IT 2 - TIA, Stroke Tromboemboli - AWS
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8/12/2019 IT 2 - TIA, Stroke Tromboemboli - AWS
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PENYAKIT
SEREBROVASKULAR
dr. Alwi Shahab, SpSBagian Neurologi
FK. UNSRI/RSUP. Dr. M. HoesinPALEMBANG
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SINONIM : CVD = GPDO
: STROKE
BATASAN : GANGGUAN FUNGSI
NEUROLOGIS AKUT YANG
DISEBABKAN OLEH
GANGGUAN ALIRAN
DARAH OTAK
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STROKE MENYEBABKAN KEMATIAN
DAN KECACATAN
BEBAN BAGI KELUARGA /
MASYARAKAT
PERLU DETEKSI DINI DAN
PENANGANAN CEPAT / TEPAT
OLEH SETIAP DOKTER
MERUPAKAN KASUS
GAWAT DARURAT
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Stroke : Di negara Maju
- Penyebab kematian nomor 3- Penyebab kecacatan yang tinggi
- Insiden : 2 – 5% / jumlah
penduduk/tahun
DI INDONESIA ?
-DIPERKIRAKAN 340.000/THN ( Junaidi )-ADA KECENDERUNGAN MENINGKAT
( Teguh Ranakusuma )
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DATA JUMLAH PENDERITA STROKE
DI RSMH & RS.CHARITAS
Rawat Inap
Tahun R.S.M.H RS.CHARITAS Jumlah
19971998
1999
2000
20012002
539383
384
508
542814
351246
421
466
533
405
890629
805
974
1075
1219
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DATA JUMLAH PENDERITA STROKE
DI RSMH
Rawat InapTahun S. Iskemik S. Haemorragic Jumlah
2003
2004
2005
2006
2007
107
143
195
180
199
102
169
152
164
116
209
312
347
344
315
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Cerebrovascular Disease:
Stroke Subtype
Albers GW et al. Chest . 1998;114:683S-698S.Rosamond WD et al. Stroke. 1999;30:736-743.
Ischemic strokeHemorrhagic stro ke
Atherothrombotic
disease (20%)
Embolism (20%)
Lacunar small vessel
disease (25%)
Cryptogenic (30%)
Intracerebral
hemorrhage (59%)
SAH (41%)(sub-Arachnoid
Hemorrhagic)
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Cerebrovascular disease is a heterogeneous disease. Strokes arecategorized as either hemorrhagic or ischemic.1,2 Hemorrhagic
strokes occur as a result of bleeding intothe brain caused by an injury to the head or a rupturedaneurysm and are furthercategorized as intracerebral or subarachnoid. Ischemic strokesalso can be further
divided into subcategories: atherosclerotic cerebrovascularstroke, cerebral embolism, lacunar infarcts, or cryptogenicinfarcts (refers to ischemic strokes in which the underlyingetiology remains obscure).Of the strokes reported in the National Heart, Lung, and Blood
Institute’s (NHLBI) Atherosclerosis Risk In Communities (ARIC)study2: 83% were ischemic, 10% were intracerebral, and 7%were subarachnoid hemorrhages. Among the 178 confirmedthrombotic brain infarctions, 38% were classified as lacunarstrokes occurring in small blood vessels of the brain.
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Ischemic Stroke
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Faktor Resiko Stroke
Tak dapat dirubah
Usia
Jenis kelamin Ras
Keturunan
Dapat dirubah
Hipertensi
Penyakit jantung DM
Hypercholesterole
mia Merokok
TIA / pernahstroke
Penyakit A.Carotis
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Faktor Resiko stroke di Indonesia
Hipertensi 73.9% merokok 20.45 %
prior stroke 19.9 %
Penyakit jantung iskemik 19.9%
Diabetes Melitus 17.3%
hiperkolesterolemia 16.4 %
Atrial fibrilasi 5.8 %
penyakit katup jantung 3.4 %
polisitemia 1.7 %
pil kontraseptif 1.5 % Alkohol 1.4 %
Jusuf Misbach;Penelitian multisenter RS di Indonesia;1996
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Faktor resiko terbanyak hipertensi :- RS seluruhIndonesia:73,9%(1996)
- RSCM: 74,6%(2001)
- RSMH: 83,6%(2005) Stroke menandakan penanganan
hipertensi yang tidak efektif.
