pemakaian antikoagulan pada iskemik stroke1
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aspiletTRANSCRIPT
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PEMAKAIAN LMWH PADA ISKEMIK STROKE
DODIK TUGASWORO
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PENGGUNAAN ANTIKOAGULAN
MASIH KONTROVERSIAL
WALAUPUN DEMIKIAN
DILAPORKAN BAHWA
HEPARIN DIPAKAI
PADA (10-90) %
RS. AKADEMIK DI
AMERIKA UNTUK
TREATMENT
STROKE AKUT
DI UNIT STROKE
DIGUNAKAN UNTUK
MENCEGAH RECURENT
STROKE DAN
STROKE EMBOLI
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ANTIKOAGULAN
SAFE EFEKTIF
TIDAK TERJADI
PERDARAHAN
KARENA
ANTIKOAGULAN
BERHASIL
MENCEGAH DAN
MENGOBATI
TROMBOSIS
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1ST
CAST
TOAST
TIDAK
MEMPERLIHATKAN
KEUNTUNGAN
PENGGUNAAN
HEPARIN
ANTI KOAGULANT I.V.
KONTROVERSIAL
PROSPECTIVE CLINICAL TRIAL
(225 PASIEN DGN HEPARIN I.V.)
OUTCOME TIDAK
ADA PERBEDAAN
BERMAKNA
PADA STROKE
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PAN EUROPEAN
CONSENSUS
MEETING
ON STROKE
MANAGEMENT
(1995)
ASIAN PASIFIC
CONSENSUS FORUM
ON STROKE
MANAGEMENT (1997)
HEPARIN
UNTUK STROKE
KARDIO EMBOLI
AKUT
TIA BERULANG
PROGRESSING
STROKE
HEPARIN SC
TIDAK MEMPERBAIKI
STROKE
AKUT HANYA
PROFILAKSIS
VENA DALAM
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KONSENSUS NASIONAL
(1999)
PENATALAKSANAAN
STROKE ISKEMIK
• TROMBOLISIS
• ANTI KOAGULAN
• ASETOSAL
GUIDELINE STROKE
(2000)
INDIKASI ANTIKOAGULAN
• PREVENSI PENDERITA
PASCA TIA
• PREVENSI PASCA STROKE
ISKEMIK (RISK : EMBOLI
OTAK BERULANG)
• PREVENSI DVT & PE
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GUIDELINES STROKE PERDOSSI 2004
INDIKASI LOW MOLECULAR WEIGHT HEPARIN
(LMWH)
STROKE KARDIOEMBOLI
LMWH 0,4cc 2 kali/hari selama 5-7 hari
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Acute Stroke Management (EUSI 2003)
1. Treatment of general conditions that need to be stabilised.
2. Specific therapy directed against particular aspect of stroke
pathogenesis, either recanalisation of a vessel occlusion or
prevention of mechanism leading to neuronal death in
ischaemic brain (neuroprotection)
3. Prophylaxis and treatment of complications which maybe
either neurological (such as secondary haemorrhage, space-
occupying oedema or seizures) or medical (such as
aspiration, infections, decubital ulcers, deep vein thrombosis
or pulmonary embolism)
4. Early secondary prevention, which is aimed at reducing the
incidence of early stroke recurrence.
5. Early rehabilitation.
Hacke, Cerebrovasc Dis 2003; 16: 311-337
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TUJUAN PEMAKAIAN
ANTIKOAGULAN
Mencegah perambatan (propagasi) trombus
Meningkatkan lisis spontan trombus
Mencegah re-embolisasi pada arteri bagian proximal
Mencegah melambannya darah dipembuluh darah kecil dan sirkulasi vena
Mencegah DVT dan Emboli Pulmonal
warlow 1996
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Analog Proses pembekuan darah
menyerupai kesibukan diperempatan setelah setelah lampu lalu lintas dimatikan
* Polisi lalu lintas (anticoagulant) membuat arah aliran (blood flow) untuk mencegah terjadinya hambatan diperempatan (blood clot)
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MEKANISME KOAGULASI DARAH
DASAR TEORI MEKANISME UMUM
PROKOAGULAN ANTIKOAGULAN
(N)
PREDOMINAN
LEBIH
AKTIF
BILA
RUPTUR
P. DARAH
RUPTUR
AKTIVATOR
PROTOMBIN + Ca++
PROTOMBIN TROMBIN
FIBRINOGEN FIBRIN
PEMBEKUAN (-)
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Fibrin
Coagulation Pathway
Extrinsic pathway(Tissue factor)
Prothrombin Thrombin
Fibrinogen
Intrinsic pathway(Contact)
X XaXa
Thrombin
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XII
Contact (Eg: with glass)
XIIa
XI XIa
IX IXa
X Xa
VIIIa
PL
Ca++
Intrinsic Pathway
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Tissue factor (TF)
VII VIIa- TF
IX IXa
X Xa
XIa
VIIIa
Extrinsic Pathway
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Intrinsic Pathway
Semua faktor pembekuan dalam pembuluh darah
Activated partial thromboplastin test (aPTT)
Extrinsic Pathway
Semua faktor diluar pembuluh darah – faktor jaringan.
