HOMEOSTASIS

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HEMOSTATIC MECHANISM

The classic mechanism include :

1. Tissue factor
2. Vascular response
3. Platelet adhesion
platelet aggregation
4. Clot formation
clot stabilization
limitation of clotting
5. Fibrinolysis
 Function of HEMOSTASIS

 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

STABLE HEMOSTATIC PLUG FIBRIN

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 The primary haemostatic system:
haemostasis and platelet plug formation
Primary haemostasis
Platelet aggregation

trombosit
Adhesion
endothelial cells
Activation
sub endothelial tissue

Vascular Aggregation
injury
White clot

Formation of
platelet plug

exposed sub 6
endothelial tissue
 The haemostatic system:
secondary haemostasis and clot formation

Prothrombin Thrombin Activation of the

Factor Xa coagulation cascade leads
Intrinsic Extrinsic Fibrinogen Fibrin
to generation of thrombin
pathway pathway and, in turn, fibrin

Coagulation cascade
leads to clot formation

Clot
growth
Fibrin threads

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 Hemostatic Plug Formation

PRIMARY
AGGREGATION

Platelet Aggregation Clotting

Hemostatic
Clot

Fibrin
SECONDARY
COAGULATION Thrombin

0 min 5 min 10 min

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Adapted from Ferguson JJ, et al. Antiplatelet Therapy in Clinical Practice. 2000:15-35.
Hereditary Clotting factor Deficiencies
( Bleeding Disorders )

1. COMMON INHERITED DEFICIENCY

- F. VIII  HEMOPHILIA A
- vWB  Von Willebrand Diasese
- F. IX  HEMOPHILIA B
- F. XI  HEMOPHILIA C

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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

 HEMORRHAGIC DISEASE OF NEWBORN

(HDN)  CLASSIFIED INTO:
- EARLY  OCCUR 24 HOURS OF LIFE
- CLASSICAL  AFTER FIRST WEEK OF LIFE
(WEEK 2nd – 8TH)
- LATE  INCIDENCE 4.4/100.000 BIRTHS

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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 )

Consumption of clotting factors, platelets

and anticoagulant protein

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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 17
 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

HEREDITARY THROMBOTIC DISORDERS

Antithrombin III deficiency
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Homozygous protein C deficiency
NEWBORN CONTINUE….
Maternal toxemia
Group B streptococcal infections
Abruptio placentae
Severe respiratory disease syndrome
Necrotizing enterocolities
Congenital viral disease (Cytomegalovirus, Herpes simplex)
Erytroblastosis fetalis

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

 Bleeding from site of venipuncture

 Petechiae and ecchymoses
 Laboratory
 PT, APTT, TT 
 Platelet count ↓
 FDP (fibrin degradation product)
 Hemolytic anemia

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Treatment

 Identification and treatment of the triggering

event
 Replacement therapy
- PLATELET CONCENTRATES ( 1U/10 KG)
- CRYOPRECIPIATE ( 50-100 MG/KG
FIBRINOGEN )
- FRESH-FROZEN PLASMA ( 10-15 ML/KG,
INITIALLY ; MAY NEED 5 ML/KG/6JAM)

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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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