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FAAL HEMOSTASIS

Oleh : diah

dr. Diah Hermayanti, SpPK

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TIU Memahami pemeriksaan faal hemostasis

TIK Memahami proses hemostasis

Memahami proses hemostasis pada jejas vaskuler

Memahami dan dapat menginterpretasi

pemeriksaan laboratorium hemostasis
 HEMOSTASI
Proses fisiologisS
yg seimbang :

❑ mencegah perdarahan >>>

(setelah perlukaan vaskuler)

❑ mempertahankan sirkulasi
(dg menjaga darah tetap cair)

Trombosis Perdarahan

KOAGULASI HEMOSTASIS FIBRINOLISIS

Perdarahan Trombosis
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TAHAPAN PROSES BILA TJD TRAUMA VASKULER

1. Vasokonstriksi

2. Primary hemostasis (detik)

3. Secondary hemostasis (menit)

4. Proses perbaikan & fibrinolisis

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SECONDARY HEMOSTASIS

PRIM ARY HEMOSTASIS

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PROSES
diah

HEMOSTASIS
Vascular
injury
Exposure of colagen
Tissue factor
Platelet adhesion
&
Serotonin Release reaction Release of
Platelet phopholipid

TX2 , ADP

Vasoconstriction Platelet
Coagulation
aggregation
cascade

Primary
Blood flow ↓
Hemostatic plug Thrombin

Secondary hemostatic plug

Fibrin
(stable hemostatic plug )
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HMWK JALUR KOAGULASI
Prekalikrein diah

DARAH
XII XIIa
XI XIa TF + VIIa
IX IXa X JALUR EKSTRINSIK
JALUR INTRINSIK
+ Ca 2+
Ca 2+
VIII VIIIa
Xa + Va + phospholipid

XIII
2+
II (prothrombin) Ca IIa (thrombin)
PL

XIIIa

I (fibrinogen) Fibrin Cross-

linked
fibrin
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FAKTOR KOAGULASI diah

PLASMA
Faktor Nama

I Fibrinogen
II Prothrombin
III Tissue thromboplastin
IV Calcium
V Proaccelerin (labile factor)
VII Proconvertin (stable factor)
VIII Antihemophilic A factor
IX Antihemophilic B factor
X Stuart factor
XI Plasma thromboplastin antecedent
XII Hageman factor, contact factor
XIII Fibrin stabilizing factor
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JALUR FIBRINOLISIS
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PLASMINOGEN
Aktivator :
o intrinsik : Anti aktivator :
F.XII, kinin, trombin, o C-1 Esterase inhibitor
urokinase o PAI (plaminogen activator
o Ekstrinsik : inhibitor )
t-PA, excercise, stress
o Terapeutik :
streptokinase
PLASMIN
Antiplasmin :
o α2 antiplasmin
o α2 makroglobulin

FIBRIN FIBRIN DEGRADATION PRODUCTS

(FDP)
D-Dimer
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PEMERIKSAAN LABORATORIUM
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UNTUK MENILAI FAAL

HEMOSTASIS
TUJUAN PEMBELAJARAN :
❑ Memahami prinsip pemeriksaan laboratorik
hemostasis sederhana

❑ Mengkaitkan dg penyakit gangguan faal hemostasis

(interpretasi & diagnostik)

Pendekatan :
1. Anamnesis
2. Pemeriksaan fisik
3. Laboratorik
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ENDOTEL MENGATUR FLUIDITAS HEMOSTASIS

Trombosis Bleeding

Pro-trombotik : Anti-trombotik :
trombosit-vaskuler ➢ antikoagulan inhibitor
koagulasi plasma
BLOOD ➢ fibrinolisis
FLOW

Bleeding Trombosis

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ANAMNESIS
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Eksplorasi riwayat penyakit :

❖ keturunan (herediter)
❖ didapat (acquired )

Anamnesa :
. Perdarahan circumsisi / tali pusat / persalinan ?
2. Epistaksis / memar (easy bruising) ?; persendian
(joint bleeding)?
3. Perdarahan cabut gigi ?
4. Menstruasi berkepanjangan ?
5. Memar tanpa sebab yg jelas ?
6. Darah di urin / feses ?
7. Riwayat transfusi (terutama trombosit) ?
8. Minum obat aspirin / derivatnya (7 hari terakhir ) ?
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PEMERIKSAAN FISIK diah

