dr. Moch. Bahrudin.

SpS
STROKE
Is based on clinical findings which meet the
Critoria of WHO definition (1986) :

Stroke is clinical symptoms of acute
developing focal (or global) cerebral
dysfunction lasting 24 hours or longer, or
lasting to death, without any apparent
cause other than vascular origin.

* Indonesia (> 55 th) =
276,3 / 100.000 PDDK
( survei KES.RT.1984, YOGYA )
* EROPA : 200 pend.baru/100.000 pddk/thn
* AMERIKA (USA) : 275 300 ribu /thn


stroke


Angka kecacatan no. 1
Angka kematian no. 3
no. 2. seluruh dunia (who 1999)
PENDAHULUAN
Otak memerlukan darah ~ (tu/o
2
& glukosa)

Aliran darah otak (ADO) = CBF (cerebral blood flow)
Tgt 3 faktor :
1. Perfusi
2. Tahanan PD perifer otak
3. Drh : viskositas & daya koagulasi darah
dan Pa O2/CO2

CAROTID
SYSTEM

VERTEBRO-
BASILAR
SYSTEM
CEREBRAL ARTERIES & BRAIN TERRITORIES SUPPLIED
CAROTID SYSTEM

Anterior CA :~ Ant & post. medial surface
of frontal lobe
~ Corpus callosum
Middle C.A : ~ Lat. Post. of front. lobe
~ Lat. pact & post, parietal lobe
~ Sup & post temporal lobe
~ Perforating branches :
- Basal ganglia
- Intern caps
- Thalamus

VERTEBRO - BASILAR SYSTEM :

* Post. C.A : ~ Pericallosal cortex
~ Inf + post med, Occip. lobe
~ Corpus callosum : post part
~ Inf. part of temporal lobe
* PICA,AICA,SCA : ~ Cerebellum
* Branches to : ~ Brainstem
Risk factors for ischaemia stroke
Non-modifiable risk
factors
Age
Sex
Race
Family history
Previous stroke
Well-documented
modifiable risk factors
Hypertension
Smoking
Diabetes mellitus
Asymptomatic carotid
stenosis
Hyperlipidaemia
Sickle cell disease
Nonvalvular atrial
fibrillation
Less well-documented
or potentially
modifiable risk factors :
Obesity
Physical inactivity
Alcohol abuse
Hyperhomocysteinaemia
Drug abuse
Hypercoagulability :
oantiphospholipid
antibodies
ofactor V leiden
oprothrombin 20210
mutation
oprotein C deficiency
oprotein S deficiency
oantithrombin III
deficiency
Hormone replacement
therapy
Oral contraceptives use
Inflammatory processes
Classification of Stroke by mechanism,
frequency Albers, Chest 2001

Penyumbatan PB.Darah otak : tu/aterosklerosis &
aterioskeloris

- Lumen pb drh < (stenosis)
- Oklusi mendadak o/trombus/aterom
- trombus lepas embolus
- Dinding pd lemah aneurisma / robek
CBF menurun
Adhesion
Key Mediators in Platelet Adhesion,
Activation and Aggregation
1. Ferguson JJ. The Physiology of Normal Platelet Function. In: Ferguson JJ, Chronos N, Harrington
RA (Eds). Antiplatelet Therapy in Clinical Practice. London: Martin Dunitz; 2000: pp.1535.
INJURY
vWF
Thrombin
Collagen
Fibronectin
Shear Forces
vWF
ADP-receptor
THROMBUS
Activation
Aggregation
Membrane changes
Granule secretion
GPIIb/IIIa expression
Multiple agonists
Feedback loops
GPIIb/IIIa-mediated
Fibrinogen
vWF
ISCHEMIA

ATP
DEPLETION
ACTIVATION of :
NMDAr, AMPAr and KAINATEr
and METABOTROPIC Receptors
Ca
++
i
the first 3 minutes.to one hour
Ca
++
i
Ca
++
i
Ca
++
i
Ca
++
i
Ca
++
i
ACTIVATION of :
Voltage dependent ion
channels
Ca
++
i
ISCHEMIC CORE AND ISCHEMIC PENUMBRA
(Friedlander 2003)
(necrosis)
(caspase apoptosis: programmed cell death)
BENTUK KLINIS