Prothrombin test (PT)
Pada LMWH karena rantai polisakaridenya kurang dari 18 – 20Maka pemeriksaan ini kurang mempunyai efek
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Diagnosis pemeriksaan koagulasi
APTT memanjang Kerusakan jalur Intrinsik Tidak ada perubahan PT
Tidak ada perubahan APTT Kerusakan jalur Intrinsik
Ektrinsik PT memanjang
APTT memanjang Kerusakan semua jalurPT memanjang
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LMWH
Bleeding
Clotting
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Indikasi Penggunaan LMWH pada stroke iskemik
Iskemik stroke dengan kardioemboli.
Iskemik stroke + narrowing of extracranial arteries.
Iskemik stroke pada pasien denganhypercoagulable state: diabetes yang tidak terkontrol, dislipidemia, sticky platelet syndrome, dll
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INDIKASI LMWH
Stroke Non Hemoragik, dibuktikan dengan CT.
SBP tidak lebih dari 180 mm Hg, DBP tidak lebih dari 120 mm Hg.
Usia < 75 tahun (tdk mutlak)
Waktu pemberian tidak lebih dari 24 hours, beberapa kasus lebih dari 12 jam. GCS > 10.
Direkomendasikan untuk stroke berulang: TIA berulang, emboli stroke, AF.
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Keadaan dimana LMWH harus digunakan dengan hati-hati
Infark luas pada CT atau MRI-scan.
Hipertensi tak terkontrol
Riwayat kecenderungan perdarahan
Keadaan lain dimana penggunaan antikoagulan merupakan kontraindikasi.
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LMWH.
Biasanya tidak diberikan sebagai monoterapi
Biasanya diberikan bersama pengobatan stroke lainnya.
Mulai awal, diberikan selama5-7 hari.
LMWH jangan diberikan pada :
- TDS > 180 mmHg.
- Infark luas atau adanya perdarahan
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MEKANISME KERJA LMWH
Dihasilkan oleh proses enzimatik atau depolarisasi kimia membentuk rantai dengan BM 5000.
LMWH mempunyai efek antikoagulan dengan mengaktifkan antitrombin III
LMWH mempunyai aktivitas lebih besar terhadap faktor Xa.
Efektifitas LMWH dipengaruhi oleh BM. Makin kecil BM efektifitas antikoagulan semakin tinggi.
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LMWH
LEBIH JARANG MENYEBABKAN
PENDARAHAN DIBANDING HEPARIN
KARENA
LMWH
MENGHAMBAT
FS. PLATELET
KURANG DARI
HEPARIN
LMWH
TIDAK
MEKAN
PERMEABILITAS
MIKR VASKULER
AKTIVITAS
LEBIH RENDAH
TERHADAP
SEL ENDOTEL
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Fibrin
ProthrombinThrombin
Fibrinogen
X Xa
IX IXa
VII VIIa- TF
Tissue factor (TF)
Site of Action of Drugs
Heparin
Warfarin VIIIa
Va-
--
-
--
-
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Jalur Terjadinya Trombosis
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Thrombin
AT III
Heparin
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Factor X aA T III
LMWH
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Citrate
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EDTA
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Heparin
Thromboplastin
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Coumarin
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pp 539
Detail of Coagulation
Cascade
Intrinsic and Extrinsic mechanisms convergehere
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Aspirin
(Platelets)
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Intrinsic Extrinsic
Later
slide
Thromboxane (paracrine) aggregates platelet
pg. 537, See also pg. 129 in packet
Thromboplastin
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Hemostasis: 3 Processes
1. Damage to blood vessel wall causes VASOSPASM
2. PLATELET PLUG FORMATION
3. 2 possible CLOTTING pathways:
A. Intrinsic initiation of coagulation cascade:1) Collagen exposure (platelets)
2) Release of platelet factors
B. Extrinsic initiation of coagulation cascade:1) Tissue damage
2) Release of thromboplastin
• Fibrinogen Fibrin threadsThrombin
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WARFARIN: MECHANISM OF ACTION
Inactive factors II,
VII, IX, and X
Proteins S and C
Active factors II,
VII, IX, and X
Proteins S and C
Vitamin K epoxide
Vitamin K reduced
Prevents the reduction of vitamin K, which is essential for
activation of certain factors
Has no effect on previously formed thrombus
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MONITORING OF WARFARIN THERAPY
Prothrombin time
PT ratio
INR (International Normalized Ratio)
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PROTHROMBIN TIME (PT)
Time required for blood to coagulate is called PT
Performed by adding a mixture of calcium and thromboplastin to citrated plasma
As a control, a normal blood sample is tested continuously
PT ratio (PTR) = Patient’s PT
Control PT
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PROBLEMS WITH PT/PTR
Thromboplastins are extracts from brain, lung or placenta of animals
Thromboplastins from various manufacturers differ in their sensitivity to prolong PT
May result in erratic control of anticoagulant therapy
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INTERNATIONAL NORMALISED RATIO (INR)
INR = [PTpt] ISI
[PTRef]
PTpt – prothrombin time of patient
PTRef – prothrombin time of normal pooled sample
ISI – International Sensitivity Index
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OPTIMIZING WARFARIN THERAPY
Dosage to be individualized according to patient’s INR response.