PTEKIAE : bercak merah kecil di kulit (Ф ujung jarum)

(ekstravasasi darah dari vaskuler yg intak
karena peningkatan permeabilitas)
PURPURA : kumpulan ptekiae

EKIMOSIS : area lebam (kebiruan) (Ф > purpura)

HEMATOMA : lebam luas yg menginfiltrasi subkutan atau

otot, shg menyebabkan deformitas
HEMARTROSIS : perdarahan di persendian (perdarahan berat)
gangguan koagulasi (hemofili)
HEMATURIA : perdarahan di urin (trauma lokal batu; overdosis
antikoagulan; hemofili)
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PEMERIKSAAN
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TES SKRINING LABORATORIUM

:

➢ Jumlah & morfologi menilai primary

trombosit hemostatic plug
➢ Bleeding time

➢ Clotting time menilai koagulasi /

➢ aPTT (activated partial secondary hemostatic
thromboplastin time) plug
➢ PT (prothrombin time)
TES KONFIRMASI / KHUSUS :
➢ Fungsi trombosit (adesi, sekresi, agregasi)
➢ Pengukuran faktor koagulan
➢ Pemeriksaan inhibitor
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TES SKRINING PRIMARY HEMOSTATIC
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PLUG
(TROMBOSIT-VASKULER )
Tujuan : menentukan kelainan trombosit / vaskuler

TROMBOSIT :
o morfologi
o jumlah
o fungsi

Capillary resistance test (Rumple-Leed test)

Bleeding time (Ivy ; Duke)

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RUMPLE – LEEDE TEST
(Capillary resistance test) diah

VOLAR
(dibaca 15 menit setelah
Tekanan dilepas)
Systole
HASIL :
(-) : jumlah ptekiae < 10
10-20 : meragukan
Diastole(+) : > 20
5 minutes
(± 100 mmHg) POSITIF :
1. Trombositopenia
2. Gangguan vaskuler
3. Gangguan fungsi trombosit
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BLEEDING TIME / BT
(waktu perdarahan) diah

BT menilai Pembentukan hemostatic

plug

1. Kelainan trombosit
2. Kelainan vaskuler

Normal (Duke) : 1-3 menit

Memanjang :
1. Kelainan konstriksi vaskuler
2. Trombositopenia
3. Gangguan adhesi trombosit
4. Gangguan pelepasan ADP trombosit
5. Gangguan aggregasi trombosit
6. Gangguan avaibilitas PF3
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Bleeding Time
diah

Volar
Cuping
telinga 40 mmHg
Cara Duke Cara Ivy
Normal Normal
1-3 menit 1-7 menit

22 Kerta
1½ s
1 ½ 3 saring
½

Star Star Bleeding time

Normal t Abnormal
t (memanjang)
menilai :
Dacie et al. 1975, Hirsh et al. 1979, Sirridge et al.
1983
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TES SKRINING KOAGULASI
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(secondary hemostatic plug /fibrin clot formation)

Tujuan :
❖ deteksi gangguan koagulasi
❖ menentukan tahapan proses yg terganggu

Pemeriksaan :
❑ clotting/coagulation time (CT)
❑ aPTT (activated partial thromboplastin time)
❑ PPT (plasma prothrombin time)
❑ TT (thrombin time)
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CLOTTING FACTOR (CT) diah

MENILAI pembentukan tahap awal dr thrombin

WAKTU untuk menghasilkan bekuan yg terlihat mata
(Jalur intrinsik & jalur umum)

CT >>> - defisiensi faktor pembekuan yg berat

pada jalur intrinsik dan jalur umum (common
pathway)
(Tidak dipengaruhi oleh F VII)
- pemakaian heparin

Normal : 5-15 ‘
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ACTIVATED PARTIAL THROMBOPLASTIN TIME (aPTT)

Tes koagulasi
jalur intrinsik (prekalikrein, HMWK, F. XII,XI, IX, VIII)
jalur umum (F. X,V, prothrombin, fibrinogen)

aPTT deteksi :
1. Defisiensi faktor di atas
2. Skrining antikoagulan lupus
3. Monitor terapi heparin