1. TIA
2. RIND
REVERSIBLE ISCHEMIC NEUROLOGICAL
DEFICITS
gejala berlangsung > 24 jam < 1 minggu
PRIND (PROLONGED RIND)
gej. s/d 3 mgg
RIND & PRIND DEFISIT KLINIS NEUROL
MINIMAL
3.STROKE PROGRESIP
(PROGRESSING STROKE) (STROKE IN EVOLUTION)
gejala neurologik berlgsg & bertambah berat

4.STROKE KOMPLIT
(COMPLETED STROKE / PERMANENT STROKE)
stroke dgn gejala klinis sudah menetap.

Hemiplegi/ hemiparese kontralateral (derajat kelumpuhan lengan &
tungkai berbeda)
Parese N.cranialis kontralateral (N.VII & XII) UMN
Hemihipestesia kontralateral
Gangguan inervasi nn. Cranialis kontralateral
Aphasia (+/-), tergantung letak lesi
LESI CORTEX
Hemiplegi/ hemiparese kontralateral (derajat
kelumpuhan lengan & Tungkai sama)
Parese N.cranialis kontralateral (N.VII & XII)
UMN
Hemihipestesia kontralateral
Gangguan inervasi nn. Cranialis kontralateral
Aphasia (-), Disartria (+)
Rigiditas, atetosis, distonia, tremor, hemianopia
Gerakan sekutu patologis (+)

LESI SUB KORTEX

ADA 2 JENIS ( WHO International )

Classification of Disease rev (1965)
1. Perdarahan Intraserebral (PIS)
ICD 431
2. Perdarahan Subarakhnoidal (PSA)
ICD 430

PIS perdarahan primer akibat rusak / robeknya
pemb. drh parenkim otak
bukan karena trauma (dari luar).

KLINIS : Akut (memburuk /krisis dlm 24 Jam)
Subakut (bila memburuk 3 < 7 Hari)
Subkronik (bila krisis selama s/d > 7 hari)

EPIDEMIOLOGI :
- DEKADE 5 - 8 (rata-rata : 55 tahun)
- laki-laki & Perempuan (K.L. lk = pr)
- Angka Kematian : 60-90% ( > 3 hari = 10 % )
( > 1 MG = 72 % )

PATOLOGI & PATOFISIOLOGI :


Penyebab :
1. Hemodinamik
2. Defek pembuluh darah
3. Gangguan faal pembekuan

- 70 % di kapsula interna
(A.C. media a.lenticulo strieta)

- 20 % di serebelum & btg otak
(fossa post)

- 10 % di hemisfer diluar kaps. int.
Aneurysma Cerebral
AVM
STROKE ATAU NON STROKE ??????
TEMUAN KLINIS :
(anamn. + pem.fisik)

STROKE





1. Timbul mendadak / cepat (akut)
2. Defisit neurologi fokal / global
3. Berlsg > 24 jam, atau maut
4. Tanpa penyebab-penyebab lain ggn vaskular
(mis. trauma serebral, infeksi & psikogen)



DIAGNOSA
STROKE
PERDARAHAN

Sangat akut
Aktifitas
Tanpa peringatan
Sakit kepala
Muntah
Kejang
Tidak sadar
Lok. Subkortikal
INFARK
Subakut
Bangun pagi
Ada peringatan
Tidak sakit kepala
Tidak muntah
Tidak kejang
Sadar
Lok. kortikal
SUBKORTIKAL
Afasia -
Astereognosis
2 point discri.
Graphestesia
Extinction phen.
Loss of body image
Lumpuh lengan dan tungkai sama
Dystonic postur ++
Gangguan sensibilitas ++
Kedua mata melihat hidung

KORTIKAL
Afasia
Astereognosis
2 point discri.
Graphestesia
Extinction phen.
Loss of body image
Lumpuh lengan dan tungkai tak sama
Dystonic postur -
Gangguan sensibilitas -
Kedua mata di tengah

