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YUNELDI ANWAR SPSDEPARTEMEN NEUROLOGI FK USUDEPARTEMEN NEUROLOGI FK USU
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Stroke
Adalah manifestasi klinik dari gangguan fungsi otak, baik fokal maupun global, yang berlangsung dengan cepat, gejala > 24 jam atau meninggal, tanpa penyebab lain selain gangguan vaskuler.
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KlasifikasiKlinis:1. T I A = Transient ischemic attacks St k h ik St k i k ik2. Stroke non hemoragik = Stroke iskemik:
* Thrombosis serebri* Embolia serebri Embolia serebri
3. Stroke hemoragik:* Perdarahan intra‐serebral (PIS)( )* Perdarahan sub‐arakhnoidal (PSA)
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Stadium.
T I Ak i l i ( i k )Stroke in evolution (progressing‐stroke)
Completed stroke : ‐ Non‐hemoragik‐Hemoragik
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T I A
Serangan defisit neurologik yg bersifat temporer akibat ggn peredaran darah temporer akibat ggn. peredaran darah otak, timbul mendadak, menghilang dgn cepat (<24 jam) tanpa gejala sisadgn cepat (<24 jam) tanpa gejala sisa.Biasanya: 5 – 60 menit / gejala max. bi ’biasanya 2’T I A : ‐ tipe karotid
‐ tipe vertebro‐basiler
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R I N D
= Reversible Ischemic Neurologic Deficitg
= T I A tapi > 24 jam= T I A , tapi > 24 jam
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Gejala TIA karotid:
Amaurosis fugaxHemiparesis
Hemi‐hipastesiHemi hipastesiAfasia
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Gejala TIA vertebrobasiler:Gejala TIA vertebrobasiler:
DiplopiaDiplopiaVertigo
DysarthriaDrop attacksp
Hemiparesis alternansHemi hipaestesiHemi‐hipaestesi
Ataxiadysphagia
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Etiologi:1. Penyakit pembuluh darah:
‐ plaque atherosklerotik‐ plaque atherosklerotik‐ arteriosklerosis
t iti dll‐ arteritis dll.2. Kelainan darah:h l b l‐ hypercoagulability
‐ embolism
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P f i b l
ETIOLOGI3. Penurunan perfusi serebral:‐ cardiac output ber(‐)‐ steal syndrome‐ kompresi pemb.darah ekstra‐kranial.kompresi pemb.darah ekstra kranial.
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PROSEDUR DIAGNOSTIKPROSEDUR DIAGNOSTIK. Lab.lengkapLab.lengkapECGThorax photoThorax photoEEGCT SCT ScanArteriografiTCDDll.
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D DD D :
1. Epilepsi2. Cardiac disorders3. Postural hypotension4. Hypoglycaemia4. Hypoglycaemia5. Syncope6 Migraine6. Migraine7. SOL8 K l iki t i Dll8. Kel.psikiatris Dll.
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Terapi:
1. Pengobatan terhadap faktor resikoP b i b i h b ik2. Pemberian obat2 anti thrombotik:= Platelet inhibitor:‐ aspirin ‐ dipyridamole‐ ticlopidinep‐ clopidogrel
= anti‐coagulansia: ‐ heparin anti coagulansia: heparin‐ coumadin
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Prognosis.Banyak penderita TIA dengan 1 atau beberapa kali serangan sebelum stroke tanpa menjumpai dokterResiko stroke paling tinggi pd. tahun p g gg ppertama stlh. TIA (10‐25%)Tahun berikutnya 5%Tahun berikutnya 5%TIA faktor resiko mayor utk. Infark otak, juga jantungjuga jantung.
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STROKE NON HEMORAGIKSTROKE ISKHEMIK= STROKE ISKHEMIK == INFARK SEREBRI =
Infark serebri terjadi bila suatu daerah diotakInfark serebri terjadi bila suatu daerah diotakmengalami iskhemia dan nekrosis, akibat ‐b k li d h k k i diberkurangnya aliran darah keotak sampai di‐bawah level kritis yang dibutuhkan untuk ke‐h d lhidupan sel.
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Etiologi
Thrombosis serebri
Emboli serebriEmboli serebri
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Th b i b iThrombosis serebri.b b d h klSebagian besar penderita atherosklerosis
= yg mempunyai faktor resiko yg h klmempercepat atherosklerosis.
* Penyebab lain:‐ arteritis pemb. darah otak‐ kelainan darah‐ kelainan darah‐ perfusi keotak menurun kritis.
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Emboli serebriEmboli serebri.
Sumber emboli:1. kardiovaskuler.‐ plaque atherosklerotik pd.pemb.darahotak yg besaryg‐ sisa pemb.darah yg telah mengalamioklusioklusi‐ trauma pemb.darah leher
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‐ Mural thrombosis o.k. infark miokard, aritmia kordis dan post operatif bedah j tjantung.
‐ Peny. Valvula jantung spt. Peny. Jantung tik l it l l rematik, prolaps mitral valve,
endokarditis.CHD d R t L h t‐ CHD dgn. R to L shunt
‐ Yang jarang: atrial myxoma,collagen di k di i ti d d di l disease,kardiomiopati dan endocardial fibrosis.