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Faktor risiko stroke dan risiko relatif
Risk factors Relative risk Modification effect
Hypertension 6 X Beneficial, proven
Smoking 2 X Beneficial, proven
Diabetes mellitus 2 - 4 X Beneficial, unproven
Atrial fibrillation 3 X Beneficial, proven
Coronary artery disease 2 - 6 X Beneficial, unproven
Recent TIA or stroke 10 X Beneficial, proven
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Aterosklerosis
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Hypertensi → Stroke
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Hypertension – Stroke risk factor
Hypertension
Hemmorhagic StrokeIschemic Stroke
Vessel wall abnormality
Defects in hemostasis
Smoking
Lipid disorder
Diabetes
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SEL MATI
FUNGSI
100%
FUNGSI N
NORMAL
50%
PATOFISIOLOGI
15%
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PATOFISIOLOGI
I. PERUBAHAN VASKULAR :- HEMATOLOGIK
- KARDIOLOGIK
- TEKANAN DARAH
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PATOFISIOLOGI
II. PERUBAHAN BIOKIMIAWI PADA
OTAK :
- Pengurangan ATP
- Penimbunan Glutamat
- Penimbunan Asam Laktat
- Rusaknya perimbangan
asam-basa- Rusaknya perimbangan
ion Na, K, Ca
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PENDARAHAN PADA STROKE DAN TRAUMA
Pendarahan
Efek Toksik
Darah
Peningkatan
Tekanan
Intkaranial
Pelepasan
AgentsVasokonstriktor
Iskemia
Global
Influks
Ca++
Nekrosis
Sel Saraf
Influks Ca++
Vasospasme
Iskemia Fokal
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Bagan 1
Patofisiologi Infark Otak
Iskemia Kerusakan
Membran
Asam lemak bebas
Asam arakhidonat
Nekrosis
Sel
Gangguan
Sel
( Dikutip dari Hacke W. Hennerici M 1991 )
Ca Influk
Prostaglandin
Thomboksan
lekotrin
Free radical
CDP Cholin
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PATOLOGIPENUMBRA
INTI ISKEMIA -- INFARK
PERFUSI
BERLEBIHAN
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Gambaran Klinis
Tergantung dari :
Pembuluh darah yang terganggu.
• Cabang-cabang A. carotis interna
• Cabang-cabang A. Basilaris
Luas daerah otak yang terganggu
Ada atau tidaknya anastomosa Jenis stroke
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PERBAIKAN TERGANTUNG PADA :
- JENIS STROKE
- LUASNYA DAERAH ISKEMIA- SISTEM KOLATERAL
- KECEPATAN TINDAKAN
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DIAGNOSA ( I )
1. STROKE / BUKAN STROKE :
- TRAUMA
- INFEKSI- SOL
2. HEMORAGIK / NON HEMORAGIK
3. PENYAKIT PENYERTA / FAKTOR
RESIKO
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DIAGNOSA ( II )
I. CT SCAN OTAK( Standar Baku )
II. KLINIS
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Periksa Penderita Adakah :
- Kesadaran Menurun
- Nyeri Kepala
- Reflex Babinsky
2 gejala positif
Nyeri kepala Stroke Hemoragik Kesadaran menurun
GAJAH MADA STROKE ALGORITMA
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PENGOBATAN MULTI DICIPLINE
PARTNERSHIP
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STRATEGI PENGOBATAN
1. REPERFUSI2. MELINDUNGI /
MENCEGAH
KERUSAKAN SEL OTAK
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TUJUAN
1. MENJAMIN 02/ ENERGI KE OTAK TETAP BAIK
2. MEMPERBAIKI METABOLISME SEL OTAK
PENATALAKSANAAN UMUM
PRINSIP :
- AIRWAY : - JALAN NAFAS TETAP LANCAR- BRAIN : - CEGAH / ATASI EDEMA
- ATASI KEJANG
- CIRCULATION : - FUNGSI JANTUNG
- TEKANAN DARAH
- VISKOSITAS DARAH
- INFECTION : - CEGAH / ATASI INFEKSI
