Hemostasis 1
Hemostasis 1
Hemostasis 1
ARREST BLEEDING
MAINTAIN BLOOD IN FLUID STATE
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Stage of the Hemostatic Process
Primary Hemostasis
Blood vessel contraction
Platelet Plug Formation
Secondary Hemostasis
Activation of Clotting Cascade
Deposition & Stabilization of Fibrin
Tertiary Hemostasis
Dissolution of Fibrin Clot
Dependent on Plasminogen Activation
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NORMAL
NORMALHAEMOSTASIS
HEMOSTASIS 4
VESSEL
VESSELINJURY
INJURY
TISSUE
TISSUE
COLLAGEN EXPOSURE TROMBOPLASTIN
TROMBOPLASTIN
F. XII
PLATELET RELEASE
REACTION
SEROTONIN PLATELET
FACTORS
BLOOD
VACOKONSTRICTION TROMBOXANE A2, ADP COAGULATION
REDUCED PLATELET AGGREGATION
BLOOD FLOW THROMBIN
PRIMARY HAEMOSTATIC PLUG
PLATELET FUSION
trombosit
Adhesion
endothelial cells
Activation
sub endothelial tissue
Vascular Aggregation
injury
White clot
Formation of
platelet plug
exposed sub 5
endothelial tissue
The haemostatic system:
secondary haemostasis and clot formation
Coagulation cascade
leads to clot formation
Clot
growth
Fibrin threads
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Hemostatic Plug Formation
PRIMARY
AGGREGATION
Fibrin
SECONDARY
COAGULATION Thrombin
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Adapted from Ferguson JJ, et al. Antiplatelet Therapy in Clinical Practice. 2000:15-35.
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Hemostatic mechanism 9
Hereditary Clotting factor Deficiencies
( Bleeding Disorders )
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2. UNCOMMON INHERITED DEFICIENCIES
- FIBRINOGEN & DYSFIBRINOGEN
- PROTHROMBRIN (F.II) &
DYSPROTHOMBRIN
- F. V ( PARAHEMOPHILIA )
- F. VII
- F. X
- F.XII
- F.XIII
- COMBINED DEFICIENCIES
- OTHER
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3. ACQUIRED DEFICIENCIES
- VIT. K
- CONSUMPTION COAGULOPATHY
- PARENCHYMAL LIVER DISEASE
- CONGENITAL HEART DISEASE
- CARDIOPULMONARY BYPASS
- RENAL DISEASE
- ACQUIRED INHIBITORS
( CIRCULATING ANTICOAGULANTS )
- OTHER
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4. NEONATAL DEFICIENCIES
- HEMORRHAGIC DISEASE OF THE
NEWBORN
- INHERITED DEFICIENCIES
- ACQUIRED DEFICIENCIES
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HEMORRHAGIC DISEASE OF
THE NEWBORN
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RISK FACTOR
Breast feeding
failure to receive vitamine K at birth
Clinical features
bleeding is relatively infrequent occurs mild to
moderate and typified by brusing, oozing from
venepuncture sites and rarely internal bleeding.
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Laboratorium
Prolongation of PT
Prolonging aPTT Not specific
Decarboxy-prothrombin (PIVKA II)
Treatment
- Suspect vitamin K deficiency
parenteral administration of vit.K 1 mg/dose
- With bleeding FFP 10-15 ml/kg
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DIC
Disseminated intravascular coagulation
(Consumptive Coagulopathy )
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CAUSE OF DISSEMINATED INTRAVASCULAR
COAGULATION
INFECTIOUS
Meningococcemia purpura fulminant
Other gram negative bacteria (haemophilus, salmonella, escherchia
coli)
Gram negative bacteria (group B streptococci, staphilococci)
Rickettsia (Rocky Mountain spotted fever)
Virus (Cytomegalovirus, herpes simplex, hemorrhagic fevers)
Malaria
Fungus
TISSUE INJURY
Central nervous system trauma (massive head injury)
Multiple fracture with fat embol
Crush injury
Profound shock or asphyxia
Hypoxemia or hyperthermia
Massive burn 18
CONTINUE.
MALIGNANCY
Acute promyelocytic leucemia
Acute monoblastic or myelocytic leucemia
Widespread malignancies (Neuroblastoma)
VENOM OR TOXIN
Snake bites
Insect bites
MICROANGIOPATHIC DISORDERS
Severe thrombotic thrombocytopenic purpura or hemolytic uremic syn
Giant hemangioma (Kasebach- Merritt syndrome)
GASTROINTESTINAL DISORDERS
Fulminant hepatitis
Severe inflamatory bowel disease
Reye syndrome
MISCELLANEOUS
Severe acute graft rejection
Acute hemolytic trasfusion resection
Severe collagen vascular disease
Kawasaki disease
Heparin-induced thrombosis
Infusion of activated prothrombin complex concentrates
Hyperpyrexia / encephalopathy, hemorrhagic shock syndrome
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Clinical manifestation
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Treatment
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INTRAVENOUS HEPARINIZATION:
- INTERMITTEN SCHEDULE :
100 U/KG/4 hours
- CONTINUOUS SCHEDULE :
50 U/KG INITIAL BOLUS, than
25 U/KG/hours with CONTINUOUS
INFUSON
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