Normal : 25 - 39 detik (tergantung laboratorium)

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PLASMA PROTHROMBIN TIME (PPT) diah

Tes koagulasi
Jalur ekstrinsik (F.VII)
Jalur umum ( F.X, V, II, I)

PPT deteksi :
1. kontrol antikoagulan oral koumarin
(F.II, VII, X adalah vit K dependent yg
terdepresi oleh obat koumarin)
2. defisiensi F. VII & X

Normal : 10 -14 detik (tergantung laboratorium)

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diah

INTERNATIONAL NORMALISED RATIO

(INR)

Dipergunakan untuk menstandarsisasi hasil pengukuran

PPT
yg sangat tergantung pada masing-masing laboratorium
ISI
INR = PTtest

PTnormal

ISI : International sensitivity index (tergantung batch)

Normal : 0,8 -1,2 (normal, tanpa terapi antikoagulan)

2 -3 (pengobatan antikoagulan/Warfarin)
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THROMBINE TIME (TT) diah

Tes koagulasi
mengukur kecepatan pembentukan fibrin

TT abnormal :
1. defisiensi F.I (fibrinogen)
2. kelainan kualitatif fibrinogen
3. heparin
4. disseminated intravascular coagulation (DIC)
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PENDEKATAN
(Anamnesa, fisik, laboratorik)
diah

Gg.Perdarahan Gg.Trombosis
(bleeding disorders) (thrombotic disorders)

Congenital
(herediter)

Acquired
(didapat)
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Gg. KOAGULASI (CLOTTING DISORDERS)
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HEREDITER

Von Willebrand synd. 1:200 - 5.000

Hemophilia A (VIII def) 1:5.000 - 10.000
Hemophilia B (IX def) 1:50.000 - 100.000
Factor XI deficiency 1:100.000 - 500.000
Factor II deficiency < 1:10 6
Factor V deficiency < 1:10 6
Factor VII deficiency < 1:106
Factor X deficiency < 1:106
Factor XII deficiency < 1:106
Prekallikrein deficiency < 1:106
HMWK deficiency < 1:106
Afibrinogenia < 1:106
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Gg. KOAGULASI DIDAPAT (ACQUIRED) diah

ACQUIRED DEFICIENCY STATE :

Liver disease
vit K deficiency
oral anticoagulant
amyloidosis
consumptive coagulopathies
hematin
snake venom

INHIBITION of CLOT FORMATION :

Heparin lupus anticoagulant
macromolecules neutralizing factor inhibitors
(dextran) non- neutralizing factor inhibitors
dysfibrinogenemia
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DIFERENSIAL SKRINING KOAGULASI diah

Prolonged APTT Prolonged PT Prolonged APTT&PT

COMMON
Heparin Vit K deficiency Vit K deficiency
Lupus anticoagulant Oral anticoagulant Oral anticoagulant
Hemophilia A Liver disease Liver disease
Hemophilia B Consumptive
VWD (with long BT) -coagulopathies

UNCOMMON
Specific factor inhibitors Factor VII deficiency F. II, V, or X def
F. XI or XII deficiency Hereditary –
Prekalikrein def dysfibrinogenemia
HMWK deficiency Afibrinogenemia
Specific factor-
inhibitors
Amyloidosis
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GANGGUAN TROMBOSIT diah

Gangguan kualitas
(trombositopati) :
Gangguan kuantitas : ❑ Primer
❑ Jumlah turun ❑ Sekunder
(trombositopenia) : Fungsi yg terganggu :
- produksi << ➢ Adesi
- usia <; destruksi > ➢ Release
- pooling >> ➢ Agregasi
(di Limpa) ➢ Koagulasi
❑ Jumlah meningkat
(trombositosis)
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KELAINAN TROMBOSIT HEREDITER diah

Kelainan Laboratorium

Kelainan adhesi
von Willebrand synd vWF, Platelet aggregation
Bernard-Soulier synd vWF, Platelet aggregation
Collagen disorders BT, normal platelet aggregation
Kelainan agregasi
Glansmann’s thrombasthenia BT, platelet aggregation, GP IIB-IIIA
Afibrinogenemia BT, platelet aggregation, fibrinogen
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KELAINAN TROMBOSIT DIDAPAT diah

