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FAAL HEMOSTASIS
Oleh :
dr. Diah Hermayanti, SpPK

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HEMOSTASIS
Proses fisiologis yg seimbang :

mencegah perdarahan >>>

(setelah perlukaan vaskuler)

mempertahankan sirkulasi
(dg menjaga darah tetap cair)

Trombosis
KOAGULASI
Perdarahan

Perdarahan

HEMOSTASIS
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Trombos
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TAHAPAN PROSES BILA TJD TRAUMA VASKULE

1. Vasokonstriksi
2. Primary hemostasis (detik)
3. Secondary hemostasis (menit)
4. Proses perbaikan & fibrinolisis

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SECONDARY HEMOSTASIS

PRIM ARY HEMOSTASIS

PROSES
HEMOSTASIS
Vascular

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injury
Exposure of colagen

Serotonin

Platelet adhesion
&
Release reaction

Tissue factor
Release of
Platelet phopholipid

TX2, ADP

Vasoconstriction

Blood flow

Platelet
aggregation

Primary
Hemostatic plug

Secondary hemostatic plug

(stable hemostatic plug)

Coagulation
cascade

Thrombin

Fibrin

Surface contac :
HMWK
Prekalikrein

JALUR KOAGULASI DARA

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XII
XI
XIIa
IX
XIa INTRINSIK
JALUR
+
VIII
VIIIa

TF + VIIa
IXa

X
Ca

Ca

2+

JALUR EKSTRINSIK

2+

Xa

Ca
II (prothrombin)
2+
PL

I (fibrinogen)

Va

+ phospholipid

XIII
IIa (thrombin)
XIIIa
Fibrin
linked
fibrin

FAKTOR KOAGULASI PLASMA

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Faktor
I
II
III
IV
V
VII
VIII
IX
X
XI
XII
XIII

Nama

Fibrinogen
Prothrombin
Tissue thromboplastin
Calcium
Proaccelerin (labile factor)
Proconvertin (stable factor)
Antihemophilic A factor
Antihemophilic B factor
Stuart factor
Plasma thromboplastin antecede
Hageman factor, contact factor
Fibrin stabilizing factor

JALUR FIBRINOLIS
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Aktivator :
o intrinsik :
F.XII, kinin, trombin,
urokinase
oEkstrinsik :
t-PA, excercise, stress
oTerapeutik :
streptokinase

PLASMINO
GEN
Anti aktivator :
o C-1 Esterase inhibitor
o PAI (plaminogen activator
inhibitor )

PLASMIN

Antiplasmin :
Antiplasmin
:
o 2
antiplasmin
o
antiplasmin
o 22
makroglobulin
o 2 makroglobulin

FIBRIN

FIBRIN DEGRADATION
(FDP)

PEMERIKSAAN LABORATORIUM
UNTUK MENILAI FAAL HEMOSTASIS

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TUJUAN PEMBELAJARAN :
Memahami prinsip pemeriksaan laboratorik
hemostasis sederhana

Mengkaitkan dg penyakit gangguan faal hem

(interpretasi & diagnostik)

Pendekatan :
1. Anamnesis
2. Pemeriksaan fisik
3. Laboratorik

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ENDOTEL MENGATUR FLUIDITAS HEMOST

Trombosis
Pro-trombotik :
trombosit-vaskuler
koagulasi plasma

BLOOD

Anti-trombotik :
antikoagulan inhibitor
FLOW
fibrinolisis

Bleeding

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ANAMNE
SIS
Eksplorasi
riwayat
penyakit :
keturunan
(herediter)
didapat
Anamnesa :
1.Perdarahan circumsisi
/ tali pusat
(acquired
) / persalinan ?

