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TROMBOSIS : DIAGNOSIS &

PENATALAKSANAAN

IRZA WAHID
SUBAGIAN HEMATOLOGI & ONKOLOGI MEDIK
FK UNAND / RS DR M DJAMIL PADANG
HEMOSTASIS - DIATESIS HEMORAGIS
- TROMBOSIS

Vaskular

Trombosit Koagulasi
A. VASKULAR
* Vasokonstriksi
* Aktifasi trombosit
* Aktifasi faktor Koagulasi

B. TROMBOSIT
* Adesi
* Agregasi
* RX pelepasan isi trombosit
 Granula padat : ADP, ATP, Ca, Epinefrin, Norepinefrin,
 Granula alfa : Fibrinogen, vWF, FV, PF 4, TG,
 Lisosom : Enzim asam hidrolase

C. SISTIM KOAGULASI VS FIBRINOLISIS


NOMENCLATUR FAKTOR PEMBEKUAN DARAH

I Fibrinogen
II Protrombin
III Tissue factor
IV Ion calsium
V Proaccelerin
VI -
VII Proconvertin
VIII Anti hemophilic factor
IX Plasma tromboplastin component
X Stuart factor
XI Plasma tromboplastin antecedent
XII Hageman factor
XIII Fibrin stabilizing factor
- High moleculer weight kininogen
- Pre kalikrein
Jalur Jalur
intrinsik Ekstrinsik

XII VII
Kontak
XIIa Tromboplastin
Ca
HMWK Jaringan
XI XIa

IX IXa
VIIa
PF3, VIII, Ca
X Xa
V, PF3, Ca
Fibrinogen
Protrombin Trombin
Fibrin Monomer

Fibrin Polimer
Solubel
XIII XIIIa
Ca Fibrin Polimer
Insoluber
Intrinsik Extrinsik Eksogen

XIIa, Kalikrein t-PA Urokinase


Aktifator Plasminogen

Plasminogen terikat Plasmin terikat Fibrin

FDP

Plasminogen bebas Plasmin bebas Fibrinogen


Fc V, Fc VIII

Anti Plasmin
TROMBOSIS
What is thrombosis ?
• Thrombosis is the formation or presence
of a blood clot inside a blood vessel or
cavity of the heart
* Triad Virchow
 Kelainan dinding pembuluh darah
* kerusakan endotel : hipertensi,
kateterisasi, anoksis , rokok,
RX ag – ab, hiperkolesterolemia,
hiperhomosisteinemia

 Perubahan aliran darah  kerusakan endotel, perlambatan

 Perubahan daya beku darah : Ggn keseimbangan sisitim


koagulasi dan fibrinolisiss
Pathophysiology thrombosis
Thrombosis
• Arterial thrombosis (white thrombus)
• Venous thrombosis (red thrombus)
HIGH FLOW : ARTERIAL CIRCULATION

Fibrin RBCs Platelets

White Thrombus
SLOW FLOW : VENOUS CIRCULATION

Fibrin RBCs Platelets

Red Thrombus
Incidence of thrombosis in United
States of America
Disease US incidence Total in US /year Definable
/100.000 cases reason

• Deep Vein Thrombosis 159/100.000 398.000  80%


• Pulmonary Embolus 139/100.000 347.000  80 %
• Fatal Pulmonary Emb. 94/100.000 235.000  80 %
• Myocardial Infarction 600/100.000 1.500.000  67 %
• Fatal MI 300/100.000 750.000  67 %
• Cerebrovascular thromb. 600/100.000 1.500.000  30 %
• Fatal Cereb. Trhromb. 396/100.000 990.000  30 %
• Total serious thromb. In US 1498/100.000 3.742.000  50 %
• Total deaths from above thrmb. 790/100.000 1.990.000  50 %

• Bick RL, Clin Appl Throm Hemos 3, Suppl 1, 1997


Diagnosis

1. Anamnesis  Riwayat penyakit (Faktor risiko


medis & bedah), Manifestasi klinis
2. Pemeriksaan fisik
3. Pemeriksaan Laboratorium
4. Pemeriksaan lain:
• Venografi (“Golden Standard”)
• USG/ Doppler
• Duplex scan
• Impedance Plethysmography
FAKTOR RISIKO TROMBOSIS ARTERI
Hipertensi, hiperkolesterolemia,
hiperlipoproteinemia, merokok, diabetes melitus,
hiperhomosisteinemia, trombositosis, polisitemia

