Scribd Logo
Upload

Welcome to Scribd!

  • 90 views

    DIC (Dr. Dimas Bayu)

    Uploaded by

    Nur Muhammad Khatim
    Disseminated intravascular coagulation (DIC) is a clinicopathologic syndrome where widespread intravascular coagulation occurs secondary to underlying conditions like sepsis, trauma, cancer, or obstetric complications. This leads to microvascular thrombosis, tissue hypoxia, and organ damage. DIC results from a systemic activation of coagulation that exceeds the body's natural anticoagulant mechanisms, causing depletion of platelets and coagulation factors and potentially resulting in bleeding or organ failure. Diagnosis involves assessing clinical signs of thrombosis or bleeding along with laboratory tests showing low platelets, prolonged clotting times, and elevated fibrin degradation products. Treatment focuses on resolving the underlying cause while providing supportive care like plasma or platelet transfusions.

    Copyright:

    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd

    DIC (Dr. Dimas Bayu)

    Uploaded by

    Nur Muhammad Khatim
    90 views48 pages
    Disseminated intravascular coagulation (DIC) is a clinicopathologic syndrome where widespread intravascular coagulation occurs secondary to underlying conditions like sepsis, trauma, cancer, or obstetric complications. This leads to microvascular thrombosis, tissue hypoxia, and organ damage. DIC results from a systemic activation of coagulation that exceeds the body's natural anticoagulant mechanisms, causing depletion of platelets and coagulation factors and potentially resulting in bleeding or organ failure. Diagnosis involves assessing clinical signs of thrombosis or bleeding along with laboratory tests showing low platelets, prolonged clotting times, and elevated fibrin degradation products. Treatment focuses on resolving the underlying cause while providing supportive care like plasma or platelet transfusions.

    Original Description:

    AAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAA

    Original Title

    8. DIC (dr. Dimas Bayu)

    Copyright

    © © All Rights Reserved

    Available Formats

    PDF, TXT or read online from Scribd

    Did you find this document useful?

    Is this content inappropriate?

    Disseminated intravascular coagulation (DIC) is a clinicopathologic syndrome where widespread intravascular coagulation occurs secondary to underlying conditions like sepsis, trauma, cancer, or obstetric complications. This leads to microvascular thrombosis, tissue hypoxia, and organ damage. DIC results from a systemic activation of coagulation that exceeds the body's natural anticoagulant mechanisms, causing depletion of platelets and coagulation factors and potentially resulting in bleeding or organ failure. Diagnosis involves assessing clinical signs of thrombosis or bleeding along with laboratory tests showing low platelets, prolonged clotting times, and elevated fibrin degradation products. Treatment focuses on resolving the underlying cause while providing supportive care like plasma or platelet transfusions.

    Copyright:

    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
    Download as pdf or txt
    90 views48 pages

    DIC (Dr. Dimas Bayu)

    Uploaded by

    Nur Muhammad Khatim
    Disseminated intravascular coagulation (DIC) is a clinicopathologic syndrome where widespread intravascular coagulation occurs secondary to underlying conditions like sepsis, trauma, cancer, or obstetric complications. This leads to microvascular thrombosis, tissue hypoxia, and organ damage. DIC results from a systemic activation of coagulation that exceeds the body's natural anticoagulant mechanisms, causing depletion of platelets and coagulation factors and potentially resulting in bleeding or organ failure. Diagnosis involves assessing clinical signs of thrombosis or bleeding along with laboratory tests showing low platelets, prolonged clotting times, and elevated fibrin degradation products. Treatment focuses on resolving the underlying cause while providing supportive care like plasma or platelet transfusions.

    Copyright:

    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
    Download as pdf or txt
    You are on page 1of 48

    Disseminated Intravascular

    Coagulation
    (DIC)

    Dimas Bayu
    Tutik Harjianti
    A. Fachruddin Benyamin
    Div of Hematology & Med Oncology - Dept of Int Medicine
    Medical Faculty , Hasanuddin University
    Outline

    1 Introduction
    2 Ethio-Pathogenesis
    3 Clinical Manifestation
    4 Diagnostic Criteria
    5 Treatment

    4 Summary
    I. Introduction
    NORMAL HEMOSTASIS

    Normal hemostasis :

    Maintains blood in a fluid


    State and produces a local
    hemostatic plug at sites of
    vascular injury
    HEMOSTASIS

    I. Primary Hemostasis
    - Blood vessel contraction
    - Platelet Plug Formation
    II. Secondary Hemostasis
    - Activation of Clotting Cascade
    - Deposition & Stabilization of Fibrin
    III. Tertiary Hemostasis
    - Dissolution of Fibrin Clot
    - Dependent on Plasminogen Activation
    Hemostasis

    Consist of :
    1. Vascular & endothelium
    2. Platelet
    3. Coagulation
    4. Anticlotting Mechanisms
    5. Fibrinolytic System
    6. Fibrinolytic Inhibitors
    1. Vasoconstriction
    2. Platelet activation
    3. Haemostatic plug
    Platelet activation