- NUTRITION : - SESUAI KEBUTUHAN
- PERHATIKAN PENYAKIT PENYERTA
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TINDAKAN AWAL DI UGDPENDERITA DI DUGA STROKE
PASANG INFUS NaCI 0,9% ATAU RL
O2
ECG
CT SCAN OTAK X-FOTO THORAX
LABORATORIUM DARAH :
- Rutin, Trombosit, BSS, Ureum, Creatinin,
Elektrolit, Faktor pembekuan
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NON HEMORAGIK BI LA :- Tekanan Darah Sistolik > 220 mmHg
- Tekanan Darah Diastolik > 120 mmHg
- MABP > 130 mmHg
- Kegawatan Organ Vital Lain
- Obat-obat yang dapat dipakai ACE Inhibitor,
Clonidin Drip, Nicardipin Drip, Diltiazem Drip
MENURUNKAN T.D. PADA STROKE
HEMORAGIK BILA :
- Turunkan sampai Hypertensi ringan
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Management of Hypertensive Emergencies
Rekomendasi : JNC-VI
Turunkan TD tidak lebih dari 25%
selama 2 jam, kemudian TDsampai 160/100 mm Hg selama 2-6 jam
Hindari penurunan TD yang cepatdan berlebihan
Titrase dengan antihipertensi
IV/Drip
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KOREKSI BILA :
- BSS > 250 mg%
- HIPOGLIKEMIA
PERHATIKAN KADAR GULA DARAH
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PENGOBATAN KHUSUS
STROKE N. H. :
- TROMBOLISIS
- ANTI COAGULAN
- ANTI PLATELET
- OBAT HEMOREOLOGIK
- NEUROPROTEKTOR
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THROMBOLITIC AGENT
TPA – ALTEPLASE
< 2 JAM SERANGAN 0,9 MG / KG BB
10% BOLUS SISANYA PER DRIP
SELAMA 1 JAM PASTIKAN BUKAN H. STROKE- CT
Scan Kepala
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THROMBOLITIC AGENT
TPA – ALTEPLASE
< 3 JAM SERANGAN 0,9 MG / KG BB
10% BOLUS SISANYA PER DRIP
SELAMA 1 JAM PASTIKAN BUKAN H. STROKE, CT
Scan Kepala
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HEMOREOLOGIC AGENT
PENTOXIFILIN 12 JAM – 24 JAM I
- 50 mg I.V DRIP 16 mg / KgBB/HARI
HARI KE 4 – 25 : ORAL 3 DD 400 mg
EFEK : - DEFORMABILIT RBC
- MUNURUNKAN
FIBRINOGEN PLASMA
VISKOSITAS MENURUN
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ANTICOAGULAN LMWH
ENOXAPARINE 2 X 40 Mg
EMBOLI JANTUNG USIA RELATIF MUDA
PASTIKAN BUKAN H. STROKE
TD SISTOLLIK < 180 MM HG
5 – 7 HARI, Ganti Oral : Warfarin
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ANTI PLATELET AGENT
ASPIRIN
TICLOPIDIN CLOPIDOGREL
CILOSTAZOL GINKOBILOBA
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1. CDP-CHOLIN
2.
PIRASETAM3. NIMODIPIN
NEUROPROTEKTOR
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1. ISTIRAHAT DIKAMAR YANG TENANG
2. MONITOR KETAT STATUS NEUROLOGIS
3. PERTIMBANGKAN MONITORING
JANTUNG4. POSISI KEPALA / LEHER TERHADAP
TEMPAT TIDUR 300
5. JANGAN MENGEJAN
6. NUTRISI ORAL UNTUK PASIEN YANG
SADAR
PERAWATAN PENDERITA SROKE
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7. NUTRISI NGT UNTUK PENDERITA YANG
TIDAK SADAR8. KESEIMBANGAN AIR ELEKROLIT
9. BILA GELISAH DIBERIKAN SEDATIF YANG
RINGAN
10. KURANGI RASA NYERI DENGANANALGETIK
11. TURUNKAN TEKANAN DARAH SECARA
HATI-HATI DAN MONITOR KETAT
12. BILA PERLU TEKANAN INTRAKRANIALYANG MENINGGI DITURUNKAN
13. BILA TERJADI KEJANG SEGERA DIATASI
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Pencegahan Stroke
Usaha Promotif P. Primer P. Sekunder
Sasaran Orang sehat, FR (factor Pasca TIA,
FR: Negatif resiko): positif pasca stroke
Tujuan Mencegah Mencegah Mencegah TIAFR TIA/Stroke stroke ulang
Cara Gaya Hidup Gaya HS, Gaya HS,
Sehat (HS) kendalikan FR kendalikan FR
Terapi obatTerapi bedah