FAKTOR RISIKO TROMBOSIS VENA


Imobilisasi, operasi, trauma jaringan yang luas,
kehamilan, pil kontrasepsi, defisiensi AT3 / protein C/S
/ Fc XII, PNH
MANIFESTASI KLINIS &
PEMERIKSAAN KLINIS

ARTERI / VENA
ORGAN
ORGAN
• OTAK
• MATA
• THT
• JANTUNG
• PARU
• ORGAN VISERAL
• EXTREMITAS
DVT >< AIL
Patogenesis, Perjalanan Penyakit,
Komplikasi, Prognosis

DVT AIL

• Dasar STASIS ISKEMIA

• Perjalanan Akut Kronik


penyakit (kel. tungkai/tempat lain)

Kronik Akut
(tromboemboli/trombosis)

• Komplikasi akut PE Nekrosis  amputasi

• Prognosis Baik / fatal Fatal lokal / sistemik


DVT >< AIL
Diagnosis: Keluhan dan Tanda

DVT AIL
• Keluhan (stasis) (iskemia)
utama/awal - edema tungkai nyeri:
biasanya unilateral - tromboemboli: onset akut
- silent DVT - trombotik: pelan-pelan
- nyeri dan keras (intermittent claudication)

• Keluhan & - nyeri - “6 Ps”: pain, pallor, pares-


tanda - pitting edema thesia,paralysis,pulseless-
- flebitis:inflamasi ness, poikylothermia
- dilatasi v.superfisial - awal: nyeri & parestesia
- sianosis (ileofemoral) - palpasi denyut arteri -
PEMERIKSAAN LABORATORIUM

• DVT: - D-dimer:
- D-dimer < 500 ng/ml  menyingkirkan DVT
atau PE
- nilai prediktif negatif pada DVT & PE: 98 %
- sensitif tetapi tidak spesifik: pasca bedah,
DIC, infeksi, dll  D-dimer (+)
- metoda ELISA: cepat dan akurat
- Pemeriksaan hemostasis lain: kelainan
dasar DVT ?  trombofilia herediter/didapat ?
(defisiensi AT III, Protein C, APS, dll)
 penentuan lamanya terapi antitrombosis
PENATALAKSANAAN

- MEDIS
- BEDAH
ANTITHROMBOTIC DRUGS:

• ANTIPLATELET DRUGS
• ANTICOAGULANT DRUGS
• THROMBOLYTIC AGENTS
ANTIPLATELET DRUGS

• ASPIRIN
• DIPYRIDAMOL
• CLOPIDOGREL AND TICLOPIDINE
ANTICOAGULANT DRUGS

• WARFARIN
• HEPARIN
• HIRUDIN AND DIRECT THROMBIN INHIBITORS
COMPARATIVE CHARACTERISTICS
OF ANTICOAGULANTS

Oral Fixed Fast onset Predictive No coagulation


administration dosing and offset kinetics monitoring

Warfarin 
Heparin 
LMWH    
Dose and administration
• UFH : initial dose: bolus 75-100 u/kgBB
followed by continous infusion
to achieve aPTT between
1.5 to 2.5 times control
• LMWH :1 mg/kgBB or 0.1 ml/10kgBB sc
twice daily
• Fondaparinux : 7.5 mg for 50-100 kgBB
sc daily
Warfarin - Action
• Inhibits the synthesis of (in order of potency)
– Factor II
– Factor X
– Factor VII
– Factor IX
Conversion from Heparin to Warfarin
• May begin concomitantly with heparin therapy
• Heparin should be continued for a minimum of four
days
– Time to peak antithrombotic effect of warfarin is delayed
96 hours (despite INR)
• When INR reaches desired therapeutic range,
discontinue heparin (after a minimum of four days)
THROMBOLYTIC AGENTS

• STREPTOKINASE
• TISSUE PLASMINOGEN ACTIVATOR