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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
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PTEKIAE

: bercak merah kecil di kulit ( ujung ja

(ekstravasasi darah dari vaskuler yg in
karena peningkatan permeabilitas)
PURPURA : kumpulan ptekiae
EKIMOSIS : area lebam (kebiruan) ( > purpura)
HEMATOMA

: lebam luas yg menginfiltrasi subk

otot, shg menyebabkan deformitas
HEMARTROSIS : perdarahan di persendian (perdar
gangguan koagulasi (hemofili)
HEMATURIA
: perdarahan di urin (trauma lokal
antikoagulan; hemofili)

PEMERIKSAAN LABORATORIUM

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TES SKRINING :
Jumlah & morfologi
trombosit
Bleeding time
Clotting time
aPTT (activated partial
thromboplastin time)
PT (prothrombin time)

menilai prima
hemostatic p

menilai koagulasi
secondary he
plug

TES KONFIRMASI / KHUSUS :

Fungsi trombosit (adesi, sekresi, agregasi)
Pengukuran faktor koagulan
Pemeriksaan inhibitor

TES SKRINING PRIMARY HEMOSTATIC PLUG

(TROMBOSIT-VASKULER )

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Tujuan : menentukan kelainan trombosit /

TROMBOSIT :
o morfologi
o jumlah
o fungsi

Capillary resistance test (Rumple-Leed tes

Bleeding time (Ivy ; Duke)

RUMPLE LEEDE TEST

(Capillary resistance test)
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VOLAR
(dibaca 15 menit setelah
Systole Tekanan dilepas)

5 minutes
( 100 mmHg)

HASIL :
(-)
: jumlah ptekiae < 10
10-20 : meragukan
Diastole
(+)
: > 20
POSITIF :
1.Trombositopenia
2.Gangguan vaskuler
3.Gangguan fungsi trombosit

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BLEEDING TIME / BT
(waktu perdarahan)
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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

Volar
Cuping
telinga

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40 mmHg
Ivy

Duke

Cara
Normal
1-7 menit

Cara
Normal
1-3 menit

2
1 2
1

Kertas
saring

Start

Normal

Start

Dacie et al. 1975, Hirsh et al. 1979, Sirridge et al. 1983

Abnormal
(memanjang)

Bleeding time
menilai :

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TES SKRINING KOAGULASI

secondary hemostatic plug /fibrin clot formatio
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Tujuan :
deteksi gangguan koagulasi
menentukan tahapan proses yg terga

Pemeriksaan :
clotting/coagulation time (CT)
aPTT (activated partial thromboplast
PPT (plasma prothrombin time)
TT
(thrombin time)

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CLOTTING FACTOR (CT)

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MENILAI
WAKTU

pembentukan tahap awal dr thrombin

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

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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

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PLASMA PROTHROMBIN TIME (PPT)

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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

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THROMBINE TIME (TT)

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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)
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Gg.Perdarahan
(bleeding disorders)
Congenital
(herediter)

Acquired
(didapat)

Gg.Trombosis
(thrombotic disorders)

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Gg. KOAGULASI (CLOTTING DISORDERS)

HEREDITER

Von Willebrand synd.

Hemophilia A (VIII def)
Hemophilia B (IX def)
Factor XI deficiency
Factor II deficiency
Factor V deficiency
Factor VII deficiency
Factor X deficiency
Factor XII deficiency
Prekallikrein deficiency
HMWK deficiency
Afibrinogenia

1:200 - 5.000
1:5.000 - 10.000
1:50.000
- 100.000
1:100.000
- 500.000
< 1:106
< 1:106
< 1:106
< 1:106
< 1:106
< 1:106
< 1:106
< 1:106

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Gg. KOAGULASI DIDAPAT (ACQUIRED)

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

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Prolonged APTT
COMMON
Heparin
Lupus anticoagulant
Hemophilia A
Hemophilia B
VWD (with long BT)
UNCOMMON
Specific factor inhibitors
F. XI or XII deficiency
Prekalikrein def
HMWK deficiency

