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DIC [Compatibility Mode]

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    DISSEMINATED INTRAVASCULAR

    COAGULATION

    (DIC)

    Clinic Departement of Nursing FacultyUNPAD

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    DEFINITION OF DISSEMINATEDINTRAVASCULAR COAGULATION

    DIC is an acquired syndromecharacterized by the intravascular

    ISTHs Scientific Subcommittee on DIC, July 2001

    localization arising from different causes.It can originate from and cause damage to

    the microvasculature, which if sufficientlysevere, can produce organ dysfunction

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    INCIDENCE / ETIOLOGY

    DIC is reported to occur in 1% of hospitalized

    patients. Of those patients, the underlying cause was:

    enera ze n ect on n ~ o casesMalignancy in ~15%

    Surgery or trauma in ~20%

    Hepatic disease in ~10%

    Miscellaneous in ~25%

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    INFECTION

    There are some mechanisms specific to infection in

    animals, there is evidence that Protein C is downregulated, as

    well as thrombomodulin.

    diminishes not only hemodilution, but to stasis as well.

    Tissue damage then occurs, which in itself causes

    thombin formation.

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    MALIGNANCY

    Malignancy is a coagulopathic state. The features of

    malignancy most closely associated with DIC include:

    High levels of tissue factor expressed by tumor cells

    T e express on y tumor ce s o cancer procoagu ant, acalcium-dependent cysteine protease which is not found in

    normal tissue (but is found in fetal tissue). It activates factor

    X directly.

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    TRAUMA

    Trauma causes the release of tissue enzymes and

    phospholipids into the circulation in turn, these trigger the

    activation of cytokines and the coagulation system.

    DIC than other body parts. Head trauma is associated withcoagulopathy in twice as many patients with CT evidence of

    injury (41%) as in those without this evidence the

    coagulopathy was consistent with DIC by labs (more on labslater).

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    OBSTETRICAL

    DIC occurs in a variety of obstetrical complications,

    including:

    Amniotic fluid embolization

    Abruptio placentae

    Eclampsia & severe pre-eclampsia

    Blah blah blah

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    DISSEMINATED INTRAVASCULAR COAGULATION

    (DIC)MECHANISM

    Systemic activation

    of coagulation

    Intravasculardeposition of fibrin

    Depletion of plateletsand coagulation factors

    BleedingThrombosis of small

    and midsize vessels

    with organ failure

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    PPROGRESSIONROGRESSION OFOFSEPSISSEPSIS

    MonocytesEndothelial

    cells

    Endothelial

    cells

    Platelets

    Leuko-

    Non-adhesivesur

    Adhesivesurfa

    Cytokines

    Tissue

    factor

    Activation of coagulation Thrombin Fibrin

    cy es

    f

    ace

    ce

    Accelerates

    coagulation

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    THE CLASSIC COAGULATION SYSTEM

    Surface contact Tissue factor

    XII XIIa

    XI XIa

    APTT Prothrombin time

    IX IXa

    X Xa X

    II IIa

    I Ia (fibrin)

    Phospholipid, Ca++, VIII

    Phospholipid, Ca++, V

    VIIa VII

    Ca++

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    CLINICAL

    OF DIC

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    SYMPTOMS OF DIC

    Dysfunction of multiple organs The pulmonary microembolism syndrome

    Acute: vascular and bronchial constriction Late: ARDS

    Acute renal failure Oli uria increasin serum creatinine haematuria

    Cerebral dysfunction Confusion, blurred consciousness, coma

    Cutane haemorrhagic Failure of liver.

