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DISSEMINATED INTRAVASCULAR COAGULATION

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Dr.Aidah Abu Elsoud Alkaissi Link ping University /Sweden An-Najah National University/- Palestine DISSEMINATED INTRAVASCULAR COAGULATION CONSUMPTION COAGULOPATHY – PowerPoint PPT presentation

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Title: DISSEMINATED INTRAVASCULAR COAGULATION


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DISSEMINATED INTRAVASCULAR COAGULATION
CONSUMPTION COAGULOPATHY DEFIBRINATION
SYNDROME ACQUIRED BLEEDING DISORDER
  • Dr.Aidah Abu Elsoud Alkaissi
  • Linköping University /Sweden
  • An-Najah National University/- Palestine

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Dr. Aidah Abu Elsoud Alkaissi Linköping
University- Swedebn
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Definition
  • Disseminated intravascular coagulation (DIC) is a
    pathophysiological process and not a disease in
    itself.
  • a systemic process producing both thrombosis and
    hemorrhage.
  • Is a Paradoxical Clinical Presentation clotting
    and hemorrhage
  • (Porth, C.M. (2004) Essentials of
    Pathophysiology) (Otto, S. (2001). Oncology
    Nursing)

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Dr. Aidah Abu Elsoud Alkaissi Linköping
University- Swedebn
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Dr. Aidah Abu Elsoud Alkaissi Linköping
University- Swedebn
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Pathophysiology
Dr. Aidah Abu Elsoud Alkaissi Linköping
University- Swedebn
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Clinical manifestations of coagulation
abnormalities in disseminated intravascular
coagulation.
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Dr. Aidah Abu Elsoud Alkaissi Linköping
University- Swedebn
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Dr. Aidah Abu Elsoud Alkaissi Linköping
University- Swedebn
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Dr. Aidah Abu Elsoud Alkaissi Linköping
University- Swedebn
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Dr. Aidah Abu Elsoud Alkaissi Linköping
University- Swedebn
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Pathophysiology
  • Fibrinolysis-period of hypocoagulability (the
    hemorrhagic phase)
  • Activates the complement system (helps, or
    complements, the ability of antibodies to clear
    pathogens from an organism).
  • Byproducts of fibrinolysis (fibrin/fibrin
    degradation products(FDP)) further enhance
    bleeding by interfering with platelet
    aggregation, fibrin polymerization, thrombin
    activity
  • Leads to Hemorrhage
  • Thrombosis-brief period of hypercoagulability
  • Coagulation cascade is initiated, causing
    widespread fibrin formation
  • Microthrombi are deposited throughout he
    microcirculatory
  • Fibrin deposits result in tissue ischemia,
    hypoxia, necrosis
  • Leads to multi organ dysfunction
  • (Porth, 2004) (Otto, 2001)

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Dr. Aidah Abu Elsoud Alkaissi Linköping
University- Swedebn
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Underlying pathology creates a triggering event
Either- endothelial tissue injury (Extrinsic)
blood vessel injury (Intrinsic)
  • (Porth, 2004)

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Dr. Aidah Abu Elsoud Alkaissi Linköping
University- Swedebn
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Dr. Aidah Abu Elsoud Alkaissi Linköping
University- Swedebn
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Signs and Symptoms
Dr. Aidah Abu Elsoud Alkaissi Linköping
University- Swedebn
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Integumentary system
  • SIGNS AND SYMPTOMS OF
  • MICROVASCULAR AND FRANK BLEEDING
  • Petechiae, including periorbital and oral mucosa
    bleeding
  • gums, oozing from wounds, previous injection
    sites, around catheters (IVs, tracheostomies)
    epistaxis
  • diffuse ecchymoses subcutaneous hemorrhage
    joint pain
  • SIGNS AND SYMPTOMS
  • OF MICROVASCULAR THROMBOSIS
  • ? Temperature, sensation ? pain cyanosis in
    extremities, nose, earlobes focal ischemia,
    superficial gangrene

