deficit neurologic

43
 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
Effects of Vasospasme

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

45
 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
 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) 48
 Piracetam
•
Mechanism (neuronal)
–
Repair cell membran fluidity
–
Repair neurotransmission
–
Stimulation adenylate kinase
•
Mechanism (vascular)
–
Increase eritrocyte deformability
–
Decrease platelet hyperagregation
–
Repair microcirculation

(Perdossi, 2004) 49
 Mekanisme Kerja Ganda Piracetam

Melindungi Sel Memperbaiki Fungsi

Jaringan
Neuron

Piracetam

Jaringan
Serebrovaskuler
Meningkatkan Aliran Darah Efek Sitoprotektif Dalam
Otak Pembuluh Darah Otak

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
HIPERTENSI
 Hipertensi
Ensefalopati
Akut Pemb.drh kecil Spasme
hipertensif
Mikro PIS
Hipertensi aneurisma
Pemb drh kecil Lipohialinosis pecah
Infark
Trombosis
lakunar
Kronis

TIA,trombosis,
Pemb drh sedang Aterosklerosis Emboli serebri
Faktor resiko lain
DM,hiperlipidemi
MANAJEMEN
 Management

•
Medical Management
•
Surgical Management

54
 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

55
 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

56

Hasil optimal terapi Stroke perdarahan
sampai 96 jam setelah onset

Puncak vasospasme antara hari ke 5-10)

57
57
 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) 58
58
 Acute stroke care-General management
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

(Lamsudin, 2004) 59
59
 Acute stroke care-General management
Blood pressure (BP)
Indications for immediate AH therapy in acute
stroke
Intracerebral haemorrhage
Cardic failure
Acute coronary syndrome
Aortic dissection
Hypertensive enchephalophaty

(Lamsudin, 2004) 60
60
 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 300, patient’s 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
61
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 200
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 1st to
10th 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)
 Blood Pressure (BP) Management Protocol in
Acute Stroke
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
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

70
Guidelines for treating elevating Blood
Pressure in ICH (2)

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.

71
 Pembedahan
•
Bukan tindakan rutin
•
GCS 7-10
•
Pemulihan fungsional tetap jelek
•
Dilakukan bila gagal mengendalikan
peningkatan TIK
•
Perdarahan serebeler sering dilakukan
pembedahan

72
 Rekomendasi pembedahan pada perdarahan
intraserebral
(konsensus Nasional Pengelolaan Stroke di Indonesia)

•
Kandidat yang tidak dioperasi
1. Perdarahan dengan volume <10 cm3 atau dgn defisit neurologis yg mini
mal tidak dilakukan tindakan pembedahan
2. GCS <4. Tetapi penderita dgn GCS<4 dgn perdarahan serebelum dan ko
mpresi batang otak adalah kandidat operasi pada beberapa kasus

•
Kandidat yang dioperasi
1. Perdarahan serebelum dgn diameter >3 cm dgn deteriosasi atau mengal
ami 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 cm3 dengan tanda-tanda peninggian tekanan intr
akranial akut dan ancaman herniasi

73