(mengganggu fungsi trombosit)

Obat (aspirin, indometasin, ibuprofen, penisilin)

Antibodi trombosit
Penyakit ginjal
Myeloproliferative disorders
Myeloma
Fibrinolysis
Macromolecules
Fibrin split product
Monoclonal proteins
In vivo release
hypothyroidism
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GANGGUAN TROMBOSIS diah

HEREDITER

Sistem Kelainan

Serine protease inhibitor Defisiensi Antitrombin III

(SERPINS) Def. Heparin kofaktor II

Sistem fibrinolitik Def. Protein C heterozygous

Def. Protein C homozygous
Def. Protein S heterozygous

Trombosit Hyperactive platelet synd

Miscellaneous dll
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Gangguan Trombotik Didapat

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Kondisi sistemik : Kelainan hemostatik :

Atherosclerotic vascular disease Lupus anticoagulant

diabetes mellitus DIC
malignat neoplasma Thrombotic thrombocyto-
myeloproliferative disorders penic purpura
paroxismal nocturnal hemoglobinuria Hemolytic-uremic synd
estrogen & oral contraceptive Snake venoms
Pregnancy Coagulation factor-
venous stasis concentrates
nephrotic syndrome
hyperlipidemia
artificial vascular prostheses
hyperviscosity
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COMPLEX HEMOSTATIC DISORDERS
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DISORDER LABORATORY MANIFESTATIONS

Disseminated intravascular thrombocytopenia low fibrinogen

Coagulation (DIC) long PT long APTT
increased FDPs low AT III

Thrombotic thrombocytopenic thrombocytopenia normal fibrinogen

Purpura (TTP) microangiopathic peripheral blood film
Hemolytic uremic syndrome normal AT III
(HUS)

Liver disease long PT low AT III

normal to low fibrinogen

Brandt 1999
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DISSEMINATED INTRAVASCULAR COAGULATION
(DIC) diah

INITIATING STIMULUS

ACTIVATION ACTIVATION

THROMBIN PLASMIN

FIBRIN PLATELET FACTOR FIBRINOLYSIS

FORMATION ACTIVATION CONSUMPTION

MICROVASCULAR HEMORRHAGE
THROMBOSIS

FIBRINOGEN PLATELET
DEPLETION DEPLETION

Brandt 1999
HEMORRHAGE
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DIC STIMULATOR :
diah

1. Tissue factor coagulants :

trauma
hemolysis
carcinoma

2. Factor producing platelet aggregation :

septicemia
uremia
immune complexes

3. Endothelial damage :
burn
vasculitis
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GANGGUAN HEMOSTATIK
diah
PADA PENYAKIT LIVER

ABNORMALITAS MANIFESTASI LABORATORIUM MANIFESTASI KLINIK

TROMBOSITOPENI TROMBOSITOPENI PERDARAHAN

SINTESA FAKTOR PT & APTT >>>>> PERDARAHAN

KOAGULASI <<<

SINTESA PROTEIN AT III <<, PROTEIN C << THROMBOSIS, DIC

REGULATOR <<<

DISFIBRINOGENEMIA TT / PT / APTT >>>>> NONE / PERDARAHAN

FDP FALSE (+) RINGAN

ABNORMAL PROTEIN PT >>>> PERDARAHAN (?)

DEPENDEN VIT K

Brandt,
1999
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VITAMIN – K DEFICIENCY diah

VIT-K dibutuhkan oleh hati untuk sintesa :

Vit-K dependent coagulation factors
(F. II , VII, IX, X)

SUMBER VIT-K :
- makanan (tu. Tumbuhan)
- sifat : fat soluble

PENYEBAB DEFISIENSI :
- malabsorpsi lemak
- obstruksi bilier (gg.sekresi empedu)
- pancreatic disease (gg.produksi lipase
pankreas)
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RINGKASAN diah

TES MENILAI INTEGRITAS

Bleeding time (BT) Trombosit – Vaskuler

Capilary resistance
test
Thrombine time Fibrinogen /fibrine
(TT) conversion
Prothrombine time Jalur ekstrinsik
(PT)
Activated partial Jalur intrinsik
thromboplastin
time (APTT)
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SEMOGA BERMANFAAT
diah