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Respiratory system
  • SIGNS AND SYMPTOMS
  • OF MICROVASCULAR THROMBOSIS
  • SIGNS AND SYMPTOMS OF
  • MICROVASCULAR AND FRANK BLEEDING
  • Hypoxia (secondary to clot in lung) dyspnea
  • chest pain with deep inspiration ? breath sounds
    over areas of large embolism
  • High-pitched bronchial breath sounds tachypnea
  • ? consolidation signs and symptoms of acute
    respiratory distress syndrome

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Gastrointestinal system
  • SIGNS AND SYMPTOMS
  • OF MICROVASCULAR THROMBOSIS
  • SIGNS AND SYMPTOMS OF
  • MICROVASCULAR AND FRANK BLEEDING
  • Gastric pain heartburn
  • Hematomesis (heme? NG output) melana (heme?
  • stools?tarry stools ?bright-red blood from
    rectum)
  • retroperitoneal bleeding (abdomen firm and tender
    to palpation distended ? abdominal girth)

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Renal system
  • SIGNS AND SYMPTOMS
  • OF MICROVASCULAR THROMBOSIS
  • SIGNS AND SYMPTOMS OF
  • MICROVASCULAR AND FRANK BLEEDING
  • ? Urine output ? creatinine, ? blood urea
  • nitrogen
  • Hematuria

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WELCOME TO LINKÖPING- SWEDEN
Dr. Aidah Abu Elsoud Alkaissi Linköping
University- Swedebn
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Dr. Aidah Abu Elsoud Alkaissi Linköping
University- Swedebn
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  • Fibrin degradation product (FDPs), also known as
    fibrin split products, are components of the
    blood produced by clot degeneration.
  • These are produced by the action of plasmin on
    deposited fibrin. The most notable subtype of
    fibrin degradation products is D-dimer.
  • The levels of these FDPs rises after any
    thrombotic event.
  • It can be used to test for disseminated
    intravascular coagulation.

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  • D-dimer is a fibrin degradation product, a small
    protein fragment present in the blood after a
    blood clot is degraded by fibrinolysis. It is so
    named because it contains two crosslinked D
    fragments of the fibrinogen protein.

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  • D-dimer concentration may be determined by a
    blood test to help diagnose thrombosis. Since its
    introduction in the 1990s, it has become an
    important test performed in patients suspected of
    thrombotic disorders. While a negative result
    practically rules out thrombosis, a positive
    result can indicate thrombosis but does not rule
    out other potential causes. Its main use,
    therefore, is to exclude thromboembolic disease
    where the probability is low. In addition, it is
    used in the diagnosis of the blood disorder
    disseminated intravascular coagulation.

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  • D-dimers are not normally present in human blood
    plasma, except when the coagulation system has
    been activated, for instance because of the
    presence of thrombosis or disseminated
    intravascular coagulation. The D-dimer assay
    depends on the binding of a monoclonal antibody
    to a particular epitope on the D-dimer fragment.
    Several detection kits are commercially available

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Lab Diagnosis
  • Elevated d-dimer levels (D-dimer är en
    degradation product of fibrin, reflecting cross
    linked fibrin degradation are the most common
    abnormal parameter in patients with DIC. blood
    test to diagnose thrombosis
  • Prolonged prothrombin time (PT) Prothrombin time
    refelects reduced activity of the components of
    the extrinsic and common pathway. These include
    factors VII, X, V, and prothrombin, which are the
    most freq decreased clotting proteins

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Dr. Aidah Abu Elsoud Alkaissi Linköping
University- Swedebn
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Lab Diagnosis
  • Prolonged Activated partial thromboplastin
    time(aPTT) measures the intrinsic and common
    pathways of coagulation. - sensitive to
    deficiencies of factors XII, XI, IX, and VIII.
  • Fibrinogen - low in acute DIC, - may be elevated
    as an acute phase reactant in certain chronic
    conditions, including pregnancy