CARA MEMBEDAKAN SUBKORTIKAL DAN KORTIKAL ??
Kriteria
Diagnosa
PIS PSA Thrombosis Emboli
Umur > 40 tahun
Tak tentu
20-30
50 70 tahun Semua umur
Onset
Perjalanan
Aktivitas
Cepat
Aktivitas
Cepat
Bangun tidur
Bertahap
- Tak tentu
- Cepat
Gejala penyerta
Sakit kepala
Muntah
Vertigo

++
++
_

++++
++++
_

_
_
+ / -

_
_
+ / -
Risk faktor
Hipertensi
Penyakit jantung
DM
Hiperlipid

HT
berat/maligna
HHD
_
_

+ / -
_
_
_

+ / -
ASHD
++
++

_
RhHD
_
_
Kriteria
Diagnosa
PIS SAH Thrombosis Emboli
Kesadaran / coma pelan N / N /
Kaku kuduk +/- ++++ _ _
Kelumpuhan
Hemiplegi
Tangan = kaki

/
Hemiparese +/-
Sdh 3-5 hari

Hemiparese
Tangan kaki

Hemiparese
Tangan kaki
Afasia _ _ ++/- ++/-
LP darah +/- +++++ _ _
Arteriografi Shift midline Aneerysma + Oklusi /
Stenosis
Oklusi
CT Scan Hiperdens ++++
Intraserebral
N / Hiperden
Ekstraserebral
Hipodens
Sdh 4 7 hari
Hipodens
Sdh 4 7 hari
SKOR
JOENAIDI SKOR
Algoritma Gajah Mada
Siriraj Skor
DIAGNOSA PASTI STROKE ???
Ct Scan
MRI
Gold Standart
Stroke Perdarahan (ICH) : Hiperdens
SAH ACUTE
1. Tampak pada CT Scan
2. Tidak tampak pada MRI

Hiperden
Diagnostic studies
All Patient :
Brain CT (brain MRI at qualified centers)
ECG
Glucose
Electrolytes
Renal Function Test
lipid
Complete Blood Count, platelet count
Prothrombin time/ineternational normalized ratio INR
activated partial thromboplastin time
Selected patient :
LFT
Toxicology
Alcohol
Oxygen saturation or arterial BGA (if hypoxia suspected)
Chest Foto (if lung disease suspected)
Lumbar puncture (if subarachnoid hemorrage suspected and CT is negative for blood)
EEG (if seizure is suspected)
Special laboratory test ( selected patient):
Protein C, S,
Homocystein
Vasculitis screening (ANA, Lupus)
CSF

To minimise volume brain tissue that is irreversible
infarcted
To prevent complications
To reduce disability and handicap
To prevent recurrent stroke

EUSI 2003
TERAPI STROKE INFARK
PENANGANAN STROKE INFARK

1.UMUM

2. KHUSUS

Penanganan umum 5 B

B1. A (AIRWAY CLEAR) :
jalan nafas harus bebas, resp.
terjamin
B2. B (BLOOD) :
Jantung hrs baik /ekg
Anemi koreksi
TD stabilkan / optimalkan ek.perfusi

Jangan R/ Tensi pd Fase Akut !
B3 = BRAIN
C (CEREBRAL FUNCTION) :
Koma - dipantau, diatasi
Kejang - diobati Anti Konvulsan
Kadar Gula DRH (GD) - bila tinggi : kan
Balans cairan, Elektrolit, Asam-Basa
pantau/ Koreksi bila perlu

Fungsi ginjal dipelihara; hindari infeksi,
batu, ggn balans elektrolit, pH, air, dsb.
Atasi retensi / inkontinensi kateter, ganti
berkala
B5 = BOWEL FUNCTION
Nutrisi yg cukup / optimal, fungsi TGI baik,
atasi obstipasi (retensi alvi) & inkontinensi
alvi, dispepsi dikoreksi, dll.
1. No antihypertensives *,
2. No diuretics,
3. No dexamethasone,
4. No glucose infusion,
5. No anticoagulant 4 hours after onset of stroke.