Use of large loading dose may lead to hemorrhage and other complications.
Initial dose: 2-5 mg once daily
Maintenance dose: 2-10 mg once daily
Immediate anticoagulation required: Start heparin along with loading dose of warfarin 10 mg. Heparin is usually discontinued after 4-5 days. Before discontinuing, ensure INR is in therapeutic range for 2 consecutive days
Monitor daily until INR is in therapeutic range, then 3 times weekly for 1-2 weeks, then less often (every 4 to 6 weeks)
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OPTIMAL THERAPEUTIC RANGE
Indication INR
Prophylaxis of venous
thromboembolism2.0-3.0
Treatment of venous
thromboembolism2.0-3.0
Atrial fibrillation 2.0-3.0
Mitral valve stenosis 2.0-3.0
Heart valve replacement
Bioprosthetic valve
Mechanical valve
2.0-3.0
2.5-3.5
Myocardial infarction 2.0-3.0
2.5-3.5 (high risk patients)
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FACTORS INFLUENCING DOSE RESPONSE
Inaccurate lab testing
Poor patient compliance
Concomitant medications
Levels of dietary vitamin K
Alcohol
Hepatic dysfunction
Fever
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DURATION OF THERAPY
Venous thromboembolism: Minimum 3 months, usually 6 months
AMI: During initial 10-14 days of hospitalization or until patient is ambulatory
Mitral valve disease/Mechanical heart valves: Lifelong
Bioprosthetic heart valves: 3 months
Atrial fibrillation: Lifelong
Prevention of cerebral embolism: 3-6 months
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CONTARINDICATIONS AND
PRECAUTIONS
Hypersensitivity to warfarin
Condition with risk of hemorrhage
Hemorrhagic tendency
Inadequate laboratory techniques
Protein C & S deficiency
Vitamin K deficiency
Intramuscular injections
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SIDE EFFECTS
Hemorrhage
Skin necrosis
Purple toe syndrome
Microembolization
Teratogenecity
Agranulocytosis, leukopenia, diarrhoea,
nausea, anorexia.
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SWITCHOVER FROM ONE BRAND OF WARFARIN TO ANOTHER/
ACENOCOUMAROL
Check patient’s INR
Start with dose of 2 mg; increase dose slowly as required
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Heparin
Perlu monitor APTT
Cara pemberiannya sulit (intravena)
Banyak ESO.
LMWH
• APTT tidak perlu
• Masa kerja panjang.
• Mudah pemberiannya.
• Diberikan 1 atau 2 kali sehari.
• ESO sedikit.
HEPARIN ATAU LMWH ?
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Nadroparin Optimized nitrous acid depolymerization
Enoxaparin Benzylation & alkaline hydrolysis
Dalteparin Nitrous acid depolimerization
Ardeparin Peroxidative cleavage
Tinzaparin Heparinase digestion
Certoparin Isoamylnitrate digestion
Reviparin Optimized nitrous acid
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JENIS PREPARAT LMWH
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DOSIS DAN DURASI
Dosis: 40 mg, 2 X 1 dalam 5 hari sampai 7 hari.
Pasien Obese , BB > 75 kg: 60 mg, 2 kali satu, dalam 5 sampai 7 hari.
Pasien kurus, BB < 40 kg. 30 mg, 2 kali satu, dalam 5 sampai 7 hari.
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Study mengenai LMWH
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Nadroparin+Aspirin showed better outcome than Aspirin alone
0
10
20
30
40
50
Complete recovery Independence in activities of
daily living
Nadroparin+Aspirin
Aspirin
40%
25%
45%
25%
p<0.05
%
Positive outcome in Nadroparin+Aspirin group
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Nadroparin+Aspirin showed better outcome than Aspirin alone
0
10
20
30
40
50
Severe disability
Nadroparin+Aspirin
Aspirin
15%
45%
p<0.05
%
Severe disability due to minimal/no recovery
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KESIMPULAN
LMWH 40 mg o.d. lebih efektif daripada heparin 5.000 IU t.id. dalam mencegah kejadian tromboembolik (DVT dan PE) pada pasien dengan acute ischemic stroke
Lebih sedikit transformasi perdarahan (haemorrhagic transformation) terlihat pada CT- scan dengan LMWH dibandingkan heparin
LMWH sama amannya dengan heparin berkaitan dengan perdarahan
Lebih sedikit kematian pada kelompok LMWH dibandingkan heparin pada 3-bulan follow-up
Terlihat adanya kecenderungan hasil neurologis yang lebih baik dengan LMWH pada pasien yang diseleksi secara benar: terapi dimulai lebih awal.