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Disseminated Intravascular Coagulation Final (Komed)

Apr 07, 2018

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Adie Kristanto
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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