    Fibrinogen
    4. Coagulation
    5. Stable clot formation
    6. Clot dissolution
    DIC

    A clinicopathologic
    syndrome in which
    widespread A syndrome associated
    intravascular with many underlying
    coagulation is induced conditions &
    by procoagulants that manifested as
    are introduced into or microvascular
    produced in the blood thrombosis, tissue
    secondary to 1 or more hypoxia,& organ damage
    underlying
    condition(s)
    Disseminated Intravascular Coagulation

    1. common features :
    §  a triggering stimulus
    §  tissue damage
    •  microvascular thrombosis & occlusion
    §  failure of perfusion of vital organs
    §  depletion of hemostatic factors
    2. common sequelae
    §  damage to brain, kidneys & lungs
    §  abnormal bleeding
    §  death
    SYSTEMIC ACTIVATION
    OF COAGULATION

    Intravascular deposition Depletion of platelets &


    of fibrin coagulation factors

    Thrombosis of small & Bleeding


    midsize vessels

    1
    Organ failure DEATH
    Why DIC can be occured ?

    Overstimulation of coagulation
    è suppresion of control mechanism
    è DIC.
    Important Clue :

    §  The presence of thrombin circulating


    in bloodline.
    __________________________________
    Normally : thrombin can only be found
    in area of lesion (where the coagulation
    process is still running)
    II. ETIO-PATHOGENESIS
    Cause of DIC

    1. Systemic §  Sepsis


    inflammatory ( any
    microorgansim )
    response, leading to §  Trauma
    activation of ( polytrauma,
    cytokine neurotrauma,
    fat embolism )

    §  Cancer ( Both


    solid &
    2. Release or exposure hematology
    of procoagulant tumor )
    material into the §  Obstetric
    bloodstream problems
    §  Vascular
    abnormality
    Cause of DIC (2)

    3. Less common cause


    §  severe hepatic failure
    §  Snake bites
    §  Transfusion reactions
    §  Transplant rejection
    §  Deficiency of protein C & protein S
    Pathophysiology of DIC

    1
    1 Activation of Blood Coagulation

    1
    2 Suppression of Anticoag Pathway

    3 Impaired Fibrinolysis

    4 Cytokines release & activation


    NORMAL HAEMOSTASIS

    Endothelial d
    Intravascular Haemostatic
    clot formation mechanisms
    TF
    TF
    TF
    Cytokines

    amage
    TF TF

    Activated
    Monocyte
    monocyte
    Activation of monocytes

    SYSTEMIC INFLAMMATION
    III. Clinical
    Manifestation
    Clinical Manifestations of DIC

    Ischemic
    Findings ORGAN ISCHEMIC HEMOR.
    are earliest!
    Skin Pur. Fulminans Petechiae
    Gangrene Echymosis
    Acral cyanosis Oozing
    CNS Delirium/Coma Intracranial
    Infarcts bleeding
    Renal Oliguria/Azotemia Hematuria
    Cortical Necrosis
    Cardiovascular Myocardial Dysfxn
    Pulmonary Dyspnea/Hypoxia Hemorrhagic Bleeding is the
    Infarct lung Most obvious
    GI Ulcers, Infarcts Massive clinical finding
    Endocrine Adrenal infarcts hemorrhage.
    Clinical Features

    1.  Acute DIC

    •  Develops rapidly over


    a period of hours
    •  Presents w/ sudden
    bleeding from
    multiple sites
    •  Treated as a medical
    emergency
    Clinical Features

    2. Chronic DIC

    •  Develops over a period


    of months
    •  May be subclinical
    •  Eventually evolves into
    an acute DIC pattern
    Clinical Manifestations of DIC
    Purpura Fulminans
    IV. DIAGNOSTIC CRITERIA
    Diagnosis of DIC

    Presence of disease associated


    with DIC
    Appropriate clinical setting
    §  Clinical evidence of thrombosis,
    hemorrhage or both.
    Laboratory studies
    §  no single test is accurate
    §  serial test are more helpful than
    single test
    Scoring system for overt DIC

    Underlying disorder known to be YES NO


    associated with overt DIC
    continue stop
    §  Platelet count
    §  (>100=0, <100=1, <50=2) ..............................
    §  Soluble fibrin/D-dimer
    §  (normal=0, é=2, éé=3) .............................
    §  Prolongation of PT
    §  (<3s=0, 3-6s=1, >6s=2) ................................
    §  Fibrinogen
    §  (>1g/l=0, <1g/l=1) ..........................................

    §  Calculate sum ........................................