* Except aortic dissection, acute myocardial infarction,
heart failure, acute renal failure, hypertensive
encephalopathy, thrombolytic therapy (T 185/110
mm Hg).
Brott 2000
Sulter et al. (2003).
PENANGANAN KHUSUS
I. REPERFUSION
To restore Blood Flow to Ischemic region
II. NEUROPROTECTION Protect/salvage cells from ischemic damage

EAA (glutamate) antagonists
GABA antagonists
Ca channel antagonists
Antioxidants
Growth factors
Leucocyte adhesion and infiltration inhibitors
Nitric oxide inhibitors

Anti platelet, anticoagulan, rtPA
Opioid antagonists
Phosphatidylcholine precusors
Serotonin agonists
Sodium channel blockers
Potassium channel openers
Mechanism(s) unknown or uncertain
ANTITHROMBOTIC AGENTS
THROMBOLYTIC
AGENTs
ANTI-PLATELET
AGENTs
ANTI-
COAGULANTs
Streptokinase
Urokinase
tPA
PARENTERAL
Coumarin
Warfarrin
Melagatran


Heparin
LMWH
Hirudin
Argatroban
Fondaparinox
ORAL PARENTERAL
GPIIb/IIIa
Antagonists
Abciximab
Tirofiban
Eptifibatide
ORAL PARENTERAL
Aspirin
Dipyridamol
Ticlopidin
Clopidogrel
Cilostazol
Sulfinpyrazone
Systemic thrombolysis: Intravenous recombinant tissue
plasminogen activator (rt-PA): Within 3 hrs of onset of stroke. Dose
0.9 mg/kg, max 90 mg.

Antiplatelet agents: Aspirin 50-325 mg within 24- 48 hrs (not during
first 24 hrs following thrombolytic therapy). Some other
antiplatelets or combinations are alternative.

Anticoagulants: Heparin/LMWH are not recommended in acute
treatment of ischemic stroke. Recommended in setting of atrial
fibrillation, acute MI risk, prosthetic valves, coagulopathies.

Intra-arterial thrombolytics: An option for treatment of selected
patients with major stroke of < 6 hrs duration due to large vessel
occlusion.

I. ANTI TROMBUS
1. Rapid Reperfusion: r tPA
2. Slow : ASA, Ticlo, Clodip.
II. MEMPERBAIKI PENUMBRA
dengan Neuroprotektif
1. Citicholine 3. Growth factor
2. Piracetam 4. Anti oksidan

III. SISTEM KOLATERAL & HEMOROLOGI:
Pentoksifilin
IV. HEMODINAMIK:
CBF = CPP -- Tensi
CVR -- Autoregulasi
-- Anti Oedema
KHUSUS : ?
Operasi ?????
TERAPI STROKE PERDARAHAN
Rekomendasi Terapi Operatif Perdarahan Intraserebral
( Broderick,1999 )



Tidak dioperasi
1. Perdarahan kecil ( < 10 cm
3
) atau dengan defisit neurologi
minimal
2. GCS < 4. Tetapi penderita dengan GCS < 4 dengan
perdarahan serebelum dan kompresi batang otak adalah
kandidat operasi pada beberapa kasus

Dioperasi
1. Perdarahan serebelum dengan diameter > 3 cm dengan
deteriorasi 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. Penderita muda dengan perdarahan lobar sedang atau besar ( >
50 cm
3
) yang mengalami deteriorasi

REHABILITASI MEDIK

~ Fisioterapi sejak Hari-I
* posisi
* grkan Pasif Aktif
~ Bina Wicara (speech therapy)

Psikoterapi & Sosialisasi
~ Terapi Kerja
FASE PASCA AKUT

Sasaran : 1. Rehab.Pend. !
2. Cegah Strok Ulang !

1. Rehab : lanjutkan fase akut bebas /
Latihan (Rehab. Fisik, Mental / Psikik &
Sosial !)
2. Preventif : * ASA : 80 - 300 mg/hari
( u/ Anti Agregasi Pletelet)
Stroke infarc

* Terapi F.Risiko :
- HT - Rokok - Diet
- DM - Lemak - OR
- Jantung - dsb
1. Derajat kesadaran : Koma 100% ; sadar 16
2. Usia : usia angka (> 70 th Mortalitas )
3. Jenis : Lk > banyak (61%) > Pr (41 %)
4. Umum : Tek DRH : TD Prog > jelek
5. R/ : > lambat Prog > buruk