Dr. Aidah Abu Elsoud Alkaissi Linköping
University- Swedebn
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Lab Diagnosis
  • Thrombocytopenia.
  • Increased fibrin formation
  • Stimulates compensatory process of secondary
    fibrinolysis,
  • Plasminogen activators generate plasmin to digest
    fibrin (and fibrinogen) into fibrin(ogen)
    degradation products (FDPs).
  • FDPs are potent circulating anticoagulants that
    contribute further to the bleeding manifestations
    of DIC.
  • Intravascular fibrin deposition can cause
    fragmentation of red blood cells and lead to the
    appearance of schistocytes in blood smears

Schafer, A., I., Cecil Textbook of Medicine,
Saunders, 2004, chapter 179, HEMORRHAGIC
DISORDERS DISSEMINATED INTRAVASCULAR
COAGULATION, LIVER FAILURE, AND VITAMIN K
DEFICIENCY
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Dr. Aidah Abu Elsoud Alkaissi Linköping
University- Swedebn
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Dr. Aidah Abu Elsoud Alkaissi Linköping
University- Swedebn
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Dr. Aidah Abu Elsoud Alkaissi Linköping
University- Swedebn
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Dr. Aidah Abu Elsoud Alkaissi Linköping
University- Swedebn
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  • Platelets transfusion and fresh frozen plasma
  • No evidence to support the administration of
    platelets and coagulation factors in patients who
    are not at high risk for bleeding
  • In patient with bleeding and hypofibrinogenemia
  • Attempt to maintatin fibrinogen gt100 mg/dl
  • give content of fibrinogen 250 mg
  • Gnereally 4 g are required to increase the
    fibrinogen concentration by 100 mg/dl

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Dr. Aidah Abu Elsoud Alkaissi Linköping
University- Swedebn
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Heparin
  • The use and dosage of heparin in DIC is
    controversial.
  • Heparin inhibition of thrombin may theoretically
    inhibit formation of microvascular thrombi, which
    fuel DIC.
  • The goal of heparin use is to suppress
    coagulation, increase fibrinogen levels, and
    decrease D-dimer levels.

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Dr. Aidah Abu Elsoud Alkaissi Linköping
University- Swedebn
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Heparin
  • Uncontrolled trials using low-molecular-weight
    heparins in DIC have also been reported.

Dr. Aidah Abu Elsoud Alkaissi Linköping
University- Swedebn
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Activated Protein C
Antithrombotic effect
  • Inhibits Factors Va and VIIIa.
  • Indirect profibrinolytic activity through its
    ability to inhibit plasminogen activator
    inhibitor-1 (PAI-1)
  • Limits generation of activated thrombin-activatabl
    e-fibrinolysis-inhibitor.
  • may exert an anti-inflammatory effect
  • Limits the thrombin-induced inflammatory
    responses within the microvascular endothelium.

Dr. Aidah Abu Elsoud Alkaissi Linköping
University- Swedebn
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Antithrombin IIIatenativ -
  • Is a natural inhibitor of coagulation that
    inactivates thrombin and factor Xa.
  • Few randomized trials have been performed, and
    improvement in laboratory tests has not led to
    clinically relevant benefits.

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Dr. Aidah Abu Elsoud Alkaissi Linköping
University- Swedebn
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Study
  • Treatment of DIC with antithrombin III
    concentrates.
  • Sakata Y, Yoshida N, Matsuda M, Aoki N.
  • Abstract
  • administered AT III concentrates to 21 patients
    with DIC who failed to respond initially to
    heparin therapy.
  • About 60 of these 21 patients were effectively
    treated with AT III concentrates by enhancing the
    effect of heparin and alleviating the burden of
    excessive plasma transfusions on the
    cardiovascular system

Dr. Aidah Abu Elsoud Alkaissi Linköping
University- Swedebn
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rFVIIa Recombinant Factor VIIA
  • Factor VII is a natural initiator of haemostasis,
    which binds to Tissue Factor (TF) at the site of
    vascular injury leading to the generation of
    thrombin.
  • rFVIIa activates factor X on the surface of
    activated platelets at the site of vascular
    injury, resulting in a localised thrombin burst,
    leading to a rapid formation of stable fibrin
    clots at the site of vascular injury.

