Post on 07-Apr-2018
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DISSEMINATED
INTRAVASCULARCOAGULATIONDokter Magang Interna FK UNPAD
RSUD Karawang
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Definition
An acquired sydrome where coagulation system
and/or fibrinolytic is activated systematically that
cause coagulation intravascular that exceed natural
anti coagulant mechanism
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Hemostasis Review
Patophysiology of Hemostasis:
Primary Hemostasis :
VascularPlatelet
Secondary Hemostasis :
Coagulation Factor
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Hemostasis Review
Primary Hemostasis:
Vascular Vasoconstriction
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Hemostasis Review
Platelet Adhesion and Agreggation
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Hemostasis Review
Secondary Hemostasis: Coagulation Factor
fibrinogenfibrin
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Hemostasis Review
Secondary Hemostasis
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Hemostasis Review
Antithrombotic counter-regulation
Thrombomodulin
Blocks coagulation
t-PA
Fibrinolysis
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Hemostasis Review
Hemostasis Balance
Procoagulant Anticoagulant
Clotting Factors
Tissue factor*
Antiplasmin
PAI-1
ATIII
Fibrinolytic System
TFPI
Prot. C
Prot. S
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Pathophysiology of DIC
- Activation of blood coagulation
- Suppression of physiologic anticoagulant pathways
-
Impaired fibrinolysis
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Pathophysiology of DIC
Systemic activation of coagulation
Intravascular
deposition of
fibrin
Thrombosis ofsmall and
midsize vessels
Depletion ofplatelets and
coagulation
factors
Bleeding
Organ failure
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Conditions Associated with DIC
- Infectious/septicemia
- Malignancy
-
Obstetric- Tissue injury
- Intravascular hemolysis
- Acute liver disease
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Clinical Manifestations of DIC
ORGAN ISCHEMIC HEMOR.
Skin Pur. FulminansGangreneAcral cyanosis
Petechiae
EchymosisOozing
CNS Delirium/ComaInfarcts
Intracranialbleeding
Renal Oliguria/AzotemiaCortical Necrosis
Hematuria
Cardiovascular MyocardialDysfxn
Pulmonary Dyspnea/HypoxiaInfarct
Hemorrhagiclung
GIEndocrine
Ulcers, InfarctsAdrenal infarcts
Massivehemorrhage.
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Clinical Manifestations of DIC
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Diagnosis of DIC
- Presence of disease associated with DIC
- Appropriate clinical setting
clinical evidence of thrombosis, hemorrhage, orboth
- Laboratory studies
serial test are more helpful than single test
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Laboratory Test Used in DIC
- Platelet count
- Prothrombin time
-
aPTT- Thrombin time
- D-dimer
- Antithrombin III
- Fibrinogen
- Fragment
Prothrombin 1+2
-
Fibrin degradationproduct
- Platelet factor 4
- Protamine test
- Reptilase time
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Laboratory diagnosis in DIC
Prolongation of prothrombin time
Prolongation of activated partial thromboplastin
time
Decrease in platelet count
Peripheral smear examination: schistocytes
Decrease in fibrinogen
Low levels of coagulation factors
Decrease in factor V, Decrease in factor VIII
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Laboratory diagnosis of DIC
Increase in D-dimer
Increase in prothrombin fragment 1+2
Increase in fibrinopeptide A Increase in fibrinopeptide B
Increase in thrombin-antithrombin complex
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Differential Diagnosis
- Severe liver failure
- Vitamin K deficiency
-
Liver disease- Thrombotic thrombocytopenic purpura
- Congenital abnormalities of fibrinogen
- HELLP syndrome
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Treatment of DIC
Stop the triggering factor
Supportive therapy
Plasma and platelet substitution therapy Anticoagulants
Physiologic coagulation inhibitors
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Plasma Therapy
Fresh Frozen Plasma
- Provides clotting factors, fibrinogen, inhibitors, and
platelets in balanced amounts.
- Usual dose is 10-15 ml/kg
Indications:
- Active bleeding
- Patient at high risk for bleeding complications
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Platelet therapy
Platelets
approximate dose 1 unit/10 kg
Indications- Active bleeding
- Patient at high risk for bleeding complications
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Blood
Replaced as needed to maintain adequate oxygen
delivery.
Blood loss due to bleeding
RBC destruction (hemolysis)
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Coagulation Inhibitor Therapy
Antithrombin III
Protein C concentrate
Tissue Factor Pathway Inhibitor (TFPI)
Heparin
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Heparin
Use is very controversial.
Indicated in patients with clinical evidence of fibrin
deposition or significant thrombosis.
Possible indicated in Retained Death Fetus
Syndrome, Aorta Aneurysm, Acute Promyelocytic
Leukemia
Dose of heparin is determined by clinicalmanifestation