Dr. Takdir Setiawan MSc, Sp.

S
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)

Risk Factors for Stroke

Non-Modifiable
Risk Factors for Stroke
Age
Sex
Race/ethnicity
Family history

Modifiable Risk Factors for

Stroke6
Hypertension
Diabetes
Smoking
Hyperlipidemia
Carotid stenosis
Atrial fibrillation

Perbedaan klinis
Anamnesis

Gejala

Onset
Saat onset
Warning
Nyeri Kepala
Kejang
Muntah
Kesadaran

Perdarahan

Mendadak
Sedang aktif
-+++
+
+
+++

Infark

Mendadak
Istirahat
+ + (TIA)
+/+/-

Perbedaan klinis
Tanda-tanda

Tanda-tanda
Bradikardi
Udem papil
Kaku kuduk
Tanda
Kernig
Brudzinski

Perdarahan
++(dari

permulaan)

sering +
+
+++
+++

Infark

+/6

SCORE SIRIRAJ
(2,5xS)+ (2xM)+ (2xN)+ (0,1D)- (3xA)- 12
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

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/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++

Jarang

Kadang

PERBEDAAN STROKE HEMORAGIK DAN ISKEMIK

VARIABEL

PIS

PSA

TROMBOSIS

EMBOLI

Reflek Patologis

Segera

Variasi

Lambat

Lambat

Hipertensi

Selalu +

Variasi

Kadang
N/Hipotensi

Jarang

Jantung

Hipertrofi LV

Variasi

Riwayat

Hipertensi

Hipotensi/
Diabetes/
Dehidrasi

Aritmia, AF,
Infark miokard,
asma kardial,
angina pektoris

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

Arteriografi

Shift

Aneurisma,
AVM

Oklusi/stenosis

Oklusi/ stenosis

Doppler

Aliran lambat

Aliran lambat

Hematology

Hematokrit/
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

Lifestyle
Smoking
Diet
Lack of exercise

Generalized
Disorders
Age
Obesity

Genetic Traits
Gender
PlA2

Atherothrombotic
Manifestations
(MI, stroke,
vascular death)

Inflammation
Elevated CRP
CD40 Ligand, IL-6
Prothrombotic factors (F I and II)
Fibrinogen
MI, myocardial infarction.
Adapted from Yusuf S, et al. Circulation. 2001;104:2746-2753.
Drouet L. Cerebrovasc Dis. 2002;13(suppl 1):1-6.

Systemic
Conditions
Hypertension
Hyperlipidemia
Diabetes
Hypercoagulable
states
Homocysteinemia

Local Factors
Blood flow patterns
Shear stress
Vessel diameter
Arterial wall structure
% arterial stenosis

Pembentukan Plak Aterosklerotik

1. Akumulasi lipoprotein pd tunika
intima

2. Stres oksidatif

3. Aktivasi Citokine

4. Penetrasi Monocyte

5. Migrasi makrofag

foam cell

7. Akumulasi matriks ekstraseluler

6. Muscle Cell Smooth

8. Kalsifikasi dan
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

aterosklerotik

22

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.
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
Hypertension
Amyloid angiopathy

Secondary
Aneurysms
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
27
WHO ICD-NA, 1987

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
toxic

Increase
Intracranial press
Global ischemic

Influks Ca+

Necrosis
Neuron

Release
Vasoconstrictor agen
Serotonin, Prostaglandin,

Influks Ca+

Vasospasme

Focal Ischemic

42

Vasospasme Process on Haemorrhage

vasoconstrictor agens & blood componen release

Vasospasme

Influks Ca+

smooth muscle
vasculer

Lumen
vasculer

stronge
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
Otak

Efek Sitoprotektif Dalam

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
Akut

Hipertensi

Pemb.drh kecil

Spasme

Ensefalopati
hipertensif

Mikro
PIS
aneurisma
pecah
Pemb drh kecil Lipohialinosis
Trombosis

Infark
lakunar

Kronis

Pemb drh sedang

Aterosklerosis

Faktor resiko lain

DM,hiperlipidemi

TIA,trombosis,
Emboli serebri

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, 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
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

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 710 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)
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
1.

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
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 cm3 dengan tanda-tanda peninggian tekanan
intrakranial akut dan ancaman herniasi

73