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    DIAGNOSTIC

    DIC

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    BLOOD TESTS WHEN DIC IS SUSPECTED

    Simple screening

    Extended screening

    Platelet count

    Activated partial thromboplastin time (APTT)

    Prothrombin time (PT)

    Fibrin D-dimer fragment

    Antithrombin

    Supplementary testsFibrinogen

    Further evidence for activation of coagulation

    and fibrinolysis

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    Activation of coagulation

    Prothrombin

    THROMBIN

    Antithrombin

    Fibrinogen

    Fibrin

    D fragmentsE fragments

    Fragment 1+2

    Fibrino-peptideA + B

    Thrombin-Antithrombin

    complex

    (TAT)

    FXIII FXIIIa

    D dimerE fragments

    Cross-linkedfibrin

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    PREDICTOR FORDIC IN

    NEONATAL SEPSIS

    Healthy neonates: 24,5 6,09 mg/l Sepsis, no DIC: 33,7 11,9 mg/l

    Sepsis + DIC*: 73,2 31,6 mg/l

    Critical level: 48,5 mg/l

    Sensitivity: 100%

    Specificity: 93%

    Overall accuracy: 97,5% Selim et al. Haematologica 2005;90:419-20

    *ISTH DIC score 5

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    CONSIDERATIONS IN PRACTICAL

    DIAGNOSTIC APPROACH TO DIC

    Presence of an underlying disorder

    The severity of haemostatic changes Decompensated haemostatic system: Overt DIC Compensated haemostatic system: Non-overt DIC

    The duration of activation Temporary: e.g. Abruptio placentae, transfusion reaction Prolonged: e.g. Sepsis, malignancy, polytrauma

    Laboratory tests Global tests / Molecular markers

    Diagnostic value / Prognostic value Use of scoring systems

    DIC scoring system Other scoring systems

    ISTHs Scientific Subcommittee on DIC, July 2001

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    SCORING SYSTEM FOR OVERTDIC

    Platelet count (>100=0,

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    SCORING SYSTEM FOR OVERTDIC

    Platelet count (>100=0,

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    SCORING SYSTEM FOR NON-OVERTDI

    Presence of underlying disorder (no=0, yes=2) ..........................................................

    Platelet count + changes (100=0, 3s=1) + ( =-1, stable=0,

    =1) ........... Antithrombin (normal=-1, low=1) .................................................

    Protein C (normal=-1, low=1) .................................................

    TAT complexes (normal=-1, high=1)

    .................................................

    Calculate sum ................................................ISTHs Scientific Subcommittee on DIC, July 2001

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    SCORING SYSTEM FOR OVERTDIC

    If the calculated score is 5: compatible with

    overt DIC

    repea scor ng a y

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    OFDIC

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    DICTREATMENT APPROACHES

    Treatment of underlying disorder

    Anticoagulation with heparin

    Platelet transfusion

    Fresh frozen plasma

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    TREATMENT OFDICDIRECTED AGAINST ETIOLOGICAL FACTORS

    Infections

    Trauma

    Antibiotics

    Removal of damaged tissue

    Obstetriccomplications

    stabilisation of fractures

    Evacuation of the uterus

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    ASSESMENT

    abnormal bleeding

    from any or all body

    orifices bleeding into

    the skin (petechiae,

    ecch moses

    confusion dyspnea and

    tachycardia potential

    nausea, vomiting

    potential severe

    hematomas) bleeding from surgical

    or invasive procedure

    sites (incisions,

    venipuncture sites)

    mental status changes

    muscle, back andabdominal pain chest

    pain hemoptysis

    epistaxis seizures

    oliguria possible GIbleeding hematuria

    complicationsrenal

    failure

    hepatic damage, stroke,

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    LAB

    Fibrinogen > Platelet

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    NX DIAGNOSE

    Defisit fluid volume

    Ineffective tissue perfusion Impaired gas exchange: infant

    Anxiety

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    INTERVENTION

    IV fluid with 16 0r 18 gauge cannula

    Folley catheter Intake out put monitoring

    ,

    frozen plasmato replace fibrinogen andclothing factor

    Monitoring of transfusion reaction

    Asses client for abnormal bleeding:

    injection site, mucosa, etc

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    Posisi client of left side and monitori fetus well

    being

    Monitor laboratory values as obtained for

    improvement or worsening condition

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    THE FACE OF SEPSIS


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