    Scoring system for overt DIC
    - Example -
    Underlying disorder known to be YES NO
    associated with overt DIC
    Polytrauma cont st
    inue op
    §  Platelet count 85 1
    §  (>100=0, <100=1, <50=2) ..............................
    §  Soluble fibrin/D-dimer
    8 3
    §  (normal=0, é=2, éé=3) .................................
    §  Prolongation of PT
    §  (<3s=0, 3-6s=1, >6s=2) ................................. +3 1
    §  Fibrinogen
    §  2,2
    (>1g/l=0, <1g/l=1) ............................................. 0

    §  Calculate sum ............................................ 5


    Scoring system for overt DIC

    §  If the calculated score is


    §  ≥5 : compatible with overt DIC
    repeat scoring daily
    §  <5: suggestive (not affirmative)
    for
    non-overt DIC repeat next 1-2 days.
    Laboratory Tests Used in DIC

    §  D-dimer* §  Thrombin time


    §  Antithrombin III* §  Fibrinogen
    §  F. 1+2* §  Prothrombin time
    §  Fibrinopeptide A* §  Activated PTT
    §  Platelet factor 4* §  Protamine test
    §  Fibrin §  Reptilase time
    Degradation Prod §  Coagulation
    §  Platelet count factor levels
    §  Protamine test
    *Most reliable test
    Laboratory diagnosis

    §  Thrombocytopenia
    §  plat count <100,000 or rapidly
    declining
    §  Prolonged clotting times (PT, APTT)
    §  Presence of Fibrin degradation
    products or positive D-dimer
    §  Low levels of coagulation inhibitors
    §  AT III, protein C
    §  Low levels of coagulation factors
    §  Factors V,VIII,X,XIII
    §  Fibrinogen levels not useful
    diagnostically
    Differential Diagnosis

    §  Severe liver failure


    §  Vitamin K deficiency
    §  Liver disease
    §  Thrombotic thrombocytopenic
    purpura
    §  Congenital abnormalities of
    fibrinogen
    §  HELLP syndrome
    V. TREATMENT of DIC
    Treatment of DIC

    §  Stop the triggering process


    §  The only proven treatment!
    §  Supportive therapy
    §  No specific treatments
    §  Plasma & platelet substitution therapy
    §  Anticoagulants
    §  Physiologic coagulation inhibitors
    Plasma therapy

    §  Indications
    §  Active bleeding
    §  Patient requiring invasive
    procedures
    §  Patient at high risk for
    bleeding complications
    §  Fresh frozen plasma(FFP):
    §  provides clotting factors,
    fibrinogen, inhibitors &
    platelets in balanced
    amounts.
    §  Usual dose is 10-15 ml/kg
    Platelet therapy

    §  Indications
    §  Active bleeding
    §  Patient requiring
    invasive procedures
    §  Patient at high risk
    for bleeding
    complications
    §  Platelets
    §  dose 1 unit/10kg
    Blood

    §  Replaced as needed to maintain


    adequate oxygen delivery.
    §  Blood loss due to bleeding
    §  RBC destruction (hemolysis)
    Coagulation Inhibitor Therapy

    §  Antithrombin III


    §  Protein C concentrate
    §  Tissue Factor Pathway Inhibitor
    (TFPI)
    §  Heparin
    Heparin

    §  Use is very controversial. Data is mixed.


    §  May be indicated in patients with clinical
    evidence of fibrin deposition or
    significant thrombosis.
    §  Generally contraindicated in patients
    with significant bleeding and CNS insults.
    §  Dosing and route of administration
    varies.
    §  Requires normal levels of ATIII.
    Summary

    §  DIC : syndrome characterized by


    systemic intravascular coagulation.
    §  Initial event : coagulation
    §  The extent of intravascular thrombosis
    has the greatest impact on morbidity &
    mortality
    §  Important link between inflammation &
    coagulation.
    §  Morbidity & mortality remain high.
    §  The only proven treatment is reversal or control
    of the underlying cause.
    6. Vessel wall with activated endothelium
    (colour-enhanced scanning electron micrograph)
    This scanning electron micrograph shows how the endothelium has reacted to
    compression and damage during surgery. The endothelial cells are activated
    and the clotting cascade has started. The formation of thrombin is the pivotal
    step in fibrin formation and thrombus development.
    Pathophysiology of DIC…..

    1. Activation of Blood Coagulation


    §  Tissue factor/factor VIIa mediated thrombin
    generation via the extrinsic pathway
    •  complex activates factor IX & X
    §  TF
    •  Endothelial cells
    •  Monocytes
    •  Extravascular: - Lung
    - Kidney
    - Epithelial cells
    Pathophysiology of DIC….

    2. Suppression of Physiologic Anticoagulant


    Pathways
    §  reduced antithrombin III levels
    §  reduced activity of the protein C-protein S
    system
    §  Insufficient regulation of tissue factor activity
    by tissue factor pathway inhibitor (TFPI)
    •  inhibits TF/FVIIa/Fxa complex activity
    Pathophysiology of DIC…..

    3. Impaired Fibrinolysis
    §  relatively suppressed at time of maximal activation of
    coagulation due to increased plasminogen activator
    inhibitor type 1

    4. Cytokines
    §  IL-6, and IL-1 mediates coagulation activation in DIC
    §  TNF-α
    •  mediates dysregulation of physiologic anticoagulant
    pathways and fibrinolysis
    •  modulates IL-6 activity
    §  IL-10 may modulate the activation of coagulation

    You might also like