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Dr. Aidah Abu Elsoud Alkaissi Linköping
University- Swedebn
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Antifibrinolytic agents
  • e-aminocaproic acid and tranexamic acid
    (Cyklokapron)
  • Generally are contraindicated
  • May precipitate thrombosis
  • May be effective in decreasing life-threatening
    bleeding

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Dr. Aidah Abu Elsoud Alkaissi Linköping
University- Swedebn
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XIGRIS (Lilly)
  • Drotrecogin alfa (activated)
  • Recombinant form of human
  • Activated Protein C

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Dr. Aidah Abu Elsoud Alkaissi Linköping
University- Swedebn
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XIGRIS
  • Clinical study (PROWESS)
  • 1690 patients with severe sepsis
  • Entry criteria included a systemic inflammatory
    response presumed due to infection and at least
    one associated acute organ dysfunction
  • The study was terminated after a planned interim
    analysis due to significantly lower mortality in
    patients on Xigris than in patients on placebo

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Dr. Aidah Abu Elsoud Alkaissi Linköping
University- Swedebn
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XIGRIS
  • INDICATIONS AND USAGE
  • Xigris is indicated for the reduction of
    mortality in adult patients with severe sepsis
    (sepsis associated with acute organ dysfunction)
    who have a high risk of death

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Dr. Aidah Abu Elsoud Alkaissi Linköping
University- Swedebn
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XIGRIS
  • Contraindications
  • Active internal bleeding
  • Recent (within 3 months) hemorrhagic stroke
  • Recent (within 2 months) intracranial or
    intraspinal surgery, or severe head trauma
  • Trauma with an increased risk of life-threatening
    bleeding
  • Presence of an epidural catheter
  • Intracranial neoplasm or mass lesion or evidence
    of cerebral herniation

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Dr. Aidah Abu Elsoud Alkaissi Linköping
University- Swedebn
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Xigris
  • DOSAGE AND ADMINISTRATION
  • Xigris should be administered intravenously at an
    infusion rate of 24 µg/kg/hr for a total duration
    of infusion of 96 hours.

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Dr. Aidah Abu Elsoud Alkaissi Linköping
University- Swedebn
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Xigris
  • Drotrecogin alfa (activated) (Xigris, is a
    recombinant form of human activated protein C
    that has anti-thrombotic, anti-inflammatory, and
    profibrinolytic properties.
  • Drotrecogin alpha (activated) belongs to the
    class of serine proteases.
  • It is used mainly in intensive care medicine as a
    treatment for severe sepsis. However, further
    evidence is required before it becomes the
    standard of care

Dr. Aidah Abu Elsoud Alkaissi Linköping
University- Swedebn
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Nursing Diagnosis
  • Risk for deficient fluid volume related to
    bleeding
  • Risk for impaired skin integrity related to
    ischemia or bleeding
  • Potential for excess fluid volume related to
    excessive blood/factor component replacement
  • Ineffective tissue perfusion related to
    microthrombi
  • Anxiety and fear of the unknown and possible
    death

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COLLABORATIVE PROBLEMS/POTENTIAL COMPLICATIONS
  • may include
  • Renal failure
  • Gangrene
  • Pulmonary embolism or hemorrhage
  • Altered level of consciousness
  • Acute respiratory distress syndrome
  • Stroke

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Thank You
Dr. Aidah Abu Elsoud Alkaissi Linköping
University- Swedebn
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