Prolonged PT

Prolonged APTT&PT

Vit K deficiency
Oral anticoagulant
Liver disease

Vit K deficiency
Oral anticoagulant
Liver disease
Consumptive
-coagulopathies

Factor VII deficiency

F. II, V, or X def
Hereditary
dysfibrinogenemia
Afibrinogenemia
Specific factorinhibitors
Amyloidosis

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GANGGUAN TROMBOSIT

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Gangguan kualitas
(trombositopati) :
Gangguan kuantitas :
Jumlah turun
(trombositopenia) :
- produksi <<
- usia <; destruksi >
- pooling >>
(di Limpa)
Jumlah meningkat
(trombositosis)

Primer
Sekunder

Fungsi yg terganggu :
Adesi
Release
Agregasi
Koagulasi

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KELAINAN TROMBOSIT HEREDITER

Kelainan
Kelainan adhesi
von Willebrand synd
Bernard-Soulier synd
Collagen disorders
Kelainan agregasi
Glansmanns thrombasthenia
Afibrinogenemia
dll

Laboratorium
vWF, Platelet aggregation
vWF, Platelet aggregation
BT, normal platelet aggregation
BT, platelet aggregation, GP IIB-IIIA
BT, platelet aggregation, fibrinogen

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KELAINAN TROMBOSIT DIDAPAT

(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
HEREDITER
Sistem

Kelainan

Serine protease inhibitor

(SERPINS)

Defisiensi Antitrombin III

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

Kondisi sistemik :
Atherosclerotic vascular disease
diabetes mellitus
malignat neoplasma
myeloproliferative disorders
paroxismal nocturnal hemoglobinuria
estrogen & oral contraceptive
Pregnancy
venous stasis
nephrotic syndrome
hyperlipidemia
artificial vascular prostheses
hyperviscosity

Kelainan hemostatik :
Lupus anticoagulant
DIC
Thrombotic thrombocytopenic purpura
Hemolytic-uremic synd
Snake venoms
Coagulation factorconcentrates

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COMPLEX HEMOSTATIC DISORDERS

DISORDER

LABORATORY MANIFESTATIONS

Disseminated intravascular
Coagulation (DIC)

thrombocytopenia
long PT
increased FDPs

low fibrinogen
long APTT
low AT III

Thrombotic thrombocytopenic
Purpura (TTP)
Hemolytic uremic syndrome
(HUS)

thrombocytopenia
normal fibrinogen
microangiopathic peripheral blood film
normal AT III

Liver disease

long PT
low AT III
normal to low fibrinogen
Brandt 1999

DISSEMINATED INTRAVASCULAR COAGULATION

(DIC)

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INITIATING STIMULUS
ACTIVATION

ACTIVATION

THROMBIN

FIBRIN
FORMATION

PLATELET
ACTIVATION

MICROVASCULAR
THROMBOSIS

FIBRINOGEN
DEPLETION

PLASMIN

FACTOR
CONSUMPTION

FIBRINOLYSIS

HEMORRHAGE

PLATELET
DEPLETION
Brandt 1999

HEMORRHAGE

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DIC STIMULATOR :
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
PADA PENYAKIT LIVER

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ABNORMALITAS

MANIFESTASI LABORATORIUM

MANIFESTASI KLINIK

TROMBOSITOPENI

TROMBOSITOPENI

PERDARAHAN

SINTESA FAKTOR
KOAGULASI <<<

PT & APTT >>>>>

PERDARAHAN

SINTESA PROTEIN
REGULATOR <<<

AT III <<, PROTEIN C <<

THROMBOSIS, DIC

DISFIBRINOGENEMIA

TT / PT / APTT >>>>>
FDP FALSE (+)

NONE / PERDARAHAN
RINGAN

ABNORMAL PROTEIN
DEPENDEN VIT K

PT >>>>

PERDARAHAN (?)

Brandt, 1999

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VITAMIN K DEFICIENCY
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
TES

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MENILAI INTEGRITAS

Bleeding time (BT)

Capilary resistance
test

Trombosit Vaskuler

Thrombine time
(TT)

Fibrinogen /fibrine
conversion

Prothrombine time
(PT)

Jalur ekstrinsik

Activated partial
thromboplastin
time (APTT)

Jalur intrinsik

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SEMOGA BERMANFAAT
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