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3 . Sistemik.‐ emboli sepsis dari paru, abdomen danp p ,pelvisemboli lemak‐ emboli lemak‐ emboli udara‐ sel metastase‐ benda asing g
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G j l kli ikGejala klinik
Tergantung lokasi dan luasnya infark.Sindroma klinik sesuai dg.pemb.darah , Sindroma klinik sesuai dg.pemb.darah , daerah infark:‐ hemiparesis ‐ hemihipastesi‐ hemiparesis ‐ hemihipastesi‐ disfasia‐afasia ‐ ggn.penglihatand l f l‐ diplopia ‐ fasialis parese‐ dll.
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Embolia serebriEmbolia serebri.
defisit neurologik timbul mendadak dan sekaligus mencapai mendadak dan sekaligus mencapai
puncakt kt ktifonset sewaktu aktif
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Thrombosis serebri
defisit neurologik timbul mendadak, tapi berkembang agak lebih lambattapi berkembang agak lebih lambat.
onset sewaktu istirahat / bangun tidur
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PengobatanPengobatan.Prinsip:memperbaiki CBF mencegah p gperluasanInfark.a .
= Pengobatan umum Pengobatan spesifik= Pengobatan spesifik
= Rehabilitasi.
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Pengobatan umumPengobatan umum
Fungsi paru / jalan nafasFungsi paru / jalan nafasJantung & tekanan darahCairan & elektrolitCairan & elektrolitKadar glukosa & temperatur
kMakananMencegah / pengobatan komplikasi a.l:‐ edema serebri ‐ seizure ‐ pneumonia‐ UTI ‐ emboli paru / DVT pFisioterapi / speech therapi
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Tekanan darahTekanan darah‐Kenaikan TD fase akut jangan diobati Kenaikan TD fase akut jangan diobati, akan turun sendiri dalam beberapa hari, kecuali: ‐ TD sistol > 220 mm Hg kecuali: TD sistol > 220 mm Hg
‐ TD diastol > 120 mm HgP TD h l bih d h d‐ Penurunan TD harus lebih rendah pada:* setelah pemberian rt‐PA < 185/110* pada MI / CHF TD diturunkan lebih –rendahrendah
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Temperatur
Setiap demam apapun penyebabnya p p p p y ypada stroke akut harus diturunkan
Temperatur yang tinggi memperburuk outcomememperburuk outcome
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Hiperglikemia
Hiperglikemia mengganggu daerah p g gg ggiskemik penumbra metabolisme anaerobic lactic acidosis lokal infark bertambah luas.Kontrol KGD memperbaiki outcome Kontrol KGD memperbaiki outcome
KGD harus dibawah 150 mg/dl ( studi experimental)experimental)
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Pengobatan spesifikStrategy := Reperfusion memulihkan aliran Reperfusion memulihkan aliran darah kedaerah iskhemik
= Neuroprotection melindungi jaringan= Neuroprotection melindungi jaringanotak terhadap kerusakan akibat i kh iiskhemi
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r CBF( / / ) JARINGAN OTAK
KASKADE ISKEMIKKASKADE ISKEMIK(ml/100g / menit) JARINGAN OTAK
NormalGangguan Biokimiawi
( i t t i )
50-60
Gangguan metab. Glukosa(Glikolisis anaerobik)
Laktoasidosis
(sintesa protein)35
Gangguan metab. Enersi
“Ion Pump Failure”Glutamate Release ↑, → Ca influx,
Free radicals dst
20
Gangguan fungsional(depolarisasi membran)
“Electrical Failure”
Free radicals, dst
15
( p )
Kerusakan Histologis(Pannekrosis)
Neuron glia Endotel“Energy Failure”
10
STRATEGI TERAPI NeuroproteksiReperfusi
Neuron, glia, Endotel0-4
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“Core”IskhemiaIskhemia
PenumbraPenumbra
Luxury perfusiony
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penumbracore
1 hour 2 hour 3 4 hour 4 6 hour1 hour 2 hour 3-4 hour 4-6 hour
Corepenumbra
= ~ 1 : 1 ~ 2-3 : 1 ~ 4-5 : 1 ? 10-20 : 1
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Terapi thrombolitik.
melarutkan clot dan memulihkan sirkulasi limitasi kerusakan otak perbaikan outcomert‐PA (recombinant tissue plasminogen rt PA (recombinant tissue plasminogen activator)Onset < 6 jam (therapeutic‐window)Onset < 6 jam (therapeutic‐window)rt‐PA 3 jam, dilaporkan perbaikan
t t k l k t toutcome ‐ protokol yg ketat.
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Antikoagulansia.Untuk embolia serebri mencegah embolisasi ulanggA.l. heparin, warfarinHarus pengawasan pem lab yg ketatHarus pengawasan pem.lab yg ketat.
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ASPIRIN
Aspirin dapat diberikan pada fase akutp p p fpada pasien dengan CT Scan perdarahan (‐) antara 12 ‐24 jam perdarahan ( ) antara 12 24 jam memperbaiki outcoma (berdasarkan 2 penelitian besar)(berdasarkan 2 penelitian besar)
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NeuroprotectionGlutamat antagonistCalcium channel blockerCalcium channel blockerFree radical scavengerGABA t i tGABA antagonistOpioid antagonistNa‐channel blockerCDP‐choline dll.C choline dll.
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Pengobatan post stroke:Kontrol faktor resikoPemberian obat2 anti‐thrombotik‐ aspirin ‐ dipyridamole‐ ticlopidineticlopidine‐ clopidogrelPemberian antikoagulansia : Pemberian antikoagulansia : ‐warfarinFi i t i / h bilit iFisioterapi / rehabilitasi